Marshall Protocol Knowledge Base - home:diseases

Acute respiratory infections

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 05:14:49 +0000

04.26.2020		current
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	====== Acute respiratory infections ======		====== Acute respiratory infections ======

-	<relatedarticle> [[home:pathogenesis:microbiota:acute_infections\|Acute infections]], [[https:home:pathogenesis:microbiota:interaction#viruses\|Effects of bacteria and viruses on their human host]] </article>	+	<relatedarticles> [[home:pathogenesis:microbiota:acute_infections\|Acute infections]], [[https:home:pathogenesis:microbiota:interaction#viruses\|Effects of bacteria and viruses on their human host]] </article>


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	</blockquote>		</blockquote>

-	Are viruses alive (({{pubmed>long:26965225}}))	+	Are viruses alive (({{pmid>long:26965225}}))
	==== Research ====		==== Research ====

-	Our findings provide direct evidence that TFH play a critical role in vaccine-induced immunity in humans and suggest a novel strategy for promoting such cells by use of intranasal vaccines against respiratory infections. (({{pubmed>long:29563292}}))	+	Our findings provide direct evidence that TFH play a critical role in vaccine-induced immunity in humans and suggest a novel strategy for promoting such cells by use of intranasal vaccines against respiratory infections. (({{pmid>long:29563292}}))

-	Members of the NOD-like receptor (NLR) family of pathogen recognition receptors have important roles in orchestrating this response (to invading pathogens) (({{pubmed>long:28615208}}))	+	Members of the NOD-like receptor (NLR) family of pathogen recognition receptors have important roles in orchestrating this response (to invading pathogens) (({{pmid>long:28615208}}))
	===== Read more =====		===== Read more =====

-	* [[http://www.nytimes.com/2010/10/05/opinion/05ackerman.html?_r=2&emc=eta1\|How not to fight colds]] – Why do children, the population with the most pristine health, get up to a dozen colds a year? This //New York Times// article argues that "susceptibility to cold symptoms is not a sign of a weakened immune system, but quite the opposite."	+	* [[https://www.nytimes.com/2010/10/05/opinion/05ackerman.html?_r=2&emc=eta1\|How not to fight colds]] – Why do children, the population with the most pristine health, get up to a dozen colds a year? This //New York Times// article argues that "susceptibility to cold symptoms is not a sign of a weakened immune system, but quite the opposite."


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	=====Notes and comments =====		=====Notes and comments =====

-	(({{pubmed>long:000}}))	+	(({{pmid>long:000}}))

	broken link		broken link
-	* [[http://www.scientificblogging.com/news_releases/cold_virus_manipulates_genes\|Cold Virus 'Manipulates' Genes]] - Sneezing, runny nose and chills? You might blame the human rhinovirus (HRV), which causes 30 to 50 percent of common colds. But in reality, it's not the virus itself but HRV's ability to manipulate your genes that is the true cause of some of the most annoying cold symptoms. For the first time, researchers have shown that HRV hijacks many of your genes and causes an overblown immune response that ends up with your nose being overblown.	+	* [[https://www.scientificblogging.com/news_releases/cold_virus_manipulates_genes\|Cold Virus 'Manipulates' Genes]] - Sneezing, runny nose and chills? You might blame the human rhinovirus (HRV), which causes 30 to 50 percent of common colds. But in reality, it's not the virus itself but HRV's ability to manipulate your genes that is the true cause of some of the most annoying cold symptoms. For the first time, researchers have shown that HRV hijacks many of your genes and causes an overblown immune response that ends up with your nose being overblown.

Addison's disease

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

01.18.2019		current
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-	[[http://www.mayoclinic.org/diseases-conditions/addisons-disease/home/ovc-20155636\|Addison's disease -overview by Mayo Clinic Staff]]	+	[[https://www.mayoclinic.org/diseases-conditions/addisons-disease/home/ovc-20155636\|Addison's disease -overview by Mayo Clinic Staff]]

	==== Evidence of infection ====		==== Evidence of infection ====

-	The adrenal crisis had been precipitated by influenza virus type B infection.(({{pubmed>long:26240101}}))	+	The adrenal crisis had been precipitated by influenza virus type B infection.(({{pmid>long:26240101}}))
	==== hyperkalemia ====		==== hyperkalemia ====

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	===== delay in Diagnosis =====		===== delay in Diagnosis =====

-	Addison's Disease: A Diagnostic Dilemma. (({{pubmed>long:28919626}}))	+	Addison's Disease: A Diagnostic Dilemma. (({{pmid>long:28919626}}))

-	Addison's disease is a rare endocrinal disorder, with several oral and systemic manifestations. A variety of pathological processes may cause Addison's disease.(({{pubmed>long:23633816}}))	+	Addison's disease is a rare endocrinal disorder, with several oral and systemic manifestations. A variety of pathological processes may cause Addison's disease.(({{pmid>long:23633816}}))


-	A LONG FOLLOW-UP STUDY ON 143 PATIENTS.(({{pubmed>long:30608902}}))	+	A LONG FOLLOW-UP STUDY ON 143 PATIENTS.(({{pmid>long:30608902}}))


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-	PAI is frequently not considered resulting in a delayed diagnosis. Successful therapy is mainly based on adequate patient education as a cornerstone in the prevention and management of adrenal crisis. (({{pubmed>long:30562824}}))</blockquote>	+	PAI is frequently not considered resulting in a delayed diagnosis. Successful therapy is mainly based on adequate patient education as a cornerstone in the prevention and management of adrenal crisis. (({{pmid>long:30562824}}))</blockquote>


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	===== Recent research =====		===== Recent research =====

-	Even though efficient and safe pharmaceutical preparations for the substitution of endogenous gluco- and mineralocorticoids are established in therapy, the mortality in patients with primary adrenal insufficiency (PAI) is still increased and the health-related quality of life (HRQoL) is often reduced. PAI is a rare disease but recent data report an increasing prevalence. In addition to the common "classical" causes of PAI like autoimmune, infectious, neoplastic and genetic disorders, other iatrogenic conditions - mostly pharmacological side effects (e. g., adrenal haemorrhage associated with anticoagulants, drugs affecting glucocorticoid synthesis, action or metabolism and some of the novel anti-cancer checkpoint inhibitors) are contributing factors to this phenomenon. Due to the rarity of the disease and often non-specific symptoms at least in the early stages, PAI is frequently not considered resulting in a delayed diagnosis. (({{pubmed>long:30562824}}))	+	Even though efficient and safe pharmaceutical preparations for the substitution of endogenous gluco- and mineralocorticoids are established in therapy, the mortality in patients with primary adrenal insufficiency (PAI) is still increased and the health-related quality of life (HRQoL) is often reduced. PAI is a rare disease but recent data report an increasing prevalence. In addition to the common "classical" causes of PAI like autoimmune, infectious, neoplastic and genetic disorders, other iatrogenic conditions - mostly pharmacological side effects (e. g., adrenal haemorrhage associated with anticoagulants, drugs affecting glucocorticoid synthesis, action or metabolism and some of the novel anti-cancer checkpoint inhibitors) are contributing factors to this phenomenon. Due to the rarity of the disease and often non-specific symptoms at least in the early stages, PAI is frequently not considered resulting in a delayed diagnosis. (({{pmid>long:30562824}}))

-	Acute adrenal crisis is a life-threatening condition that requires immediate treatment. Standard replacement therapy consists of multiple daily doses of hydrocortisone or cortisone acetate combined with fludrocortisone. Annual follow-up by an endocrinologist is recommended with the focus on optimization of replacement therapy and detection of new autoimmune diseases. (({{pubmed>long:2433003}}))	+	Acute adrenal crisis is a life-threatening condition that requires immediate treatment. Standard replacement therapy consists of multiple daily doses of hydrocortisone or cortisone acetate combined with fludrocortisone. Annual follow-up by an endocrinologist is recommended with the focus on optimization of replacement therapy and detection of new autoimmune diseases. (({{pmid>long:2433003}}))


-	The most common causes of PAI are autoimmune adrenalitis (Addison's disease), infectious diseases, adrenalectomy, neoplasia, medications, and various rare genetic syndromes and inborn errors of metabolism that typically present in childhood although late-onset presentations are becoming increasingly recognized. (({{pubmed>long:29956047}})) Fady Hannah-Shmouni and Constantine A. Stratakis : An overview of inborn errors of metabolism manifesting with primary adrenal insufficiency	+	The most common causes of PAI are autoimmune adrenalitis (Addison's disease), infectious diseases, adrenalectomy, neoplasia, medications, and various rare genetic syndromes and inborn errors of metabolism that typically present in childhood although late-onset presentations are becoming increasingly recognized. (({{pmid>long:29956047}})) Fady Hannah-Shmouni and Constantine A. Stratakis : An overview of inborn errors of metabolism manifesting with primary adrenal insufficiency

-	Main presenting symptoms of Addison's disease such as fatigue, anorexia, vomiting and convulsion often mimics central nervous system (CNS) infections. (({{pubmed>long:28919626}}))	+	Main presenting symptoms of Addison's disease such as fatigue, anorexia, vomiting and convulsion often mimics central nervous system (CNS) infections. (({{pmid>long:28919626}}))

-	New-onset autoimmune Addison's disease should be considered as a potentially reversible condition in some patients. Future studies of immunomodulation in autoimmune Addison's disease may be warranted. (({{pubmed>long:22767640}}))	+	New-onset autoimmune Addison's disease should be considered as a potentially reversible condition in some patients. Future studies of immunomodulation in autoimmune Addison's disease may be warranted. (({{pmid>long:22767640}}))

-	The prevalence of the metabolic syndrome in patients with AM was 35.71% after a period of treatment longer than 15 years. (({{pubmed>long:30627312}}))	+	The prevalence of the metabolic syndrome in patients with AM was 35.71% after a period of treatment longer than 15 years. (({{pmid>long:30627312}}))
	===== Patient's reports =====		===== Patient's reports =====

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		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====
		+
		+	(({{pmid>long:000}}))


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	===== Presentations and publications=====		===== Presentations and publications=====

-	===== References =====	+	===== References =====</nodisp>

Aging (senescence)

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

Allergies and sensitivities

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

02.11.2019		current
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-	Papadopoulos //et al.// have written that atopy should be treated as a suboptimal innate immune response.(({{pubmed>long:17188832}})) Consistent with that thinking, the Marshall Protocol is a treatment for allergies. Other treatments (some of which are contraindicated) include the following.	+	Papadopoulos //et al.// have written that atopy should be treated as a suboptimal innate immune response.(({{pmid>long:17188832}})) Consistent with that thinking, the Marshall Protocol is a treatment for allergies. Other treatments (some of which are contraindicated) include the following.


-	vitamin D supplementation can cause allergies(({{pubmed>long:15699498}}))	+	vitamin D supplementation can cause allergies(({{pmid>long:15699498}}))


-	Hyppönen //et al.// performed a retrospective cohort study of 7,648 Finnish infants born in 1967. The prevalence of atopy and allergic rhinitis at age 31 years was 46% higher in participants who had received vitamin D supplementation regularly during the first year compared to others.(({{pubmed>long:15699498}}))	+	Hyppönen //et al.// performed a retrospective cohort study of 7,648 Finnish infants born in 1967. The prevalence of atopy and allergic rhinitis at age 31 years was 46% higher in participants who had received vitamin D supplementation regularly during the first year compared to others.(({{pmid>long:15699498}}))

	see also [[home:mp:allergies\|allergies to MP antibiotics]]		see also [[home:mp:allergies\|allergies to MP antibiotics]]
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	=====Asthma=====		=====Asthma=====

-	[[http://en.wikipedia.org/wiki/Asthma\|Asthma]] is a chronic or recurring // inflammatory // condition in which the airway develops increased responsiveness to various stimuli, characterized by bronchial hyper-responsiveness, // inflammation // , increased mucus production, and intermittent airway obstruction. Only a minority of asthma sufferers have an identifiable allergy trigger. Sounds a lot like Th1 disease, doesn't it? The Marshall Protocol will often resolve your asthma. (({{pubmed>long:25649083}}))	+	[[https://en.wikipedia.org/wiki/Asthma\|Asthma]] is a chronic or recurring // inflammatory // condition in which the airway develops increased responsiveness to various stimuli, characterized by bronchial hyper-responsiveness, // inflammation // , increased mucus production, and intermittent airway obstruction. Only a minority of asthma sufferers have an identifiable allergy trigger. Sounds a lot like Th1 disease, doesn't it? The Marshall Protocol will often resolve your asthma. (({{pmid>long:25649083}}))

	=====Sinus symptoms=====		=====Sinus symptoms=====
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-	===== Evidence of infectious cause =====

-	Sample PubMed cite(({{pubmed>long:18200565}}))


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	Active patients		Active patients
-	* [[http://www.marshallprotocol.com/view_user.php?id=953&posts=1\|Bevin Black]]	+	* [[https://www.marshallprotocol.com/view_user.php?id=953&posts=1\|Bevin Black]]
-	* [[http://www.marshallprotocol.com/view_user.php?id=371&posts=1\|Julia]]	+	* [[https://www.marshallprotocol.com/view_user.php?id=371&posts=1\|Julia]]

	//Last updated: January 4, 2009//		//Last updated: January 4, 2009//
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	Patient interviews		Patient interviews

-	* [[http://bacteriality.com/2007/12/28/interview14/\|P. Bear]] <html> </html> [[http://bacteriality.com\|{{:home:bacteriality.gif}}]]	+	* [[https://bacteriality.com/2007/12/28/interview14/\|P. Bear]] <html> </html> [[https://bacteriality.com\|{{:home:bacteriality.gif}}]]

	Marshall Protocol member comments		Marshall Protocol member comments
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	<blockquote>I think it's just experience that tells us things are herx. We nearly all start by arguing that something 'couldn't be herx because...' and we all end up saying 'ok, you were right, it was herx' when we see what a limited timescale it has, and how its coming and going relates to the medication programme.		<blockquote>I think it's just experience that tells us things are herx. We nearly all start by arguing that something 'couldn't be herx because...' and we all end up saying 'ok, you were right, it was herx' when we see what a limited timescale it has, and how its coming and going relates to the medication programme.

-	Anyway, it doesn't make any practical difference to what you do, does it? I mean, the MP is the way forward, no matter what's causing your symptoms. And you'll gradually see them fading, or going altogether. [[http://www.marshallprotocol.com/forum2/6606.html\|Keep a good record]] of daily symptoms, so that you track your progress.	+	Anyway, it doesn't make any practical difference to what you do, does it? I mean, the MP is the way forward, no matter what's causing your symptoms. And you'll gradually see them fading, or going altogether. [[https://www.marshallprotocol.com/forum2/6606.html\|Keep a good record]] of daily symptoms, so that you track your progress.

	I had a lot of true allergies before I started the MP; I had no idea they could be sarc-related. Now they've gone - except that sometimes I get a few hours or even a day or two of returned allergy, on the same days of my Z cycle each time. Allergies are an over-reaction of our distressed immune system; it stands to reason that some herxes will be allergy-like symptoms.		I had a lot of true allergies before I started the MP; I had no idea they could be sarc-related. Now they've gone - except that sometimes I get a few hours or even a day or two of returned allergy, on the same days of my Z cycle each time. Allergies are an over-reaction of our distressed immune system; it stands to reason that some herxes will be allergy-like symptoms.
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	===== Read More =====		===== Read More =====

-	[[http://www.foodsmatter.com/es/health_risks/articles/goldsworthy-biological-effects-04-12.pdf\|biological effects]]	+	[[https://www.foodsmatter.com/es/health_risks/articles/goldsworthy-biological-effects-04-12.pdf\|biological effects]]

	{{tag>diseases allergy}}		{{tag>diseases allergy}}
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		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

	broken links abounded --- //Sallie Q 02.11.2019//		broken links abounded --- //Sallie Q 02.11.2019//
-	[[http://www.marshallprotocol.com/view_topic.php?id=2810&forum_id=2&jump_to=74772#p74772\|innate immunity, and not by acquired immmunity.]]	+	[[https://www.marshallprotocol.com/view_topic.php?id=2810&forum_id=2&jump_to=74772#p74772\|innate immunity, and not by acquired immmunity.]]

-	the [[http://www.marshallprotocol.com/forum2/10.html\|Medication To Avoid While on the Marshall Protocol]]	+	the [[https://www.marshallprotocol.com/forum2/10.html\|Medication To Avoid While on the Marshall Protocol]]

-	[[http://www.marshallprotocol.com/view_topic.php?id=10371&forum_id=32&jump_to=125033#p125033\|My immune response / symptoms are too strong. What should I do?]]	+	[[https://www.marshallprotocol.com/view_topic.php?id=10371&forum_id=32&jump_to=125033#p125033\|My immune response / symptoms are too strong. What should I do?]]

-	[[http://www.rxlist.com/cgi/generic/monteluk.htm\|Singulair]]	+	[[https://www.rxlist.com/cgi/generic/monteluk.htm\|Singulair]]

-	[[http://www.marshallprotocol.com/view_topic.php?id=4175&forum_id=23&jump_to=72854#p72854\|inhaler]]	+	[[https://www.marshallprotocol.com/view_topic.php?id=4175&forum_id=23&jump_to=72854#p72854\|inhaler]]


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	* Legacy content		* Legacy content
-	* [[http://www.marshallprotocol.com/forum32/5430.html]] F283	+	* [[https://www.marshallprotocol.com/forum32/5430.html]] F283
-	* new posts on this thread may have better member's experiences: http://www.marshallprotocol.com/forum11/8833-2.html --- //Joyful 2009/01/01 20:53//	+	* new posts on this thread may have better member's experiences: https://www.marshallprotocol.com/forum11/8833-2.html --- //Joyful 2009/01/01 20:53//


	<blockquote>Allergy Asthma Clin Immunol. 2009 Nov 19;5(1):8.		<blockquote>Allergy Asthma Clin Immunol. 2009 Nov 19;5(1):8.

-	Introduction of oral vitamin D supplementation and the rise of the allergy pandemic.(({{pubmed>long:20016691}}))	+	Introduction of oral vitamin D supplementation and the rise of the allergy pandemic.(({{pmid>long:20016691}}))

	Wjst M.		Wjst M.
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	TNF alpha is also elevated in celiac disease and improves when the Gluten free diet is followed:		TNF alpha is also elevated in celiac disease and improves when the Gluten free diet is followed:

-	http://www.ncbi.nlm.nih.gov/pubmed/17681027	+	https://www.ncbi.nlm.nih.gov/pubmed/17681027

	The following abstract shows that reducing TNF alpha (olmesartan does that at least some and food allergy reduction should do it), then the VDR will be more active against bacteria.		The following abstract shows that reducing TNF alpha (olmesartan does that at least some and food allergy reduction should do it), then the VDR will be more active against bacteria.

	</blockquote>		</blockquote>
-	===== References =====	+	===== References =====</nodisp>

Baldness (alopecia)

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

02.19.2019		current
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	Here, we sketch basic background information and key concepts that one needs to keep in mind when exploring the enigmatic "hair cycle clock"(HCC), and summarize competing models of the HCC. We invite the reader on a very subjective guided tour, which focuses on our own trials, errors, and findings toward the distant goal of unravelling one of the most fascinating mysteries of biology: Why does the hair follicle cycle at all? How does it do it? What are the key players in the underlying molecular controls? Attempting to offer at least some meaningful answers, we share our prejudices and perspectives, and define crucial open questions.		Here, we sketch basic background information and key concepts that one needs to keep in mind when exploring the enigmatic "hair cycle clock"(HCC), and summarize competing models of the HCC. We invite the reader on a very subjective guided tour, which focuses on our own trials, errors, and findings toward the distant goal of unravelling one of the most fascinating mysteries of biology: Why does the hair follicle cycle at all? How does it do it? What are the key players in the underlying molecular controls? Attempting to offer at least some meaningful answers, we share our prejudices and perspectives, and define crucial open questions.
-	(({{pubmed>long: 15617561}}))	+	(({{pmid>long: 15617561}}))


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	Maryborough, in central Victoria has an approximate population of 8000 and census data is well matched for Australia overall. Australia has compulsory voting and registration on the electoral roll. To determine the age-related prevalence of balding among men and women in Maryborough we conducted a postal survey of 5000 men and women aged 20 or older, and 427 were invited to attend for examination.		Maryborough, in central Victoria has an approximate population of 8000 and census data is well matched for Australia overall. Australia has compulsory voting and registration on the electoral roll. To determine the age-related prevalence of balding among men and women in Maryborough we conducted a postal survey of 5000 men and women aged 20 or older, and 427 were invited to attend for examination.

-	Additional data was collected on dandruff, presence of gray hair. Supplementary questionnaires were sent to 340 children aged 5-9, attending a coeducational primary school. 1456 adults (34.1%) responded to the questionnaire. 396 attended for examination. The prevalence of androgenetic alopecia (AGA) increased with advancing age. 98.6% of men had bitemporal recession and severity was significantly associated with vertex and mid-frontal hair loss (p <0.01) but not age (p = 0.06). In all, 64.4% of women had bitemporal hair loss, and similar to men there was a significant association with mid-frontal hair loss (p =0.042) but not age (p =0.467). One hundred and forty children with completed questionnaires were examined. All 72 females and 68 males were assessed as stage 1 on the mid-line part and with no bitemporal recession (frequency stage 1 = 100%, 95% CI (confidence interval) 97.4%-100%). A significant but weak positive association existed between presence of gray hair and history of dandruff (p<0.01). The prevalence of mid-frontal hair loss increases with age and affects 57% of women and 73.5% of men aged 80 and over. (({{pubmed>long:16382660}}))	+	Additional data was collected on dandruff, presence of gray hair. Supplementary questionnaires were sent to 340 children aged 5-9, attending a coeducational primary school. 1456 adults (34.1%) responded to the questionnaire. 396 attended for examination. The prevalence of androgenetic alopecia (AGA) increased with advancing age. 98.6% of men had bitemporal recession and severity was significantly associated with vertex and mid-frontal hair loss (p <0.01) but not age (p = 0.06). In all, 64.4% of women had bitemporal hair loss, and similar to men there was a significant association with mid-frontal hair loss (p =0.042) but not age (p =0.467). One hundred and forty children with completed questionnaires were examined. All 72 females and 68 males were assessed as stage 1 on the mid-line part and with no bitemporal recession (frequency stage 1 = 100%, 95% CI (confidence interval) 97.4%-100%). A significant but weak positive association existed between presence of gray hair and history of dandruff (p<0.01). The prevalence of mid-frontal hair loss increases with age and affects 57% of women and 73.5% of men aged 80 and over. (({{pmid>long:16382660}}))


-	"Vertex baldness, but not frontal baldness, is associated with an increased risk of chronic heart disease. The association with CHD depends on the severity of vertex baldness and also exists among younger men"(({{pubmed>long:23554099}}))	+	"Vertex baldness, but not frontal baldness, is associated with an increased risk of chronic heart disease. The association with CHD depends on the severity of vertex baldness and also exists among younger men"(({{pmid>long:23554099}}))


-	[[http://www.bbc.co.uk/news/health-12112673\|Cause of male baldness discovered, experts say]]	+	[[https://www.bbc.co.uk/news/health-12112673\|Cause of male baldness discovered, experts say]]

	===== Members' experiences =====		===== Members' experiences =====
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	Br J Vener Dis. 1977 Dec;53(6):389-90.Syphilitic alopecia and Jarisch-Herxheimer reaction.		Br J Vener Dis. 1977 Dec;53(6):389-90.Syphilitic alopecia and Jarisch-Herxheimer reaction.
-	Pareek SS. (({{pubmed>long:606336}}))	+	Pareek SS. (({{pmid>long:606336}}))


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	Alopecia syphilitica with detection of Treponema pallidum in the hair follicle.		Alopecia syphilitica with detection of Treponema pallidum in the hair follicle.
	Nam-Cha SH, Guhl G, Fernández-Peña P, Fraga J.		Nam-Cha SH, Guhl G, Fernández-Peña P, Fraga J.
-	J Cutan Pathol. 2007 Dec;34 Suppl 1:37-40. (({{pubmed>long:17997737}}))	+	J Cutan Pathol. 2007 Dec;34 Suppl 1:37-40. (({{pmid>long:17997737}}))


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	Cutaneous Mycobacterium neoaurum infection causing scarring alopecia in an immunocompetent host.		Cutaneous Mycobacterium neoaurum infection causing scarring alopecia in an immunocompetent host.
	Martin LK, Lawrence R, Kossard S, Murrell DF.		Martin LK, Lawrence R, Kossard S, Murrell DF.
-	Br J Dermatol. 2007 Jul;157(1):204-6. Epub 2007 May 14. No abstract available. (({{pubmed>long:17501949}}))	+	Br J Dermatol. 2007 Jul;157(1):204-6. Epub 2007 May 14. No abstract available. (({{pmid>long:17501949}}))


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	[Scarring tinea profunda in the pubic area due to Trichophyton verrucosum]		[Scarring tinea profunda in the pubic area due to Trichophyton verrucosum]
	Grunewald S, Paasch U, Gräser Y, Glander HJ, Simon JC, Nenoff P.		Grunewald S, Paasch U, Gräser Y, Glander HJ, Simon JC, Nenoff P.
-	Hautarzt. 2006 Sep;57(9):811-3. German. (({{pubmed>long:16402270}}))	+	Hautarzt. 2006 Sep;57(9):811-3. German. (({{pmid>long:16402270}}))


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	PSA screening for prostate cancer is generally not begun until men are in their 40s and 50s, but Giraud and Yassa suggested that it might be useful to start it somewhat earlier for men who go bald in their 20s because of their increased risk. Experts cautioned, however, that the number of people involved in the study was small, so the results should be interpreted with care.		PSA screening for prostate cancer is generally not begun until men are in their 40s and 50s, but Giraud and Yassa suggested that it might be useful to start it somewhat earlier for men who go bald in their 20s because of their increased risk. Experts cautioned, however, that the number of people involved in the study was small, so the results should be interpreted with care.

-	Other risk factors for prostate cancer include age, family history of the disease, diet, lifestyle and ethnicity. (({{pubmed>long:30764008}}))	+	Other risk factors for prostate cancer include age, family history of the disease, diet, lifestyle and ethnicity. (({{pmid>long:30764008}}))
	</blockquote>		</blockquote>

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	METHODS: A MEDLINE search (1955-July 2009) was preformed to find relevant articles pertaining to vitamin D, the vitamin D receptor, and hair loss. RESULTS: The vitamin D receptor, independent of vitamin D, plays an important role in hair cycling, specifically anagen initiation. The role of vitamin D in hair follicle cycling is not as well understood.		METHODS: A MEDLINE search (1955-July 2009) was preformed to find relevant articles pertaining to vitamin D, the vitamin D receptor, and hair loss. RESULTS: The vitamin D receptor, independent of vitamin D, plays an important role in hair cycling, specifically anagen initiation. The role of vitamin D in hair follicle cycling is not as well understood.

-	LIMITATIONS: The review is broad and there are limited human studies available to date. CONCLUSION: Additional studies to evaluate the role of vitamin D in the hair cycle should be done. Treatments that up regulate the vitamin D receptor may be successful in treating hair disorders and are a potential area of further study. (({{pubmed>long:20178699}}))	+	LIMITATIONS: The review is broad and there are limited human studies available to date. CONCLUSION: Additional studies to evaluate the role of vitamin D in the hair cycle should be done. Treatments that up regulate the vitamin D receptor may be successful in treating hair disorders and are a potential area of further study. (({{pmid>long:20178699}}))

	From: Bane, date: 2011-10-20 [[https://www.marshallprotocol.com/forum43/10978.html\|VDR's transcription of genes]]		From: Bane, date: 2011-10-20 [[https://www.marshallprotocol.com/forum43/10978.html\|VDR's transcription of genes]]


-	<blockquote>The hair cycle and Vitamin D receptor. (({{pubmed>long:22008469}}))	+	<blockquote>The hair cycle and Vitamin D receptor. (({{pmid>long:22008469}}))

	The Vitamin D receptor (VDR) plays a critical role in epidermal homeostasis. The ligand-dependent actions of the VDR attenuate epidermal keratinocyte proliferation and promote keratinocyte differentiation. Calcium can compensate for the absence of the VDR in maintaining a normal program of epidermal keratinocyte differentiation both in vitro and in vivo. In contrast, the effects of VDR ablation on the hair follicle cannot be prevented by maintaining normal calcium levels and are independent of 1,25-dihydroxyvitamin D. These actions of the VDR are critical in the keratinocyte stem cell population that resides in the bulge region of the hair follicle. Absence of a functional VDR leads to a self-renewal and lineage progression defect in this population of stem cells, resulting in the absence of post-morphogenic hair cycles. The molecular partners and downstream target genes of the VDR in this unique population of cells have not yet been identified.		The Vitamin D receptor (VDR) plays a critical role in epidermal homeostasis. The ligand-dependent actions of the VDR attenuate epidermal keratinocyte proliferation and promote keratinocyte differentiation. Calcium can compensate for the absence of the VDR in maintaining a normal program of epidermal keratinocyte differentiation both in vitro and in vivo. In contrast, the effects of VDR ablation on the hair follicle cannot be prevented by maintaining normal calcium levels and are independent of 1,25-dihydroxyvitamin D. These actions of the VDR are critical in the keratinocyte stem cell population that resides in the bulge region of the hair follicle. Absence of a functional VDR leads to a self-renewal and lineage progression defect in this population of stem cells, resulting in the absence of post-morphogenic hair cycles. The molecular partners and downstream target genes of the VDR in this unique population of cells have not yet been identified.
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-	{{tag>diseases arrange}}	+	{{tag>diseases }}




		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

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	* legacy content		* legacy content
	*		*
-	* [[http://www.bbc.co.uk/news/health-12112673\|Cause of male baldness discovered, experts say]]	+	* [[https://www.bbc.co.uk/news/health-12112673\|Cause of male baldness discovered, experts say]]



-	===== References =====	+	===== References =====</nodisp>

ALS (Lou Gehrig's Disease)

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

02.11.2019		current
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	Lou Gehrig was known as The Gentleman of Baseball. He played for the NY Yankees in the '20s and '30s. He had Amyotrophic Lateral Sclerosis (ALS) and, because of his fame and courage in fighting it, the disease also became known as Lou Gehrig's Disease. They made a movie about his life and his famous speech telling his beloved fans he had to quit.		Lou Gehrig was known as The Gentleman of Baseball. He played for the NY Yankees in the '20s and '30s. He had Amyotrophic Lateral Sclerosis (ALS) and, because of his fame and courage in fighting it, the disease also became known as Lou Gehrig's Disease. They made a movie about his life and his famous speech telling his beloved fans he had to quit.

-	Here is [[http://en.wikipedia.org/wiki/Lou_Gehrig\|his bio]].	+	Here is [[https://en.wikipedia.org/wiki/Lou_Gehrig\|his bio]].

-	A Washington Post columnist [[http://www.washingtonpost.com/wp-dyn/articles/A19187-2005Apr1.html\|recently reviewed]] a new book about Lou Gehrig. He included an interesting quote from the book, "Luckiest Man: The Life and Death of Lou Gehrig" by Jonathan Eig, explaining that Gehrig's untimely death at age 39 from ALS changed it from an almost-unknown disease to a near-universally known disease.	+	A Washington Post columnist [[https://www.washingtonpost.com/wp-dyn/articles/A19187-2005Apr1.html\|recently reviewed]] a new book about Lou Gehrig. He included an interesting quote from the book, "Luckiest Man: The Life and Death of Lou Gehrig" by Jonathan Eig, explaining that Gehrig's untimely death at age 39 from ALS changed it from an almost-unknown disease to a near-universally known disease.

	Lida Mattman's slides of ALS blood show very aggressive CWD-bacteria. Dr. Mattman suggested that the bacteria causing ALS multiply rapidly and are, therefore, very aggressive. It isn't known if that translates into their being resistant to the MP or readily killed. Or if they are easily killed, if they would release more endotoxins. All these unknowns mean that treating ALS with the MP will have to be done very carefully. It is best in these situations for Dr to discuss the actual case with Dr Marshall.		Lida Mattman's slides of ALS blood show very aggressive CWD-bacteria. Dr. Mattman suggested that the bacteria causing ALS multiply rapidly and are, therefore, very aggressive. It isn't known if that translates into their being resistant to the MP or readily killed. Or if they are easily killed, if they would release more endotoxins. All these unknowns mean that treating ALS with the MP will have to be done very carefully. It is best in these situations for Dr to discuss the actual case with Dr Marshall.
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	Neuropharmacology Vol.13 No 8 12 June 2002 Ludo Van Den Bosch, Petra Tilkin, Griet Lemmns and Wim Robberecht Laboratory of Neurology, Campus Gasthuisberg, Herestraat 49, B-3000, Leuven, Belium		Neuropharmacology Vol.13 No 8 12 June 2002 Ludo Van Den Bosch, Petra Tilkin, Griet Lemmns and Wim Robberecht Laboratory of Neurology, Campus Gasthuisberg, Herestraat 49, B-3000, Leuven, Belium

-	<blockquote>[[http://www.labspaces.net/107755/Mysterious_cells_may_play_role_in_ALS\|Mysterious cells may play role in ALS]]	+	<blockquote>[[https://www.labspaces.net/107755/Mysterious_cells_may_play_role_in_ALS\|Mysterious cells may play role in ALS]]

	Although we found that the potential of these cells is more limited than previously thought, it might be possible to coax them to adopt different fates," Bergles says. "We only need to know what factors are restricting their development in the intact nervous system.		Although we found that the potential of these cells is more limited than previously thought, it might be possible to coax them to adopt different fates," Bergles says. "We only need to know what factors are restricting their development in the intact nervous system.
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	* Chris Mavo:		* Chris Mavo:

-	//Last contact: July, 2018// see [[http://www.marshallprotocol.com/forum30/13432.html\|summary thread]] [[https://www.marshallprotocol.com/forum35/13463.html\|progress thread]]	+	//Last contact: July, 2018// see [[https://www.marshallprotocol.com/forum30/13432.html\|summary thread]] [[https://www.marshallprotocol.com/forum35/13463.html\|progress thread]]


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	An interesting thing is that my photosensitivity has returned so it is not the benicar alone that causes it in me, it is benicar and abx.</blockquote>		An interesting thing is that my photosensitivity has returned so it is not the benicar alone that causes it in me, it is benicar and abx.</blockquote>

-	Editor's note: photosensitivity seems to actually be related to the amount of infection being fought, and produced by something in the die-off of microbes. I experienced photosensitivity for many years before finding MP, including childhood measles.	+	//Editor's note: photosensitivity seems to actually be related to the amount of infection being fought, and produced by something in the die-off of microbes. I experienced photosensitivity for many years before finding MP, including childhood measles.//


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-	Marijuana is a substance with many properties that may be applicable to the management of amyotrophic lateral sclerosis (({{pubmed>long:11467101}}))	+	Marijuana is a substance with many properties that may be applicable to the management of amyotrophic lateral sclerosis (({{pmid>long:11467101}}))

	Be aware that cannibinoids are immune suppressant.		Be aware that cannibinoids are immune suppressant.
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	===== Research notes =====		===== Research notes =====

-	<blockquote>All this frenetic oligodendrocyte-generating activity takes place in the central nervous system's gray matter where other cells — the motor neurons — are dying. A body of research shows that after acute trauma to the central nervous system, a short-term upswing in NG2+ activity takes place that may help reduce the extent of damage. Whether this change in behavior of NG2+ cells is protective, or accelerates the death of motor neurons in ALS, is not yet known. //[[http://www.labspaces.net/107755/Mysterious_cells_may_play_role_in_ALS\|Thanks to Johns Hopkins Medical Institutions for this article.]] // 2010</blockquote>	+	<blockquote>All this frenetic oligodendrocyte-generating activity takes place in the central nervous system's gray matter where other cells — the motor neurons — are dying. A body of research shows that after acute trauma to the central nervous system, a short-term upswing in NG2+ activity takes place that may help reduce the extent of damage. Whether this change in behavior of NG2+ cells is protective, or accelerates the death of motor neurons in ALS, is not yet known. //[[https://www.labspaces.net/107755/Mysterious_cells_may_play_role_in_ALS\|Thanks to Johns Hopkins Medical Institutions for this article.]] // 2010</blockquote>

	{{tag>diseases neurological }}		{{tag>diseases neurological }}
		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

-	this link is to old TH1 thread [[http://www.marshallprotocol.com/forum19/13414.html\|getting started]] for Chris Mavo, pity we do not have access to GET CONTENT	+	this link is to old TH1 thread [[https://www.marshallprotocol.com/forum19/13414.html\|getting started]] for Chris Mavo, pity we do not have access to GET CONTENT

	<DiseaseHierarchy>		<DiseaseHierarchy>
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	* Legacy content		* Legacy content
-	* [[http://www.marshallprotocol.com/view_topic.php?id=2697&forum_id=37&jump_to=37083#p37083]] e245	+	* [[https://www.marshallprotocol.com/view_topic.php?id=2697&forum_id=37&jump_to=37083#p37083]] e245
-	* [[http://www.marshallprotocol.com/forum37/9805.html#p113372]] s322	+	* [[https://www.marshallprotocol.com/forum37/9805.html#p113372]] s322
-	* [[http://www.marshallprotocol.com/view_topic.php?id=9805&forum_id=37&jump_to=113373#p113373]] s323	+	* [[https://www.marshallprotocol.com/view_topic.php?id=9805&forum_id=37&jump_to=113373#p113373]] s323
-	* [[http://www.marshallprotocol.com/view_topic.php?id=9805&forum_id=37&jump_to=113374#p113374]] s324	+	* [[https://www.marshallprotocol.com/view_topic.php?id=9805&forum_id=37&jump_to=113374#p113374]] s324

	.		.
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	From: Scottk		From: Scottk
	Date: 2009-11-27 20:53:34		Date: 2009-11-27 20:53:34
-	Reply: http://www.marshallprotocol.com/reply.php?topic_id=12013	+	Reply: https://www.marshallprotocol.com/reply.php?topic_id=12013

	I continued benicar throughout. after a day of MMS I could straighten my toes which I could not before and I still can now that I have stopped MMS and resumed the full mp. My walking improved also but I am unsure if that was from stopping the abx/ip. so far the improvement in my walking has remained.		I continued benicar throughout. after a day of MMS I could straighten my toes which I could not before and I still can now that I have stopped MMS and resumed the full mp. My walking improved also but I am unsure if that was from stopping the abx/ip. so far the improvement in my walking has remained.
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-	We don't have an official position on this anti-microbial specifically (http://mpkb.org/doku.php/home:othertreatments), but for an ALS patient, would his experimentation be considered a specially allowed case due to this disease having more of an 'acute infection' timeline?	+	We don't have an official position on this anti-microbial specifically (https://mpkb.org/doku.php/home:othertreatments), but for an ALS patient, would his experimentation be considered a specially allowed case due to this disease having more of an 'acute infection' timeline?


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	<blockquote>Mysterious cells may play role in ALS		<blockquote>Mysterious cells may play role in ALS

-	http://www.labspaces.net/107755/Mysterious_cells_may_play_role_in_ALS	+	https://www.labspaces.net/107755/Mysterious_cells_may_play_role_in_ALS

	Although we found that the potential of these cells is more limited than previously thought, it might be possible to coax them to adopt different fates," Bergles says. "We only need to know what factors are restricting their development in the intact nervous system.		Although we found that the potential of these cells is more limited than previously thought, it might be possible to coax them to adopt different fates," Bergles says. "We only need to know what factors are restricting their development in the intact nervous system.
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-	===== References =====	+	===== References =====</nodisp>

Alzheimer's disease and dementia

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

Anemia

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

Ankylosing spondylitis

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

08.12.2019		current
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	CONCLUSION: The role of K. pneumoniae and anti-collagen antibodies in the aetiopathogenesis of CD and AS requires further study.		CONCLUSION: The role of K. pneumoniae and anti-collagen antibodies in the aetiopathogenesis of CD and AS requires further study.
-	(({{pubmed>long:11157137}}))</blockquote>	+	(({{pmid>long:11157137}}))</blockquote>

	[[https://ard.bmj.com/content/76/6/1123.abstract?utm_term=usage-012019&utm_content=consumer&utm_campaign=ard&utm_medium=cpc&utm_source=trendmd\|Dysbiosis and zonulin upregulation alter gut epithelial and vascular barriers in patients with ankylosing spondylitis ]]		[[https://ard.bmj.com/content/76/6/1123.abstract?utm_term=usage-012019&utm_content=consumer&utm_campaign=ard&utm_medium=cpc&utm_source=trendmd\|Dysbiosis and zonulin upregulation alter gut epithelial and vascular barriers in patients with ankylosing spondylitis ]]
	===== Management =====		===== Management =====

-	The prevalence rate of hip involvement in AS patients varies from 10 to 23%, depending on the type of hip assessment. TNF-α blocking therapy significantly improved tender hip joints, and inflammatory US lesions including positive power Doppler. (({{pubmed>long:30624693}}))	+	The prevalence rate of hip involvement in AS patients varies from 10 to 23%, depending on the type of hip assessment. TNF-α blocking therapy significantly improved tender hip joints, and inflammatory US lesions including positive power Doppler. (({{pmid>long:30624693}}))


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	Patients with ankylosing spondylitis (AS) warrant a comprehensive clinical assessment because of the lack of biomarkers of disease activity, prognosis and response to biologic therapy. Multiple AS-related questionnaires have been developed to assess the disease status accurately, but feasibility remains a problem in clinical practice.		Patients with ankylosing spondylitis (AS) warrant a comprehensive clinical assessment because of the lack of biomarkers of disease activity, prognosis and response to biologic therapy. Multiple AS-related questionnaires have been developed to assess the disease status accurately, but feasibility remains a problem in clinical practice.

-	The Bath Ankylosing Disease Activity Index remains the gold standard for assessing disease activity in a routine practice, despite poor correlation with C-reactive protein (CRP) levels and MRI inflammation. (({{pubmed>long:30624284}}))	+	The Bath Ankylosing Disease Activity Index remains the gold standard for assessing disease activity in a routine practice, despite poor correlation with C-reactive protein (CRP) levels and MRI inflammation. (({{pmid>long:30624284}}))


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	==== TNF inhibitor dose ====		==== TNF inhibitor dose ====

-	In patients with ankylosing spondylitis in clinical remission for at least 6 months, dose reduction is non-inferior to full TNF inhibitor doses to maintain LDA after 1 year. Serious adverse events may be less frequent with reduced doses. (({{pubmed>long:30621746}}))	+	In patients with ankylosing spondylitis in clinical remission for at least 6 months, dose reduction is non-inferior to full TNF inhibitor doses to maintain LDA after 1 year. Serious adverse events may be less frequent with reduced doses. (({{pmid>long:30621746}}))


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	<blockquote> I was on Fosamax for 2 years, which lead to acid reflux and the need for Prilosec. My primary doc was obviously wrong then, as I believe he is now when he recommends 1000mg of Vitamin D daily. Been there and done that already with very bad results. I don't argue with my doc, but I make my own educated health decisions. Most of our current medical insight seems to be blinded by the "sunshine vitamin syndrome" //Jasmine//</blockquote>		<blockquote> I was on Fosamax for 2 years, which lead to acid reflux and the need for Prilosec. My primary doc was obviously wrong then, as I believe he is now when he recommends 1000mg of Vitamin D daily. Been there and done that already with very bad results. I don't argue with my doc, but I make my own educated health decisions. Most of our current medical insight seems to be blinded by the "sunshine vitamin syndrome" //Jasmine//</blockquote>
		+
		+	==== D-free calcium ====
		+
		+	<blockquote> I have found an orange juice with calcium and NO D! I also found a lactose fat free milk (LandOLakes) D free ....with calcium. It is called Dairy Ease. Perfect for this lactose intolerant, D free, calcium deficient
		+
		+	I do fair better with fortified calcium foods than I do calcium supplements! I tend to get pains in my back if I take more than 800 mgs of calcium daily in pill form. But I am determined to get my bones stronger</blockquote>


	==== Related research on osteonecrosis ====		==== Related research on osteonecrosis ====

-	The findings from this study indicated that even short-term oral use of alendronate led to ONJ in a subset of patients after certain dental procedures were performed. These findings have important therapeutic and preventive implications. (({{pubmed>long:19119168}}))	+	The findings from this study indicated that even short-term oral use of alendronate led to ONJ in a subset of patients after certain dental procedures were performed. These findings have important therapeutic and preventive implications. (({{pmid>long:19119168}}))

-	Oral bisphosphonate use and the prevalence of osteonecrosis of the jaw (({{pubmed>long:30534822}}))	+	Oral bisphosphonate use and the prevalence of osteonecrosis of the jaw (({{pmid>long:30534822}}))


	{{tag>diseases }}		{{tag>diseases }}

		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

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	<blockquote>Arthritis Rheum. 2009 Nov;60(11):3519-20; author reply 3520-1.		<blockquote>Arthritis Rheum. 2009 Nov;60(11):3519-20; author reply 3520-1.

-	Time to prove the infective etiology of ankylosing spondylitis and related spondylarthritides: Comment on the article by Carter et al.(({{pubmed>long:19877074}}))	+	Time to prove the infective etiology of ankylosing spondylitis and related spondylarthritides: Comment on the article by Carter et al.(({{pmid>long:19877074}}))

	Zeidler H, Rihl M.		Zeidler H, Rihl M.
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	</blockquote>		</blockquote>

-	===== References =====	+	===== References =====</nodisp>

Anorexia and bulimia

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

08.12.2019		current
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	Discussion in The Economist print edition 29 Sep 2005		Discussion in The Economist print edition 29 Sep 2005
-	[[http://www.economist.com/displaystory.cfm?story_id=4455455\|Molecular self-loathing]]	+	[[https://www.economist.com/displaystory.cfm?story_id=4455455\|Molecular self-loathing]]

	===== Evidence of infectious cause =====		===== Evidence of infectious cause =====

-	The intrinsic ability of bacteria to regulate their growth and to maintain their population within the gut suggests that gut bacteria can interfere with molecular pathways controlling energy balance in the host. (({{pubmed>long:27616451}}))	+	The intrinsic ability of bacteria to regulate their growth and to maintain their population within the gut suggests that gut bacteria can interfere with molecular pathways controlling energy balance in the host. (({{pmid>long:27616451}}))

	===== Immune overload =====		===== Immune overload =====
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	An immune overload hypothesis would suggest that compensating withdrawal from some activities would help recovery from eating disorders, and certainly a reduction of unnecessary parental pressure may be needed.		An immune overload hypothesis would suggest that compensating withdrawal from some activities would help recovery from eating disorders, and certainly a reduction of unnecessary parental pressure may be needed.

-	[[http://www.eurekalert.org/pub_releases/2009-07/uoc--rpn072109.php\|New imaging technology]] at U.Cal. San Diego provides insight into abnormalities in the brain circuitry of patients with anorexia nervosa that may contribute to the puzzling symptoms found in people with the eating disorder.	+	[[https://www.eurekalert.org/pub_releases/2009-07/uoc--rpn072109.php\|New imaging technology]] at U.Cal. San Diego provides insight into abnormalities in the brain circuitry of patients with anorexia nervosa that may contribute to the puzzling symptoms found in people with the eating disorder.
	<blockquote>Under Kaye's leadership, the eating disorders treatment program at UC San Diego is developing treatments based on understanding the temperament and personality that drives anorexia, and helping patients to use such traits in constructive, rather then self-defeating ways.</blockquote>		<blockquote>Under Kaye's leadership, the eating disorders treatment program at UC San Diego is developing treatments based on understanding the temperament and personality that drives anorexia, and helping patients to use such traits in constructive, rather then self-defeating ways.</blockquote>

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	So that is it. I am starting to feel normal again. I even have less of the nerve issues in my hands now. I didn't think things like that would ever go back to normal. But I can feel them normalizing. The word for me is beginning to be…NORMAL. 4.5 years on the Marshall, (was on one antibiotic protocol or another since July of 2005).		So that is it. I am starting to feel normal again. I even have less of the nerve issues in my hands now. I didn't think things like that would ever go back to normal. But I can feel them normalizing. The word for me is beginning to be…NORMAL. 4.5 years on the Marshall, (was on one antibiotic protocol or another since July of 2005).
		+
		+
		+	==== Alayne's strategy ====
		+
		+	The trick is to have as many kinds of foods around as possible because when one's appetite is down, having just one thing to choose from generally doesn't work. I went through years of having little or no appetite myself, so understand the problem pretty well myself - it's very frustrating!
		+
		+	Here's some of what Jack manages to choke down and hasn't lost anymore weight on:
		+
		+	Breakfasts - 2 slices of whole grain toast or rolls with peanut butter/almond butter with agave nectar (like honey) and high fat cheese.
		+
		+	Mixed whole grain hot cereals with half & half, dried or whatever kinds of fruits you have and nuts.
		+
		+	Smoothies - Frozen and unfrozen fruits (lots of vitamins). He also adds almonds or some softer nuts to the blenderized drink. Always add some protein to the mix as well. We like to make an eggwhite omelet to accompany the smoothie (3-5 eggwhites with garlic, grated cheese, green onions, tomatoes…or whatever else is in the fridge).
		+
		+	Other meals - sandwiches with guacamole and whole milk cheese or chicken or both. We also use vegenaise which is a great substitute for mayo (tastes like the real thing).
		+
		+	Brown rice, wild rice, basmati rice pilafs with quick cooked organic beef or lamb stew with lots of veggies and spices.
		+
		+	Buffalo, beef, or lamb burgers (spiced with various herbs and onion, garlic, etc.) on whole grain rolls or just with veggies.
		+
		+	Grill a marinated beef or buffalo steak and have on hand for snacks and meals.
		+
		+	Roast a chicken once or twice a week and have on hand for snacks and meals. We make a great chicken salad with the vegenaise, pickles, onions, and whatever else we like. Spread on crackers, bread, or use in salads lettuces.
		+
		+	Whole fat cheese on crackers (try different types of cheeses and crackers for variation)
		+
		+	Apples and celery with peanut butter or almond butter. Cashew butter's also great.
		+
		+	Jacks makes almond milk and cashew yogurt which are nice and high in calories. If you're interested, can give you the recipes. Kind of a pain to make though.
		+
		+	Lots of sugar free dark chocolate.
		+
		+	Mixed nuts (I know you're heartily sick of them…there are ways to flavor them differently so they're a tad more interesting. Although it's not known whether or not pumpkin and sunflower seeds have Vit D, Jacks eats them on many things. His 25-D dropped to <5, so I think they probably have little D, if any.
		+
		+	Tortilla chips with salsas and guacamole.

	===== Further Research =====		===== Further Research =====

-	We found significantly altered correlations between alpha-MSH autoAb levels and the total Eating Disorder Inventory-2 score, as well as most of its subscale dimensions in AN and BN patients vs. controls. Remarkably, these correlations were opposite in AN vs. BN patients. In contrast, levels of autoAbs reacting with adrenocorticotropic hormone, OT, or VP had only few altered correlations with the Eating Disorder Inventory-2 subscale dimensions in AN and BN patients. Thus, our data reveal that core psychobehavioral abnormalities characteristic for eating disorders correlate with the levels of autoAbs against alpha-MSH, suggesting that AN and BN may be associated with autoAb-mediated dysfunctions of primarily the melanocortin system. //Fetissov SO, et al//(({{pubmed>long:16195379}}))	+	We found significantly altered correlations between alpha-MSH autoAb levels and the total Eating Disorder Inventory-2 score, as well as most of its subscale dimensions in AN and BN patients vs. controls. Remarkably, these correlations were opposite in AN vs. BN patients. In contrast, levels of autoAbs reacting with adrenocorticotropic hormone, OT, or VP had only few altered correlations with the Eating Disorder Inventory-2 subscale dimensions in AN and BN patients. Thus, our data reveal that core psychobehavioral abnormalities characteristic for eating disorders correlate with the levels of autoAbs against alpha-MSH, suggesting that AN and BN may be associated with autoAb-mediated dysfunctions of primarily the melanocortin system. //Fetissov SO, et al//(({{pmid>long:16195379}}))

-	Hypovolemia-induced obesity and diabetes. (({{pubmed>long:19709692}})) Hypovolemia is a diminished volume of circulating blood in the body. Therefore is it obviously important to guard against dehydration.	+	Hypovolemia-induced obesity and diabetes. (({{pmid>long:19709692}})) Hypovolemia is a diminished volume of circulating blood in the body. Therefore is it obviously important to guard against dehydration.

-	Imaging studies reveal[[http://www.eurekalert.org/pub_releases/2009-07/uoc--rpn072109.php\|Differences]] in the brain circuitry of patients with anorexia nervosa (commonly known as anorexia) that may contribute to the puzzling symptoms found in people with the eating disorder. (({{pubmed>long:21243469}}))	+	Imaging studies reveal[[https://www.eurekalert.org/pub_releases/2009-07/uoc--rpn072109.php\|Differences]] in the brain circuitry of patients with anorexia nervosa (commonly known as anorexia) that may contribute to the puzzling symptoms found in people with the eating disorder. (({{pmid>long:21243469}}))


-	[[http://www.plosone.org/article/info:doi/10.1371/journal.pone.0007125\|Monitoring Bacterial Community]] of Human Gut Microbiota Reveals an Increase in Lactobacillus in Obese Patients and Methanogens in Anorexic Patients (({{pubmed>long:19774074}}))	+	[[https://www.plosone.org/article/info:doi/10.1371/journal.pone.0007125\|Monitoring Bacterial Community]] of Human Gut Microbiota Reveals an Increase in Lactobacillus in Obese Patients and Methanogens in Anorexic Patients (({{pmid>long:19774074}}))

-	Famine may affect the microbiome in a lasting way(({{pubmed>long:14696131}}))	+	Famine may affect the microbiome in a lasting way(({{pmid>long:14696131}}))
-	[[http://www.ncbi.nlm.nih.gov/pubmed/14696131\|psychological traits in eating disorders]]	+	[[https://www.ncbi.nlm.nih.gov/pubmed/14696131\|psychological traits in eating disorders]]

-	in New Insights in Anorexia Nervosa (({{pubmed>long:27445651}}))	+	in New Insights in Anorexia Nervosa (({{pmid>long:27445651}}))
	P. Gorwood, J. Epelbaum and colleagues assemble seven possible models, each accompanied by illustrative figures.		P. Gorwood, J. Epelbaum and colleagues assemble seven possible models, each accompanied by illustrative figures.

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		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

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	* legacy content		* legacy content
-	* [[http://www.marshallprotocol.com/view_topic.php?id=4243&forum_id=37&jump_to=39895#p39895]] s60	+	* [[https://www.marshallprotocol.com/view_topic.php?id=4243&forum_id=37&jump_to=39895#p39895]] s60



	(//Paul and/or Amy// ??) I'm not sure I can completely tease out the significance of this study, but this sort of result suggests that famine may affect the microbiome in a lasting way:		(//Paul and/or Amy// ??) I'm not sure I can completely tease out the significance of this study, but this sort of result suggests that famine may affect the microbiome in a lasting way:
-	[[http://www.ncbi.nlm.nih.gov/pubmed/14696131\|psychological traits in eating disorders]]	+	[[https://www.ncbi.nlm.nih.gov/pubmed/14696131\|psychological traits in eating disorders]]

	Final point: IMO, we should all be careful not to define the chain of events. What if a disruption in the microbiome preceded anorexia and the anorexia "phenotype" was only expressed in certain cultures?		Final point: IMO, we should all be careful not to define the chain of events. What if a disruption in the microbiome preceded anorexia and the anorexia "phenotype" was only expressed in certain cultures?

-	===== References =====	+	===== References =====</nodisp>

Anxiety

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

01.26.2020		current
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-	Finally there's certain evidence that olmesartan (Benicar) may be useful against stress disorders. A National Institutes of Health paper says an important stress hormone, ANGII, and by extension stress disorders, could be managed by the use of ARBs, of which olmesartan is one.(({{pubmed>long:17514587}}))	+	Finally there's certain evidence that olmesartan (Benicar) may be useful against stress disorders. A National Institutes of Health paper says an important stress hormone, ANGII, and by extension stress disorders, could be managed by the use of ARBs, of which olmesartan is one.(({{pmid>long:17514587}}))


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	autism, ADHD, depression, severe anxiety, chronic fatigue syndrome (CFS)		autism, ADHD, depression, severe anxiety, chronic fatigue syndrome (CFS)

-	Read the [[http://bacteriality.com/2008/03/15/interview18/\|interview]]	+	Read the [[https://bacteriality.com/2008/03/15/interview18/\|interview]]

	<html></div></div>		<html></div></div>
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	<blockquote>Infection and inflammation lead to changes in mood and cognition. Although the "classic" sickness behavior syndrome, involving fatigue, social withdrawal, and loss of appetites are most familiar, other emotional responses accompany immune activation, including anxiety. Recent studies have shown that gastrointestinal bacterial infections lead to enhanced anxiety-like behavior in mice. The bacteria-induced signal is most likely carried by vagal sensory neurons, and occurs early on (within 6h) during the infection. These signals induce evidence of activation in brain regions that integrate viscerosensory information with mood, and potentiate activation in brain regions established as key players in fear and anxiety.		<blockquote>Infection and inflammation lead to changes in mood and cognition. Although the "classic" sickness behavior syndrome, involving fatigue, social withdrawal, and loss of appetites are most familiar, other emotional responses accompany immune activation, including anxiety. Recent studies have shown that gastrointestinal bacterial infections lead to enhanced anxiety-like behavior in mice. The bacteria-induced signal is most likely carried by vagal sensory neurons, and occurs early on (within 6h) during the infection. These signals induce evidence of activation in brain regions that integrate viscerosensory information with mood, and potentiate activation in brain regions established as key players in fear and anxiety.

-	//L.E. Goehler et al.//(({{pubmed>long:17428636}}))</blockquote>	+	//L.E. Goehler et al.//(({{pmid>long:17428636}}))</blockquote>

-	Further, Neufeld //et al.// showed that germ-free mice exhibited reduced anxiety-like behavior as well as significant neurochemical changes in the brain compared to specific-pathogen-free mice. (({{pubmed>long:21054680}}))	+	Further, Neufeld //et al.// showed that germ-free mice exhibited reduced anxiety-like behavior as well as significant neurochemical changes in the brain compared to specific-pathogen-free mice. (({{pmid>long:21054680}}))



-	The frequency with which patients of certain Th1 diseases also experience anxiety(({{pubmed>long:8818377}})) (({{pubmed>long:18774427}})) (({{pubmed>long:18774427}})) (({{pubmed>long:9361174}})) (({{pubmed>long:15569892}})) (({{pubmed>long:7883407}})) (({{pubmed>long:9707157}})) (({{pubmed>long:12011605}})) (({{pubmed>long:11391746}})) may also suggest a single underlying cause.	+	The frequency with which patients of certain Th1 diseases also experience anxiety(({{pmid>long:8818377}})) (({{pmid>long:18774427}})) (({{pmid>long:18774427}})) (({{pmid>long:9361174}})) (({{pmid>long:15569892}})) (({{pmid>long:7883407}})) (({{pmid>long:9707157}})) (({{pmid>long:12011605}})) (({{pmid>long:11391746}})) may also suggest a single underlying cause.


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	{{tag>diseases symptoms neurological}}		{{tag>diseases symptoms neurological}}

		+	Findings suggest that a low dose of THC produces subjective stress-relieving effects in line with those commonly reported among cannabis users, but that higher doses may non-specifically increase negative mood. (({{pmid>long:28599212}})) [[https://www.sciencedirect.com/science/article/abs/pii/S037687161730220X?via%3Dihub\|effects of delta-9-THC on responses to the Trier Social Stress Test (TSST)]]

-	findings suggest that a low dose of THC produces subjective stress-relieving effects in line with those commonly reported among cannabis users, but that higher doses may non-specifically increase negative mood. [[https://www.sciencedirect.com/science/article/abs/pii/S037687161730220X?via%3Dihub\|effects of delta-9-THC on responses to the Trier Social Stress Test (TSST)Link]]	+	Baseline symptoms of depression (but not anxiety or stress) appeared to be exacerbated across time/tracked sessions. [[https://www.sciencedirect.com/science/article/pii/S0165032718303100?via%3Dihub\|Journal of Affective Disorders]] (({{pmid>long:29656267}}))

-	baseline symptoms of depression (but not anxiety or stress) appeared to be exacerbated across time/tracked sessions. [[https://www.sciencedirect.com/science/article/pii/S0165032718303100?via%3Dihub\|Journal of Affective Disorders]] (({{pubmed>long:29656267}}))	+	Perhaps most well-studied is the role the CeA plays in unconditioned and conditioned fear generation (Ciocchi et al., 2010, Li et al., 2013, Tye et al., 2011), fear extinction, and conditioned inhibition (Amano et al., 2010), as well as conditioned orienting responses to emotionally salient stimuli (El-Amamy and Holland, 2007, Groshek et al., 2005). [[https://www.cell.com/neuron/fulltext/S0896-6273(14)00017-8?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0896627314000178%3Fshowall%3Dtrue\|The central amygdala Link]] (({{pmid>long:24607231}}))
-		+
-	Perhaps most well-studied is the role the CeA plays in unconditioned and conditioned fear generation (Ciocchi et al., 2010, Li et al., 2013, Tye et al., 2011), fear extinction, and conditioned inhibition (Amano et al., 2010), as well as conditioned orienting responses to emotionally salient stimuli (El-Amamy and Holland, 2007, Groshek et al., 2005). [[https://www.cell.com/neuron/fulltext/S0896-6273(14)00017-8?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0896627314000178%3Fshowall%3Dtrue\|The central amygdala Link]] (({{pubmed>long:24607231}}))	+

	the mechanisms by which stress increases amygdala-dmPFC synaptic strength and generates anxiety-like behaviors are not well understood. Here, we show that the mouse basolateral amygdala (BLA)-prelimbic prefrontal cortex (plPFC) circuit is engaged by stress and activation of this pathway in anxiogenic. [[https://www.cell.com/neuron/pdf/S0896-6273(19)31090-6.pdf\|Functional coupling between the amygdala and the dorsomedial prefrontal cortex Link]]		the mechanisms by which stress increases amygdala-dmPFC synaptic strength and generates anxiety-like behaviors are not well understood. Here, we show that the mouse basolateral amygdala (BLA)-prelimbic prefrontal cortex (plPFC) circuit is engaged by stress and activation of this pathway in anxiogenic. [[https://www.cell.com/neuron/pdf/S0896-6273(19)31090-6.pdf\|Functional coupling between the amygdala and the dorsomedial prefrontal cortex Link]]
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-	(({{pubmed>long:29656267}}))

-	(({{pubmed>long:000}}))

-	(({{pubmed>long:000}}))

-	(({{pubmed>long:000}}))	+	(({{pmid>long:000}}))
		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

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	* Legacy content		* Legacy content
-	* http://www.marshallprotocol.com/view_topic.php?id=2696&forum_id=32&jump_to=45601#p23751 f102	+	* https://www.marshallprotocol.com/view_topic.php?id=2696&forum_id=32&jump_to=45601#p23751 f102
-	* http://www.marshallprotocol.com/forum32/7148.html f248	+	* https://www.marshallprotocol.com/forum32/7148.html f248
-	* http://www.marshallprotocol.com/view_topic.php?id=4243&forum_id=37&jump_to=41630#p41630 s62	+	* https://www.marshallprotocol.com/view_topic.php?id=4243&forum_id=37&jump_to=41630#p41630 s62


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	Bacteria’s presence or absence affected how the mice used certain brain chemicals and genes involved in brain development. Taken together, the results indicate that intestinal bacteria somehow shape the brain and make mice more anxious — or cautious, depending how you look at it, Pettersson says.		Bacteria’s presence or absence affected how the mice used certain brain chemicals and genes involved in brain development. Taken together, the results indicate that intestinal bacteria somehow shape the brain and make mice more anxious — or cautious, depending how you look at it, Pettersson says.
	</blockquote>		</blockquote>
-	===== References =====	+	===== References =====</nodisp>

Asthma

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

10.19.2018		current
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-	Papadopoulos //et al.// have written that asthma should be treated as a suboptimal innate immune response.(({{pubmed>long:17188832}})) Consistent with that thinking, the Marshall Protocol (MP) is a treatment for asthma. While many physicians still consider immunosuppressive medications such as corticosteroids as a first-line treatment for asthma, these drugs interfere with the body's immune response. The Marshall Protocol is designed to stimulate the innate immune response. In the process may cause immunopathology, the bacterial die-off reaction.	+	Papadopoulos //et al.// have written that asthma should be treated as a suboptimal innate immune response.(({{pmid>long:17188832}})) Consistent with that thinking, the Marshall Protocol (MP) is a treatment for asthma. While many physicians still consider immunosuppressive medications such as corticosteroids as a first-line treatment for asthma, these drugs interfere with the body's immune response. The Marshall Protocol is designed to stimulate the innate immune response. In the process may cause immunopathology, the bacterial die-off reaction.


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	===== Lung microbiome =====		===== Lung microbiome =====

-	Until recently, estimates of the resident microbial flora in the lungs were far too low. A 1998 infectious disease textbook stated that the lungs were sterile.((Noskin, Gary A. 1998. //Management of infectious complication in cancer patients.// Boston: Kluwer Academic Publishers.)) However, such conclusions were made on the basis of culture-based tests, which we now know identify a small minority of microbes. Since then, metagenomic analyses have indicated the presence of a persistent lung microbiome, the composition of which differs in health and disease. For example, Erb-Downward found bacterial 16S sequences in the lung tissues of all subjects in a 2011 based study of healthy patients as well as those with chronic obstructive pulmonary disease (COPD).(({{pubmed>long:21364979}}))	+	Until recently, estimates of the resident microbial flora in the lungs were far too low. A 1998 infectious disease textbook stated that the lungs were sterile.((Noskin, Gary A. 1998. //Management of infectious complication in cancer patients.// Boston: Kluwer Academic Publishers.)) However, such conclusions were made on the basis of culture-based tests, which we now know identify a small minority of microbes. Since then, metagenomic analyses have indicated the presence of a persistent lung microbiome, the composition of which differs in health and disease. For example, Erb-Downward found bacterial 16S sequences in the lung tissues of all subjects in a 2011 based study of healthy patients as well as those with chronic obstructive pulmonary disease (COPD).(({{pmid>long:21364979}}))


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	People thought that asthma was caused by inhalation of allergens but this study shows that it may be more complicated than that – asthma may involve colonization of the airways by multiple bacteria.		People thought that asthma was caused by inhalation of allergens but this study shows that it may be more complicated than that – asthma may involve colonization of the airways by multiple bacteria.

-	//Homer Boushey, MD, [[http://www.sciencedaily.com/releases/2011/02/110217151457.htm\|UCSF professor of medicine]]//</blockquote>	+	//Homer Boushey, MD, [[https://www.sciencedaily.com/releases/2011/02/110217151457.htm\|UCSF professor of medicine]]//</blockquote>

-	[{{ :home:diseases:nihms254341f1.jpeg?400\|16S rRNA bacterial burden in bronchial brushings from asthmatic and healthy subjects. (Source: [[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3037020/\|Huang 2010]])}}]	+	[{{ :home:diseases:nihms254341f1.jpeg?400\|16S rRNA bacterial burden in bronchial brushings from asthmatic and healthy subjects. (Source: [[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3037020/\|Huang 2010]])}}]


-	In their three-year pilot project, Huang //et al.// collected samples from the airway linings of 65 adults with mild to moderate asthma and 10 healthy subjects.(({{pubmed>long:21194740}})) Then, using 16S rRNA – a tool that can identify approximately 8,500 distinct groups of bacteria in a single assay – the scientists profiled the organisms present in each sample to look for relationships between bacterial community composition and clinical characteristics of the patients' asthma.	+	In their three-year pilot project, Huang //et al.// collected samples from the airway linings of 65 adults with mild to moderate asthma and 10 healthy subjects.(({{pmid>long:21194740}})) Then, using 16S rRNA – a tool that can identify approximately 8,500 distinct groups of bacteria in a single assay – the scientists profiled the organisms present in each sample to look for relationships between bacterial community composition and clinical characteristics of the patients' asthma.


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	There is broad support for the conclusion that early infections, especially acute infections, predispose a person to later onset of chronic diseases such as asthma. Successive infection is the process by which an infectious cascade of pathogens slow the immune response and allow for subsequent infections (and the diseases which they cause) to proliferate. For example:		There is broad support for the conclusion that early infections, especially acute infections, predispose a person to later onset of chronic diseases such as asthma. Successive infection is the process by which an infectious cascade of pathogens slow the immune response and allow for subsequent infections (and the diseases which they cause) to proliferate. For example:
-	* rhinoviruses in infancy – Children who experience repeated rhinovirus-induced wheezing episodes in infancy have a significantly increased risk of developing asthma.(({{pubmed>long:22053589}}))	+	* rhinoviruses in infancy – Children who experience repeated rhinovirus-induced wheezing episodes in infancy have a significantly increased risk of developing asthma.(({{pmid>long:22053589}}))
-	* neonates and common infections – Neonates colonized in the hypopharyngeal region with //S. pneumoniae, H. influenzae,// or //M. catarrhalis,// or with a combination of these organisms, are at increased risk for recurrent wheeze and asthma early in life.(({{pubmed>long:17928596}}))	+	* neonates and common infections – Neonates colonized in the hypopharyngeal region with //S. pneumoniae, H. influenzae,// or //M. catarrhalis,// or with a combination of these organisms, are at increased risk for recurrent wheeze and asthma early in life.(({{pmid>long:17928596}}))


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-	Papadopoulos //et al.// have written that asthma should be treated as a suboptimal innate immune response.(({{pubmed>long:17188832}})) Consistent with that thinking, the Marshall Protocol is a treatment for asthma. Other treatments (some of which are contraindicated) include the following.	+	Papadopoulos //et al.// have written that asthma should be treated as a suboptimal innate immune response.(({{pmid>long:17188832}})) Consistent with that thinking, the Marshall Protocol is a treatment for asthma. Other treatments (some of which are contraindicated) include the following.

	==== Immunosuppressive medications ====		==== Immunosuppressive medications ====
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-	* corticosteroids – There are no studies which show that glucocoritcoids (corticosteroids) improve long-term prognosis in the treatment of illness. Van den Bosch and Grutters write(({{pubmed>long:16946094}})), "Remarkably, despite over 50 years of use, there is no proof of long-term (survival) benefit from corticosteroid treatment." For even short periods of time, steroid use can become genuinely addictive. Research shows that any kind of short-term symptomatic improvement from corticosteroid use does not last, and that over the longer term, use of the drugs entales a litany of side effects. For their own safety, patients on the MP must [[home:othertreatments:corticosteroids:weaningoffsteroids\|wean off]] of them as opposed to discontinuing them outright.	+	* corticosteroids – There are no studies which show that glucocoritcoids (corticosteroids) improve long-term prognosis in the treatment of illness. Van den Bosch and Grutters write(({{pmid>long:16946094}})), "Remarkably, despite over 50 years of use, there is no proof of long-term (survival) benefit from corticosteroid treatment." For even short periods of time, steroid use can become genuinely addictive. Research shows that any kind of short-term symptomatic improvement from corticosteroid use does not last, and that over the longer term, use of the drugs entales a litany of side effects. For their own safety, patients on the MP must [[home:othertreatments:corticosteroids:weaningoffsteroids\|wean off]] them as opposed to discontinuing them outright.
	* [[home:othertreatments:steroid_inhalers\|inhalers, steroid]] – Steroid inhalers suppress the innate immune response and delay progress on the MP. MP patients taking steroid inhalers should work with their physicians to switch drugs such as a [[home:othertreatments:bronchodilator_inhalers\|bronchiodilator inhaler]].		* [[home:othertreatments:steroid_inhalers\|inhalers, steroid]] – Steroid inhalers suppress the innate immune response and delay progress on the MP. MP patients taking steroid inhalers should work with their physicians to switch drugs such as a [[home:othertreatments:bronchodilator_inhalers\|bronchiodilator inhaler]].

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	==== Vitamin D ====		==== Vitamin D ====

-	Several studies have shown that patients with asthma have low levels of the vitamin D metabolite, 25-D.(({{pubmed>long:19179486}})) (({{pubmed>long:19365260}})) While some in the medical community have been quick to conclude this suggests a need for supplementation, supplemental vitamin D [[home:pathogenesis:vitamind#supplemental_vitamin_d_tends_to_be_immunosuppressive\|interferes with the immune response]] precisely when it needs to respond to microbes and may therefore contribute to asthma.	+	Several studies have shown that patients with asthma have low levels of the vitamin D metabolite, 25-D.(({{pmid>long:19179486}})) (({{pmid>long:19365260}})) While some in the medical community have been quick to conclude this suggests a need for supplementation, supplemental vitamin D [[home:pathogenesis:vitamind#supplemental_vitamin_d_tends_to_be_immunosuppressive\|interferes with the immune response]] precisely when it needs to respond to microbes and may therefore contribute to asthma.

-	Hansen //et al.// study with 965 pregnant women enrolled in 1988-1989 does not provide support for a protective effect of a high maternal 25(OH)D concentration on outcomes of allergic airway disease and lung function at 20 to 25 years of age. In contrast, a high maternal 25(OH)D concentration might be associated with an increased risk of allergic diseases in offspring. (({{pubmed>long:25649083}}))	+	Hansen //et al.// study with 965 pregnant women enrolled in 1988-1989 does not provide support for a protective effect of a high maternal 25(OH)D concentration on outcomes of allergic airway disease and lung function at 20 to 25 years of age. In contrast, a high maternal 25(OH)D concentration might be associated with an increased risk of allergic diseases in offspring. (({{pmid>long:25649083}}))

-	Hyppönen //et al.// performed a retrospective cohort study of 7,648 Finnish infants born in 1967. The prevalence of asthma at age 31 years was 35% higher in participants who had received vitamin D supplementation regularly during the first year compared to others.(({{pubmed>long:15699498}})) A stronger relationship between cod liver oil supplementation (which is high in vitamin D) and asthma was likewise identified in an Australian study.(({{pubmed>long:20880353}}))	+	Hyppönen //et al.// performed a retrospective cohort study of 7,648 Finnish infants born in 1967. The prevalence of asthma at age 31 years was 35% higher in participants who had received vitamin D supplementation regularly during the first year compared to others.(({{pmid>long:15699498}})) A stronger relationship between cod liver oil supplementation (which is high in vitamin D) and asthma was likewise identified in an Australian study.(({{pmid>long:20880353}}))


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	===== Epidemiology =====		===== Epidemiology =====

-	Asthma is one of the most common diseases in the world, with approximately 300 million asthmatics globally, including 24 million in the United States, according to the Centers for Disease Control. The disease has been on the rise for the last 60 years. "It has gone from 3 percent of the population to slightly more than 8 percent of the population in the U.S.," according to [[http://www.sciencedaily.com/releases/2011/02/110217151457.htm\|Homer Boushey]].	+	Asthma is one of the most common diseases in the world, with approximately 300 million asthmatics globally, including 24 million in the United States, according to the Centers for Disease Control. The disease has been on the rise for the last 60 years. "It has gone from 3 percent of the population to slightly more than 8 percent of the population in the U.S.," according to [[https://www.sciencedaily.com/releases/2011/02/110217151457.htm\|Homer Boushey]].


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		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====



-	===== References =====	+	===== References =====</nodisp>

Autism spectrum disorder

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

Bipolar Disorder (manic-depression)

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

04.09.2020		current
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	=====Poster from Ljubljana International Congress on Autoimmunity=====		=====Poster from Ljubljana International Congress on Autoimmunity=====

-	[[http://autoimmunityResearch.org/abstracts/Ljubljana_Bipolar_Poster.pdf\|This poster presentation]] relates some experiences of MP community members who suffered from Bipolar disorder.	+	[[https://autoimmunityResearch.org/abstracts/Ljubljana_Bipolar_Poster.pdf\|This poster presentation]] relates some experiences of MP community members who suffered from Bipolar disorder.


	=====Presentation on MP in Psychiatric Disorders=====		=====Presentation on MP in Psychiatric Disorders=====

-	Prof. Trevor Marshall conducted a seminar at the Institute of Psychiatry, Kings College London, on 13 May 2010. There is a video record of that seminar: "Observations of Olmesartan in Psychiatric Disease," available from this [[http://www.youtube.com/watch?v=uha9lyVoEf0\|YouTube link]]	+	Prof. Trevor Marshall conducted a seminar at the Institute of Psychiatry, Kings College London, on 13 May 2010. There is a video record of that seminar: "Observations of Olmesartan in Psychiatric Disease," available from this [[https://www.youtube.com/watch?v=uha9lyVoEf0\|YouTube link]]

	=====Lithium=====		=====Lithium=====

-	[[http://www.medicinenet.com/lithium/article.htm\|Lithium]] is commonly used to treat bipolar disorder. If you have been taking it, you may need to to continue. It will make recovery more difficult.	+	[[https://www.medicinenet.com/lithium/article.htm\|Lithium]] is commonly used to treat bipolar disorder. If you have been taking it, you may need to to continue. It will make recovery more difficult.

	Due to slow renal clearing, lithium toxicity may occur when taking Benicar (or verapamil). Lithium blood levels should be monitored very closely by your Dr (perhaps weekly when Benicar is started) and then regularly as long as you are on the MP. We recommend Members not change their Lithium dose without the consent and supervision of their doctor.		Due to slow renal clearing, lithium toxicity may occur when taking Benicar (or verapamil). Lithium blood levels should be monitored very closely by your Dr (perhaps weekly when Benicar is started) and then regularly as long as you are on the MP. We recommend Members not change their Lithium dose without the consent and supervision of their doctor.
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	===== Evidence of infectious cause =====		===== Evidence of infectious cause =====

-	2018 electron microscope study [[http://nautil.us/issue/66/clockwork/are-there-bacteria-in-your-brain\|bacteria-in-your-brain]]	+	2018 electron microscope study [[https://nautil.us/issue/66/clockwork/are-there-bacteria-in-your-brain\|bacteria-in-your-brain]]


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	===== Recent research =====		===== Recent research =====

-	It is possible that increased UA levels are a trait marker of higher vulnerability to bipolar disorder, and are even more increased during mania (mostly in the first manic episode of drug-naïve patients). (({{pubmed>long:25462413}}))	+	It is possible that increased UA levels are a trait marker of higher vulnerability to bipolar disorder, and are even more increased during mania (mostly in the first manic episode of drug-naïve patients). (({{pmid>long:25462413}}))

-	magnetic resonance imaging confirms that hyperuricemia in rats and humans are associated with gliosis* in the hippocampus (({{pubmed>long:27798180}}))	+	magnetic resonance imaging confirms that hyperuricemia in rats and humans are associated with gliosis* in the hippocampus (({{pmid>long:27798180}}))


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	Uric acid may play an important role in mental health by modulating the emotional response to stress.		Uric acid may play an important role in mental health by modulating the emotional response to stress.

-	The current study provides novel evidence that brain function varies with baseline uric acid level. Specifically, these results demonstrate that uric acid is associated with a greater hippocampal response to psychosocial stress. (({{pubmed>long:27725214}}))	+	The current study provides novel evidence that brain function varies with baseline uric acid level. Specifically, these results demonstrate that uric acid is associated with a greater hippocampal response to psychosocial stress. (({{pmid>long:27725214}}))

-	==== astroglia ====	+	==== Astroglia ====

	Astrocytes perform many functions, including biochemical support of endothelial cells that form the blood–brain barrier, provision of nutrients to the nervous tissue, maintenance of extracellular ion balance, and a role in the repair and scarring process of the brain and spinal cord following traumatic injuries.		Astrocytes perform many functions, including biochemical support of endothelial cells that form the blood–brain barrier, provision of nutrients to the nervous tissue, maintenance of extracellular ion balance, and a role in the repair and scarring process of the brain and spinal cord following traumatic injuries.
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		+	{{tag>diseases neurological}}

		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

-	(({{pubmed>long:000}}))	+	(({{pmid>long:000}}))

	--- //Sallie Q 08.25.2017// removed		--- //Sallie Q 08.25.2017// removed

-	[[http://www.marshallprotocol.com/forum32/7350.html\|My potassium is elevated. What should I do?]]	+	[[https://www.marshallprotocol.com/forum32/7350.html\|My potassium is elevated. What should I do?]]
	Here is an interesting paper by a Harvard/Mass General Hospital group implicating lithium, Calcium, Chromium and Mercuric salts as a pleomorphic factor for some of these L-form organisms:		Here is an interesting paper by a Harvard/Mass General Hospital group implicating lithium, Calcium, Chromium and Mercuric salts as a pleomorphic factor for some of these L-form organisms:

-	[[http://www.pubmedcentral.gov/picrender.fcgi?artid=373960&blobtype=pdf\|"The Significance of Pleomorphism in Bacteroides Strains"]]	+	[[https://www.pubmedcentral.gov/picrender.fcgi?artid=373960&blobtype=pdf\|"The Significance of Pleomorphism in Bacteroides Strains"]]


Line 198:		Line 199:

	* Legacy content		* Legacy content
-	* http://www.marshallprotocol.com/view_topic.php?id=4243&forum_id=37&jump_to=74205#p74205 s67	+	* https://www.marshallprotocol.com/view_topic.php?id=4243&forum_id=37&jump_to=74205#p74205 s67
-	* http://www.marshallprotocol.com/view_topic.php?id=4243&forum_id=37&jump_to=144057#p144057 s71	+	* https://www.marshallprotocol.com/view_topic.php?id=4243&forum_id=37&jump_to=144057#p144057 s71


Line 213:		Line 214:
	It is worth to be read as it explains the disease, the immune system etc etc in a rather clear language.		It is worth to be read as it explains the disease, the immune system etc etc in a rather clear language.

-	http://publishing.eur.nl/ir/repub/asset/14920/090225_Padmos,%20Roos%20Carlijn.pdf	+	https://publishing.eur.nl/ir/repub/asset/14920/090225_Padmos,%20Roos%20Carlijn.pdf

	Titta		Titta
Line 219:		Line 220:
	As it is published in the internet I think I am allowed to inform you where to find it.</blockquote>		As it is published in the internet I think I am allowed to inform you where to find it.</blockquote>

-	===== References =====	+	===== References =====</nodisp>

Cancer

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 05:14:49 +0000

Cardiovascular diseases

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

Cat scratch fever

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

02.18.2019		current
Line 10:		Line 10:


-	Lymphatic Circulation Disseminates Bartonella Infection Into Bloodstream (({{pubmed>long:27803173}}))	+	Lymphatic Circulation Disseminates Bartonella Infection Into Bloodstream (({{pmid>long:27803173}}))

	<blockquote>The hallmark of Bartonella infection is long-lasting intraerythrocytic parasitism.		<blockquote>The hallmark of Bartonella infection is long-lasting intraerythrocytic parasitism.
Line 16:		Line 16:
	Bartonella was poorly phagocytized by peritoneal macrophages in vitro. Intracellular Bartonella survived and replicated in macrophages at an early stage of infection. Intracellular Bartonella inhibited spontaneous cell death of macrophages. They also inhibited Salmonella-induced pyroptosis and mildly reduced inflammasome activation through an unidentified mechanism. </blockquote>		Bartonella was poorly phagocytized by peritoneal macrophages in vitro. Intracellular Bartonella survived and replicated in macrophages at an early stage of infection. Intracellular Bartonella inhibited spontaneous cell death of macrophages. They also inhibited Salmonella-induced pyroptosis and mildly reduced inflammasome activation through an unidentified mechanism. </blockquote>

-	Prevalence of Bartonella spp. by culture, PCR and serology, in veterinary personnel from Spain. (({{pubmed>long:29116007}}))	+	Prevalence of Bartonella spp. by culture, PCR and serology, in veterinary personnel from Spain. (({{pmid>long:29116007}}))

	<blockquote>The genus Bartonella includes fastidious, facultative intracellular bacteria mainly transmitted by arthropods and distributed among mammalian reservoirs. Bartonella spp. implicated as etiological agents of zoonoses are increasing. Apart from the classical Bartonella henselae, B. bacilliformis or B. quintana, other species (B. elizabethae, B. rochalimae, B. vinsonii arupensis and B. v. berkhoffii, B. tamiae or B. koehlerae, among others) have also been associated with human and/or animal diseases.</blockquote>		<blockquote>The genus Bartonella includes fastidious, facultative intracellular bacteria mainly transmitted by arthropods and distributed among mammalian reservoirs. Bartonella spp. implicated as etiological agents of zoonoses are increasing. Apart from the classical Bartonella henselae, B. bacilliformis or B. quintana, other species (B. elizabethae, B. rochalimae, B. vinsonii arupensis and B. v. berkhoffii, B. tamiae or B. koehlerae, among others) have also been associated with human and/or animal diseases.</blockquote>

-	Molecular survey of Bartonella henselae and Bartonella clarridgeiae in pet cats across Japan by species-specific nested-PCR. (({{pubmed>long:28780918}}))	+	Molecular survey of Bartonella henselae and Bartonella clarridgeiae in pet cats across Japan by species-specific nested-PCR. (({{pmid>long:28780918}}))

	<blockquote>Cats are known to be the main reservoir for Bartonella henselae and Bartonella clarridgeiae, which are the agents of 'cat-scratch disease' in humans.		<blockquote>Cats are known to be the main reservoir for Bartonella henselae and Bartonella clarridgeiae, which are the agents of 'cat-scratch disease' in humans.
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	sarcoidosis, cat scratch fever, restless leg syndrome		sarcoidosis, cat scratch fever, restless leg syndrome

-	Read the [[http://bacteriality.com/2007/11/19/interview13/\|interview]]	+	Read the [[https://bacteriality.com/2007/11/19/interview13/\|interview]]

	<html></div></div>		<html></div></div>
Line 59:		Line 59:

	Interviews of patients with other diseases are [[home:patients:patient_interviews\|also available]].		Interviews of patients with other diseases are [[home:patients:patient_interviews\|also available]].
-
-
-
-
-
-
-


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-	<note>Dear MPKB Reader: You have arrived at one of the articles that has not yet completed the development and review process in the knowledge base. Some of the content here may be helpful, but please know that this page is not complete. There are about 400 articles in the KB, and this is one we are still working on. Thanks for your patience.</note>




		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

Line 92:		Line 85:
	*		*

-	===== References =====	+	===== References =====</nodisp>

Celiac disease

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

07.20.2019		current
Line 8:		Line 8:


-	People with celiac disease react to gluten, which is found in wheat, rye, spelt and barley. Villus atrophy in the small intestine is one of the most significant findings in celiac disease, rendering the patient with a poor absorptive capacity. The vast majority of celiac patients produce antibodies to tissue transglutaminase and have either the gene variant HLA-DQ-2 or HLA-DQ-8. However, these gene variants are much more common than the occurence of celiac disease. Thus, there must be additional factors that can explain why celiac disease develops. (({{pubmed>long:18667914}}))	+	People with celiac disease react to gluten, which is found in wheat, rye, spelt and barley. Villus atrophy in the small intestine is one of the most significant findings in celiac disease, rendering the patient with a poor absorptive capacity. The vast majority of celiac patients produce antibodies to tissue transglutaminase and have either the gene variant HLA-DQ-2 or HLA-DQ-8. However, these gene variants are much more common than the occurence of celiac disease. Thus, there must be additional factors that can explain why celiac disease develops. (({{pmid>long:18667914}}))
	===== Epidemiology =====		===== Epidemiology =====

Line 29:		Line 29:


-	CONCLUSIONS: The mode of delivery and associated alterations in the development of the enteric homeostasis during the neonatal period might influence the incidence of celiac disease. (({{pubmed>long:20478942}}))	+	CONCLUSIONS: The mode of delivery and associated alterations in the development of the enteric homeostasis during the neonatal period might influence the incidence of celiac disease. (({{pmid>long:20478942}}))
	</blockquote>		</blockquote>

-	The emerging data on viral and bacterial microbe-host interactions and their alterations in celiac disease provides a plausible mechanism linking environmental risk and disease development. (({{pubmed>long:30519552}}))	+	The emerging data on viral and bacterial microbe-host interactions and their alterations in celiac disease provides a plausible mechanism linking environmental risk and disease development. (({{pmid>long:30519552}}))


	===== Celiac and D metabolite levels =====		===== Celiac and D metabolite levels =====

-	Some patients with celiac disease have low/normal 25D but elevated 1,25D apparently related to celiac. (({{pubmed>long:8186825}}))	+	Some patients with celiac disease have low/normal 25D but elevated 1,25D apparently related to celiac. (({{pmid>long:8186825}}))

-	Our patient had hypocalcemia caused by celiac disease and values for serum 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D that were normal and elevated, respectively. Correction was demonstrated after dietary gluten withdrawal. (({{pubmed>long:15310538}}))	+	Our patient had hypocalcemia caused by celiac disease and values for serum 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D that were normal and elevated, respectively. Correction was demonstrated after dietary gluten withdrawal. (({{pmid>long:15310538}}))

-	Calcium and vitamin D supplement intake may increase arterial stiffness in systemic lupus erythematosus patients. (({{pubmed>long:30628012}}))	+	Calcium and vitamin D supplement intake may increase arterial stiffness in systemic lupus erythematosus patients. (({{pmid>long:30628012}}))

-	(({{pubmed>long:000}}))	+	(({{pmid>long:000}}))

	===== Evidence of infectious cause =====		===== Evidence of infectious cause =====

-	<blockquote>"The finding of rod-shaped bacteria attached to the small intestinal epithelium of some untreated and treated celiac-disease patients, but not to the epithelium of healthy controls, ignites the notion that bacteria may be involved in the pathogenesis of celiac disease." Am J Gastroenterol. 2004 May;99(5):905-6. A role for bacteria in celiac disease? Sollid LM, Gray GM (({{pubmed>long:15128358}}))	+	<blockquote>"The finding of rod-shaped bacteria attached to the small intestinal epithelium of some untreated and treated celiac-disease patients, but not to the epithelium of healthy controls, ignites the notion that bacteria may be involved in the pathogenesis of celiac disease." Am J Gastroenterol. 2004 May;99(5):905-6. A role for bacteria in celiac disease? Sollid LM, Gray GM (({{pmid>long:15128358}}))
	</blockquote>		</blockquote>

	<blockquote>"As presence of Campylobacter jejuni in other diseases with antigangliosides antibody formation has been established, we propose the possible role of Campylobacter jejuni in development of CD in association with other genetic and environmental factors by the mechanism that molecular mimicry of gangliosides-like epitopes common to both lipo-polysacharide coats of certain strains of Campylobacter jejuni and gangliosides in cell structure of gastrointestinal mucosa may cause an autoimmune response and consequently lead to atrophy and degeneration of mucosa possibly by apoptosis." World J Gastroenterol. 2007 Sep 21;13(35):4784-5. Can Campylobacter jejuni play a role in development of celiac disease?		<blockquote>"As presence of Campylobacter jejuni in other diseases with antigangliosides antibody formation has been established, we propose the possible role of Campylobacter jejuni in development of CD in association with other genetic and environmental factors by the mechanism that molecular mimicry of gangliosides-like epitopes common to both lipo-polysacharide coats of certain strains of Campylobacter jejuni and gangliosides in cell structure of gastrointestinal mucosa may cause an autoimmune response and consequently lead to atrophy and degeneration of mucosa possibly by apoptosis." World J Gastroenterol. 2007 Sep 21;13(35):4784-5. Can Campylobacter jejuni play a role in development of celiac disease?
-	Sabayan B, Foroughinia F, Imanieh MH (({{pubmed>long:17729402}})) </blockquote>	+	Sabayan B, Foroughinia F, Imanieh MH (({{pmid>long:17729402}})) </blockquote>

-	Specific duodenal and faecal bacterial groups are associated with paediatric celiac disease.(({{pubmed>long:18996905}}))	+	Specific duodenal and faecal bacterial groups are associated with paediatric celiac disease.(({{pmid>long:18996905}}))

-	Lymphocytic gastritis and celiac disease in indian children: evidence of a positive relation.(({{pubmed>long:18979579}}))	+	Lymphocytic gastritis and celiac disease in indian children: evidence of a positive relation.(({{pmid>long:18979579}}))

-	Autoantibodies involved in celiac disease are not specific, as infection may increase levels of anti-transglutaminase antibodies. These antibodies are not detectable once the infection is gone.(({{pubmed>long:19912255}}))	+	Autoantibodies involved in celiac disease are not specific, as infection may increase levels of anti-transglutaminase antibodies. These antibodies are not detectable once the infection is gone.(({{pmid>long:19912255}}))

	==== recent research ====		==== recent research ====
Line 63:		Line 63:
	Could a common virus trigger coeliac disease in some children? //Tye-Din JA et al//, Norway February 2019		Could a common virus trigger coeliac disease in some children? //Tye-Din JA et al//, Norway February 2019

-	[[http://science.sciencemag.org/content/356/6333/44\| study in humans supports a role for infection with reovirus, a seemingly innocuous virus, in triggering the development of CeD]]	+	[[https://science.sciencemag.org/content/356/6333/44\| study in humans supports a role for infection with reovirus, a seemingly innocuous virus, in triggering the development of CeD]]
-	(({{pubmed>long:28386004}})) (({{pubmed>long:26060107}}))	+	(({{pmid>long:28386004}})) (({{pmid>long:26060107}}))

-	Findings suggest that neither olmesartan nor other ARBs were associated with diarrhea among patients undergoing endoscopy. The spruelike enteropathy recently associated with olmesartan is likely a rare adverse effect and milder presentations are unlikely. (({{pubmed>long:25023670}}))	+	Findings suggest that neither olmesartan nor other ARBs were associated with diarrhea among patients undergoing endoscopy. The spruelike enteropathy recently associated with olmesartan is likely a rare adverse effect and milder presentations are unlikely. (({{pmid>long:25023670}}))

	In 2015 I saw that 6 individuals in the USA were suing maker of Benicar. (//presumably for bowel immunopathology caused by cytokines//). //Somewhere else I found that 1.9 million individuals are currently taking Olmesartan Medoxomil.// //6 in 1.9 million ? Seems pretty rare to me.// (//Editor//)		In 2015 I saw that 6 individuals in the USA were suing maker of Benicar. (//presumably for bowel immunopathology caused by cytokines//). //Somewhere else I found that 1.9 million individuals are currently taking Olmesartan Medoxomil.// //6 in 1.9 million ? Seems pretty rare to me.// (//Editor//)

-	Gluten in "gluten-free" manufactured foods in Australia: a cross-sectional study. (({{pubmed>long:30404591}})) PMID 30404591	+	Gluten in "gluten-free" manufactured foods in Australia: a cross-sectional study. (({{pmid>long:30404591}})) PMID 30404591


	2018 data show that OLM is an Nrf2 activator, NFkB inhibitor and apoptosis inhibitor in an experimental model of ulcerative colitis. Overall, the study indicates that OLM shows promise as a potential therapy for the treatment of human inflammatory bowel diseases.		2018 data show that OLM is an Nrf2 activator, NFkB inhibitor and apoptosis inhibitor in an experimental model of ulcerative colitis. Overall, the study indicates that OLM shows promise as a potential therapy for the treatment of human inflammatory bowel diseases.
-	(({{pubmed>long:30594690}}))	+	(({{pmid>long:30594690}}))
		+
		+	Research associated with J Tye-Din (({{pmid>long: 20650871}})) , (({{pmid>long:17629515}})) , (({{pmid>long:888}})) , (({{pmid>long: 19942485}})) , (({{pmid>long:23981538}})) , (({{pmid>long:16099789}})) , (({{pmid>long:888}}))
		+

	{{tag>diseases }}		{{tag>diseases }}
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		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

Line 123:		Line 128:
	Romain Bouziat1,2,, Reinhard Hinterleitner1,2,, Judy J. Brown3,4,*, Jennifer E. Stencel-Baerenwald3,4, Mine Ikizler4,5,		Romain Bouziat1,2,, Reinhard Hinterleitner1,2,, Judy J. Brown3,4,*, Jennifer E. Stencel-Baerenwald3,4, Mine Ikizler4,5,
	as link will likely break (news media)		as link will likely break (news media)
-	===== References =====	+	===== References =====</nodisp>

Chronic fatigue syndrome (myalgic encephalomyelitis)

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

Co-infections

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

01.03.2012		current
Line 24:		Line 24:
	//Candida albicans// is a fungus (a form of yeast) that plays a role in opportunistic oral and genital infections in humans. //C. albicans// biofilms readily form on the surface of implantable medical devices. Systemic fungal infections (fungemias) have emerged as important causes of morbidity and mortality in patients traditionally labelled as immunocompromised, e.g., AIDS, cancer chemotherapy, organ or bone marrow transplantation. (According to the Marshall Pathogenesis, patients suffering from chronic inflammatory diseases are likewise immunocompromised.)		//Candida albicans// is a fungus (a form of yeast) that plays a role in opportunistic oral and genital infections in humans. //C. albicans// biofilms readily form on the surface of implantable medical devices. Systemic fungal infections (fungemias) have emerged as important causes of morbidity and mortality in patients traditionally labelled as immunocompromised, e.g., AIDS, cancer chemotherapy, organ or bone marrow transplantation. (According to the Marshall Pathogenesis, patients suffering from chronic inflammatory diseases are likewise immunocompromised.)

-	As the section devoted to antimicrobial peptides (AmPs) explains, the AmP cathelicidin is a component of the innate immune system, and is responsive to fungi.(({{pubmed>long:19817855}}))	+	Extrapolating to humans, these findings suggest that coconut oil could become the first dietary intervention to reduce C. albicans GI colonization. [[https://msphere.asm.org/content/1/1/e00020-15\|Dietary coconut oil also altered the metabolic program of colonizing C. albicans cells.]]
		+
		+
		+
		+	As the section devoted to antimicrobial peptides (AmPs) explains, the AmP cathelicidin is a component of the innate immune system, and is responsive to fungi.(({{pmid>long:19817855}}))

	Antifungal agents such as fluconazole (Diflucan) are sometimes prescribed to treat fungal infections. While some patients have reported feeling better after taking antifungal agents, antifungals interfere with immune function.		Antifungal agents such as fluconazole (Diflucan) are sometimes prescribed to treat fungal infections. While some patients have reported feeling better after taking antifungal agents, antifungals interfere with immune function.
Line 33:		Line 37:
	Patient symptom scores were a poor predictor of yeast infections based on yeast culture results. ... Self-reported symptoms are not reliable for diagnosis.		Patient symptom scores were a poor predictor of yeast infections based on yeast culture results. ... Self-reported symptoms are not reliable for diagnosis.

-	//Susan Hoffstetter et al.// (({{pubmed>long:18664056}})) </blockquote>	+	//Susan Hoffstetter et al.// (({{pmid>long:18664056}})) </blockquote>


Line 42:		Line 46:
	In parasitology, a coinfection is defined as the simultaneous infection of a host by multiple pathogens with one pathogen being the primary disease-causing agent. The term is something of a legacy of Koch's postulates in which infectious diseases are only caused by a single species of microbe.		In parasitology, a coinfection is defined as the simultaneous infection of a host by multiple pathogens with one pathogen being the primary disease-causing agent. The term is something of a legacy of Koch's postulates in which infectious diseases are only caused by a single species of microbe.

-	According to the Marshall Pathogenesis, however, pointing to a single microbe as being the cause of disease and the rest as largely ancillary does not adequately represent the complexity of successive infection and the role that many microbes, combined, may have in causing disease. Even Epstein-Barr virus, which is the minds of many a classical co-infection, has been show to act directly on the body's nuclear receptors including the VDR.(({{pubmed>long:19550398}})) A 2011 paper further showed that EBV not only down-regulates expression of the VDR protein itself, but also acts to block transcription by the VDR.(({{pubmed>long:20593215}}))	+	According to the Marshall Pathogenesis, however, pointing to a single microbe as being the cause of disease and the rest as largely ancillary does not adequately represent the complexity of successive infection and the role that many microbes, combined, may have in causing disease. Even Epstein-Barr virus, which is the minds of many a classical co-infection, has been show to act directly on the body's nuclear receptors including the VDR.(({{pmid>long:19550398}})) A 2011 paper further showed that EBV not only down-regulates expression of the VDR protein itself, but also acts to block transcription by the VDR.(({{pmid>long:20593215}}))


Line 65:		Line 69:


-	Some evidence has emerged that using a therapy to target a given infection aids the body in its ability to eliminate otherwise unrelated pathogens. For example, a 2011 //Science// study gave two groups of mice an injection of poliovirus, a gut virus. One group was treated with antibiotics, thus depleting their intestinal microbiome. This group was less susceptible to poliovirus disease and supported minimal viral replication in the intestine. Further, the pathogenesis of reovirus, an unrelated gut virus, was also more severe in the presence of intestinal microbes.(({{pubmed>long:2199839}}))	+	Some evidence has emerged that using a therapy to target a given infection aids the body in its ability to eliminate otherwise unrelated pathogens. For example, a 2011 //Science// study gave two groups of mice an injection of poliovirus, a gut virus. One group was treated with antibiotics, thus depleting their intestinal microbiome. This group was less susceptible to poliovirus disease and supported minimal viral replication in the intestine. Further, the pathogenesis of reovirus, an unrelated gut virus, was also more severe in the presence of intestinal microbes.(({{pmid>long:2199839}}))


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	{{tag>diseases}}		{{tag>diseases}}

		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

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-	===== References =====	+	===== References =====</nodisp>

Cystic fibrosis

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

02.18.2019		current
Line 4:		Line 4:
	====== Cystic fibrosis ======		====== Cystic fibrosis ======

-	[[http://www.mayoclinic.org/diseases-conditions/cystic-fibrosis/home/ovc-20211890}\|Mayo Clinic overview]]	+	[[https://www.mayoclinic.org/diseases-conditions/cystic-fibrosis/home/ovc-20211890}\|Mayo Clinic overview]]


-	[[http://www.nhlbi.nih.gov/health/health-topics/topics/cf\|NIH]]	+	[[https://www.nhlbi.nih.gov/health/health-topics/topics/cf\|NIH]]


Line 13:		Line 13:
	===== Evidence of infectious cause =====		===== Evidence of infectious cause =====

-	Pseudomonal infection in cystic fibrosis: the battle continues.(({{pubmed>long:15482158}}))	+	Pseudomonal infection in cystic fibrosis: the battle continues.(({{pmid>long:15482158}}))
	<blockquote>		<blockquote>
	Pseudomonas aeruginosa lung infection is the major cause of morbidity and mortality in patients with cystic fibrosis. Infection usually begins in childhood and is responsible for respiratory failure and death in most patients with cystic fibrosis. The organism triggers an exuberant chronic inflammatory reaction which damages the airways and leads to progressive loss of lung function.		Pseudomonas aeruginosa lung infection is the major cause of morbidity and mortality in patients with cystic fibrosis. Infection usually begins in childhood and is responsible for respiratory failure and death in most patients with cystic fibrosis. The organism triggers an exuberant chronic inflammatory reaction which damages the airways and leads to progressive loss of lung function.
Line 20:		Line 20:


-	Evolution of airway microbiology in the infant with cystic fibrosis: role of nonpseudomonal and pseudomonal pathogens.(({{pubmed>long:1475540}}))	+	Evolution of airway microbiology in the infant with cystic fibrosis: role of nonpseudomonal and pseudomonal pathogens.(({{pmid>long:1475540}}))
	<blockquote>Bacterial colonization of the airways of the infant with cystic fibrosis is usually established early in life, and, once established, is difficult to eradicate and is associated with progressive lung disease.		<blockquote>Bacterial colonization of the airways of the infant with cystic fibrosis is usually established early in life, and, once established, is difficult to eradicate and is associated with progressive lung disease.

Line 26:		Line 26:
	</blockquote>		</blockquote>

-	ChIP-seq reveals the global regulator AlgR mediating cyclic di-GMP synthesis in Pseudomonas aeruginosa (({{pubmed>long: 26206672}}))	+	ChIP-seq reveals the global regulator AlgR mediating cyclic di-GMP synthesis in Pseudomonas aeruginosa (({{pmid>long: 26206672}}))
	<blockquote>AlgR is a key transcriptional regulator required for the expression of multiple virulence factors, including type IV pili and alginate in Pseudomonas aeruginosa.		<blockquote>AlgR is a key transcriptional regulator required for the expression of multiple virulence factors, including type IV pili and alginate in Pseudomonas aeruginosa.

	A ΔalgR strain produced lesser biofilm than did the wild-type strain, which is consistent with a phenotype controlled by c-di-GMP.		A ΔalgR strain produced lesser biofilm than did the wild-type strain, which is consistent with a phenotype controlled by c-di-GMP.
		+	</blockquote>
		+
		+	Quorum sensing and virulence of Pseudomonas aeruginosa during lung infection of cystic fibrosis patients. (({{pmid>long: 20404933}}))
		+	<blockquote>The concomitant development of QS malfunction significantly correlated with the reduced production of rhamnolipids and elastase and with the occurrence of mutations in the regulatory genes lasR and rhlR.
	</blockquote>		</blockquote>

Line 38:		Line 42:


		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

Line 49:		Line 54:


-	===== References =====	+	===== References =====</nodisp>

Depression

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

04.09.2020		current
Line 5:		Line 5:
	Looking out for friends and loved ones is an important part of preventing suicide. You can call to speak with a crisis worker on behalf of someone you are concerned about. The crisis workers have access to local resources, and can help you identify ways to get help to your loved ones.		Looking out for friends and loved ones is an important part of preventing suicide. You can call to speak with a crisis worker on behalf of someone you are concerned about. The crisis workers have access to local resources, and can help you identify ways to get help to your loved ones.

-	To find out more about the difference you can make in a friend or loved one's life, visit [[http://www.suicidepreventionlifeline.org/GetHelp/WhatIfSomeoneIKnowNeedsHelp.aspx\|What If Someone I Know Needs Help]].</note>	+	To find out more about the difference you can make in a friend or loved one's life, visit [[https://www.suicidepreventionlifeline.org/GetHelp/WhatIfSomeoneIKnowNeedsHelp.aspx\|What If Someone I Know Needs Help]].</note>

	====== Depression ======		====== Depression ======
Line 13:		Line 13:


-	Why are depressed patients inflamed? (({{pubmed>long:28479211}}))	+	Why are depressed patients inflamed? (({{pmid>long:28479211}}))

	<blockquote>It is my opinion that early and prominent symptoms of Th1 disease are psychological which have been interpreted as anxiety, depression, insomnia, learning disabilities etc. These symptoms like physical ones are exacerbated during effective treatment of Th1 [diseases].		<blockquote>It is my opinion that early and prominent symptoms of Th1 disease are psychological which have been interpreted as anxiety, depression, insomnia, learning disabilities etc. These symptoms like physical ones are exacerbated during effective treatment of Th1 [diseases].
Line 21:		Line 21:
	//Greg Blaney, MD// </blockquote>		//Greg Blaney, MD// </blockquote>

-	[[http://np-privatepracticeassoc.com/2016/04/depression-and-insomnia/\|Depression and Insomnia study (Trudi Heil) with Recovery Charts on Olmesartan]]	+	[[https://np-privatepracticeassoc.com/2016/04/depression-and-insomnia/\|Depression and Insomnia study (Trudi Heil) with Recovery Charts on Olmesartan]]

	Some research indicates that parasites can affect levels of neurotransmitters, and hence behaviour. The implication is that this could apply to humans too.((Journal reference: Proceedings of the Royal Society B (DOI: 10.1098/rspb.2008.1597) ))		Some research indicates that parasites can affect levels of neurotransmitters, and hence behaviour. The implication is that this could apply to humans too.((Journal reference: Proceedings of the Royal Society B (DOI: 10.1098/rspb.2008.1597) ))
Line 27:		Line 27:
	<blockquote>Understanding how parasites and pathogens alter brain function and behaviour may also help us understand the suspected links between some infectious diseases and mental illness in humans.		<blockquote>Understanding how parasites and pathogens alter brain function and behaviour may also help us understand the suspected links between some infectious diseases and mental illness in humans.

-	//Shelly Adamo, [[http://www.newscientist.com/article/dn16283-prozac-may-counter-parasite-mind-control.html?DCMP=OTC-rss&nsref=online-news\|New Scientist]]// </blockquote>	+	//Shelly Adamo, [[https://www.newscientist.com/article/dn16283-prozac-may-counter-parasite-mind-control.html?DCMP=OTC-rss&nsref=online-news\|New Scientist]]// </blockquote>

	[[https://onlinelibrary.wiley.com/doi/full/10.1111/nmo.12198\|Impact of microbiota on brain function]]		[[https://onlinelibrary.wiley.com/doi/full/10.1111/nmo.12198\|Impact of microbiota on brain function]]

-	2019 There is strong epidemiological evidence that poor diet is associated with depression. The reverse has also been shown, namely that eating a healthy diet rich in fruit, vegetables, fish and lean meat, is associated with reduced [[https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0222768#pone.0222768.ref012\|risk of depression]].(({{pubmed>long:88888888}}))	+	2019 There is strong epidemiological evidence that poor diet is associated with depression. The reverse has also been shown, namely that eating a healthy diet rich in fruit, vegetables, fish and lean meat, is associated with reduced [[https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0222768#pone.0222768.ref012\|risk of depression]].(({{pmid>long:88888888}}))
	===== Virtues of depression =====		===== Virtues of depression =====

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	[[https://onlinelibrary.wiley.com/doi/full/10.1111/nmo.12198\|Melancholic microbes]]		[[https://onlinelibrary.wiley.com/doi/full/10.1111/nmo.12198\|Melancholic microbes]]

-	[[https://www.ncbi.nlm.nih.gov/pubmed/28736331\|The gut microbiota plays an important role in modulating small RNAs that influence hippocampal gene expression, a process critical to hippocampal development.]](({{pubmed>long:28736331}}))	+	[[https://www.ncbi.nlm.nih.gov/pubmed/28736331\|The gut microbiota plays an important role in modulating small RNAs that influence hippocampal gene expression, a process critical to hippocampal development.]](({{pmid>long:28736331}}))

	[[https://www.sciencedirect.com/topics/immunology-and-microbiology/psychoneuroimmunology\|Psychoneuroimmunology is starting to think that the immune system can also affect our psychology]]		[[https://www.sciencedirect.com/topics/immunology-and-microbiology/psychoneuroimmunology\|Psychoneuroimmunology is starting to think that the immune system can also affect our psychology]]


-	In the research field of psychoneuroimmunology, accumulating evidence has indicated the existence of reciprocal communication pathways between nervous, endocrine and immune systems. In this respect, there has been increasing interest in the putative involvement of the immune system in psychiatric disorders. Cytokines and major depression (({{pubmed>long:15694227}}))	+	In the research field of psychoneuroimmunology, accumulating evidence has indicated the existence of reciprocal communication pathways between nervous, endocrine and immune systems. In this respect, there has been increasing interest in the putative involvement of the immune system in psychiatric disorders. Cytokines and major depression (({{pmid>long:15694227}}))

	==== Immune suppression ====		==== Immune suppression ====
		+
		+	Two U.S. government reports from the 1970s to 1980s provide evidence for many neuropsychiatric effects of non-thermal microwave EMFs, based on occupational exposure studies.[[https://www.ncbi.nlm.nih.gov/pubmed/26300312\|(EMFs) produce widespread neuropsychiatric effects including depression.]]
		+
		+	In summary, then, the mechanism of action of microwave EMFs, the role of the VGCCs in the brain, the impact of non-thermal EMFs on the brain, extensive epidemiological studies performed over the past 50 years, and five criteria testing for causality, all collectively show that various non-thermal microwave EMF exposures produce diverse neuropsychiatric effects.
		+

	===== Immune signaling =====		===== Immune signaling =====


-	A novel form of immune signaling revealed by transmission of the inflammatory mediator serotonin between dendritic cells and T cells (({{pubmed>long:16223770}}))	+	A novel form of immune signaling revealed by transmission of the inflammatory mediator serotonin between dendritic cells and T cells (({{pmid>long:16223770}}))


	===== Co-morbidity =====		===== Co-morbidity =====

-	Association with R.A. (({{pubmed>long:30366684}}))	+	Association with R.A. (({{pmid>long:30366684}}))

	===== Management =====		===== Management =====
Line 80:		Line 85:
	If slowing the immune response is ineffective, you may need to try an antidepressant. Many of the prescription antidepressant medications are compatible with the MP meds if depression is not resolved by reducing immunopathology.		If slowing the immune response is ineffective, you may need to try an antidepressant. Many of the prescription antidepressant medications are compatible with the MP meds if depression is not resolved by reducing immunopathology.

-	Preliminary results suggest that chronic depression, in contrast to acute melancholic depression, might be characterized by increased ACTH response to CRH challenge. Short-term treatment with vagus nerve stimulation was associated with normalization of this response. (({{pubmed>long:16005439}}))	+	Preliminary results suggest that chronic depression, in contrast to acute melancholic depression, might be characterized by increased ACTH response to CRH challenge. Short-term treatment with vagus nerve stimulation was associated with normalization of this response. (({{pmid>long:16005439}}))

-	Action of SSRIs (({{pubmed>long:22251606}}))	+	Action of SSRIs (({{pmid>long:22251606}}))

	<blockquote>High-Dose Vitamin D Does Not Prevent Depression		<blockquote>High-Dose Vitamin D Does Not Prevent Depression
Line 131:		Line 136:


-	[[http://www.jneuropsychiatry.org/peer-review/depression-and-inflammation-disentangling-a-clear-yet-complex-and-multifaceted-link.html\|depression and inflammation seem closely connected. Specifically that patients with inflammatory diseases are more likely to have MDD, a large number of people with major depression show inflammatory biomarkers, and patients treated with cytokines are at increased risk of developing depression. Also inflammatory mediators have been found to alter glutamate and monoamine neurotransmission, glucocorticoid receptor resistance and hippocampal neurogenesis. Also, inflammation is able to alter brain signalling patterns, to affect cognition.]]	+	[[https://www.jneuropsychiatry.org/peer-review/depression-and-inflammation-disentangling-a-clear-yet-complex-and-multifaceted-link.html\|depression and inflammation seem closely connected. Specifically that patients with inflammatory diseases are more likely to have MDD, a large number of people with major depression show inflammatory biomarkers, and patients treated with cytokines are at increased risk of developing depression. Also inflammatory mediators have been found to alter glutamate and monoamine neurotransmission, glucocorticoid receptor resistance and hippocampal neurogenesis. Also, inflammation is able to alter brain signalling patterns, to affect cognition.]]


-	The 'cytokine hypothesis of depression' implies that proinflammatory cytokines, acting as neuromodulators, represent the key factor in the (central) mediation of the behavioural, neuroendocrine and neurochemical features of depressive disorders. This view is supported by various findings. Several medical illnesses, which are characterised by chronic inflammatory responses, e.g. rheumatoid arthritis, have been reported to be accompanied by depression. (({{pubmed>long: 15694227}}))	+	The 'cytokine hypothesis of depression' implies that proinflammatory cytokines, acting as neuromodulators, represent the key factor in the (central) mediation of the behavioural, neuroendocrine and neurochemical features of depressive disorders. This view is supported by various findings. Several medical illnesses, which are characterised by chronic inflammatory responses, e.g. rheumatoid arthritis, have been reported to be accompanied by depression. (({{pmid>long: 15694227}}))


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	autism, ADHD, depression, severe anxiety, chronic fatigue syndrome (CFS)		autism, ADHD, depression, severe anxiety, chronic fatigue syndrome (CFS)

-	Read the [[http://bacteriality.com/2008/03/15/interview18/\|interview]]	+	Read the [[https://bacteriality.com/2008/03/15/interview18/\|interview]]

	<html></div></div></html>		<html></div></div></html>
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	chronic fatigue syndrome (CFS), depression, food sensitivities		chronic fatigue syndrome (CFS), depression, food sensitivities

-	Read the [[http://bacteriality.com/2007/11/10/interview10/\|interview]]	+	Read the [[https://bacteriality.com/2007/11/10/interview10/\|interview]]

	<html></div></div>		<html></div></div>
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		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

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	<blockquote>		<blockquote>
	Here is another scholarly article making the connection between depression and inflamation.		Here is another scholarly article making the connection between depression and inflamation.
-	http://psychcentral.com/news/2009/04/01/chronic-infection-may-spawn-depression/5079.html	+	https://psychcentral.com/news/2009/04/01/chronic-infection-may-spawn-depression/5079.html
	</blockquote>		</blockquote>

Line 252:		Line 258:

	<blockquote>Why do clinical trials exclude depressed people?		<blockquote>Why do clinical trials exclude depressed people?
-	http://www.reuters.com/article/2011/03/18/us-trials-idUSTRE72H31320110318	+	https://www.reuters.com/article/2011/03/18/us-trials-idUSTRE72H31320110318

	..trevor..		..trevor..
Line 275:		Line 281:
	See:		See:
	Pro-inflammatory cytokines activate enzymes that consume the precursor to seratonin.		Pro-inflammatory cytokines activate enzymes that consume the precursor to seratonin.
-	http://www.ncbi.nlm.nih.gov/pubmed/17928982	+	https://www.ncbi.nlm.nih.gov/pubmed/17928982


Line 289:		Line 295:

	It seems that SAM-e may produce homocysteine without supplemental folic acid. Among their other caveats, the newsletter says, "The most important problem: SAM-e is converted into homocysteine in the body. High homocysteine levels appear to raise the risk of heart disease."		It seems that SAM-e may produce homocysteine without supplemental folic acid. Among their other caveats, the newsletter says, "The most important problem: SAM-e is converted into homocysteine in the body. High homocysteine levels appear to raise the risk of heart disease."
-	http://www.berkeleywellness.com/html/ds/dsSAMe.php	+	https://www.berkeleywellness.com/html/ds/dsSAMe.php

-	High homocysteine levels have also been linked to Alzheimer's. http://www.blackmores.com.au/news/news_detail.asp?art=90	+	High homocysteine levels have also been linked to Alzheimer's. https://www.blackmores.com.au/news/news_detail.asp?art=90

	If your doctor has ordered SAM-e and it is effective for intolerable depression, it's okay to continue it. Monitor your mood carefully and wean from this supplement as your depression resolves.		If your doctor has ordered SAM-e and it is effective for intolerable depression, it's okay to continue it. Monitor your mood carefully and wean from this supplement as your depression resolves.
Line 593:		Line 599:
	Hi Rich. I think contemplative prayer sounds great; it is similar to other types of meditation, I think. I have done a little of that recently in sessions at a beautiful church -- the beauty of the surroundings helps a lot, though I'd imagine you could set up your own space with a candle, etc. (though I've found that candles hurt my eyes now that I'm on the MP).		Hi Rich. I think contemplative prayer sounds great; it is similar to other types of meditation, I think. I have done a little of that recently in sessions at a beautiful church -- the beauty of the surroundings helps a lot, though I'd imagine you could set up your own space with a candle, etc. (though I've found that candles hurt my eyes now that I'm on the MP).

-	One thing that I find immediately helps with wound up emotional states is something called EFT, or Emotional Freedom Technique. It is essentially a quick tapping routine whilst repeating the negative thought, whatever it is that's bothering you. You tap at acupuncture meridian points which supposedly releases the negative impact of the emotion as you state it. It actually works pretty instantaneously for all sorts of stress situations. Check out http://www.mercola.com/forms/eftcourse.htm to see how it's done. I just do the abbreviated, 7-point tap, only takes a minute.	+	One thing that I find immediately helps with wound up emotional states is something called EFT, or Emotional Freedom Technique. It is essentially a quick tapping routine whilst repeating the negative thought, whatever it is that's bothering you. You tap at acupuncture meridian points which supposedly releases the negative impact of the emotion as you state it. It actually works pretty instantaneously for all sorts of stress situations. Check out https://www.mercola.com/forms/eftcourse.htm to see how it's done. I just do the abbreviated, 7-point tap, only takes a minute.

	Best regards,		Best regards,
Line 623:		Line 629:
	Whenever I get moody I will stop and think (meditate) about what in this situation can I be grateful for. It rarely doesn't work; but it can be tough depending on my immune response!		Whenever I get moody I will stop and think (meditate) about what in this situation can I be grateful for. It rarely doesn't work; but it can be tough depending on my immune response!

-	I also listen to nature sound cds--without music, like these http://www.somersetent.com/store/SearchResult.aspx?CategoryID=20	+	I also listen to nature sound cds--without music, like these https://www.somersetent.com/store/SearchResult.aspx?CategoryID=20
	from Dan Gibson. I love music, but it can be a real stressor if my immune response is high.		from Dan Gibson. I love music, but it can be a real stressor if my immune response is high.

Line 738:		Line 744:

	Scientists build on case connecting inflammatory disease and depression		Scientists build on case connecting inflammatory disease and depression
-	http://www.eurekalert.org/pub_releases/2004-07/uoia-sbo072704.php	+	https://www.eurekalert.org/pub_releases/2004-07/uoia-sbo072704.php
	and		and
-	http://www.sciencedaily.com/releases/2004/07/040728084924.htm	+	https://www.sciencedaily.com/releases/2004/07/040728084924.htm

	Dr. Marshall's comment:		Dr. Marshall's comment:
Line 1391:		Line 1397:

	Meg		Meg
-	===== References =====	+	===== References =====</nodisp>

Diabetes, Type I

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

05.24.2019		current
Line 12:		Line 12:
	===== Evidence for infectious cause =====		===== Evidence for infectious cause =====

-	The advent of culture-independent approaches for detecting the presence of microbes has given increasing evidence of the possible role of microbes in type I diabetes. For example, a 2012 paper correlated hemoglobin A1c (HbA1c) levels, an indicator of a hyperglycaemic state, on //C. pneumoniae// infection and disease chronicity.(({{pubmed>long:22859582}})) Using Real Time-Polymerase Chain Reaction (RT-PCR), //C. pneumoniae// DNA was detected in 46.5% of the patients with T1DM compared to 10.5% of non-diabetic paediatric controls. Further, IgG/IgA //C. pneumoniae// antibody positivity was significantly more common in patients in poor metabolic control (HbA1c > 9%) versus patients in good metabolic control (HbA1c < 7%).	+	The advent of culture-independent approaches for detecting the presence of microbes has given increasing evidence of the possible role of microbes in type I diabetes. For example, a 2012 paper correlated hemoglobin A1c (HbA1c) levels, an indicator of a hyperglycaemic state, on //C. pneumoniae// infection and disease chronicity.(({{pmid>long:22859582}})) Using Real Time-Polymerase Chain Reaction (RT-PCR), //C. pneumoniae// DNA was detected in 46.5% of the patients with T1DM compared to 10.5% of non-diabetic paediatric controls. Further, IgG/IgA //C. pneumoniae// antibody positivity was significantly more common in patients in poor metabolic control (HbA1c > 9%) versus patients in good metabolic control (HbA1c < 7%).


Line 19:		Line 19:
	==== Successive infection ====		==== Successive infection ====

-	A 2010 Norwegian paper showed that progression from islet autoimmunity to type 1 diabetes may increase after an enterovirus infection, characterized by the presence of viral RNA in blood.(({{pubmed>long:20858685}}))	+	A 2010 Norwegian paper showed that progression from islet autoimmunity to type 1 diabetes may increase after an enterovirus infection, characterized by the presence of viral RNA in blood.(({{pmid>long:20858685}}))


Line 27:		Line 27:
	==== Intestinal microbiome ====		==== Intestinal microbiome ====

-	Growing evidence suggests a role for intestinal microbiome alterations in autoimmune disease development, including type 1 diabetes.(({{pubmed>long:22211896}})) In a 2011 paper, Giongo //et al.// collected stool samples at three points each from eight Finnish children. Four of the children remained clinically healthy throughout the study, and four were diagnosed with type I diabetes //at or near the time of the third sampling//.(({{pubmed>long:20613793}})) As the diabetic children’s disease progressed, so did the irregular makeup of their gut bacteria. The researchers concluded that level of bacterial diversity diminishes over time in these autoimmune subjects relative to that of age-matched nonautoimmune individuals. A single species, //Bacteroides ovatus//, comprised nearly 24% of the total increase in the phylum //Bacteroidetes// in cases compared with controls. Conversely, another species in controls, represented by the human firmicute strain CO19, represented nearly 20% of the increase in //Firmicutes// compared with cases over time.	+	Growing evidence suggests a role for intestinal microbiome alterations in autoimmune disease development, including type 1 diabetes.(({{pmid>long:22211896}})) In a 2011 paper, Giongo //et al.// collected stool samples at three points each from eight Finnish children. Four of the children remained clinically healthy throughout the study, and four were diagnosed with type I diabetes //at or near the time of the third sampling//.(({{pmid>long:20613793}})) As the diabetic children’s disease progressed, so did the irregular makeup of their gut bacteria. The researchers concluded that level of bacterial diversity diminishes over time in these autoimmune subjects relative to that of age-matched nonautoimmune individuals. A single species, //Bacteroides ovatus//, comprised nearly 24% of the total increase in the phylum //Bacteroidetes// in cases compared with controls. Conversely, another species in controls, represented by the human firmicute strain CO19, represented nearly 20% of the increase in //Firmicutes// compared with cases over time.

-	Also, patients with type I diabetes have increased small intestinal permeability compared to controls.(({{pubmed>long:12713453}})) Such higher permeability would allow microbes easier access to the remainder of the body.	+	Also, patients with type I diabetes have increased small intestinal permeability compared to controls.(({{pmid>long:12713453}})) Such higher permeability would allow microbes easier access to the remainder of the body.

	==== Research ====		==== Research ====

-	Restoration of impaired intestinal barrier function by the hydrolysed casein diet contributes to the prevention of type 1 diabetes in the diabetes-prone BioBreeding rat. (({{pubmed>long:20853098}}))	+	Restoration of impaired intestinal barrier function by the hydrolysed casein diet contributes to the prevention of type 1 diabetes in the diabetes-prone BioBreeding rat. (({{pmid>long:20853098}}))

	As the average amount of plasma glucose increases, the fraction of glycated hemoglobin increases in a predictable way. In diabetes, higher amounts of glycated hemoglobin, indicating poorer control of blood glucose levels, have been associated with cardiovascular disease, nephropathy, neuropathy, and retinopathy. [[https://en.wikipedia.org/wiki/Glycated_hemoglobin\|Glycated hemoglobin (wikipedia)]]		As the average amount of plasma glucose increases, the fraction of glycated hemoglobin increases in a predictable way. In diabetes, higher amounts of glycated hemoglobin, indicating poorer control of blood glucose levels, have been associated with cardiovascular disease, nephropathy, neuropathy, and retinopathy. [[https://en.wikipedia.org/wiki/Glycated_hemoglobin\|Glycated hemoglobin (wikipedia)]]

		+	The overall quality score of clinical practice guidelines ranges between 3 and 6.25. While NICE's guidelines scored the highest, the guidelines of the National Diabetes Foundation scored the lowest. (({{pmid>long: 31121273}}))


		+	18β-GA provides a potential implication to diabetes mellitus and its complications. (({{pmid>long: 31120605}}))
		+
		+	Hyperuricaemia was associated with an unfavourable cardiovascular risk profile in HF patients. Treatment with low doses of allopurinol did not improve the prognosis of HF patients. (({{pmid>long: 31119751}}))


Line 45:		Line 49:
	==== Animal models ====		==== Animal models ====

-	Several studies have shown that gut bacteria have a role in diabetes in murine models. Specific bacteria have been correlated with the onset of diabetes in a rat model.(({{pubmed>long:20613793}})) The incidence of diabetes can be reduced in diabetes-prone rats by preventing an increase in small intestine epithelial permeability.(({{pubmed>long:15710870}}))	+	Several studies have shown that gut bacteria have a role in diabetes in murine models. Specific bacteria have been correlated with the onset of diabetes in a rat model.(({{pmid>long:20613793}})) The incidence of diabetes can be reduced in diabetes-prone rats by preventing an increase in small intestine epithelial permeability.(({{pmid>long:15710870}}))


Line 51:		Line 55:
	==== Streptozotocin ====		==== Streptozotocin ====

-	Due to its high toxicity to beta cells, the microbial byproduct [[http://en.wikipedia.org/wiki/Streptozotocin\|streptozotocin]] has also been long used for inducing insulitis and diabetes on experimental animals. Streptozotocin was originally identified in the late 1950s as an antibiotic.(({{pubmed>long:9421374}})) The drug was discovered in a strain of the soil microbe //Streptomyces achromogenes// by scientists at the drug company Upjohn (now part of Pfizer) in Kalamazoo, Michigan. The soil sample in which the microbe turned up had been taken from Blue Rapids, Kansas, which can therefore be considered the birthplace of streptozotocin. Upjohn filed for patent protection for the drug in August 1958 and U.S. Patent 3,027,300 was granted in March 1962.	+	Due to its high toxicity to beta cells, the microbial byproduct [[https://en.wikipedia.org/wiki/Streptozotocin\|streptozotocin]] has also been long used for inducing insulitis and diabetes on experimental animals. Streptozotocin was originally identified in the late 1950s as an antibiotic.(({{pmid>long:9421374}})) The drug was discovered in a strain of the soil microbe //Streptomyces achromogenes// by scientists at the drug company Upjohn (now part of Pfizer) in Kalamazoo, Michigan. The soil sample in which the microbe turned up had been taken from Blue Rapids, Kansas, which can therefore be considered the birthplace of streptozotocin. Upjohn filed for patent protection for the drug in August 1958 and U.S. Patent 3,027,300 was granted in March 1962.

-	In the mid-1960s streptozotocin was found to be selectively toxic to the beta cells of the pancreatic islets, the cells that normally regulate blood glucose levels by producing the hormone insulin. This suggested the drug's use as an animal model of diabetes,(({{pubmed>long:7926307}})) (({{pubmed>long:13841501}})) and as a medical treatment for cancers of the beta cells.(({{pubmed>long:4170654}})) In the 1960s and 1970s the National Cancer Institute investigated streptozotocin's use in cancer chemotherapy. Upjohn filed for FDA approval of streptozotocin as a treatment for pancreatic islet cell cancer in November 1976, and approval was granted in July 1982. The drug was subsequently marketed as Zanosar. Streptozotocin is now marketed by the generic drug company Sicor (Teva).	+	In the mid-1960s streptozotocin was found to be selectively toxic to the beta cells of the pancreatic islets, the cells that normally regulate blood glucose levels by producing the hormone insulin. This suggested the drug's use as an animal model of diabetes,(({{pmid>long:7926307}})) (({{pmid>long:13841501}})) and as a medical treatment for cancers of the beta cells.(({{pmid>long:4170654}})) In the 1960s and 1970s the National Cancer Institute investigated streptozotocin's use in cancer chemotherapy. Upjohn filed for FDA approval of streptozotocin as a treatment for pancreatic islet cell cancer in November 1976, and approval was granted in July 1982. The drug was subsequently marketed as Zanosar. Streptozotocin is now marketed by the generic drug company Sicor (Teva).

-	Lammi //et al.// have hypothesized that //Streptomyces// produce another toxin, bafilomycin A1, that could be the cause of pancreatic beta-cell damage.(({{pubmed>long:15735577}}))	+	Lammi //et al.// have hypothesized that //Streptomyces// produce another toxin, bafilomycin A1, that could be the cause of pancreatic beta-cell damage.(({{pmid>long:15735577}}))


Line 73:		Line 77:
	===== Read more =====		===== Read more =====

-	* [[http://phys.org/news198243171.html\|Children's gut bacteria linked to type 1 diabetes]]	+	* [[https://phys.org/news198243171.html\|Children's gut bacteria linked to type 1 diabetes]]
-	* [[http://articles.latimes.com/2011/jun/25/health/la-he-bcg-diabetes-20110625\|Research shows promise in reversing Type 1 diabetes]] – Experiments in a small number of people show that an inexpensive vaccine normally used against tuberculosis – Bacille Calmette-Guerin or BCG – may stop the immune system from attacking pancreas cells. However, a live microbe like BCG clearly contributes to the pathogenic load, leading to increased risk for other diseases such as sarcoidosis.	+	* [[https://articles.latimes.com/2011/jun/25/health/la-he-bcg-diabetes-20110625\|Research shows promise in reversing Type 1 diabetes]] – Experiments in a small number of people show that an inexpensive vaccine normally used against tuberculosis – Bacille Calmette-Guerin or BCG – may stop the immune system from attacking pancreas cells. However, a live microbe like BCG clearly contributes to the pathogenic load, leading to increased risk for other diseases such as sarcoidosis.


Line 80:		Line 84:
	{{tag>diseases no_current_patients}}		{{tag>diseases no_current_patients}}

		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

-	We have a T1 Diabetic in our Porto data: http://mpkb.org/_detail/home/publications/perezimprovements.gif?id=home%3Apublications%3Aperez_congress_on_autoimmunity_2008	+	We have a T1 Diabetic in our Porto data: https://mpkb.org/_detail/home/publications/perezimprovements.gif?id=home%3Apublications%3Aperez_congress_on_autoimmunity_2008

	Trevor's comment to me about T1D:		Trevor's comment to me about T1D:
Line 90:		Line 95:
	4-5 years ago: Trevor saw video of pancreas being surrounded by macrophages		4-5 years ago: Trevor saw video of pancreas being surrounded by macrophages
	we have one person (debbie y) on the MP with t1d; her insulin requirements have been dropping and it's pulsing in line with Z; there is a response;		we have one person (debbie y) on the MP with t1d; her insulin requirements have been dropping and it's pulsing in line with Z; there is a response;
-	http://www.marshallprotocol.com/view_topic.php?id=8020&forum_id=35&jump_to=197496#p197496	+	https://www.marshallprotocol.com/view_topic.php?id=8020&forum_id=35&jump_to=197496#p197496

	Search the alumni forums for people with these indications		Search the alumni forums for people with these indications
Line 101:		Line 106:


-	===== References =====	+	===== References =====</nodisp>

Diabetes, Type II

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

03.21.2019		current
Line 15:		Line 15:


-	Prevention of microalbuminuria in patients with type 2 diabetes and hypertension. (({{pubmed>long:22418908}}))	+	Prevention of microalbuminuria in patients with type 2 diabetes and hypertension. (({{pmid>long:22418908}}))


-	Prevention of electrocardiographic left ventricular remodeling by the angiotensin receptor blocker olmesartan in patients with type 2 diabetes. (({{pubmed>long:25275251}}))	+	Prevention of electrocardiographic left ventricular remodeling by the angiotensin receptor blocker olmesartan in patients with type 2 diabetes. (({{pmid>long:25275251}}))

-	Adenosine is an endogenous metabolite that is released from all tissues and cells including liver, pancreas, muscle and fat, particularly under stress, intense exercise, or during cell damage. (({{pubmed>long:23460239}}))	+	Adenosine is an endogenous metabolite that is released from all tissues and cells including liver, pancreas, muscle and fat, particularly under stress, intense exercise, or during cell damage. (({{pmid>long:23460239}}))

-	The effects of diabetes on Adenosine A2BR receptor transcription and signaling (({{pubmed>long:21270276}}))	+	The effects of diabetes on Adenosine A2BR receptor transcription and signaling (({{pmid>long:21270276}}))

-	Results indicate a relationship between muscular TLR4, p-AMPK and NF-κB content and insulin sensitivity. The study also highlights that in situations of insulin resistance, such as in diabetic subjects, metformin treatment may prevent attenuation of activation of the inflammatory pathway. (({{pubmed>long:28791487}}))	+	Results indicate a relationship between muscular TLR4, p-AMPK and NF-κB content and insulin sensitivity. The study also highlights that in situations of insulin resistance, such as in diabetic subjects, metformin treatment may prevent attenuation of activation of the inflammatory pathway. (({{pmid>long:28791487}}))

-	Here, we investigated the hypothesis that the activation of the low-affinity adenosine receptor, the A2B receptor (A(2B)R), promotes glucose uptake in neurons and astrocytes, thereby linking brain activity with energy metabolism. (({{pubmed>long:26446689}}))	+	Here, we investigated the hypothesis that the activation of the low-affinity adenosine receptor, the A2B receptor (A(2B)R), promotes glucose uptake in neurons and astrocytes, thereby linking brain activity with energy metabolism. (({{pmid>long:26446689}}))

-	Our results illustrate that macrophage A2bAR signaling is needed and sufficient for relaying the protective effect of the A2bAR against HFD-induced tissue inflammation and insulin resistance in mice. (({{pubmed>long:24892847}}))	+	Our results illustrate that macrophage A2bAR signaling is needed and sufficient for relaying the protective effect of the A2bAR against HFD-induced tissue inflammation and insulin resistance in mice. (({{pmid>long:24892847}}))

-	This trial aims to determine the effects of resistant starch (RS) subtype 2 (RS2) on glycemic status, metabolic endotoxemia and markers of oxidative stress. (({{pubmed>long: 26655398}}))	+	This trial aims to determine the effects of resistant starch (RS) subtype 2 (RS2) on glycemic status, metabolic endotoxemia and markers of oxidative stress. (({{pmid>long: 26655398}}))
		+
		+	Among persons at high risk for type 2 diabetes not selected for vitamin D insufficiency, vitamin D3 supplementation at a dose of 4000 IU per day did not result in a significantly lower risk of diabetes than placebo. (({{pmid>long:31173679}}))


Line 36:		Line 38:


-	Diet and exercise are the traditional lifestyle interventions used to prevent and treat type 2 diabetes. Different components of the diet can affect the course of type 2 diabetes, but a low carbohydrate diet appears to be giving the most significant results. (({{pubmed>long:19099589}})) (({{pubmed>long:19419563}})) (({{pubmed>long:18397522}}))	+	Diet and exercise are the traditional lifestyle interventions used to prevent and treat type 2 diabetes. Different components of the diet can affect the course of type 2 diabetes, but a low carbohydrate diet appears to be giving the most significant results. (({{pmid>long:19099589}})) (({{pmid>long:19419563}})) (({{pmid>long:18397522}}))

-	Both endurance and resistance exercise yield improvements in many aspects of the metabolic derangements in diabetes type II.(({{pubmed>long:17656625}}))	+	Both endurance and resistance exercise yield improvements in many aspects of the metabolic derangements in diabetes type II.(({{pmid>long:17656625}}))

	Sulfonylureas, biguanids, glitazones, GLP-1 analogs, DPP-4 inhibitors and insulin are the main medication groups used to treat type 2 diabetes. These medications have modulation of insulin funcion, increments in insulin sensitivity and increments in insulin production as their main mechanisms of action.		Sulfonylureas, biguanids, glitazones, GLP-1 analogs, DPP-4 inhibitors and insulin are the main medication groups used to treat type 2 diabetes. These medications have modulation of insulin funcion, increments in insulin sensitivity and increments in insulin production as their main mechanisms of action.
Line 45:		Line 47:
	===== Evidence of infectious cause =====		===== Evidence of infectious cause =====

-	Rubella virus-induced diabetes in the hamster. (({{pubmed>long:3530856}}))	+	Rubella virus-induced diabetes in the hamster. (({{pmid>long:3530856}}))
	<blockquote>The congenital rubella syndrome provides the best documentation in humans that a viral infection is associated with the subsequent development of insulin-dependent diabetes mellitus.</blockquote>		<blockquote>The congenital rubella syndrome provides the best documentation in humans that a viral infection is associated with the subsequent development of insulin-dependent diabetes mellitus.</blockquote>

Line 53:		Line 55:
	The presence of bacterial components in blood predicts the onset of diabetes mellitus in a large general population recounts lead author Jacques Amar from the Centre Hospitalier Universitaire in Toulouse, France. The investigators determined the concentration of 16S rDNA in blood at baseline and assessed its relationship with incident diabetes mellitus and obesity over a follow-up period of 9 years.		The presence of bacterial components in blood predicts the onset of diabetes mellitus in a large general population recounts lead author Jacques Amar from the Centre Hospitalier Universitaire in Toulouse, France. The investigators determined the concentration of 16S rDNA in blood at baseline and assessed its relationship with incident diabetes mellitus and obesity over a follow-up period of 9 years.

-	Linda Koch - comment in [[http://www.nature.com/nrendo/journal/v8/n1/full/nrendo.2011.192.html?WT.ec_id=NRENDO-201201\|Nature reviews: Endocrinology]]	+	Linda Koch - comment in [[https://www.nature.com/nrendo/journal/v8/n1/full/nrendo.2011.192.html?WT.ec_id=NRENDO-201201\|Nature reviews: Endocrinology]]
	</blockquote>		</blockquote>

Line 73:		Line 75:
	CONCLUSIONS/INTERPRETATION:		CONCLUSIONS/INTERPRETATION:

-	16S rDNA was shown to be an independent marker of the risk of diabetes. These findings are evidence for the concept that tissue bacteria are involved in the onset of diabetes in humans.(({{pubmed>long:21976140}}))	+	16S rDNA was shown to be an independent marker of the risk of diabetes. These findings are evidence for the concept that tissue bacteria are involved in the onset of diabetes in humans.(({{pmid>long:21976140}}))

	</blockquote>		</blockquote>
Line 81:		Line 83:

	To what extent microbes contribute to the global diabetes burden, and to what extent antimicrobial therapy can prevent or reverse the disease, has to a limited degree been investigated in clinical trials (see below).		To what extent microbes contribute to the global diabetes burden, and to what extent antimicrobial therapy can prevent or reverse the disease, has to a limited degree been investigated in clinical trials (see below).
-	However, the finding that obese and diabetic patients have higher levels of lipopolysaccharides (LPS, a bacterial product) in their bodies and that insulin level is correlated with the amount of LPS make a strong argument for infectious cause.(({{pubmed>long:17090751}}))	+	However, the finding that obese and diabetic patients have higher levels of lipopolysaccharides (LPS, a bacterial product) in their bodies and that insulin level is correlated with the amount of LPS make a strong argument for infectious cause.(({{pmid>long:17090751}}))

-	Inflammation (which is intimately associated with infection) induced by cytokines (({{pubmed>long:20056828}})) (({{pubmed>long:12453891}})) (({{pubmed>long:16427608}})) leads to insulin resistance.	+	Inflammation (which is intimately associated with infection) induced by cytokines (({{pmid>long:20056828}})) (({{pmid>long:12453891}})) (({{pmid>long:16427608}})) leads to insulin resistance.

-	Abrogation of inflammation ameliorates insulin resistance. (({{pubmed>long:20445103}})) (({{pubmed>long:2038201}})) (({{pubmed>long:20159859}})) (({{pubmed>long:19515743}}))	+	Abrogation of inflammation ameliorates insulin resistance. (({{pmid>long:20445103}})) (({{pmid>long:2038201}})) (({{pmid>long:20159859}})) (({{pmid>long:19515743}}))

-	Deletion of the insulin receptor in myeloid cell lines inhibits development of insulin resistance.(({{pubmed>long:20463885}}))	+	Deletion of the insulin receptor in myeloid cell lines inhibits development of insulin resistance.(({{pmid>long:20463885}}))

-	Further, beta amyloid, which has been identified as an antimicrobial peptide,(({{pubmed>long:20209079}})) is found in increased amounts in pancreatic beta cells of type 2 diabetics,(({{pubmed>long:18950899}})) hinting at the presence of microorganisms as a cause of the malfunction and destruction of the beta cells.	+	Further, beta amyloid, which has been identified as an antimicrobial peptide,(({{pmid>long:20209079}})) is found in increased amounts in pancreatic beta cells of type 2 diabetics,(({{pmid>long:18950899}})) hinting at the presence of microorganisms as a cause of the malfunction and destruction of the beta cells.

	<blockquote>"The VDR is responsible for expression of the Insulin receptor substrate (reference needed). Fix the VDR dysfunction and you will stymy the diabetes. In addition, those of our members who have had high blood-glucose levels have not suffered from having those high BG levels to the same extent that a 'normal' individual would have done, as the VDR activation, and the Angiotensin receptor blockade, both produced by the Olmesartan, have protected their bodies from the expected damage." Trevor Marshall </blockquote>		<blockquote>"The VDR is responsible for expression of the Insulin receptor substrate (reference needed). Fix the VDR dysfunction and you will stymy the diabetes. In addition, those of our members who have had high blood-glucose levels have not suffered from having those high BG levels to the same extent that a 'normal' individual would have done, as the VDR activation, and the Angiotensin receptor blockade, both produced by the Olmesartan, have protected their bodies from the expected damage." Trevor Marshall </blockquote>
Line 96:		Line 98:


-	Helicobacter pylori eradication led to a reduction in insulin resistance(({{pubmed>long:20134372}})).	+	Helicobacter pylori eradication led to a reduction in insulin resistance(({{pmid>long:20134372}})).
-	The use of oxytetracycline in obese mice reduced insulin resistance(({{pubmed>long:4464837}}))	+	The use of oxytetracycline in obese mice reduced insulin resistance(({{pmid>long:4464837}}))



-	Diabetes can cause a sugar coating that smothers body's immune defences (({{pubmed>long:20674073}}))	+	Diabetes can cause a sugar coating that smothers body's immune defences (({{pmid>long:20674073}}))

	The researchers looked at the similarities in chemical structure between glucose in blood and body fluids, and two other sugar called mannose and fucose. These sugars are found on the surfaces of bacteria and fungi and act as targets for receptors in our body that have evolved to detect and bind to microbial sugars to then combat the infection.		The researchers looked at the similarities in chemical structure between glucose in blood and body fluids, and two other sugar called mannose and fucose. These sugars are found on the surfaces of bacteria and fungi and act as targets for receptors in our body that have evolved to detect and bind to microbial sugars to then combat the infection.
Line 111:		Line 113:


-	[[http://tinyurl.com/yrjqa3\|Burden of Infection and Insulin Resistance in Healthy Middle-Aged Men]]	+	[[https://tinyurl.com/yrjqa3\|Burden of Infection and Insulin Resistance in Healthy Middle-Aged Men]]


Line 131:		Line 133:
	diabetes, sarcoidosis, irritable bowel syndrome		diabetes, sarcoidosis, irritable bowel syndrome

-	Read the [[http://bacteriality.com/2008/06/19/interview22/\|interview]]	+	Read the [[https://bacteriality.com/2008/06/19/interview22/\|interview]]

	<html></div></div>		<html></div></div>
Line 166:		Line 168:


		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

Line 316:		Line 319:
	s177, s178:		s177, s178:
	Read first:		Read first:
-	(({{pubmed>long:20140211}}))	+	(({{pmid>long:20140211}}))




-	http://www.ncbi.nlm.nih.gov/pubmed/19225551	+	https://www.ncbi.nlm.nih.gov/pubmed/19225551


-	egg consumption and diabetes(({{pubmed>long:18400720}}))	+	egg consumption and diabetes(({{pmid>long:18400720}}))


Line 341:		Line 344:


-	10 Kramer, Hilary. “Diabetes is Killing our Economy”. Forbes.com. 13 Jan 2010. <http://www.forbes.com/2010/01/13/kramer-obesity-nutrition-intelligent-investing-diabetes.html>;	+	10 Kramer, Hilary. “Diabetes is Killing our Economy”. Forbes.com. 13 Jan 2010. <https://www.forbes.com/2010/01/13/kramer-obesity-nutrition-intelligent-investing-diabetes.html>;


Line 388:		Line 391:
	It is well documented, over several decades, that the BCG vaccine causes Sarcoidosis, eg		It is well documented, over several decades, that the BCG vaccine causes Sarcoidosis, eg
	"Juvenile sarcoidosis after BCG vaccination (2006)"		"Juvenile sarcoidosis after BCG vaccination (2006)"
-	http://www.ncbi.nlm.nih.gov/pubmed/12734491	+	https://www.ncbi.nlm.nih.gov/pubmed/12734491

	"Juvenile sarcoidosis after BCG vaccination (1989)"		"Juvenile sarcoidosis after BCG vaccination (1989)"
-	http://www.ncbi.nlm.nih.gov/pubmed/2602688	+	https://www.ncbi.nlm.nih.gov/pubmed/2602688

	"Incidence of Intrathoracic Sarcoidosis among young adults participating in a trial of Tuberculosis vaccines (1965)"		"Incidence of Intrathoracic Sarcoidosis among young adults participating in a trial of Tuberculosis vaccines (1965)"
-	http://www.ncbi.nlm.nih.gov/pubmed/14321221	+	https://www.ncbi.nlm.nih.gov/pubmed/14321221

	The use of BCG vaccine has been banned in several countries , as being unsafe. Its use in Diabetes is not even a new idea, having been first mooted in 1991		The use of BCG vaccine has been banned in several countries , as being unsafe. Its use in Diabetes is not even a new idea, having been first mooted in 1991
-	http://www.ncbi.nlm.nih.gov/pubmed/1833072	+	https://www.ncbi.nlm.nih.gov/pubmed/1833072

	Anybody who is researching the use of live vaccines, and who doesn't know about the terrible track record of BCG, needs to have their researchers' licenses stripped from them, in my opinion. ..Trevor..		Anybody who is researching the use of live vaccines, and who doesn't know about the terrible track record of BCG, needs to have their researchers' licenses stripped from them, in my opinion. ..Trevor..
Line 495:		Line 498:

	The renin-angiotensin-aldosterone system and the eye in diabetes.		The renin-angiotensin-aldosterone system and the eye in diabetes.
-	http://tinyurl.com/67ldp	+	https://tinyurl.com/67ldp

	Immuno-localization of the calcitriol receptor, calbindin-D28k and the plasma membrane calcium pump in the human eye.		Immuno-localization of the calcitriol receptor, calbindin-D28k and the plasma membrane calcium pump in the human eye.
-	http://tinyurl.com/552tv	+	https://tinyurl.com/552tv

	Retinopathy		Retinopathy
Line 504:		Line 507:
	Retinopathy, in general, is a very common occurrence in Type 1 Diabetics, many of whom end up blinded by it.		Retinopathy, in general, is a very common occurrence in Type 1 Diabetics, many of whom end up blinded by it.

-	A similar process, macular degeneration, is an inflammatory process (see http://tinyurl.com/yjthzk ).	+	A similar process, macular degeneration, is an inflammatory process (see https://tinyurl.com/yjthzk ).

-	Reduction of retinopathy during the course of the MP (in others) would tend to indicate it is also an inflammatory process. However, several of my Diabetes-research colleagues were convinced it was caused by the body failing to assimilate exogenous insulin correctly. see diagram summarizing some of the key relationships between the body's hormones and 1,25-D. You can access it at http://autoimmunityresearch.org/hormones.pdf	+	Reduction of retinopathy during the course of the MP (in others) would tend to indicate it is also an inflammatory process. However, several of my Diabetes-research colleagues were convinced it was caused by the body failing to assimilate exogenous insulin correctly. see diagram summarizing some of the key relationships between the body's hormones and 1,25-D. You can access it at https://autoimmunityresearch.org/hormones.pdf

	Be careful of the lasers. Th1 tissues don't heal as easily, and certainly not when a lot of incident radiation has been focused on them (excess Vit D production).		Be careful of the lasers. Th1 tissues don't heal as easily, and certainly not when a lot of incident radiation has been focused on them (excess Vit D production).
Line 554:		Line 557:
	Selective vitamin D receptor activation with paricalcitol for reduction of albuminuria in patients with type 2 diabetes		Selective vitamin D receptor activation with paricalcitol for reduction of albuminuria in patients with type 2 diabetes

-	http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(10)61032-X/abstract	+	https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(10)61032-X/abstract

	2nd lot of notes & COMMENTS		2nd lot of notes & COMMENTS
Line 568:		Line 571:
	* Legacy content		* Legacy content

-	http://www.lipidsonline.org/news/article.cfm?aid=9682	+	https://www.lipidsonline.org/news/article.cfm?aid=9682




-	<blockquote>Conversely, harmful bacteria may deregulate genes mediating energy metabolism, and can produce toxins that mutate DNA, affecting the nervous and immune systems. The outcome is various forms of chronic disease, including obesity, diabetes and even cancers.(({{pubmed>long:17210919}})) (({{pubmed>long:17456850}})) (({{pubmed>long:17456850}}))	+	<blockquote>Conversely, harmful bacteria may deregulate genes mediating energy metabolism, and can produce toxins that mutate DNA, affecting the nervous and immune systems. The outcome is various forms of chronic disease, including obesity, diabetes and even cancers.(({{pmid>long:17210919}})) (({{pmid>long:17456850}})) (({{pmid>long:17456850}}))

	//Liping Zhao//</blockquote>		//Liping Zhao//</blockquote>
Line 579:		Line 582:

	<blockquote>Diabetes. 2007 Jul;56(7):1761-72. Epub 2007 Apr 24.		<blockquote>Diabetes. 2007 Jul;56(7):1761-72. Epub 2007 Apr 24.
-	Metabolic endotoxemia initiates obesity and insulin resistance.(({{pubmed>long:17456850}}))	+	Metabolic endotoxemia initiates obesity and insulin resistance.(({{pmid>long:17456850}}))

	Cani PD, Amar J, Iglesias MA, Poggi M, Knauf C, Bastelica D, Neyrinck AM, Fava F, Tuohy KM, Chabo C, Waget A, Delmée E, Cousin B, Sulpice T, Chamontin B, Ferrières J, Tanti JF, Gibson GR, Casteilla L, Delzenne NM, Alessi MC, Burcelin R.		Cani PD, Amar J, Iglesias MA, Poggi M, Knauf C, Bastelica D, Neyrinck AM, Fava F, Tuohy KM, Chabo C, Waget A, Delmée E, Cousin B, Sulpice T, Chamontin B, Ferrières J, Tanti JF, Gibson GR, Casteilla L, Delzenne NM, Alessi MC, Burcelin R.
Line 593:		Line 596:
	From: Sue Lyons		From: Sue Lyons
	Date: 2011-03-24 20:44:55		Date: 2011-03-24 20:44:55
-	Reply: http://www.marshallprotocol.com/reply.php?topic_id=7078	+	Reply: https://www.marshallprotocol.com/reply.php?topic_id=7078

	Janet, your suggestions to watch my blood sugar closely was timely as the day you wrote to me, I had a very low blood sugar episode while exercising! I immediately stopped all diabetes meds and exercising until my blood sugar became more stable! Thank you for the advise!		Janet, your suggestions to watch my blood sugar closely was timely as the day you wrote to me, I had a very low blood sugar episode while exercising! I immediately stopped all diabetes meds and exercising until my blood sugar became more stable! Thank you for the advise!
Line 642:		Line 645:
	</blockquote>		</blockquote>
	<blockquote>Effects of Olmesartan Medoxomil, an Angiotensin II Type 1 Receptor Antagonist, on Plasma Concentration of B-Type Natriuretic Peptide, in Hypertensive Patients with Type 2 Diabetes Mellitus: A Preliminary, Observational, Open-Label Study.		<blockquote>Effects of Olmesartan Medoxomil, an Angiotensin II Type 1 Receptor Antagonist, on Plasma Concentration of B-Type Natriuretic Peptide, in Hypertensive Patients with Type 2 Diabetes Mellitus: A Preliminary, Observational, Open-Label Study.
-	http://www.ncbi.nlm.nih.gov/pubmed/21184621	+	https://www.ncbi.nlm.nih.gov/pubmed/21184621

	Angiotensin II type 1 (AT(1)) receptor antagonists (angiotensin receptor blockers [ARBs]) are widely used for the treatment of not only hypertension but also cardiac dysfunction. B-type natriuretic peptide (BNP) is secreted mainly by the cardiac ventricle and plays an important role in the regulation of blood pressure (BP) and body fluid. It has been established that the plasma level of BNP is increased in patients with chronic heart failure in proportion to the severity of cardiac dysfunction. Because cardiac dysfunction is closely associated with a high risk of mortality in patients with diabetes mellitus, early identification and prevention of cardiac dysfunction are important. The objective of this study was to determine the effects of olmesartan medoxomil, a novel ARB, on the plasma level of BNP in hypertensive patients with type 2 diabetes. Methods: This was a preliminary, prospective, observational, open-label study. Sixty-eight type 2 diabetic patients with hypertension (systolic BP [SBP] 140 mmHg or diastolic BP [DBP] 90 mmHg) received olmesartan medoxomil 10-20 mg/day for 24 weeks. Plasma levels of BNP, as well as several clinical parameters of glycaemic control and lipid metabolism, were compared before and after 24 weeks of treatment. Another group consisting of 22 age- and body mass index-matched subjects not treated with olmesartan medoxomil was observed for reference purposes. Results: In the olmesartan medoxomil group, mean ± SD SBP decreased from 152.8 ± 16.4 at baseline to 146.8 ± 14.4 mmHg after 24 weeks' treatment (p < 0.05); similarly, mean ± SD DBP decreased from 85.6 ± 10.5 to 81.3 ± 11.6 mmHg (p < 0.05). In 53 subjects in whom plasma levels of BNP could be measured both before and after treatment, mean ± SD BNP decreased from 41.3 ± 49.9 to 32.5 ± 36.3 pg/mL (p < 0.05). Change in plasma BNP level over the 24-week treatment period in the olmesartan medoxomil group was not correlated with change in SBP or DBP. Multiple regression analysis revealed that change in plasma BNP level was not correlated with baseline value of or change in any other parameters. No other parameters in the olmesartan medoxomil group, and no parameters in the non-olmesartan medoxomil reference group, showed significant changes. Conclusion: The current preliminary study showed that olmesartan medoxomil treatment might decrease plasma BNP levels, independent of its BP-lowering effect, in hypertensive patients with type 2 diabetes.		Angiotensin II type 1 (AT(1)) receptor antagonists (angiotensin receptor blockers [ARBs]) are widely used for the treatment of not only hypertension but also cardiac dysfunction. B-type natriuretic peptide (BNP) is secreted mainly by the cardiac ventricle and plays an important role in the regulation of blood pressure (BP) and body fluid. It has been established that the plasma level of BNP is increased in patients with chronic heart failure in proportion to the severity of cardiac dysfunction. Because cardiac dysfunction is closely associated with a high risk of mortality in patients with diabetes mellitus, early identification and prevention of cardiac dysfunction are important. The objective of this study was to determine the effects of olmesartan medoxomil, a novel ARB, on the plasma level of BNP in hypertensive patients with type 2 diabetes. Methods: This was a preliminary, prospective, observational, open-label study. Sixty-eight type 2 diabetic patients with hypertension (systolic BP [SBP] 140 mmHg or diastolic BP [DBP] 90 mmHg) received olmesartan medoxomil 10-20 mg/day for 24 weeks. Plasma levels of BNP, as well as several clinical parameters of glycaemic control and lipid metabolism, were compared before and after 24 weeks of treatment. Another group consisting of 22 age- and body mass index-matched subjects not treated with olmesartan medoxomil was observed for reference purposes. Results: In the olmesartan medoxomil group, mean ± SD SBP decreased from 152.8 ± 16.4 at baseline to 146.8 ± 14.4 mmHg after 24 weeks' treatment (p < 0.05); similarly, mean ± SD DBP decreased from 85.6 ± 10.5 to 81.3 ± 11.6 mmHg (p < 0.05). In 53 subjects in whom plasma levels of BNP could be measured both before and after treatment, mean ± SD BNP decreased from 41.3 ± 49.9 to 32.5 ± 36.3 pg/mL (p < 0.05). Change in plasma BNP level over the 24-week treatment period in the olmesartan medoxomil group was not correlated with change in SBP or DBP. Multiple regression analysis revealed that change in plasma BNP level was not correlated with baseline value of or change in any other parameters. No other parameters in the olmesartan medoxomil group, and no parameters in the non-olmesartan medoxomil reference group, showed significant changes. Conclusion: The current preliminary study showed that olmesartan medoxomil treatment might decrease plasma BNP levels, independent of its BP-lowering effect, in hypertensive patients with type 2 diabetes.
Line 699:		Line 702:
	1. Gerstein HC, Miller ME, Byington RP, et al. Effects of intensive glucose lowering in type 2 diabetes. N Engl J Med. 2008;358(24):2545-2559.		1. Gerstein HC, Miller ME, Byington RP, et al. Effects of intensive glucose lowering in type 2 diabetes. N Engl J Med. 2008;358(24):2545-2559.

-	//H.H. Weng//(({{pubmed>long:18827215}}))	+	//H.H. Weng//(({{pmid>long:18827215}}))
	</blockquote>		</blockquote>

Line 725:		Line 728:

	find more about Barney's blood glucose - very high		find more about Barney's blood glucose - very high
-	- http://www.bbc.co.uk/blogs/today/tomfeilden/2008/10/drugs_on_test.html	+	- https://www.bbc.co.uk/blogs/today/tomfeilden/2008/10/drugs_on_test.html


Line 747:		Line 750:


-	Glucose test is [[http://labtestsonline.org/understanding/analytes/glucose/test.html\|described here]].	+	Glucose test is [[https://labtestsonline.org/understanding/analytes/glucose/test.html\|described here]].

	Blood glucose meters		Blood glucose meters
Line 797:		Line 800:

	</blockquote>		</blockquote>
-	===== References =====	+	===== References =====</nodisp>

Endometriosis

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

01.14.2019		current
Line 12:		Line 12:
	===== Introduction =====		===== Introduction =====

-	from [[https://medical-dictionary.thefreedictionary.com/endometriosis\|thefreedictionary]]	+	from [[https://medical-dictionary.thefreedictionary.com/endometriosis\|medical-dictionary.thefreedictionary]]

	<blockquote>Endometriosis was once called the "career woman's disease" because it was thought to be a product of delayed childbearing. The statistics defy such a narrow generalization; however, pregnancy may slow the progress of the condition. A more important predictor of a woman's risk is if her female relatives have endometriosis. Another influencing factor is the length of a woman's menstrual cycle. Women whose periods last longer than a week with an interval of less than 27 days between them seem to be more prone to the condition.</blockquote>		<blockquote>Endometriosis was once called the "career woman's disease" because it was thought to be a product of delayed childbearing. The statistics defy such a narrow generalization; however, pregnancy may slow the progress of the condition. A more important predictor of a woman's risk is if her female relatives have endometriosis. Another influencing factor is the length of a woman's menstrual cycle. Women whose periods last longer than a week with an interval of less than 27 days between them seem to be more prone to the condition.</blockquote>
Line 39:		Line 39:
	CONCLUSIONS:		CONCLUSIONS:

-	This exploratory study suggested that there might be an associated risk of endometriosis for those women who have worked as a flight attendant, service station attendant, or health worker, particularly a nurse. (({{pubmed>long:19377833}}))	+	This exploratory study suggested that there might be an associated risk of endometriosis for those women who have worked as a flight attendant, service station attendant, or health worker, particularly a nurse. (({{pmid>long:19377833}}))
	</blockquote>		</blockquote>


	<blockquote>		<blockquote>
-	Comorbidities: http://en.wikipedia.org/wiki/Endometriosis	+	Comorbidities: https://en.wikipedia.org/wiki/Endometriosis

-	"A trend towards higher levels of 1,25-dihydroxyvitamin-D(3) and Ca(2+) was observed in women with endometriosis, but differences did not reach statistical significance." (({{pubmed>long:17548365}}))	+	"A trend towards higher levels of 1,25-dihydroxyvitamin-D(3) and Ca(2+) was observed in women with endometriosis, but differences did not reach statistical significance." (({{pmid>long:17548365}}))
	</blockquote>		</blockquote>

-	<blockquote>Human cycling endometrium may be included among the extrarenal sites able to synthesize vitamin D. (({{pubmed>long:16720713}}))</blockquote>	+	<blockquote>Human cycling endometrium may be included among the extrarenal sites able to synthesize vitamin D. (({{pmid>long:16720713}}))</blockquote>

	===== Members' experience =====		===== Members' experience =====
Line 61:		Line 61:


		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

	look in https://www.marshallprotocol.com/search.php?s=1&q=Endometriosis&forum_id=35		look in https://www.marshallprotocol.com/search.php?s=1&q=Endometriosis&forum_id=35

		+	</nodisp>

Epilepsy (seizures)

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

Eye diseases

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

05.16.2019		current
Line 21:		Line 21:
	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5331551/		https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5331551/

		+	Getting the most out of spinach: Maximizing the antioxidant lutein
		+	https://www.sciencedaily.com/releases/2018/12/181221123810.htm
		+	Eat your spinach in the form of a smoothie or juice -- this is the best way to obtain the antioxidant lutein, according to new research. High levels of lutein are found in dark green vegetables, and researchers at the university have compared different ways of preparing fresh spinach in order to maximize the levels of lutein in finished food.
		+
		+	Lutein and Brain Function
		+	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4638416/
		+	Lutein is one of the most prevalent carotenoids in nature and in the human diet. Together with zeaxanthin, it is highly concentrated as macular pigment in the foveal retina of primates, attenuating blue light exposure, providing protection from photo-oxidation and enhancing visual performance. Recently, interest in lutein has expanded beyond the retina to its possible contributions to brain development and function. Only primates accumulate lutein within the brain, but little is known about its distribution or physiological role. Our team has begun to utilize the rhesus macaque (Macaca mulatta) model to study the uptake and bio-localization of lutein in the brain. Our overall goal has been to assess the association of lutein localization with brain function. In this review, we will first cover the evolution of the non-human primate model for lutein and brain studies, discuss prior association studies of lutein with retina and brain function, and review approaches that can be used to localize brain lutein. We also describe our approach to the biosynthesis of 13C-lutein, which will allow investigation of lutein flux, localization, metabolism and pharmacokinetics. Lastly, we describe potential future research opportunities.
		+
		+	Inhibitory Effects of Lutein on Endotoxin-Induced Uveitis in Lewis Rats
		+	https://iovs.arvojournals.org/article.aspx?articleid=2125584
		+	Lutein deposits in the macula and lens of human eyes with high concentration and is well known as an eye-protective nutrient for its beneficial effects on eye disease such as age-related macular degeneration and cataract. The purpose of the present study was to investigate the effects of lutein on endotoxin-induced uveitis (EIU) in rats.
		+	...
		+	Lutein suppressed the development of EIU in a dose-dependent fashion. The anti-inflammatory effect of 100 mg/kg lutein was as strong as that of 1 mg/kg dexamethasone. Treatment with lutein reduced the concentrations of NO, TNF-α, IL-6, PGE2, MCP-1, and MIP-2 in aqueous humor. Lutein also suppressed the activation of NF-κB in the ICB as well as iNOS and COX-2 expression and IκB degradation in RAW cells.
		+
		+	Foods highest in Lutein+Zeaxanthin: (based on levels per 200-Calorie serving)
		+	https://nutritiondata.self.com/foods-000138000000000000000.html#ixzz5o6l2k3dS
		+
		+	Individual lutein and zeaxanthin values of common foods:
		+	https://i.imgur.com/jhpvacY.png

	===== Marshall Protocol for chronic eye diseases =====		===== Marshall Protocol for chronic eye diseases =====
Line 29:		Line 48:

	When researchers at the Keio University School of Medicine used a bacterial endotoxin to create a condition similar to uveitis in mice, they found that the eye inflammation of the animals decreased significantly after they were administered [[home:othertreatments:immune_suppressants:telmisartan\|Telmisartan]],		When researchers at the Keio University School of Medicine used a bacterial endotoxin to create a condition similar to uveitis in mice, they found that the eye inflammation of the animals decreased significantly after they were administered [[home:othertreatments:immune_suppressants:telmisartan\|Telmisartan]],
-	(a dangerously different ARB).(({{pubmed>long:16043867}}))	+	(a dangerously different ARB).(({{pmid>long:16043867}}))


Line 67:		Line 86:
	=====Evidence of infectious cause=====		=====Evidence of infectious cause=====

-	Cell wall deficient bacteria have been detected on multiple occasions in the eye. Researchers at Columbia under Emil Wirostko detected non-cultivable cell wall-deficient bacterial pathogens in patients with chronic ocular inflammatory disease. In one experiment, they injected these organisms into mouse eyelids, which subsequently caused the mice to develop inflammatory eye disease. They also found that these cell wall deficient pathogens could disseminate and cause similar inflammation in the heart, gut and lungs.(({{pubmed>long:8140710}}))	+	Cell wall deficient bacteria have been detected on multiple occasions in the eye. Researchers at Columbia under Emil Wirostko detected non-cultivable cell wall-deficient bacterial pathogens in patients with chronic ocular inflammatory disease. In one experiment, they injected these organisms into mouse eyelids, which subsequently caused the mice to develop inflammatory eye disease. They also found that these cell wall deficient pathogens could disseminate and cause similar inflammation in the heart, gut and lungs.(({{pmid>long:8140710}}))

-	Additionally, photographs by Emil Wirostko show a substantial number of L-form bacteria inside the immune system cells present in the vitreous of the eye. Several years later, his son, Dr. William Wirostko, implicated bacteria such as //Staphylococcus hominis// and //Staphylococcus aureus// in inflammatory diseases of the eye.(({{pubmed>long:15043554}})) (({{pubmed>long:15860311}}))	+	Additionally, photographs by Emil Wirostko show a substantial number of L-form bacteria inside the immune system cells present in the vitreous of the eye. Several years later, his son, Dr. William Wirostko, implicated bacteria such as //Staphylococcus hominis// and //Staphylococcus aureus// in inflammatory diseases of the eye.(({{pmid>long:15043554}})) (({{pmid>long:15860311}}))


Line 78:		Line 97:
	==== Age-related macular degeneration ====		==== Age-related macular degeneration ====

-	Similarly, researchers at the Massachusetts Eye and Ear Infirmary found //Chlamydia pneumoniae// present in the diseased eye tissue of five out of nine people with age-related macular degeneration (AMD) - a disease in which the center of the inner lining of the eye, known as the macula area of the retina, suffers thinning, atrophy, and in some cases bleeding. However, the bacterium was not found in the eyes of more than 20 individuals without AMD.(({{pubmed>long:15909160}}))	+	Similarly, researchers at the Massachusetts Eye and Ear Infirmary found //Chlamydia pneumoniae// present in the diseased eye tissue of five out of nine people with age-related macular degeneration (AMD) - a disease in which the center of the inner lining of the eye, known as the macula area of the retina, suffers thinning, atrophy, and in some cases bleeding. However, the bacterium was not found in the eyes of more than 20 individuals without AMD.(({{pmid>long:15909160}}))

-	AMD can result in loss of central vision, which entails the inability to see fine details, to read, or to recognize faces. According to the American Academy of Ophthalmology, it is the leading cause of central vision loss (blindness) in the United States today for people over 50 years of age. “The paper showed that //C. pneumoniae// is capable of modifying the function of important cell types involved in regulating normal eye function,” [[http://www.sciencedaily.com/releases/2005/11/051110221819.htm\|said]] lead author Murat Kalayoglu, MD, PhD.(({{pubmed>long:15909160}}))	+	AMD can result in loss of central vision, which entails the inability to see fine details, to read, or to recognize faces. According to the American Academy of Ophthalmology, it is the leading cause of central vision loss (blindness) in the United States today for people over 50 years of age. “The paper showed that //C. pneumoniae// is capable of modifying the function of important cell types involved in regulating normal eye function,” [[https://www.sciencedaily.com/releases/2005/11/051110221819.htm\|said]] lead author Murat Kalayoglu, MD, PhD.(({{pmid>long:15909160}}))

	=== Recent research into AMD ===		=== Recent research into AMD ===
Line 87:		Line 106:

	CONCLUSIONS:		CONCLUSIONS:
-	High adherence to a Mediterranean diet and regular physical activity seem to be protective factors for AMD in a Portuguese population. The effect of the diet is likely driven by the increased consumption of vegetables, fruits, and nuts. (({{pubmed>long:29547735}}))	+	High adherence to a Mediterranean diet and regular physical activity seem to be protective factors for AMD in a Portuguese population. The effect of the diet is likely driven by the increased consumption of vegetables, fruits, and nuts. (({{pmid>long:29547735}}))


Line 94:		Line 113:
	We also found probable evidence that higher intakes of meat increased the risk of cataracts and macular degeneration. Dietary calcium and iron appeared protective against glaucoma, but not in supplemental form.		We also found probable evidence that higher intakes of meat increased the risk of cataracts and macular degeneration. Dietary calcium and iron appeared protective against glaucoma, but not in supplemental form.

-	We would caution intake of supplementary antioxidants for those with ocular disease. (({{pubmed>long:28582804}}))	+	We would caution intake of supplementary antioxidants for those with ocular disease. (({{pmid>long:28582804}}))

	==== Diabetic macular edema ====		==== Diabetic macular edema ====
Line 101:		Line 120:

	CONCLUSIONS:		CONCLUSIONS:
-	Higher homocysteine levels were associated with an increased CSMT, AMT, and AMV in diabetic patients without DME. This link may indicate that patients with type 2 diabetes with increased levels of plasma tHcy are more prone to develop a clinical manifestation of DME. (({{pubmed>long:28391536}}))	+	Higher homocysteine levels were associated with an increased CSMT, AMT, and AMV in diabetic patients without DME. This link may indicate that patients with type 2 diabetes with increased levels of plasma tHcy are more prone to develop a clinical manifestation of DME. (({{pmid>long:28391536}}))


	==== Cataracts ====		==== Cataracts ====

-	Similarly, Wirostko’s group noted that cataracts developed in the eyes of 14 of the 15 mice who had been exposed to the cell wall deficient forms, whereas no cataracts developed in the eyes of 200 control mice that had not come in contact with the pathogens. This data led the team to suggest that cell wall deficient organisms can penetrate the lens capsule to produce cataracts, and that these same organisms could cause human cataracts.(({{pubmed>long:1751463}}))	+	Similarly, Wirostko’s group noted that cataracts developed in the eyes of 14 of the 15 mice who had been exposed to the cell wall deficient forms, whereas no cataracts developed in the eyes of 200 control mice that had not come in contact with the pathogens. This data led the team to suggest that cell wall deficient organisms can penetrate the lens capsule to produce cataracts, and that these same organisms could cause human cataracts.(({{pmid>long:1751463}}))


Line 113:		Line 132:
	In a prospective, non-randomised, comparative study, Kountouras et al found that the frequency of HP infection in a group of glaucoma patients was higher than in control subjects.8 In their study, HP infection was histologically confirmed in 88.2% of glaucoma patients.		In a prospective, non-randomised, comparative study, Kountouras et al found that the frequency of HP infection in a group of glaucoma patients was higher than in control subjects.8 In their study, HP infection was histologically confirmed in 88.2% of glaucoma patients.

-	<blockquote>Uveitic glaucoma is a common complication of uveitis affecting some 20% of patients. The term uveitic glaucoma is used to describe glaucoma resulting indirectly or directly from uveitis. Glaucoma is more commonly associated with anterior uveitis and with chronic forms of uveitis. Uveitis and its treatment can lead to elevated intraocular pressure (IOP). A persistent rise in IOP can lead to glaucamatous optic neuropathy and visual field loss. Intraocular pressure (IOP) elevation in uveitis can be secondary to open angle or angle closure mechanisms. It can also be to due corticosteroid induced glaucoma. The pathogenesis may be acute in onset, with rapid onset inflammation, obstruction of intertrabecular spaces and subsequent increased IOP. The pathogenesis may also be chronic, with repeated bouts of uveitis leading to fibroblastic infiltration and formation of scar tissue that slowly obstructs the anterior chamber angle. [[http://eyewiki.aao.org/Uveitic_Glaucoma\|Uveitic glaucoma]]</blockquote>	+	<blockquote>Uveitic glaucoma is a common complication of uveitis affecting some 20% of patients. The term uveitic glaucoma is used to describe glaucoma resulting indirectly or directly from uveitis. Glaucoma is more commonly associated with anterior uveitis and with chronic forms of uveitis. Uveitis and its treatment can lead to elevated intraocular pressure (IOP). A persistent rise in IOP can lead to glaucamatous optic neuropathy and visual field loss. Intraocular pressure (IOP) elevation in uveitis can be secondary to open angle or angle closure mechanisms. It can also be to due corticosteroid induced glaucoma. The pathogenesis may be acute in onset, with rapid onset inflammation, obstruction of intertrabecular spaces and subsequent increased IOP. The pathogenesis may also be chronic, with repeated bouts of uveitis leading to fibroblastic infiltration and formation of scar tissue that slowly obstructs the anterior chamber angle. [[https://eyewiki.aao.org/Uveitic_Glaucoma\|Uveitic glaucoma]]</blockquote>


Line 121:		Line 140:
	Symptoms of uveitis include redness of the eye, blurred vision, photosensitivity (photophobia), dark floating spots along the visual field, and eye pain.		Symptoms of uveitis include redness of the eye, blurred vision, photosensitivity (photophobia), dark floating spots along the visual field, and eye pain.

-	Some cases are widely accepted to be due to bacteria or viruses. Other cases are associated with "autoimmune diseases" including Crohn's disease, multiple sclerosis, and sarcoidosis.(({{pubmed>long:16942393}}))	+	Some cases are widely accepted to be due to bacteria or viruses. Other cases are associated with "autoimmune diseases" including Crohn's disease, multiple sclerosis, and sarcoidosis.(({{pmid>long:16942393}}))

-	In a 2008 prospective study of 1,321 patients with uveitis, a team of French researchers used polymerase chain reaction (PCR) to search for evidence of microbes. Researchers found a variety of fastidious and difficult-to-grow bacteria including spirochetes, //Bartonella// species, intracellular bacteria (//Chlamydia// species, //Rickettsia// species, //Coxiella burnetii//), and //Tropheryma whipplei// along with herpes viruses and fungi. //Bartonella quintana, Coxiella burnetii, Paracoccus yeei, Aspergillus oryzae,// and //Cryptococcus albidus// were found to be associated with uveitis for the first time. The fact that PCR was not able to find microbes in all samples may be a tribute to this technology's weaknesses.(({{pubmed>long:18520326}}))	+	In a 2008 prospective study of 1,321 patients with uveitis, a team of French researchers used polymerase chain reaction (PCR) to search for evidence of microbes. Researchers found a variety of fastidious and difficult-to-grow bacteria including spirochetes, //Bartonella// species, intracellular bacteria (//Chlamydia// species, //Rickettsia// species, //Coxiella burnetii//), and //Tropheryma whipplei// along with herpes viruses and fungi. //Bartonella quintana, Coxiella burnetii, Paracoccus yeei, Aspergillus oryzae,// and //Cryptococcus albidus// were found to be associated with uveitis for the first time. The fact that PCR was not able to find microbes in all samples may be a tribute to this technology's weaknesses.(({{pmid>long:18520326}}))


Line 135:		Line 154:
	//Trevor Marshall, PhD//</blockquote>		//Trevor Marshall, PhD//</blockquote>

-	The Vitamin D Receptor is involved in the transcription of several key proteins that form the structure of the retina. According to researchers at McGill University,(({{pubmed>long:16002434}})) these proteins include:	+	The Vitamin D Receptor is involved in the transcription of several key proteins that form the structure of the retina. According to researchers at McGill University,(({{pmid>long:16002434}})) these proteins include:
	* Epidermal retinal dehydrogenase		* Epidermal retinal dehydrogenase
	* Retinal outer segment membrane protein		* Retinal outer segment membrane protein
Line 165:		Line 184:
	sarcoidosis (Hedfort Syndrome), uveitis		sarcoidosis (Hedfort Syndrome), uveitis

-	Read the [[http://bacteriality.com/2007/11/19/interview12\|interview]]	+	Read the [[https://bacteriality.com/2007/11/19/interview12\|interview]]

	<html></div></div></html>		<html></div></div></html>
Line 347:		Line 366:
	5 Cambridge Center 8th Floor		5 Cambridge Center 8th Floor
	Cambridge, MA 02142		Cambridge, MA 02142
-	http://www.mersi.us.	+	https://www.mersi.us.
	Phone 617-621-6377		Phone 617-621-6377
	Fax 617-494-1430		Fax 617-494-1430
Line 353:		Line 372:
	Dr. Foster wrote a book on uveitis; he and his research group have published a huge number of articles on it. Because he is such a well-known specialist, he has seen more cases of uveitis than pretty much anyone else.		Dr. Foster wrote a book on uveitis; he and his research group have published a huge number of articles on it. Because he is such a well-known specialist, he has seen more cases of uveitis than pretty much anyone else.

-	Here is a [[http://www.mersi.com/physicians/c-steven-foster-md-facs-facr/\|link]] to his background and publication details:	+	Here is a [[https://www.mersi.com/physicians/c-steven-foster-md-facs-facr/\|link]] to his background and publication details:

-	You can also contact the [[http://www.uveitis.org/patients/support\|online patient support group]] that Dr. Foster supports. People there may have recommendations for doctors to see in your area.	+	You can also contact the [[https://www.uveitis.org/patients/support\|online patient support group]] that Dr. Foster supports. People there may have recommendations for doctors to see in your area.

	If you are faced with eye surgery or complicated-to-manage inflammatory eye conditions , it would be a good idea to get Dr. Foster's input. You and your doctor may not want to do what he says, but he has much more experience in this area than almost anyone else. He is unfamiliar with the MP, and, in fact, considers most inflammatory eye disease to be autoimmune in nature (not caused by active bacterial infection). However, for managing essential eye surgery, we have also consulted doctors trained by Dr. Foster.		If you are faced with eye surgery or complicated-to-manage inflammatory eye conditions , it would be a good idea to get Dr. Foster's input. You and your doctor may not want to do what he says, but he has much more experience in this area than almost anyone else. He is unfamiliar with the MP, and, in fact, considers most inflammatory eye disease to be autoimmune in nature (not caused by active bacterial infection). However, for managing essential eye surgery, we have also consulted doctors trained by Dr. Foster.
Line 366:		Line 385:


		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

Line 371:		Line 391:

	Study Shows Bacterium Present in Eyes with "Wet" Age-Related Macular Degeneration		Study Shows Bacterium Present in Eyes with "Wet" Age-Related Macular Degeneration
-	http://www.meei.harvard.edu/what/press.php	+	https://www.meei.harvard.edu/what/press.php

	ARB reduces Uveitis due to bacterial toxin		ARB reduces Uveitis due to bacterial toxin
Line 398:		Line 418:
	There is an article in PubMed Central in which Wirostko explains how mollicutes, transfected from humans, infected first the eyes of mice, then their whole bodies. Somehow it has slipped my attention since I first saw it. You might be interested to take a look. The images are not as compelling as the the original publications from the 1980's, however		There is an article in PubMed Central in which Wirostko explains how mollicutes, transfected from humans, infected first the eyes of mice, then their whole bodies. Somehow it has slipped my attention since I first saw it. You might be interested to take a look. The images are not as compelling as the the original publications from the 1980's, however

-	http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1298461/?page=1	+	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1298461/?page=1


Line 447:		Line 467:

	</blockquote>		</blockquote>
-	===== References =====	+	===== References =====</nodisp>

Fibromyalgia

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

02.28.2019		current
Line 3:		Line 3:

	Fibromyalgia is a common syndrome of chronic widespread soft-tissue pain accompanied by weakness, fatigue, and sleep disturbances. It is characterized by chronic widespread aching and stiffness, involving particularly the neck, shoulders, back, and hips, which is aggravated by use of the affected muscles.		Fibromyalgia is a common syndrome of chronic widespread soft-tissue pain accompanied by weakness, fatigue, and sleep disturbances. It is characterized by chronic widespread aching and stiffness, involving particularly the neck, shoulders, back, and hips, which is aggravated by use of the affected muscles.
		+
		+	Three types of overlap occur among the disease states chronic fatigue syndrome (CFS), fibromyalgia (FM), multiple chemical sensitivity (MCS) and posttraumatic stress disorder (PTSD). They share common symptoms. (({{pmid>long:11461161}}))

	According to the Marshall Pathogenesis, fibromyalgia is caused by groups of microbes which downregulate activity of the Vitamin D Receptor, a nuclear receptor which plays a key role in maintaining the function of the innate immune response. Physical or psychological stress may exacerbate the disease, but it should not be considered ultimately responsible for it.		According to the Marshall Pathogenesis, fibromyalgia is caused by groups of microbes which downregulate activity of the Vitamin D Receptor, a nuclear receptor which plays a key role in maintaining the function of the innate immune response. Physical or psychological stress may exacerbate the disease, but it should not be considered ultimately responsible for it.
Line 94:		Line 96:
	sarcoidosis, fibromyalgia, chronic fatigue syndrome (CFS)		sarcoidosis, fibromyalgia, chronic fatigue syndrome (CFS)

-	Read the [[http://bacteriality.com/2007/11/08/interview8//\|interview]]	+	Read the [[https://bacteriality.com/2007/11/08/interview8//\|interview]]

	<html></div></div>		<html></div></div>
Line 113:		Line 115:
	{{tag>diseases}}		{{tag>diseases}}

		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

	* Legacy content		* Legacy content
-	* http://www.marshallprotocol.com/view_topic.php?id=3139&forum_id=37&jump_to=30309#p30309 s214	+	* https://www.marshallprotocol.com/view_topic.php?id=3139&forum_id=37&jump_to=30309#p30309 s214
		+
		+	===== References =====</nodisp>

-	===== References =====

Stomach and esophageal disorders

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

10.17.2018		current
Line 15:		Line 15:
	Gastroesophageal reflux disease (GERD) is a condition in which the stomach contents (food or liquid) leak backwards from the stomach into the esophagus. This action can irritate the esophagus, causing heartburn and other symptoms.		Gastroesophageal reflux disease (GERD) is a condition in which the stomach contents (food or liquid) leak backwards from the stomach into the esophagus. This action can irritate the esophagus, causing heartburn and other symptoms.

-	Interestingly, the presence of //Helicobacter pylori// may be inversely related with GERD.(({{pubmed>long:21029801}})) It is unclear what the implications of this work are, however, patients on the Marshall Protocol should expect symptoms of GERD to improve on the treatment.	+	Interestingly, the presence of //Helicobacter pylori// may be inversely related with GERD.(({{pmid>long:21029801}})) It is unclear what the implications of this work are, however, patients on the Marshall Protocol should expect symptoms of GERD to improve on the treatment.


Line 33:		Line 33:
	An antacid is any substance, generally a base or basic salt, which counteracts stomach acidity. Antacids are not contraindicated for Marshall Protocol (MP) patients. As with other over-the-counter medications and supplements, users should follow label directions carefully.		An antacid is any substance, generally a base or basic salt, which counteracts stomach acidity. Antacids are not contraindicated for Marshall Protocol (MP) patients. As with other over-the-counter medications and supplements, users should follow label directions carefully.

-	Note, however, that according to a recent literature review, antacids are no better than placebo in a literature review.(({{pubmed>long:16181387}}))	+	Note, however, that according to a recent literature review, antacids are no better than placebo in a literature review.(({{pmid>long:16181387}}))

	MP patients should not take antacids at least one hour before or two hours after taking other medications.		MP patients should not take antacids at least one hour before or two hours after taking other medications.
Line 41:		Line 41:
	Proton-pump inhibitors (PPIs) are a group of drugs whose main action is a pronounced and long-lasting reduction of gastric acid production. They are the most potent inhibitors of acid secretion available today.		Proton-pump inhibitors (PPIs) are a group of drugs whose main action is a pronounced and long-lasting reduction of gastric acid production. They are the most potent inhibitors of acid secretion available today.

-	PPIs fall into the category of drugs that can be used for temporary relief of intolerable symptoms, but should be weaned when possible. The most troubling aspect of PPIs is their effect on the body's susceptibility to infection. A 2011 systematic review of the literature concluded that the severe hypochlorhydria (lack of stomach acid) generated by PPIs use leads to "bacterial colonisation and increased susceptibility to enteric bacterial infection."(({{pubmed>long:21999643}})) The adjusted [[http://en.wikipedia.org/wiki/Relative_risk\|relative risk]] range for each microbe was calculated as follows.	+	PPIs fall into the category of drugs that can be used for temporary relief of intolerable symptoms, but should be weaned when possible. The most troubling aspect of PPIs is their effect on the body's susceptibility to infection. A 2011 systematic review of the literature concluded that the severe hypochlorhydria (lack of stomach acid) generated by PPIs use leads to "bacterial colonisation and increased susceptibility to enteric bacterial infection."(({{pmid>long:21999643}})) The adjusted [[https://en.wikipedia.org/wiki/Relative_risk\|relative risk]] range for each microbe was calculated as follows.
	* //Salmonella// (4.2-8.3, e.g., 320% to 730% greater risk of infection)		* //Salmonella// (4.2-8.3, e.g., 320% to 730% greater risk of infection)
	* //Campylobacter jejuni,// (3.5-11.7)		* //Campylobacter jejuni,// (3.5-11.7)
Line 107:		Line 107:


-	{{tag>diseases }}	+	{{tag>disease }}
		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

-	===== References =====	+	===== References =====</nodisp>

Graves' disease

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

01.04.2019		current
Line 9:		Line 9:
	===== Introduction =====		===== Introduction =====

-	[[http://www.mayoclinic.org/diseases-conditions/graves-disease/basics/definition/con-20025811\|Mayo Clinic overview]]	+	[[https://www.mayoclinic.org/diseases-conditions/graves-disease/basics/definition/con-20025811\|Mayo Clinic overview]]

	==== Thyroid markers ====		==== Thyroid markers ====
Line 23:		Line 23:


-	//Nanba, T., M. Watanabe, et al. (2009).// "Increases of the Th1/Th2 cell ratio in severe Hashimoto's disease and in the proportion of Th17 cells in intractable Graves' disease." . (({{pubmed>long:19415997}}))	+	//Nanba, T., M. Watanabe, et al. (2009).// "Increases of the Th1/Th2 cell ratio in severe Hashimoto's disease and in the proportion of Th17 cells in intractable Graves' disease." . (({{pmid>long:19415997}}))
	===== Evidence of infectious cause =====		===== Evidence of infectious cause =====

Line 29:		Line 29:
	"AUTOIMMUNE DISEASE ASSOCIATED WITH IRIS Graves Disease Several different autoimmune processes have been described in patients initiating ART, although a clear association with IRIS has yet to be defined for many. It is widely accepted that Graves disease occurring after ART initiation is a manifestation of IRIS. This occurs late in the course of immune restoration, with a median time to onset after ART initiation of 21 months. In one study the median CD4 count before initiation of therapy in patients who developed Graves disease was 10 cells/mm, indicating severe immunodeficiency at the time of ART initiation in this population."		"AUTOIMMUNE DISEASE ASSOCIATED WITH IRIS Graves Disease Several different autoimmune processes have been described in patients initiating ART, although a clear association with IRIS has yet to be defined for many. It is widely accepted that Graves disease occurring after ART initiation is a manifestation of IRIS. This occurs late in the course of immune restoration, with a median time to onset after ART initiation of 21 months. In one study the median CD4 count before initiation of therapy in patients who developed Graves disease was 10 cells/mm, indicating severe immunodeficiency at the time of ART initiation in this population."

-	<blockquote> Distinguishing between manifestations of IRIS and active infection is of paramount importance and poses a diagnostic challenge to the provider in the acute care setting. Presentations of IRIS are often atypical for the precipitating pathogen, and novel presentations are likely. Of the diseases associated with IRIS, mycobacteria and cryptococcal infections are commonly encountered, as are dermatologic symptoms in general. (({{pubmed>long:20413021}})) </blockquote>	+	<blockquote> Distinguishing between manifestations of IRIS and active infection is of paramount importance and poses a diagnostic challenge to the provider in the acute care setting. Presentations of IRIS are often atypical for the precipitating pathogen, and novel presentations are likely. Of the diseases associated with IRIS, mycobacteria and cryptococcal infections are commonly encountered, as are dermatologic symptoms in general. (({{pmid>long:20413021}})) </blockquote>

	===== Patient posted =====		===== Patient posted =====
Line 52:		Line 52:

	//Hogan//</blockquote>		//Hogan//</blockquote>
		+
		+
		+	Also test mineral status, as Selenium and Iodine are essential for thyroid hormone synthesis and function.(({{pmid>long:26088475}}))

	{{tag>diseases }}		{{tag>diseases }}
Line 59:		Line 62:


		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

Line 70:		Line 74:


-	===== References =====	+	===== References =====</nodisp>

Hashimoto's disease

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

01.01.2019		current
Line 8:		Line 8:


-	Hashimoto's disease is characterized by chronic inflammation of the thyroid gland, often leading to a less than sufficient production of the hormones T3 and T4. In some cases hormone replacement therapy may alleviate the majority of symptoms, at least for a while, while in other cases euthyroid patients suffer from a variety of symptoms; lethargy and fatigue being prominent symptoms.(({{pubmed>long:21186954}}))	+	Hashimoto's disease is characterized by chronic inflammation of the thyroid gland, often leading to a less than sufficient production of the hormones T3 and T4. In some cases hormone replacement therapy may alleviate the majority of symptoms, at least for a while, while in other cases euthyroid patients suffer from a variety of symptoms; lethargy and fatigue being prominent symptoms.(({{pmid>long:21186954}}))

-	<blockquote>Women with Hashimotos thyroiditis suffer from a high symptom load. Hypothyroidism is only a contributing factor to the development of associated conditions.(({{pubmed>long:21186954}}))</blockquote>	+	<blockquote>Women with Hashimotos thyroiditis suffer from a high symptom load. Hypothyroidism is only a contributing factor to the development of associated conditions.(({{pmid>long:21186954}}))</blockquote>

-	An infectious etiology has long been suspected in different thyroid diseases, including Hashimoto's thyroiditis. As with many other inflammatory diseases most reasearchers appear to be searching for one specific culprit, something which seems unlikely in light of the many findings of links to many different viruses and bacteria in thyroid disease. Further, in the light of the last few years' progress in metagenomics, a multimicrobial, successive type infection appears more likely to drive the disease process.(({{pubmed>long:23370376}}))	+	An infectious etiology has long been suspected in different thyroid diseases, including Hashimoto's thyroiditis. As with many other inflammatory diseases most reasearchers appear to be searching for one specific culprit, something which seems unlikely in light of the many findings of links to many different viruses and bacteria in thyroid disease. Further, in the light of the last few years' progress in metagenomics, a multimicrobial, successive type infection appears more likely to drive the disease process.(({{pmid>long:23370376}}))

	===== Evidence of infectious cause =====		===== Evidence of infectious cause =====

-	There are many links to infection in Hashimoto's disease, both sereological(({{pubmed>long:3754083}}))(({{pubmed>long:19356903}}))(({{pubmed>long:11318812}})) and DNA based.(({{pubmed>long:23055929}}))(({{pubmed>long:24008857}}))(({{pubmed>long:18788945}}))	+	There are many links to infection in Hashimoto's disease, both sereological(({{pmid>long:3754083}}))(({{pmid>long:19356903}}))(({{pmid>long:11318812}})) and DNA based.(({{pmid>long:23055929}}))(({{pmid>long:24008857}}))(({{pmid>long:18788945}}))

-	Also, inflammatory thyroid disease has also been shown to occur as part of the immmunopathology resulting from treatment of HIV infection.(({{pubmed>long:22784301}})) In line with the Marshall Pathogenesis of inflammatory disease, this is most readily explained by an enhanced function of the immune system upon initiating antiviral therapy, revealing subclinical thyroid disease and multimicrobial infection of the thyroid gland.	+	Also, inflammatory thyroid disease has also been shown to occur as part of the immmunopathology resulting from treatment of HIV infection.(({{pmid>long:22784301}})) In line with the Marshall Pathogenesis of inflammatory disease, this is most readily explained by an enhanced function of the immune system upon initiating antiviral therapy, revealing subclinical thyroid disease and multimicrobial infection of the thyroid gland.
-	==== Other evidence ====	+	==== Research ====

-	Patients suffering from Hashimoto's disease have lower levels of vitamin 25-D, and disease severity correlates with vitamin D levels.(({{pubmed>long:23337162}})) In line with the Marshall Pathogenesis of inflammatory disease, this points to microbes having subverted the function of the vitamin D receptor.	+	Patients suffering from Hashimoto's disease have lower levels of vitamin 25-D, and disease severity correlates with vitamin D levels.(({{pmid>long:23337162}})) In line with the Marshall Pathogenesis of inflammatory disease, this points to microbes having subverted the function of the vitamin D receptor.

-	The ratio of Th1/Th2 cells is higher in Hashimoto's, indicating presence of intracellular infection.(({{pubmed>long:19415997}}))	+	The ratio of Th1/Th2 cells is higher in Hashimoto's, indicating presence of intracellular infection.(({{pmid>long:19415997}}))

		+	Selenium and iodine are essential for thyroid hormone synthesis and function.(({{pmid>long:26088475}}))


		+
		+
		+
		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

Line 41:		Line 46:

	Close to our science is this paper showing that the Alpha Thyroid receptor is key to bone structure.		Close to our science is this paper showing that the Alpha Thyroid receptor is key to bone structure.
-	http://tinyurl.com/mlaea	+	https://tinyurl.com/mlaea

	A simpler summary of what is known is found here		A simpler summary of what is known is found here
-	http://tinyurl.com/nwpaj	+	https://tinyurl.com/nwpaj

	My molecular genomics shows that 1,25-D directly acts on the alpha-1-Thyroid receptor, with higher affinity even than it has for the VDR. This is clearly an important pathway towards the osteopenia we often see in Th1 disease, especially when folks exhibit hypothyroid symptoms.		My molecular genomics shows that 1,25-D directly acts on the alpha-1-Thyroid receptor, with higher affinity even than it has for the VDR. This is clearly an important pathway towards the osteopenia we often see in Th1 disease, especially when folks exhibit hypothyroid symptoms.
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	and the rebuttal:		and the rebuttal:

-	http://www.wilsonsthyroidsyndrome.com/OpinionsOnWTS.htm	+	https://www.wilsonsthyroidsyndrome.com/OpinionsOnWTS.htm

	Please research carefully and discuss this issue which your doctor.		Please research carefully and discuss this issue which your doctor.
Line 179:		Line 184:

	Dr. Marshall has created a diagram summarizing some of the key relationships between the body's hormones and 1,25-D. You can access it at		Dr. Marshall has created a diagram summarizing some of the key relationships between the body's hormones and 1,25-D. You can access it at
-	http://autoimmunityresearch.org/hormones.pdf	+	https://autoimmunityresearch.org/hormones.pdf

	Related Topics:		Related Topics:
Line 204:		Line 209:


-	<blockquote>Prevalence of Yersinia plasmid-encoded outer protein (Yop) class-specific antibodies in patients with Hashimoto's thyroiditis(({{pubmed>long:11318812}}))	+	<blockquote>Prevalence of Yersinia plasmid-encoded outer protein (Yop) class-specific antibodies in patients with Hashimoto's thyroiditis(({{pmid>long:11318812}}))

	Clin Microbiol Infect. 2001 Mar;7(3):138-43.		Clin Microbiol Infect. 2001 Mar;7(3):138-43.
Line 217:		Line 222:
	PMID: 11318812</blockquote>		PMID: 11318812</blockquote>

-	===== References =====	+	===== References =====</nodisp>

HIV and AIDS

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

Hemophagocytic lymphohistiocytosis (HLH)

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

01.03.2012		current
Line 10:		Line 10:
	Several findings link the syndrome to infections:		Several findings link the syndrome to infections:

-	* The immune system is activated. High levels of serum TNF-α, interleukins, IFN-γ have been found in HLH patients.(({{pubmed>long:11076718}})) The actual hemophagocytosis is undertaken by macrophages.	+	* The immune system is activated. High levels of serum TNF-α, interleukins, IFN-γ have been found in HLH patients.(({{pmid>long:11076718}})) The actual hemophagocytosis is undertaken by macrophages.
-	* HLH has been associated with the following microbes: Epstein-Barr virus,(({{pubmed>long:20504238}})) //Salmonella thyphi//,(({{pubmed>long:10910545}})) Herpes simplex virus 1,(({{pubmed>long:20504238}})) HHV-6,(({{pubmed>long:20400100}})) //Mycobacterium tuberculosis//(({{pubmed>long:19449255}})) and other infectious agents.(({{pubmed>long:11076718}}))	+	* HLH has been associated with the following microbes: Epstein-Barr virus,(({{pmid>long:20504238}})) //Salmonella thyphi//,(({{pmid>long:10910545}})) Herpes simplex virus 1,(({{pmid>long:20504238}})) HHV-6,(({{pmid>long:20400100}})) //Mycobacterium tuberculosis//(({{pmid>long:19449255}})) and other infectious agents.(({{pmid>long:11076718}}))
-	* Treatment of infections can reduce hemophagocytosis.(({{pubmed>long:20504238}}))	+	* Treatment of infections can reduce hemophagocytosis.(({{pmid>long:20504238}}))


	==== Possible mechanism for hemophagocytosis ====		==== Possible mechanism for hemophagocytosis ====

-	The actual hemophagocytosis may be viewed as a result of overstimulated macrophages. While blood cells may harbour infectious agents and therefore the infected individual could benefit from the macrophages attacking the blood cells, there is also the possibility that hemophagocytosis benefits the infectious agent. Bacteria in hemophagocytic macrophages could access nutrients from the ingested cells, or hemophagocytic macrophages could reduce bacteria-killing activity by killing the very cells that could attack them. Yet, other macrophages could still be sufficiently activated to generate additional hemophagocytic macrophages.(({{pubmed>long:18085823}}))	+	The actual hemophagocytosis may be viewed as a result of overstimulated macrophages. While blood cells may harbour infectious agents and therefore the infected individual could benefit from the macrophages attacking the blood cells, there is also the possibility that hemophagocytosis benefits the infectious agent. Bacteria in hemophagocytic macrophages could access nutrients from the ingested cells, or hemophagocytic macrophages could reduce bacteria-killing activity by killing the very cells that could attack them. Yet, other macrophages could still be sufficiently activated to generate additional hemophagocytic macrophages.(({{pmid>long:18085823}}))


Line 25:		Line 25:


-	{{tag>Diseases}}	+	{{tag>Disease}}

		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

Line 33:		Line 34:
	So far, so good, Inge. Note the syntax for references. --- //Paul Albert 07.15.2010//		So far, so good, Inge. Note the syntax for references. --- //Paul Albert 07.15.2010//

-	===== References =====	+	===== References =====</nodisp>

Hypercalcemia (hypercalcaemia)

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

07.27.2019		current
Line 7:		Line 7:


-	[[http://www.mayoclinic.org/diseases-conditions/hypercalcemia/basics/definition/con-20031513\|Mayo Clinic overview]]	+	[[https://www.mayoclinic.org/diseases-conditions/hypercalcemia/basics/definition/con-20031513\|Mayo Clinic overview]]

	===== Introduction =====		===== Introduction =====


-	Hypercalcaemia - presentation and management (({{pubmed>long:28572230}}))	+	Hypercalcaemia - presentation and management (({{pmid>long:28572230}}))
	<blockquote>Hypercalcaemia is a common disorder normally caused by primary hyperparathyroidism (PHPT) or malignancy. A proportion of cases present as an emergency, which carries a significant mortality. Emergency management of hypercalcaemia is based on intravenous rehydration with normal saline but when this is inadequate, bisphosphonate therapy is used; more recently the novel anti-resorbtive agent denosumab has been shown to have a useful role in treatment.		<blockquote>Hypercalcaemia is a common disorder normally caused by primary hyperparathyroidism (PHPT) or malignancy. A proportion of cases present as an emergency, which carries a significant mortality. Emergency management of hypercalcaemia is based on intravenous rehydration with normal saline but when this is inadequate, bisphosphonate therapy is used; more recently the novel anti-resorbtive agent denosumab has been shown to have a useful role in treatment.

Line 18:		Line 18:
	</blockquote>		</blockquote>

-	Hyperuricaemia was associated with an unfavourable cardiovascular risk profile in HF patients. Treatment with low doses of allopurinol did not improve the prognosis of HF patients. (({{pubmed>long: 31119751}}))	+	Hyperuricaemia was associated with an unfavourable cardiovascular risk profile in HF patients. Treatment with low doses of allopurinol did not improve the prognosis of HF patients. (({{pmid>long: 31119751}}))

-	A Quick Reference on Hypercalcemia. (({{pubmed>long:28012787}}))	+	A Quick Reference on Hypercalcemia. (({{pmid>long:28012787}}))
	<blockquote>In dogs, neoplasia is the most common cause of hypercalcemia, followed by primary hyperparathyroidism, chronic kidney disease, and hypoadrenocorticism. In cats, idiopathic hypercalcemia is the most common cause, followed by chronic kidney disease and then neoplasia.</blockquote>		<blockquote>In dogs, neoplasia is the most common cause of hypercalcemia, followed by primary hyperparathyroidism, chronic kidney disease, and hypoadrenocorticism. In cats, idiopathic hypercalcemia is the most common cause, followed by chronic kidney disease and then neoplasia.</blockquote>

-	Cancer-Related Hypercalcemia. (({{pubmed>long:27170690}}))	+	Cancer-Related Hypercalcemia. (({{pmid>long:27170690}}))
	<blockquote>The most common causes include humoral hypercalcemia of malignancy mediated by parathyroid hormone-related peptide, osteolytic cytokine production, and excess 1,25-dihydroxy vitamin D production.</blockquote>		<blockquote>The most common causes include humoral hypercalcemia of malignancy mediated by parathyroid hormone-related peptide, osteolytic cytokine production, and excess 1,25-dihydroxy vitamin D production.</blockquote>

-	The active form of vitamin D3 , calcitriol, is a potent antiproliferative compound. However, when effective antitumor doses of calcitriol are used, hypercalcemic effects are observed, thus blocking its therapeutic application. (({{pubmed>long: 31025400}}))	+	The active form of vitamin D3 , calcitriol, is a potent antiproliferative compound. However, when effective antitumor doses of calcitriol are used, hypercalcemic effects are observed, thus blocking its therapeutic application. (({{pmid>long: 31025400}}))

	==== Infants ====		==== Infants ====

-	Vitamin D: Metabolism, Molecular Mechanism of Action, and Pleiotropic Effects. (({{pubmed>long:000}}))	+	Vitamin D: Metabolism, Molecular Mechanism of Action, and Pleiotropic Effects. (({{pmid>long:26681795}}))

	<blockquote> CYP2R1 has been identified as the most important 25-hydroxylase, and a critical role for CYP24A1 in humans was noted in studies showing that inactivating mutations in CYP24A1 are a probable cause of idiopathic infantile hypercalcemia.		<blockquote> CYP2R1 has been identified as the most important 25-hydroxylase, and a critical role for CYP24A1 in humans was noted in studies showing that inactivating mutations in CYP24A1 are a probable cause of idiopathic infantile hypercalcemia.
Line 39:		Line 39:


-	Successful treatment of an intra-pelvic fungal pseudomycetoma causing constipation and hypercalcaemia in a Persian cat. (({{pubmed>long: 23985754}}))	+	Successful treatment of an intra-pelvic fungal pseudomycetoma causing constipation and hypercalcaemia in a Persian cat. (({{pmid>long: 23985754}}))
	===== Why doesn't the use of olmesartan lead to hypercalcemia? =====		===== Why doesn't the use of olmesartan lead to hypercalcemia? =====

-	Since calcitriol (the active form of vitamin D) is a Vitamin D receptor (VDR) agonist, and use of this substance can cause hypercalcemia, one may expect that olmesartan, through effects on the VDR, may also cause hypercalcemia if the dosage is high. There is however no evidence that this is an effect of olmesartan, and the reason for the differing effects appears to reside in the non-VDR effects of calcitriol. (({{pubmed>long:19631778}}))	+	Since calcitriol (the active form of vitamin D) is a Vitamin D receptor (VDR) agonist, and use of this substance can cause hypercalcemia, one may expect that olmesartan, through effects on the VDR, may also cause hypercalcemia if the dosage is high. There is however no evidence that this is an effect of olmesartan, and the reason for the differing effects appears to reside in the non-VDR effects of calcitriol. (({{pmid>long:19631778}}))


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		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

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	</blockquote>		</blockquote>

-	===== References =====	+	===== References =====</nodisp>

Secondary hyperparathyroidism

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

02.18.2019		current
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	<html><!--		<html><!--
-	Joyce Waterhouse, Ph.D. has [[http://synergyhn.com/lesions/\|described in detail]] a number of flaws in studies that use the relationship between low 25D and secondary hyperparathyroidism in order to estimate an optimal level of 25D. One problem is that they usually fail to ensure that subjects are consuming adequate calcium before assessing the relationship between 25-D and PTH.	+	Joyce Waterhouse, Ph.D. has [[https://synergyhn.com/lesions/\|described in detail]] a number of flaws in studies that use the relationship between low 25D and secondary hyperparathyroidism in order to estimate an optimal level of 25D. One problem is that they usually fail to ensure that subjects are consuming adequate calcium before assessing the relationship between 25-D and PTH.
	-->		-->
	</html>		</html>

-	When researchers at Winthrop University Hospital made sure that subjects consumed adequate calcium, they found that only a small percentage of patients with low 25-D actually had elevated levels of PTH, and that just 16 ng/ml of 25-D is usually enough to keep PTH in the correct range.(({{pubmed>long:16960175}})) This was confirmed by a recent study which found that PTH levels frequently remain normal even in patients with very low 25-D. The bone density of the elderly subjects in the study also remained the same as subjects taking higher levels of 25-D as long as their PTH remained normal.(({{pubmed>long:17854393}}))	+	When researchers at Winthrop University Hospital made sure that subjects consumed adequate calcium, they found that only a small percentage of patients with low 25-D actually had elevated levels of PTH, and that just 16 ng/ml of 25-D is usually enough to keep PTH in the correct range.(({{pmid>long:16960175}})) This was confirmed by a recent study which found that PTH levels frequently remain normal even in patients with very low 25-D. The bone density of the elderly subjects in the study also remained the same as subjects taking higher levels of 25-D as long as their PTH remained normal.(({{pmid>long:17854393}}))

	==== vitamin D ====		==== vitamin D ====


-	In reality, 25-D may account for only a very small percentage of variation in PTH levels, especially when subjects are taking adequate calcium. Several studies have shown that low magnesium, increasing age, or elevated serum phosphate and creatinine due to kidney disease also greatly contribute to the level of PTH, causing researchers at the University Hospital of New Norway to conclude that elevated PTH “is therefore probably a result of a combination of factors.” (({{pubmed>long:16369900}})) It’s not surprising then, that several studies have noted that giving vitamin D to patients with low levels of 25-D often does nothing to bring PTH back to normal levels.(({{pubmed>long:6611345}}))	+	In reality, 25-D may account for only a very small percentage of variation in PTH levels, especially when subjects are taking adequate calcium. Several studies have shown that low magnesium, increasing age, or elevated serum phosphate and creatinine due to kidney disease also greatly contribute to the level of PTH, causing researchers at the University Hospital of New Norway to conclude that elevated PTH “is therefore probably a result of a combination of factors.” (({{pmid>long:16369900}}))
		+
		+	It’s not surprising then, that several studies have noted that giving vitamin D to patients with low levels of 25-D often does nothing to bring PTH back to normal levels.(({{pmid>long:6611345}}))

	In the end, it is perfectly possible that when calcium intake is adequate, most of what remains of the association between low 25-D and elevated PTH is simply part of the pathogenesis of chronic disease and osteoporosis. Just as the low 25-D seen in patients with chronic disease is the //result// rather than the //cause// of the disease process, elevated PTH in patients with low 25-D may simply be an indicator of inflammation caused by the Th1 pathogens.		In the end, it is perfectly possible that when calcium intake is adequate, most of what remains of the association between low 25-D and elevated PTH is simply part of the pathogenesis of chronic disease and osteoporosis. Just as the low 25-D seen in patients with chronic disease is the //result// rather than the //cause// of the disease process, elevated PTH in patients with low 25-D may simply be an indicator of inflammation caused by the Th1 pathogens.
Line 47:		Line 49:


		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

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	* Legacy content		* Legacy content

-	===== References =====	+	===== References =====</nodisp>

Hypertension (high blood pressure)

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

03.30.2020		current
Line 6:		Line 6:


-	<relatedarticle> [[home:protocol:olmesartan#other beneficial effects\|section on cardiovascular_disease]] </article>	+	<relatedarticle> [[home:protocol:olmesartan#other beneficial effects\|Science behind Olmesartan, section on cardiovascular_disease]] </article>
	===== Introduction =====		===== Introduction =====

Line 53:		Line 53:
	===== Inflammation and Hypertension =====		===== Inflammation and Hypertension =====

-	Hypertension, inflammation and atherosclerosis (({{pubmed>long:15262906}}))	+	Hypertension, inflammation and atherosclerosis (({{pmid>long:15262906}}))


-	Inflammation may be a bridge connecting hypertension and atherosclerosis. (({{pubmed>long:16464884}}))	+	Inflammation may be a bridge connecting hypertension and atherosclerosis. (({{pmid>long:16464884}}))


-	[[http://ndt.oxfordjournals.org/cgi/content/full/21/4/850\|Inflammation and hypertension: the search for a link]]	+	[[https://ndt.oxfordjournals.org/cgi/content/full/21/4/850\|Inflammation and hypertension: the search for a link]]

	//Elevated high-sensitive C-reactive protein, large arterial stiffness and atherosclerosis: a relationship between inflammation and hypertension?//		//Elevated high-sensitive C-reactive protein, large arterial stiffness and atherosclerosis: a relationship between inflammation and hypertension?//
Line 68:		Line 68:
	RECENT FINDINGS: Essential hypertension is characterized by increased peripheral vascular resistance to blood flow, due in large part to vascular remodeling. Vascular changes in hypertension are associated with mechanical and humoral factors that modulate signaling events, resulting in abnormal function, media growth, extracellular matrix deposition and inflammation. Recent evidence suggests that inflammation is present in the vasculature in animal models of hypertension. Inflammatory markers, such as C-reactive protein, are associated with vascular lesions in humans, and are predictive of cardiovascular outcome. In animal and human studies, pro-inflammatory components of the renin-angiotensin-aldosterone system have been demonstrated in large conduit and small arteries in the kidney and heart. Peroxisome proliferator-activated receptor activators are drugs with metabolic properties that have been demonstrated to exert anti-inflammatory effects on the vasculature, and there is now evidence that these actions may be protective for blood vessels.		RECENT FINDINGS: Essential hypertension is characterized by increased peripheral vascular resistance to blood flow, due in large part to vascular remodeling. Vascular changes in hypertension are associated with mechanical and humoral factors that modulate signaling events, resulting in abnormal function, media growth, extracellular matrix deposition and inflammation. Recent evidence suggests that inflammation is present in the vasculature in animal models of hypertension. Inflammatory markers, such as C-reactive protein, are associated with vascular lesions in humans, and are predictive of cardiovascular outcome. In animal and human studies, pro-inflammatory components of the renin-angiotensin-aldosterone system have been demonstrated in large conduit and small arteries in the kidney and heart. Peroxisome proliferator-activated receptor activators are drugs with metabolic properties that have been demonstrated to exert anti-inflammatory effects on the vasculature, and there is now evidence that these actions may be protective for blood vessels.

-	SUMMARY: Inflammatory processes are important participants in the pathophysiology of hypertension and cardiovascular disease. The identification of the mechanisms leading to the activation of inflammation should contribute to the development of specific therapeutic approaches to apply in hypertension and its complications. (({{pubmed>long:16481882}}))</blockquote>	+	SUMMARY: Inflammatory processes are important participants in the pathophysiology of hypertension and cardiovascular disease. The identification of the mechanisms leading to the activation of inflammation should contribute to the development of specific therapeutic approaches to apply in hypertension and its complications. (({{pmid>long:16481882}}))</blockquote>

	//see also//		//see also//
	Nephrol Dial Transplant. 2006 Apr;21(4):850-3. Epub 2006 Feb 7.		Nephrol Dial Transplant. 2006 Apr;21(4):850-3. Epub 2006 Feb 7.
	Inflammation and hypertension: the search for a link.		Inflammation and hypertension: the search for a link.
-	Pauletto P, Rattazzi M. (({{pubmed>long:16464884}}))	+	Pauletto P, Rattazzi M. (({{pmid>long:16464884}}))



-	Wilke, R. A., R. U. Simpson, et al. (2009). "Genetic variation in CYP27B1 is associated with congestive heart failure in patients with hypertension." Pharmacogenomics 10(11): 1789-1797. (({{pubmed>long:19891555}}))	+	Wilke, R. A., R. U. Simpson, et al. (2009). "Genetic variation in CYP27B1 is associated with congestive heart failure in patients with hypertension." Pharmacogenomics 10(11): 1789-1797. (({{pmid>long:19891555}}))
	<blockquote>		<blockquote>

Line 87:		Line 87:


-	For some, the absence of well-defined causal connections between diseases and surrogate outcomes is a tribute to how truly complicated chronic inflammatory diseases are. Ralph B D'Agostino characterizes hypertension in this way: “There is no reason to believe that hypertension is simply elevated blood pressure. Hypertension is much more complex.” (({{pubmed>long:11714414}}))</blockquote>	+	For some, the absence of well-defined causal connections between diseases and surrogate outcomes is a tribute to how truly complicated chronic inflammatory diseases are. Ralph B D'Agostino characterizes hypertension in this way: “There is no reason to believe that hypertension is simply elevated blood pressure. Hypertension is much more complex.” (({{pmid>long:11714414}}))</blockquote>

	__		__
Line 99:		Line 99:
	intrinsic elastic properties of the carotid artery wall material. These data suggest that 40 and 80 mg olmesartan were able		intrinsic elastic properties of the carotid artery wall material. These data suggest that 40 and 80 mg olmesartan were able
	to significantly remodel and destiffen the arterial wall material during long-term treatment, partly independently of blood		to significantly remodel and destiffen the arterial wall material during long-term treatment, partly independently of blood
-	pressure, compared with 20 mg. (({{pubmed>long:25001274}}))	+	pressure, compared with 20 mg. (({{pmid>long:25001274}}))


Line 109:		Line 109:
	===== Recent research =====		===== Recent research =====

-	Comparative effectiveness of an angiotensin receptor blocker, olmesartan medoxomil, in older hypertensive patients. (({{pubmed>long:29462508}}))	+	Comparative effectiveness of an angiotensin receptor blocker, olmesartan medoxomil, in older hypertensive patients. (({{pmid>long:29462508}}))


-	The administration of olmesartan improved blood pressure, insulin, HOMA, visfatin and lipid profile in hypertensive obese women. Irbesartan improved blood pressure and lipid levels. (({{pubmed>long:21061834}}))	+	The administration of olmesartan improved blood pressure, insulin, HOMA, visfatin and lipid profile in hypertensive obese women. Irbesartan improved blood pressure and lipid levels. (({{pmid>long:21061834}}))


-	Olmesartan ameliorated arterial stiffness in patients with hypertension, which may be involved in the reduction of serum A-FABP. (({{pubmed>long:21063874}}))	+	Olmesartan ameliorated arterial stiffness in patients with hypertension, which may be involved in the reduction of serum A-FABP. (({{pmid>long:21063874}}))

-	Given the involvement of oxidative stress and its signaling in atherogenesis, and the available evidence of olmesartan's vasoprotective, anti-inflammatory and antiatherosclerotic effects derived from clinical trials in humans, the results of our study provide a mechanistic rationale for the olmesartan's antioxidant and anti-inflammatory potential translation, in the long term, toward the antiatherosclerotic and antiremodeling effects reported on the clinical ground. (({{pubmed>long:21504378}}))	+	Given the involvement of oxidative stress and its signaling in atherogenesis, and the available evidence of olmesartan's vasoprotective, anti-inflammatory and antiatherosclerotic effects derived from clinical trials in humans, the results of our study provide a mechanistic rationale for the olmesartan's antioxidant and anti-inflammatory potential translation, in the long term, toward the antiatherosclerotic and antiremodeling effects reported on the clinical ground. (({{pmid>long:21504378}}))

	{{tag>disease symptoms }}		{{tag>disease symptoms }}
Line 127:		Line 127:


		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

-	//BROKEN LINK// [[http://hyper.ahajournals.org/cgi/content/full/44/3/253\|Is Vascular Endothelial Growth Factor a Missing Link Between Hypertension and Inflammation?]]	+	//BROKEN LINK// [[https://hyper.ahajournals.org/cgi/content/full/44/3/253\|Is Vascular Endothelial Growth Factor a Missing Link Between Hypertension and Inflammation?]]

	ANOR //DEAD LINK//		ANOR //DEAD LINK//
-	[[http://hyper.ahajournals.org/content/hypertensionaha/early/2014/07/07/HYPERTENSIONAHA.114.03282.full.pdf\|Dose-Dependent Arterial Destiffening and Inward	+	[[https://hyper.ahajournals.org/content/hypertensionaha/early/2014/07/07/HYPERTENSIONAHA.114.03282.full.pdf\|Dose-Dependent Arterial Destiffening and Inward
	Remodeling After Olmesartan in Hypertensives With		Remodeling After Olmesartan in Hypertensives With
	Metabolic Syndrome]]		Metabolic Syndrome]]

-	link to current research by 2 authers [[http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Search&itool=pubmed_Abstract&term=%22Savoia%20C%22[Author]\|Savoia C]], [[http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Search&itool=pubmed_Abstract&term=%22Schiffrin%20EL%22[Author]\|Schiffrin EL.]]	+	link to current research by 2 authers [[https://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Search&itool=pubmed_Abstract&term=%22Savoia%20C%22[Author]\|Savoia C]], [[https://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Search&itool=pubmed_Abstract&term=%22Schiffrin%20EL%22[Author]\|Schiffrin EL.]]

	Vitamins		Vitamins
Line 149:		Line 150:
	--- //Sallie Q 02.22.2017// moved contents of 1st para out of view as follows		--- //Sallie Q 02.22.2017// moved contents of 1st para out of view as follows

-	http://www.newswire.ca/en/releases/archive/May2009/21/c6035.html	+	https://www.newswire.ca/en/releases/archive/May2009/21/c6035.html


Line 168:		Line 169:
	*Legacy content		*Legacy content

-	http://www.lipidsonline.org/news/article.cfm?aid=9682	+	https://www.lipidsonline.org/news/article.cfm?aid=9682



-	* salt avoidance – not recommended given that the body seems to naturally regulate sodium levels independently(({{pubmed>long:19833911}}))	+	* salt avoidance – not recommended given that the body seems to naturally regulate sodium levels independently(({{pmid>long:19833911}}))


-	<blockquote>Effects of olmesartan vs irbesartan on metabolic parameters and visfatin in hypertensive obese women. (({{pubmed>long:21061834}}))	+	<blockquote>Effects of olmesartan vs irbesartan on metabolic parameters and visfatin in hypertensive obese women. (({{pmid>long:21061834}}))

-	http://www.ncbi.nlm.nih.gov/pubmed/21061834 (USED on page --- //Sallie Q 01.04.2019// )	+	https://www.ncbi.nlm.nih.gov/pubmed/21061834 (USED on page --- //Sallie Q 01.04.2019// )

	CONCLUSION: The administration of olmesartan improved blood pressure, insulin, HOMA, visfatin and lipid profile in hypertensive obese women. Irbesartan improved blood pressure and lipid levels.		CONCLUSION: The administration of olmesartan improved blood pressure, insulin, HOMA, visfatin and lipid profile in hypertensive obese women. Irbesartan improved blood pressure and lipid levels.
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	Visfatin, glucose metabolism and vascular disease: a review of evidence		Visfatin, glucose metabolism and vascular disease: a review of evidence

-	http://www.dmsjournal.com/content/2/1/21	+	https://www.dmsjournal.com/content/2/1/21

	Visfatin is is an adipokine involved in inflammatory phenomena, atherosclerosis, and possibly in insulin secretion. Its physiology has begun to be described but its role on diabetes and CAD pathophysiology is still controversial.		Visfatin is is an adipokine involved in inflammatory phenomena, atherosclerosis, and possibly in insulin secretion. Its physiology has begun to be described but its role on diabetes and CAD pathophysiology is still controversial.
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	~~~~		~~~~
	(part below ref. USED on page --- --- //Sallie Q 01.04.2019// )		(part below ref. USED on page --- --- //Sallie Q 01.04.2019// )
-	Olmesartan reduces arterial stiffness and serum adipocyte fatty acid-binding protein in hypertensive patients. (({{pubmed>long:21063874}}))	+	Olmesartan reduces arterial stiffness and serum adipocyte fatty acid-binding protein in hypertensive patients. (({{pmid>long:21063874}}))

-	http://www.ncbi.nlm.nih.gov/pubmed/21063874	+	https://www.ncbi.nlm.nih.gov/pubmed/21063874

	Olmesartan ameliorated arterial stiffness in patients with hypertension, which may be involved in the reduction of serum A-FABP.		Olmesartan ameliorated arterial stiffness in patients with hypertension, which may be involved in the reduction of serum A-FABP.
Line 238:		Line 239:
	Abstract		Abstract

-	Abstract The role of oxidative stress in the pathophysiology of hypertension and target organ damage is widely recognized. Using a molecular biology approach, we report, in essential hypertensive patients, the effect of the angiotensin II type 1 receptor blocker olmesartan on the mononuclear cell (PBMC) protein expression of major elements in the oxidative stress and vascular remodeling-related pathways, p22(phox) and HO-1, along with the phosphorylation state of ERK1/2 and plasma oxidized low-density lipoproteins (oxLDL). Twenty untreated essential hypertensive patients (range blood pressure: 142-156/94-98 mmHg) were treated with olmesartan medoxomil (20 mg/day for 6 months) and blood samples collected at baseline, 3 and 6 months for PBMC p22(phox) and HO-1 protein expression, phosphorylation state of ERK1/2 (western blot) and oxLDL level (ELISA) evaluations. Olmesartan normalized blood pressure since the third month (149 ± 4.7/94.88 ± 1.9 mmHg vs 137.89 ± 2.08/88.44 ± 2.0 at 3 months and vs 135.44 ± 2.18/85.78 ± 1.2 at 6 months, analysis of variance: p < 0.001). p22(phox) protein level declined at 3 months (7.10 ± 2.61 vs 9.32 ± 2.43 densitometric units (d.u.; p < 0.001), further declining at 6 months (4.55 ± 1.26 d.u., p < 0.001). HO-1 levels increased at 3 months (10.87 ± 1.92 vs 7.70 ± 0.71 d.u., p = 0.001) and remained elevated (11.11 ± 1.89 d.u., p = 0.001), without further increase at 6 months. Phosphorylated ERK1/2 declined at 3 months (3.94 ± 1.44 vs 5.62 ± 1.11 d.u., p = 0.001), further declining at 6 months (1.94 ± 0.87, p < 0.001). oxLDL significantly declined at 3 and 6 months. These results demonstrate that olmesartan inhibits oxidative stress. Given the involvement of oxidative stress and its signaling in atherogenesis, and the available evidence of olmesartan's vasoprotective, anti-inflammatory and antiatherosclerotic effects derived from clinical trials in humans, the results of our study provide a mechanistic rationale for the omelsartan's antioxidant and anti-inflammatory potential translation, in the long term, toward the antiatherosclerotic and antiremodeling effects reported on the clinical ground. (({{pubmed>long:21504378}}))	+	Abstract The role of oxidative stress in the pathophysiology of hypertension and target organ damage is widely recognized. Using a molecular biology approach, we report, in essential hypertensive patients, the effect of the angiotensin II type 1 receptor blocker olmesartan on the mononuclear cell (PBMC) protein expression of major elements in the oxidative stress and vascular remodeling-related pathways, p22(phox) and HO-1, along with the phosphorylation state of ERK1/2 and plasma oxidized low-density lipoproteins (oxLDL). Twenty untreated essential hypertensive patients (range blood pressure: 142-156/94-98 mmHg) were treated with olmesartan medoxomil (20 mg/day for 6 months) and blood samples collected at baseline, 3 and 6 months for PBMC p22(phox) and HO-1 protein expression, phosphorylation state of ERK1/2 (western blot) and oxLDL level (ELISA) evaluations. Olmesartan normalized blood pressure since the third month (149 ± 4.7/94.88 ± 1.9 mmHg vs 137.89 ± 2.08/88.44 ± 2.0 at 3 months and vs 135.44 ± 2.18/85.78 ± 1.2 at 6 months, analysis of variance: p < 0.001). p22(phox) protein level declined at 3 months (7.10 ± 2.61 vs 9.32 ± 2.43 densitometric units (d.u.; p < 0.001), further declining at 6 months (4.55 ± 1.26 d.u., p < 0.001). HO-1 levels increased at 3 months (10.87 ± 1.92 vs 7.70 ± 0.71 d.u., p = 0.001) and remained elevated (11.11 ± 1.89 d.u., p = 0.001), without further increase at 6 months. Phosphorylated ERK1/2 declined at 3 months (3.94 ± 1.44 vs 5.62 ± 1.11 d.u., p = 0.001), further declining at 6 months (1.94 ± 0.87, p < 0.001). oxLDL significantly declined at 3 and 6 months. These results demonstrate that olmesartan inhibits oxidative stress. Given the involvement of oxidative stress and its signaling in atherogenesis, and the available evidence of olmesartan's vasoprotective, anti-inflammatory and antiatherosclerotic effects derived from clinical trials in humans, the results of our study provide a mechanistic rationale for the omelsartan's antioxidant and anti-inflammatory potential translation, in the long term, toward the antiatherosclerotic and antiremodeling effects reported on the clinical ground. (({{pmid>long:21504378}}))

	PMID:		PMID:
-	21504378 (part USED on page --- //Sallie Q 01.04.2019//</blockquote>	+	21504378 (part USED on page --- //Sallie Q 01.04.2019//</blockquote> </nodisp>

Inflammatory bowel disease (Crohn's disease and ulcerative colitis)

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

03.24.2019		current
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	===== Introduction =====		===== Introduction =====

-	[[http://www.mayoclinic.org/diseases-conditions/inflammatory-bowel-disease/basics/definition/con-20034908\|Mayo Clinic overview]]	+	[[https://www.mayoclinic.org/diseases-conditions/inflammatory-bowel-disease/basics/definition/con-20034908\|Mayo Clinic overview]]

-	<blockquote> The metagenomic approach allowed us to detect a reduced complexity of the bacterial phylum Firmicutes as a signature of the faecal microbiota in patients with CD. It also indicated the presence of new bacterial species. (({{pubmed>long:1856500}}))	+	<blockquote> The metagenomic approach allowed us to detect a reduced complexity of the bacterial phylum Firmicutes as a signature of the faecal microbiota in patients with CD. It also indicated the presence of new bacterial species. (({{pmid>long:1856500}}))
	</blockquote>		</blockquote>


-	<blockquote> Gut microbial induction of host immune maturation exemplifies host-microbe mutualism. We colonized germ-free (GF) mice with mouse microbiota (MMb) or human microbiota (HMb) to determine whether small intestinal immune maturation depends on a coevolved host-specific microbiota. Gut bacterial numbers and phylum abundance were similar in MMb and HMb mice, but bacterial species differed, especially the Firmicutes. HMb mouse intestines had low levels of CD4(+) and CD8(+) T cells, few proliferating T cells, few dendritic cells, and low antimicrobial peptide expression-all characteristics of GF mice. Rat microbiota also failed to fully expand intestinal T cell numbers in mice. Colonizing GF or HMb mice with mouse-segmented filamentous bacteria (SFB) partially restored T cell numbers, suggesting that SFB and other MMb organisms are required for full immune maturation in mice. Importantly, MMb conferred better protection against Salmonella infection than HMb. A host-specific microbiota appears to be critical for a healthy immune system. (({{pubmed>long:22726443}}))	+	<blockquote> Gut microbial induction of host immune maturation exemplifies host-microbe mutualism. We colonized germ-free (GF) mice with mouse microbiota (MMb) or human microbiota (HMb) to determine whether small intestinal immune maturation depends on a coevolved host-specific microbiota. Gut bacterial numbers and phylum abundance were similar in MMb and HMb mice, but bacterial species differed, especially the Firmicutes. HMb mouse intestines had low levels of CD4(+) and CD8(+) T cells, few proliferating T cells, few dendritic cells, and low antimicrobial peptide expression-all characteristics of GF mice. Rat microbiota also failed to fully expand intestinal T cell numbers in mice. Colonizing GF or HMb mice with mouse-segmented filamentous bacteria (SFB) partially restored T cell numbers, suggesting that SFB and other MMb organisms are required for full immune maturation in mice. Importantly, MMb conferred better protection against Salmonella infection than HMb. A host-specific microbiota appears to be critical for a healthy immune system. (({{pmid>long:22726443}}))
	</blockquote>		</blockquote>

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	===== Evidence of infectious cause =====		===== Evidence of infectious cause =====

-	These papers are really helpful.(({{pubmed>long:16849736}})) (({{pubmed>long:17699621}}))	+	These papers are really helpful.(({{pmid>long:16849736}})) (({{pmid>long:17699621}}))



	- [[home:patients:assessing_literature:palliative\|Patient response to immunosuppressive medications]] – Temporary symptomatic remission after taking immunosuppressive medications implies a decrease in the strength of the bacterial die-off reaction known as immunopathology. That none of these medications make patients better over the long-term is also telling. Several immunosuppressants are used to treat Crohn's including glucocorticoids such as prednisone and budesonide, aminosalicylates such as sulfasalazine and mesalamines, immunomodulators such as azathioprine and methotrexate and biologics such as remicade/infliximab and adalimumab.		- [[home:patients:assessing_literature:palliative\|Patient response to immunosuppressive medications]] – Temporary symptomatic remission after taking immunosuppressive medications implies a decrease in the strength of the bacterial die-off reaction known as immunopathology. That none of these medications make patients better over the long-term is also telling. Several immunosuppressants are used to treat Crohn's including glucocorticoids such as prednisone and budesonide, aminosalicylates such as sulfasalazine and mesalamines, immunomodulators such as azathioprine and methotrexate and biologics such as remicade/infliximab and adalimumab.
-	- Presence of microbes – Bacteria have long been suspected to be the cause of Crohn's Disease. Detection rates for bacterial DNA from L-forms (a portion of the metagenomic microbiota that cause disease) in Crohn's tissues is variable due to "the fastidious culture requirements of the cell wall-deficient forms." (({{pubmed>long:15074643}})) The following types and species of bacteria have been found in patients with Crohn's:	+	- Presence of microbes – Bacteria have long been suspected to be the cause of Crohn's Disease. Detection rates for bacterial DNA from L-forms (a portion of the metagenomic microbiota that cause disease) in Crohn's tissues is variable due to "the fastidious culture requirements of the cell wall-deficient forms." (({{pmid>long:15074643}})) The following types and species of bacteria have been found in patients with Crohn's:
-	* L-form bacteria (({{pubmed>long:6134652}}))	+	* L-form bacteria (({{pmid>long:6134652}}))
-	* //Bacteroides fragilis// (({{pubmed>long:88760}}))	+	* //Bacteroides fragilis// (({{pmid>long:88760}}))
-	* //Chlamydia trachomatis// (({{pubmed>long:83465}}))	+	* //Chlamydia trachomatis// (({{pmid>long:83465}}))
-	* //Listeria monocytogenes// (({{pubmed>long:7729631}}))	+	* //Listeria monocytogenes// (({{pmid>long:7729631}}))
-	* //Mycobacterium avium//, subspecies paratuberculosis (({{pubmed>long:12843021}}))	+	* //Mycobacterium avium//, subspecies paratuberculosis (({{pmid>long:12843021}}))
-	* //Mycobacterium kansasii// (({{pubmed>long:80630}}))	+	* //Mycobacterium kansasii// (({{pmid>long:80630}}))
-	* //Pseudomonas maltophilia// (({{pubmed>long:780185}}))	+	* //Pseudomonas maltophilia// (({{pmid>long:780185}}))

	De Hertogh //et al// provide a thorough review of the "unidentified persistent pathogen" theory, stating:		De Hertogh //et al// provide a thorough review of the "unidentified persistent pathogen" theory, stating:

-	<blockquote>Various environmental factors may play a role in the development of CD [Crohn's Disease], but microbes are most consistently implied. This theory is based on epidemiological, clinicopathological, genetic and experimental evidence. (({{pubmed>long:18240341}}))</blockquote>	+	<blockquote>Various environmental factors may play a role in the development of CD [Crohn's Disease], but microbes are most consistently implied. This theory is based on epidemiological, clinicopathological, genetic and experimental evidence. (({{pmid>long:18240341}}))</blockquote>

	Other researchers have come to similar conclusions:		Other researchers have come to similar conclusions:
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	<blockquote>//M. avium subsp paratuberculosis//, adherent-invasive //E. coli// and //Candida// are good candidates for an infectious aetiology of Crohn's disease on the basis of genetic susceptibility, which relates to impaired function in the defence against intracellular bacteria.		<blockquote>//M. avium subsp paratuberculosis//, adherent-invasive //E. coli// and //Candida// are good candidates for an infectious aetiology of Crohn's disease on the basis of genetic susceptibility, which relates to impaired function in the defence against intracellular bacteria.

-	//De Chambrunet et al.// (({{pubmed>long:18622157}}))	+	//De Chambrunet et al.// (({{pmid>long:18622157}}))
	</blockquote>		</blockquote>

	<blockquote>The bacterial community, in whole or in part, resident in the bowel of humans is considered to fuel the chronic immune inflammatory conditions characteristic of Crohn's disease and ulcerative colitis. Chronic or recurrent pouchitis in ulcerative colitis patients is responsive to antibiotic therapy, indicating that bacteria are the etiological agents.		<blockquote>The bacterial community, in whole or in part, resident in the bowel of humans is considered to fuel the chronic immune inflammatory conditions characteristic of Crohn's disease and ulcerative colitis. Chronic or recurrent pouchitis in ulcerative colitis patients is responsive to antibiotic therapy, indicating that bacteria are the etiological agents.

-	//Sokol et al.// (({{pubmed>long:18275077}})) </blockquote>	+	//Sokol et al.// (({{pmid>long:18275077}})) </blockquote>



-	<blockquote>Bacterial exotoxins downregulate cathelicidin (hCAP-18/LL-37) and human beta-defensin 1 (HBD-1) expression in the intestinal epithelial cells. (({{pubmed>long:18717821}}))	+	<blockquote>Bacterial exotoxins downregulate cathelicidin (hCAP-18/LL-37) and human beta-defensin 1 (HBD-1) expression in the intestinal epithelial cells. (({{pmid>long:18717821}}))
	</blockquote>		</blockquote>

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	==== More evidence ====		==== More evidence ====

-	[[http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=%22Inflammatory+Bowel+Diseases%2Fmicrobiology%22[Majr]+AND+Review[ptyp]\|PubMed reviews on the microbiology of inflammatory bowel diseases]]	+	[[https://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=%22Inflammatory+Bowel+Diseases%2Fmicrobiology%22[Majr]+AND+Review[ptyp]\|PubMed reviews on the microbiology of inflammatory bowel diseases]]

	58. El Zaatari FA, Osato MS, Graham DY. Etiology of		58. El Zaatari FA, Osato MS, Graham DY. Etiology of
Line 68:		Line 68:


-	[[http://rheumatology.oxfordjournals.org/cgi/content/abstract/40/1/15\|Correlation between the immune responses to collagens type I, III, IV and V and Klebsiella pneumoniae in patients with Crohn's disease and ankylosing spondylitis]]	+	[[https://rheumatology.oxfordjournals.org/cgi/content/abstract/40/1/15\|Correlation between the immune responses to collagens type I, III, IV and V and Klebsiella pneumoniae in patients with Crohn's disease and ankylosing spondylitis]]


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	Am J Clin Pathol. 1989 Mar;91(3):259-64.		Am J Clin Pathol. 1989 Mar;91(3):259-64.
	Johnson LA, Wirostko E, Wirostko WJ.		Johnson LA, Wirostko E, Wirostko WJ.
-	[[http://tinyurl.com/dh8th\Tinyurl\|Crohn's disease uveitis]]	+	[[https://tinyurl.com/dh8th\Tinyurl\|Crohn's disease uveitis]]

	"Uveitis is a symptom, and has many identified causes and associations at this point. Some cases are widely accepted to be due to bacteria or viruses. Other cases are associated with “autoimmune diseases” like Crohns disease and rheumatic arthritis. I suspect that these other cases are due to CWD bacteria. There are several interesting papers that explore this. The researchers found cell-wall deficient bacteria (sometimes called mollicute-like organisms) in the vitreous fluid of patients with sardoidosis, Crohn’s disease, ulcerative colitis, juvenile rheumatoid arthritis, etc."		"Uveitis is a symptom, and has many identified causes and associations at this point. Some cases are widely accepted to be due to bacteria or viruses. Other cases are associated with “autoimmune diseases” like Crohns disease and rheumatic arthritis. I suspect that these other cases are due to CWD bacteria. There are several interesting papers that explore this. The researchers found cell-wall deficient bacteria (sometimes called mollicute-like organisms) in the vitreous fluid of patients with sardoidosis, Crohn’s disease, ulcerative colitis, juvenile rheumatoid arthritis, etc."
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	Rifaximin is made by Salix Pharmaceuticals, Inc. Funding for the study was provided by Salix Pharmaceuticals, Inc.		Rifaximin is made by Salix Pharmaceuticals, Inc. Funding for the study was provided by Salix Pharmaceuticals, Inc.

-	One of only five hospitals in California whose nurses have been honored with the prestigious Magnet designation, Cedars-Sinai Medical Center is one of the largest nonprofit academic medical centers in the Western United States. Additional information is available at http://www.cedars-sinai.edu	+	One of only five hospitals in California whose nurses have been honored with the prestigious Magnet designation, Cedars-Sinai Medical Center is one of the largest nonprofit academic medical centers in the Western United States. Additional information is available at https://www.cedars-sinai.edu

-	[[http://www.newswise.com/articles/view/515982\|Targeted Antibiotics Lead to Long-lasting Improvement in IBS Symptoms]]	+	[[https://www.newswise.com/articles/view/515982\|Targeted Antibiotics Lead to Long-lasting Improvement in IBS Symptoms]]

-	It is apparently very rare for a patient to actually be allergic to Olmesartan (see Research below). An alternative approach where there is present a confirmed mycobacterial infection was recorded here [[http://www.mattioli1885journals.com/index.php/sarcoidosis/article/view/6769/4736\|MAP Abx]] .	+	It is apparently very rare for a patient to actually be allergic to Olmesartan (see Research below). An alternative approach where there is present a confirmed mycobacterial infection was recorded here [[https://www.mattioli1885journals.com/index.php/sarcoidosis/article/view/6769/4736\|MAP Abx]] .


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	This presentation explains how those, and the other Defensins, are important, and I think that those of you who track the science will find it very interesting indeed.		This presentation explains how those, and the other Defensins, are important, and I think that those of you who track the science will find it very interesting indeed.

-	The presentation runs for 30 minutes. [[http://autoimmunityresearch.org/crohns.ram\|Crohns]]	+	The presentation runs for 30 minutes. [[https://autoimmunityresearch.org/crohns.ram\|Crohns]]

	==== Serum levels of 'vitamin' D ====		==== Serum levels of 'vitamin' D ====
Line 154:		Line 154:
	BACKGROUND: The active form of vitamin D (1,25(OH)2D3) has been shown to inhibit development of inflammatory bowel disease (IBD) in IL-10 KO mice.		BACKGROUND: The active form of vitamin D (1,25(OH)2D3) has been shown to inhibit development of inflammatory bowel disease (IBD) in IL-10 KO mice.

-	<blockquote>Data point to a critical role for the VDR and 1,25(OH)2D3 in control of innate immunity and the response of the colon to chemical injury. (({{pubmed>long:17397543}}))</blockquote>	+	<blockquote>Data point to a critical role for the VDR and 1,25(OH)2D3 in control of innate immunity and the response of the colon to chemical injury. (({{pmid>long:17397543}}))</blockquote>


Line 161:		Line 161:
	SUBJECTS. One hundred and fifty randomly selected patients with IBD from the hospital register and 73 healthy controls.		SUBJECTS. One hundred and fifty randomly selected patients with IBD from the hospital register and 73 healthy controls.

-	<blockquote>Patients with IBD have lower serum levels of 250HD than healthy controls, but similar serum PTH concentrations and vitamin D intake. Vitamin D intake, and the serum levels of 250HD and PTH are not associated with BMD, and malabsorption is unlikely to be a major factor in the aetiology of bone loss in unselected IBD patients. (({{pubmed>long:8568480}}))</blockquote>	+	<blockquote>Patients with IBD have lower serum levels of 250HD than healthy controls, but similar serum PTH concentrations and vitamin D intake. Vitamin D intake, and the serum levels of 250HD and PTH are not associated with BMD, and malabsorption is unlikely to be a major factor in the aetiology of bone loss in unselected IBD patients. (({{pmid>long:8568480}}))</blockquote>


Line 168:		Line 168:

	<blockquote>		<blockquote>
-	The number of E. coli in situ correlated with the severity of ileal disease (rho 0.621, P<0.001) and invasive E. coli was restricted to inflamed mucosa. E. coli strains isolated from the ileum were predominantly novel in phylogeny, displayed pathogen-like behavior in vitro and harbored chromosomal and episomal elements similar to those described in extraintestinal pathogenic E. coli and pathogenic Enterobacteriaceae. These data establish that dysbiosis of the ileal mucosa-associated flora correlates with an ileal Crohn's disease (ICD) phenotype, and raise the possibility that a selective increase in a novel group of invasive E. coli is involved in the etiopathogenesis to Crohn's disease involving the ileum. (({{pubmed>long:18043660}}))</blockquote>	+	The number of E. coli in situ correlated with the severity of ileal disease (rho 0.621, P<0.001) and invasive E. coli was restricted to inflamed mucosa. E. coli strains isolated from the ileum were predominantly novel in phylogeny, displayed pathogen-like behavior in vitro and harbored chromosomal and episomal elements similar to those described in extraintestinal pathogenic E. coli and pathogenic Enterobacteriaceae. These data establish that dysbiosis of the ileal mucosa-associated flora correlates with an ileal Crohn's disease (ICD) phenotype, and raise the possibility that a selective increase in a novel group of invasive E. coli is involved in the etiopathogenesis to Crohn's disease involving the ileum. (({{pmid>long:18043660}}))</blockquote>

	<blockquote> A study suggests that the bacteria-immune system 'fight' continues after the instigator bacteria have been cleared by the body, according to Andrew Gewirtz. The fight can result in metabolic syndrome, an important factor in obesity, or inflammatory bowel disease (IBD).		<blockquote> A study suggests that the bacteria-immune system 'fight' continues after the instigator bacteria have been cleared by the body, according to Andrew Gewirtz. The fight can result in metabolic syndrome, an important factor in obesity, or inflammatory bowel disease (IBD).
Line 180:		Line 180:


-	"It is increasingly apparent that bacteria are playing a role in healthy development, and need to be properly managed by the mucosal immune system to avoid inflammatory diseases" Gewirtz explained. (({{pubmed>long:22863420}})) </blockquote>	+	"It is increasingly apparent that bacteria are playing a role in healthy development, and need to be properly managed by the mucosal immune system to avoid inflammatory diseases" Gewirtz explained. (({{pmid>long:22863420}})) </blockquote>

	===== Patient interviews =====		===== Patient interviews =====
Line 196:		Line 196:
	Lyme disease, irritable bowel syndrome/ulcerative colitis, radiculitis		Lyme disease, irritable bowel syndrome/ulcerative colitis, radiculitis

-	Read the [[http://bacteriality.com/2008/02/17/interview16/\|interview]]	+	Read the [[https://bacteriality.com/2008/02/17/interview16/\|interview]]

	<html></div></div>		<html></div></div>
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	===== Research =====		===== Research =====

-	Findings suggest that neither olmesartan nor other ARBs were associated with diarrhea among patients undergoing endoscopy. The spruelike enteropathy recently associated with olmesartan is likely a rare adverse effect and milder presentations are unlikely. (({{pubmed>long:25023670}}))	+	Findings suggest that neither olmesartan nor other ARBs were associated with diarrhea among patients undergoing endoscopy. The spruelike enteropathy recently associated with olmesartan is likely a rare adverse effect and milder presentations are unlikely. (({{pmid>long:25023670}}))

-	In a methotrexate-induced model of intestinal mucositis, olmesartan reduced inflammation and induced enteropathy characterized by severe diarrhea, weight loss, and reduced sucrose activity. (({{pubmed>long:25947920}}))	+	In a methotrexate-induced model of intestinal mucositis, olmesartan reduced inflammation and induced enteropathy characterized by severe diarrhea, weight loss, and reduced sucrose activity. (({{pmid>long:25947920}}))

-	Development, validation and implementation of an in vitro model for the study of metabolic and immune function in normal and inflamed human colonic epithelium. (({{pubmed>long:25557335}}))	+	Development, validation and implementation of an in vitro model for the study of metabolic and immune function in normal and inflamed human colonic epithelium. (({{pmid>long:25557335}}))

	<blockquote> It is now known that epithelial cells have the capacity to secrete and respond to a range of immunological mediators and this suggests that these cells play a prominent role in the pathogenesis of IBD. Current knowledge about the intestinal epithelium has mainly been obtained using models based on animal cells, transformed human intestinal cell lines and isolated cells from resected colonic bowel segments. Species difference, malignant origin and confounders related to surgery, obviously make these cell models however less applicable for patophysiological studies.		<blockquote> It is now known that epithelial cells have the capacity to secrete and respond to a range of immunological mediators and this suggests that these cells play a prominent role in the pathogenesis of IBD. Current knowledge about the intestinal epithelium has mainly been obtained using models based on animal cells, transformed human intestinal cell lines and isolated cells from resected colonic bowel segments. Species difference, malignant origin and confounders related to surgery, obviously make these cell models however less applicable for patophysiological studies.
Line 227:		Line 227:
	</blockquote>		</blockquote>

-	'Western'-style diets, high in fat/sugar, low in fibre, decrease beneficial Firmicutes that metabolise dietary plant-derived polysaccharides to SCFAs and increase mucosa-associated Proteobacteria (including enteric pathogens). (({{pubmed>long:26011307}}))	+	'Western'-style diets, high in fat/sugar, low in fibre, decrease beneficial Firmicutes that metabolise dietary plant-derived polysaccharides to SCFAs and increase mucosa-associated Proteobacteria (including enteric pathogens). (({{pmid>long:26011307}}))

	Butyric acid-producing anaerobic bacteria as a novel probiotic treatment approach for inflammatory bowel disease. [[https://jmm.microbiologyresearch.org/content/journal/jmm/10.1099/jmm.0.017541-0#tab2\|microbiology research]]		Butyric acid-producing anaerobic bacteria as a novel probiotic treatment approach for inflammatory bowel disease. [[https://jmm.microbiologyresearch.org/content/journal/jmm/10.1099/jmm.0.017541-0#tab2\|microbiology research]]

-	Butyric acid in functional constipation (({{pubmed>long:24868272}}))	+	Butyric acid in functional constipation (({{pmid>long:24868272}}))

-	Butyric acid in irritable bowel syndrome (({{pubmed>long:24868283}}))	+	Butyric acid in irritable bowel syndrome (({{pmid>long:24868283}}))

	[[https://www.sciencemag.org/news/2018/11/do-gut-bacteria-make-second-home-our-brains\|Roberts doesn’t know how these gut bacteria could have gotten into the brain. They may have crossed from blood vessels, traveling up nerves from the gut, or even come in through the nose]]		[[https://www.sciencemag.org/news/2018/11/do-gut-bacteria-make-second-home-our-brains\|Roberts doesn’t know how these gut bacteria could have gotten into the brain. They may have crossed from blood vessels, traveling up nerves from the gut, or even come in through the nose]]
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	[[https://www.karger.com/Article/FullText/477386\|Resistant Starch Regulates Gut Microbiota: Structure,		[[https://www.karger.com/Article/FullText/477386\|Resistant Starch Regulates Gut Microbiota: Structure,
	Biochemistry and Cell Signalling]]		Biochemistry and Cell Signalling]]
		+
		+	immune mechanisms and interactions between cells of the immune system and tissue environment (({{pmid>long:28126697}}))

	[{{:home:diseases:file:table_1_yang_et_al.gif\|Table 1 Yang et al }}]		[{{:home:diseases:file:table_1_yang_et_al.gif\|Table 1 Yang et al }}]
Line 246:		Line 248:


		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

-	(({{pubmed>long:000}}))	+	(({{pmid>long:000}}))


-	broken link http://mrw.interscience.wiley.com/cochrane/clsysrev/articles/CD007735/frame.html	+	broken link https://mrw.interscience.wiley.com/cochrane/clsysrev/articles/CD007735/frame.html
-	another, maybe [[http://www.wjgnet.com/1007-9327/14/845.asp\|thorough review]]	+	another, maybe [[https://www.wjgnet.com/1007-9327/14/845.asp\|thorough review]]

	<DiseaseHierarchy>		<DiseaseHierarchy>
Line 434:		Line 437:
	<blockquote>		<blockquote>

-	http://www.nejm.org/doi/full/10.1056/NEJMra1102942	+	https://www.nejm.org/doi/full/10.1056/NEJMra1102942

	Ulcerative Colitis		Ulcerative Colitis
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	<blockquote>		<blockquote>

-	Aberrant expansion of segmented filamentous bacteria in IgA-deficient gut(({{pubmed>long:14766966}}))	+	Aberrant expansion of segmented filamentous bacteria in IgA-deficient gut(({{pmid>long:14766966}}))

	The mechanism to maintain homeostasis of the gut microbiota remains largely unknown despite its critical role in the body defense. In the intestines of mice with deficiency of activation-induced cytidine deaminase (AID), the absence of hypermutated IgA is partially compensated for by the presence of large amounts of unmutated IgM and normal expression levels of defensins and angiogenins. We show here a predominant and persistent expansion of segmented filamentous bacteria throughout the small intestine of AID–/– mice. Reconstitution of lamina propria IgA production in AID–/– mice recovered the normal composition of gut flora and abolished the local and systemic activation of the immune system. The results indicate that secretions of IgAs rather than innate defense peptides are critical to regulation of commensal bacterial flora and that the segmented filamentous bacteria antigens are strong stimuli of the mucosal immune system.		The mechanism to maintain homeostasis of the gut microbiota remains largely unknown despite its critical role in the body defense. In the intestines of mice with deficiency of activation-induced cytidine deaminase (AID), the absence of hypermutated IgA is partially compensated for by the presence of large amounts of unmutated IgM and normal expression levels of defensins and angiogenins. We show here a predominant and persistent expansion of segmented filamentous bacteria throughout the small intestine of AID–/– mice. Reconstitution of lamina propria IgA production in AID–/– mice recovered the normal composition of gut flora and abolished the local and systemic activation of the immune system. The results indicate that secretions of IgAs rather than innate defense peptides are critical to regulation of commensal bacterial flora and that the segmented filamentous bacteria antigens are strong stimuli of the mucosal immune system.
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	<blockquote>		<blockquote>
-	Eur J Gastroenterol Hepatol. 2006 Jun;18(6):615-21.Heterogeneous expression of human cathelicidin hCAP18/LL-37 in inflammatory bowel diseases.(({{pubmed>long:16702850}}))	+	Eur J Gastroenterol Hepatol. 2006 Jun;18(6):615-21.Heterogeneous expression of human cathelicidin hCAP18/LL-37 in inflammatory bowel diseases.(({{pmid>long:16702850}}))
	Schauber J, Rieger D, Weiler F, Wehkamp J, Eck M, Fellermann K, Scheppach W, Gallo RL, Stange EF.		Schauber J, Rieger D, Weiler F, Wehkamp J, Eck M, Fellermann K, Scheppach W, Gallo RL, Stange EF.
	Department of Medicine II, Division of Gastroenterology cInstitute of Pathology, University of Würzburg, Germany. jschauber@ucsd.edu		Department of Medicine II, Division of Gastroenterology cInstitute of Pathology, University of Würzburg, Germany. jschauber@ucsd.edu
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	<blockquote>		<blockquote>
-	http://www.scientificamerican.com/article.cfm?id=genetics-in-the-gut	+	https://www.scientificamerican.com/article.cfm?id=genetics-in-the-gut


Line 595:		Line 598:

	After looking at various studies of human intestinal bacteria, Scientific American's Katherine Harmon (above) suggests that the microorganisms play a larger part in human health than previously thought, even at times overshadowing genetics. One key study, Harmon says, is a catalog of about 3.3 million human gut microbe genes — research being done by a team of BGI scientists (which our sister publication GenomeWeb Daily News covered here). Harmon also points to work from Emory University's Andrew Gewirtz which has focused on a particular host gene that seems affect intestinal microbes. Those researchers found that a loss of the TLR5 gene in mice leads to a shift in the microbiota communities and an increase in insulin resistance, obesity, and other metabolic disruptions. Gerwitz thinks that inflammation could be driving the cycle of obesity, in conjunction with the changes in gut microbes, in some cases allowing more calories to be extracted from food, though the exact trigger for the cycle is unknown. His group has already started comparing human genes and microbial profiles of healthy people, versus those with metabolic syndrome to see if they can achieve the same results as with the mouse study.		After looking at various studies of human intestinal bacteria, Scientific American's Katherine Harmon (above) suggests that the microorganisms play a larger part in human health than previously thought, even at times overshadowing genetics. One key study, Harmon says, is a catalog of about 3.3 million human gut microbe genes — research being done by a team of BGI scientists (which our sister publication GenomeWeb Daily News covered here). Harmon also points to work from Emory University's Andrew Gewirtz which has focused on a particular host gene that seems affect intestinal microbes. Those researchers found that a loss of the TLR5 gene in mice leads to a shift in the microbiota communities and an increase in insulin resistance, obesity, and other metabolic disruptions. Gerwitz thinks that inflammation could be driving the cycle of obesity, in conjunction with the changes in gut microbes, in some cases allowing more calories to be extracted from food, though the exact trigger for the cycle is unknown. His group has already started comparing human genes and microbial profiles of healthy people, versus those with metabolic syndrome to see if they can achieve the same results as with the mouse study.
-	http://www.genomeweb.com//node/935506?hq_e=el&hq_m=643944&hq_l=1&hq_v=891326c480	+	https://www.genomeweb.com//node/935506?hq_e=el&hq_m=643944&hq_l=1&hq_v=891326c480
	</blockquote>		</blockquote>

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	<blockquote>Nat Rev Gastroenterol Hepatol. 2010 Mar;7(3):126-8.		<blockquote>Nat Rev Gastroenterol Hepatol. 2010 Mar;7(3):126-8.
-	Crohn's disease: bacterial clearance in Crohn's disease pathogenesis.(({{pubmed>long:20203678}}))	+	Crohn's disease: bacterial clearance in Crohn's disease pathogenesis.(({{pmid>long:20203678}}))
	Fava F, Danese S.		Fava F, Danese S.

Line 618:		Line 621:


-	<blockquote>Mucosal flora in Crohn's disease and ulcerative colitis - an overview.(({{pubmed>long:20224153}}))	+	<blockquote>Mucosal flora in Crohn's disease and ulcerative colitis - an overview.(({{pmid>long:20224153}}))
	by Swidsinski A, Loening-Baucke V, Herber A		by Swidsinski A, Loening-Baucke V, Herber A
	Related Articles		Related Articles
Line 634:		Line 637:

	<blockquote>Rheumatology (Oxford). 2001 Jan;40(1):15-23.		<blockquote>Rheumatology (Oxford). 2001 Jan;40(1):15-23.
-	Correlation between the immune responses to collagens type I, III, IV and V and Klebsiella pneumoniae in patients with Crohn's disease and ankylosing spondylitis.(({{pubmed>long:11157137}}))	+	Correlation between the immune responses to collagens type I, III, IV and V and Klebsiella pneumoniae in patients with Crohn's disease and ankylosing spondylitis.(({{pmid>long:11157137}}))

	Tiwana H, Natt RS, Benitez-Brito R, Shah S, Wilson C, Bridger S, Harbord M, Sarner M, Ebringer A.		Tiwana H, Natt RS, Benitez-Brito R, Shah S, Wilson C, Bridger S, Harbord M, Sarner M, Ebringer A.
Line 648:		Line 651:

	This presentation was critical in helping me understand GI disease, it is worth reviewing in the light of what we know now:		This presentation was critical in helping me understand GI disease, it is worth reviewing in the light of what we know now:
-	http://autoimmunityresearch.org/crohns.ram	+	https://autoimmunityresearch.org/crohns.ram
	It is from the UCSD Host Defenses conferences in 2006.		It is from the UCSD Host Defenses conferences in 2006.

	Then the gene-disease links are tabulated at:		Then the gene-disease links are tabulated at:
-	http://www.ncbi.nlm.nih.gov/gene/64127?ordinalpos=1&itool=EntrezSystem2.PEntrez.Gene.Gene_ResultsPanel.Gene_RVDocSum	+	https://www.ncbi.nlm.nih.gov/gene/64127?ordinalpos=1&itool=EntrezSystem2.PEntrez.Gene.Gene_ResultsPanel.Gene_RVDocSum

	..Trevor..		..Trevor..
Line 722:		Line 725:
	</blockquote>		</blockquote>

-	[[http://www.cnn.com/2009/HEALTH/06/11/teen.self.diagnosis/\|Teen diagnoses her own disease in science class]]	+	[[https://www.cnn.com/2009/HEALTH/06/11/teen.self.diagnosis/\|Teen diagnoses her own disease in science class]]
	<blockquote>Inflamm Bowel Dis. 2011 Jan 6. [Epub ahead of print]Use of a novel vitamin d bioavailability test demonstrates that vitamin D absorption is decreased in patients with quiescent crohn's disease.		<blockquote>Inflamm Bowel Dis. 2011 Jan 6. [Epub ahead of print]Use of a novel vitamin d bioavailability test demonstrates that vitamin D absorption is decreased in patients with quiescent crohn's disease.
	Farraye FA, Nimitphong H, Stucchi A, Dendrinos K, Boulanger AB, Vijjeswarapu A, Tanennbaum A, Biancuzzo R, Chen TC, Holick MF.		Farraye FA, Nimitphong H, Stucchi A, Dendrinos K, Boulanger AB, Vijjeswarapu A, Tanennbaum A, Biancuzzo R, Chen TC, Holick MF.
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	</blockquote>		</blockquote>

-	(({{pubmed>long:99999999}}))	+	(({{pmid>long:99999999}}))
		+
		+	===== References =====</nodisp>

-	===== References =====

Irritable bowel syndrome (IBS)

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

03.13.2019		current
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-	Irritable bowel syndrome (IBS) is a gastrointestinal disorder characterized by chronic abdominal pain and altered bowel habits. It is the most commonly diagnosed gastrointestinal condition: the prevalence of IBS in North America is estimated to be approximately 10 to 15 percent Until the advent of culture-independent studies, physicians supposed IBS was a psychosomatic (functional) disorder as there was limited indication of an organic cause, with physicians complaining that patients were unmotivated to seek out cognitive behavioral therapy.(({{pubmed>long:20484720}}))	+	Irritable bowel syndrome (IBS) is a gastrointestinal disorder characterized by chronic abdominal pain and altered bowel habits. It is the most commonly diagnosed gastrointestinal condition: the prevalence of IBS in North America is estimated to be approximately 10 to 15 percent Until the advent of culture-independent studies, physicians supposed IBS was a psychosomatic (functional) disorder as there was limited indication of an organic cause, with physicians complaining that patients were unmotivated to seek out cognitive behavioral therapy.(({{pmid>long:20484720}}))

-	However, the notion that IBS is a psychological disorder has come under serious challenge.(({{pubmed>long:17040359}})) Recent research demonstrates that IBS is characterized by significant alterations in the gut microbiota.(({{pubmed>long:20937460}}))	+	However, the notion that IBS is a psychological disorder has come under serious challenge.(({{pmid>long:17040359}})) Recent research demonstrates that IBS is characterized by significant alterations in the gut microbiota.(({{pmid>long:20937460}}))

	The Marshall Protocol treats IBS by reactivating the innate immune response. In the course of treatment, patients' disease symptoms may become worse due to a process called immunopathology.		The Marshall Protocol treats IBS by reactivating the innate immune response. In the course of treatment, patients' disease symptoms may become worse due to a process called immunopathology.
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	* constipation – MP patients with constipation should have the symptom treated for immediate relief and then measures should be adopted to prevent constipation.		* constipation – MP patients with constipation should have the symptom treated for immediate relief and then measures should be adopted to prevent constipation.
-	* diarrhea – Patients with diarrhea may wish to increase fluid intake and/or take anti-diarrheal medication. (({{pubmed>long:26203094}}))	+	* diarrhea – Patients with diarrhea may wish to increase fluid intake and/or take anti-diarrheal medication. (({{pmid>long:26203094}}))
	* [[home:symptoms:gastrointestinal:appetite\|loss of appetite]] – If nausea is preventing a patient from eating, it's very important to palliate the nausea. Over the counter medications such as Gravol (dramamine) may be helpful. If not, patients should ask their doctor for a prescription antiemetic, such as hydroxyzine.		* [[home:symptoms:gastrointestinal:appetite\|loss of appetite]] – If nausea is preventing a patient from eating, it's very important to palliate the nausea. Over the counter medications such as Gravol (dramamine) may be helpful. If not, patients should ask their doctor for a prescription antiemetic, such as hydroxyzine.

-	[{{ :home:diseases:ibs.jpeg?400\|IBS is characterized by microbial dysbiosis. Electron micrograph of the cytoplasm of an enteroendocrine cell from a patient with IBS showing a structure resembling an intermediate body of //Chlamydia// (arrow) with characteristic condensed nucleoids. Dark homogenous structures are granules. M = Mitochondria, N = Nucleus, Bar = 0.5 μm. (Source: [[http://www.biomedcentral.com/1471-230X/10/19\|Dlugosz et al., 2010]])}}]	+	[{{ :home:diseases:ibs.jpeg?400\|IBS is characterized by microbial dysbiosis. Electron micrograph of the cytoplasm of an enteroendocrine cell from a patient with IBS showing a structure resembling an intermediate body of //Chlamydia// (arrow) with characteristic condensed nucleoids. Dark homogenous structures are granules. M = Mitochondria, N = Nucleus, Bar = 0.5 μm. (Source: [[https://www.biomedcentral.com/1471-230X/10/19\|Dlugosz et al., 2010]])}}]

	===== Evidence of infectious cause =====		===== Evidence of infectious cause =====
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	<blockquote>Recent studies provide increasing support for the concept that disturbances in gut flora occur in patients with irritable bowel syndrome and that such abnormalities may contribute to irritable bowel syndrome-type symptoms.		<blockquote>Recent studies provide increasing support for the concept that disturbances in gut flora occur in patients with irritable bowel syndrome and that such abnormalities may contribute to irritable bowel syndrome-type symptoms.

-	//Riordan et al.//(({{pubmed>long:17053447}}))</blockquote>	+	//Riordan et al.//(({{pmid>long:17053447}}))</blockquote>

	==== Onset following gastrointestinal infection ====		==== Onset following gastrointestinal infection ====

-	Epidemiologic studies have shown that gastrointestinal infection is the strongest environmental risk factor for the development of IBS.(({{pubmed>long:10037630}})) (({{pubmed>long:17445753}})) Although most patients with gastroenteritis become asymptomatic, a small but significant proportion of subjects (7%–31%) develop postinfectious IBS, dyspepsia, or both. A recent systematic review and meta-analysis identified that the incidence for IBS development after infectious gastroenteritis was 10%.(({{pubmed>long:17661757}}))	+	Epidemiologic studies have shown that gastrointestinal infection is the strongest environmental risk factor for the development of IBS.(({{pmid>long:10037630}})) (({{pmid>long:17445753}})) Although most patients with gastroenteritis become asymptomatic, a small but significant proportion of subjects (7%–31%) develop postinfectious IBS, dyspepsia, or both. A recent systematic review and meta-analysis identified that the incidence for IBS development after infectious gastroenteritis was 10%.(({{pmid>long:17661757}}))


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	==== Abnormal composition ====		==== Abnormal composition ====

-	Small intestinal bacterial overgrowth (SIBO) has been documented in a proportion of patients with IBS (10%–84%). For example, in 2012, Greek researchers enrolled patients needing upper gastrointestinal (GI) tract endoscopy. Among 320 subjects SIBO was diagnosed in 62 (19.4%) with 42 of those having IBS (67.7%). Of all IBS sufferers, SIBO was found in 37.5%. //Escherichia coli, Enterococcus spp.// and //Klebsiella pneumoniae// were the most common isolates within patients with SIBO. Several researchers have shown that eradicating SIBO results in symptomatic improvement.(({{pubmed>long:11151884}})) (({{pubmed>long:12591062}}))	+	Small intestinal bacterial overgrowth (SIBO) has been documented in a proportion of patients with IBS (10%–84%). For example, in 2012, Greek researchers enrolled patients needing upper gastrointestinal (GI) tract endoscopy. Among 320 subjects SIBO was diagnosed in 62 (19.4%) with 42 of those having IBS (67.7%). Of all IBS sufferers, SIBO was found in 37.5%. //Escherichia coli, Enterococcus spp.// and //Klebsiella pneumoniae// were the most common isolates within patients with SIBO. Several researchers have shown that eradicating SIBO results in symptomatic improvement.(({{pmid>long:11151884}})) (({{pmid>long:12591062}}))


	==== Higher temporal instability ====		==== Higher temporal instability ====

-	Accumulating evidence shows that patients with IBS have a higher temporal instability of the bacterial populations and that the microbiota composition is different compared with healthy controls.(({{pubmed>long:15747442}})) (({{pubmed>long:19693670}}))	+	Accumulating evidence shows that patients with IBS have a higher temporal instability of the bacterial populations and that the microbiota composition is different compared with healthy controls.(({{pmid>long:15747442}})) (({{pmid>long:19693670}}))


	==== Headline ====		==== Headline ====

-	Free versus total serum 25-hydroxyvitamin D in a murine model of colitis. (({{pubmed>long: 30710745}}))	+	Free versus total serum 25-hydroxyvitamin D in a murine model of colitis. (({{pmid>long: 30710745}}))

	==== Further research ====		==== Further research ====

-	Findings suggest that neither olmesartan nor other ARBs were associated with diarrhea among patients undergoing endoscopy. The spruelike enteropathy recently associated with olmesartan is likely a rare adverse effect and milder presentations are unlikely. (({{pubmed>long:25023670}}))	+	Findings suggest that neither olmesartan nor other ARBs were associated with diarrhea among patients undergoing endoscopy. The spruelike enteropathy recently associated with olmesartan is likely a rare adverse effect and milder presentations are unlikely. (({{pmid>long:25023670}}))
		+
		+	In a methotrexate-induced model of intestinal mucositis, olmesartan reduced inflammation and induced enteropathy characterized by severe diarrhea, weight loss, and reduced sucrose activity. (({{pmid>long:25947920}}))
		+
		+	Mast cell activation syndromes (({{pmid>long: 28780942}}))
		+
		+	Gastrointestinal (GI) symptoms are commonly reported in patients with mast cell disease. (({{pmid>long: 30007461}}))
		+
		+	Mast cells are located in close proximity to the vasculature, and vasoactive mediators released upon their activation can promote endothelial activation leading to blood brain barrier (BBB) dysfunction. (({{pmid>long: 30837844}}))
		+
		+	Mast cell activation plays an important role in stress-mediated disease pathogenesis. (({{pmid>long:30837843}}))

-	In a methotrexate-induced model of intestinal mucositis, olmesartan reduced inflammation and induced enteropathy characterized by severe diarrhea, weight loss, and reduced sucrose activity. (({{pubmed>long:25947920}}))


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	Lyme disease, irritable bowel syndrome/ulcerative colitis, radiculitis		Lyme disease, irritable bowel syndrome/ulcerative colitis, radiculitis

-	Read the [[http://bacteriality.com/2008/02/17/interview16/\|interview]]	+	Read the [[https://bacteriality.com/2008/02/17/interview16/\|interview]]

	<html></div></div></html>		<html></div></div></html>
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	diabetes, sarcoidosis, irritable bowel syndrome		diabetes, sarcoidosis, irritable bowel syndrome

-	Read the [[http://bacteriality.com/2008/06/19/interview22/\|interview]]	+	Read the [[https://bacteriality.com/2008/06/19/interview22/\|interview]]

	<html></div></div>		<html></div></div>
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	{{tag>disease}}		{{tag>disease}}

		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====



-	===== References =====	+	===== References =====</nodisp>

Kidney disease

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

02.19.2019		current
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	==== Dialysis ====		==== Dialysis ====

-	Dialysis is primarily used to provide an artificial replacement for lost kidney function in people with renal failure. The death rate from cardiovascular disease for dialysis patients is much higher than the general population, regardless of age.(({{pubmed>long:20411052}})) Patients with renal failure are not only exposed to higher volumes of water in their lifetime than the general population, but the barrier between blood and dialysis fluid is generally in the form of a nonselective semipermeable membrane, providing a direct route for any contaminants into the bloodstream. Consequently many of the permitted levels of contaminants in drinking water have the potential to cause problems in dialysis patients.(({{pubmed>long:12953025}}))	+	Dialysis is primarily used to provide an artificial replacement for lost kidney function in people with renal failure. The death rate from cardiovascular disease for dialysis patients is much higher than the general population, regardless of age.(({{pmid>long:20411052}})) Patients with renal failure are not only exposed to higher volumes of water in their lifetime than the general population, but the barrier between blood and dialysis fluid is generally in the form of a nonselective semipermeable membrane, providing a direct route for any contaminants into the bloodstream. Consequently many of the permitted levels of contaminants in drinking water have the potential to cause problems in dialysis patients.(({{pmid>long:12953025}}))

-	It is known that tap water harbors potentially pathogenic micro-organisms that can pose a signiﬁcant health threat to patients, especially those people with compromised immune systems and haemodialysis.(({{pubmed>long:9950177}}))(({{pubmed>long:16329897}})) For decades, hospital water sources have been known to be reservoirs of nosocomial pathogens, especially organisms of the //Pseudomonas sp.// yet guidelines for preventing such infections do not exist.(({{pubmed>long:12090885}}))(({{pubmed>long:12861087}}))	+	It is known that tap water harbors potentially pathogenic micro-organisms that can pose a signiﬁcant health threat to patients, especially those people with compromised immune systems and haemodialysis.(({{pmid>long:9950177}}))(({{pmid>long:16329897}})) For decades, hospital water sources have been known to be reservoirs of nosocomial pathogens, especially organisms of the //Pseudomonas sp.// yet guidelines for preventing such infections do not exist.(({{pmid>long:12090885}}))(({{pmid>long:12861087}}))

-	Today, specialists in infectious diseases are considering point-of-use filters. They presume that the filters achieve a greater than 99% reduction in total heterotrophic plate count of bacteria in the immediate and postﬂush samples.(({{pubmed>long:15940113}}))(({{pubmed>long:15940115}})) They conclude that such filtration units would prevent exposure of high-risk patients to waterborne pathogens. However, the results of Silbaq's 2009 study show that viable ultra-microcells pass through 0.2 micron filtration, and can be cultured on agar, as early as 72 hours after collection. The bacteria were identified using 16S ribosomal DNA sequences. The presence of those ultra-small bacteria in water filtrates would remain undetected by the standard and total heterotrophic plate count.	+	Today, specialists in infectious diseases are considering point-of-use filters. They presume that the filters achieve a greater than 99% reduction in total heterotrophic plate count of bacteria in the immediate and postﬂush samples.(({{pmid>long:15940113}}))(({{pmid>long:15940115}})) They conclude that such filtration units would prevent exposure of high-risk patients to waterborne pathogens. However, the results of Silbaq's 2009 study show that viable ultra-microcells pass through 0.2 micron filtration, and can be cultured on agar, as early as 72 hours after collection. The bacteria were identified using 16S ribosomal DNA sequences. The presence of those ultra-small bacteria in water filtrates would remain undetected by the standard and total heterotrophic plate count.

-	<blockquote>From the results in this study, one might conclude that the ﬁltration strategies may remove most microbes from water, but cannot prevent it. The ability of UMC to pass through the 0.2 m ﬁlters and even 0.1 m ﬁlters might select for new emerging pathogens from diverse phyla such as //S. maltophilia// and //Pandoraea sp.// which are well recognized as pathogens among cystic ﬁbrosis patients.(({{pubmed>long:15865277}}))	+	<blockquote>From the results in this study, one might conclude that the ﬁltration strategies may remove most microbes from water, but cannot prevent it. The ability of UMC to pass through the 0.2 m ﬁlters and even 0.1 m ﬁlters might select for new emerging pathogens from diverse phyla such as //S. maltophilia// and //Pandoraea sp.// which are well recognized as pathogens among cystic ﬁbrosis patients.(({{pmid>long:15865277}}))

-	//F.S. Silbaq//(({{pubmed>long:19040704}}))	+	//F.S. Silbaq//(({{pmid>long:19040704}}))
	</blockquote>		</blockquote>

Line 28:		Line 28:
	===== Role of Vitamin D Receptor in in chronic kidney disease =====		===== Role of Vitamin D Receptor in in chronic kidney disease =====

-	Excess 25(OH)D3 worsens tubulointerstitial injury by modulating macrophage phenotype. (({{pubmed>long:26176830}}))	+	Excess 25(OH)D3 worsens tubulointerstitial injury by modulating macrophage phenotype. (({{pmid>long:26176830}}))

	<blockquote>Continuously evidence indicates that deficiencies in vitamin D receptor activation represents one of key players in adversely affecting cardiovascular health, as well as inducing to secondary hyperparathyroidism in chromic kidney disease patients.... Potentially, selective VDR activators not only reduce serum parathyroid hormone levels minimizing the risk of hypercalcemia and hyperphosphatemia, but also may improve patient health, reducing the risk of cardiovascular disease.		<blockquote>Continuously evidence indicates that deficiencies in vitamin D receptor activation represents one of key players in adversely affecting cardiovascular health, as well as inducing to secondary hyperparathyroidism in chromic kidney disease patients.... Potentially, selective VDR activators not only reduce serum parathyroid hormone levels minimizing the risk of hypercalcemia and hyperphosphatemia, but also may improve patient health, reducing the risk of cardiovascular disease.

-	M. Cozzolino //et al.//(({{pubmed>long:20411052}}))</blockquote>	+	M. Cozzolino //et al.//(({{pmid>long:20411052}}))</blockquote>


-	<blockquote>Thessaloniki - Greece, June 2010 (({{pubmed>long:20540037}}))	+	<blockquote>Thessaloniki - Greece, June 2010 (({{pmid>long:20540037}}))

	Abstract		Abstract
Line 45:		Line 45:

	<blockquote>		<blockquote>
-	from Torino - Italy: Selective vitamin D receptor activation: effect on renal physiopathology. (({{pubmed>long:19941275}}))	+	from Torino - Italy: Selective vitamin D receptor activation: effect on renal physiopathology. (({{pmid>long:19941275}}))


Line 58:		Line 58:

	<blockquote>Sept. 2010		<blockquote>Sept. 2010
-	Direct evidence for a causative role of FGF23 in the abnormal renal phosphate handling and vitamin D metabolism in rats with early-stage chronic kidney disease.(({{pubmed>long:20844473}}))	+	Direct evidence for a causative role of FGF23 in the abnormal renal phosphate handling and vitamin D metabolism in rats with early-stage chronic kidney disease.(({{pmid>long:20844473}}))


Line 81:		Line 81:


-	Calcium-alkali syndrome due to vitamin D administration and magnesium oxide administration.(({{pubmed>long:19185403}}))	+	Calcium-alkali syndrome due to vitamin D administration and magnesium oxide administration.(({{pmid>long:19185403}}))


Line 96:		Line 96:
	Intricate mechanisms mediating the calcium-alkali syndrome depend on interplay among intestine, kidney, and bone. New insights regarding its pathogenesis focus on the key role of calcium-sensing receptors and TRPV5 channels in the modulation of renal calcium excretion.		Intricate mechanisms mediating the calcium-alkali syndrome depend on interplay among intestine, kidney, and bone. New insights regarding its pathogenesis focus on the key role of calcium-sensing receptors and TRPV5 channels in the modulation of renal calcium excretion.

-	Restoring extracellular blood volume, increasing GFR and calcium excretion, and discontinuing calcium supplementation provide best treatment. (({{pubmed>long:20413609}}))	+	Restoring extracellular blood volume, increasing GFR and calcium excretion, and discontinuing calcium supplementation provide best treatment. (({{pmid>long:20413609}}))


	===== Evidence of infectious cause =====		===== Evidence of infectious cause =====

-	[[http://www.nature.com/ja/journal/v65/n3/full/ja2011131a.html\|Creatinine inhibits bacterial replication]]	+	[[https://www.nature.com/ja/journal/v65/n3/full/ja2011131a.html\|Creatinine inhibits bacterial replication]]


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	//Claudia, MarshallProtocol.com//</blockquote>		//Claudia, MarshallProtocol.com//</blockquote>

		+	==== Patient's chart ====

		+	//with notes re eating meat before a test//

		+
		+	Creatinine, at 130 umole/L, was above normal range from the start. It took a few months to reach around 150 umole/L which seemed to become the basic level for the the next 11 years with peaks above that level being associated with other factors. The two anomalous peaks above 200umole/L were associated with having meat meals too close to the time of the test. The creatine and creatinine content in vertebrate muscle, or creatine supplements, can be absorbed to add to the body's potential to generate serum creatinine (70Effect of a Cooked Meat Meal on Serum Creatinine and Estimated Glomerular Filtration Rate in Diabetes-Related Kidney Disease \| Diabetes Care). After the early 200+ peak, from a sample taken after a light chicken lunch, meat was avoided for a day or two before sampling for subsequent tests.
		+
		+	The other exception was the second last one, for which meat was eaten the night before sampling. Apart from the aberrations arising from meat eating, eGFR values remained in the 30 to 40 range throughout the 11 year period. Thus the MP treatment, while inducing an initial fall in eGFR, has subsequently allowed the kidney function to remain stable.
		+
		+	{{:home:tests:kidney_tests..gif?700\|}}


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		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

Line 189:		Line 198:

	* legacy content		* legacy content
-	* http://www.marshallprotocol.com/view_topic.php?id=2487&forum_id=32&jump_to=84509#p84509 f109	+	* https://www.marshallprotocol.com/view_topic.php?id=2487&forum_id=32&jump_to=84509#p84509 f109

	* Avoid foods high in potassium for people with kidney disease?		* Avoid foods high in potassium for people with kidney disease?
Line 204:		Line 213:
	<blockquote>From: Jigsaw		<blockquote>From: Jigsaw
	Date: 2011-03-10 19:19:56		Date: 2011-03-10 19:19:56
-	Reply: http://www.marshallprotocol.com/reply.php?topic_id=1448	+	Reply: https://www.marshallprotocol.com/reply.php?topic_id=1448

	Hi Trevor. I am pleased to see your positive results from the use of sodium bicarbonate. I started using it (840 mg/ day) in August and have had one favourable result with potassium back into the normal range. Not much effect on creatinine.		Hi Trevor. I am pleased to see your positive results from the use of sodium bicarbonate. I started using it (840 mg/ day) in August and have had one favourable result with potassium back into the normal range. Not much effect on creatinine.
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	All values were from blood samples taken in the morning after overnight fasting. Seven days before the the 3/08 readings (urea, 18.3; creatinine, 148; eGFR, 40; potassium 5.5) , I had one set taken in the afternoon after a chicken lunch, where urea was 23.3, creatinine 201 and eGFR 28. Potassium was 5.4.		All values were from blood samples taken in the morning after overnight fasting. Seven days before the the 3/08 readings (urea, 18.3; creatinine, 148; eGFR, 40; potassium 5.5) , I had one set taken in the afternoon after a chicken lunch, where urea was 23.3, creatinine 201 and eGFR 28. Potassium was 5.4.

-	As I noted in a reply to Inge's thread, my cardiologist/physician and the Path lab said this would have no effect: but http://www.medicine.ox.ac.uk/bandolier/band156/b156-3.html noted that the test was standardised on samples taken in the morning from subjects after an overnight fast and quoting data showing that blood creatinine was raised an average of 25% for samples taken 1-2 hours after a meat meal One might say mine was raised by 53/148 x 100 = 35.5%..	+	As I noted in a reply to Inge's thread, my cardiologist/physician and the Path lab said this would have no effect: but https://www.medicine.ox.ac.uk/bandolier/band156/b156-3.html noted that the test was standardised on samples taken in the morning from subjects after an overnight fast and quoting data showing that blood creatinine was raised an average of 25% for samples taken 1-2 hours after a meat meal One might say mine was raised by 53/148 x 100 = 35.5%..

	I am not sure that the web link will still come up. I think the tests were done on healthy subjects and imagine that the effect would be greater where GFR is less adequate.		I am not sure that the web link will still come up. I think the tests were done on healthy subjects and imagine that the effect would be greater where GFR is less adequate.
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	Here is an article giving a glimpse into what it is like to experience true kidney failure:		Here is an article giving a glimpse into what it is like to experience true kidney failure:

-	http://www.vcstar.com/news/2011/jan/02/woman-starts-countys-first-group-for-dialysis-i/	+	https://www.vcstar.com/news/2011/jan/02/woman-starts-countys-first-group-for-dialysis-i/

	and another:		and another:

-	http://thehill.com/blogs/healthwatch/medicare/135463-medicare-agency-creates-quality-standards-for-kidney-disease-treatment	+	https://thehill.com/blogs/healthwatch/medicare/135463-medicare-agency-creates-quality-standards-for-kidney-disease-treatment

	and another from India:		and another from India:

-	http://www.indianexpress.com/news/dialysis-treatment-via-home-hemodialysis/732720/	+	https://www.indianexpress.com/news/dialysis-treatment-via-home-hemodialysis/732720/

	..Trevor..</blockquote>		..Trevor..</blockquote>
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	</blockquote>		</blockquote>

-	<note>a link to the document http://mpkb.org/home/othertreatments/sodium_bicarbonate would be appropriate somewhere here IMO	+	<note>a link to the document https://mpkb.org/home/othertreatments/sodium_bicarbonate would be appropriate somewhere here IMO
	//Sallie Q// Jan 2014</note>		//Sallie Q// Jan 2014</note>
	made Link --- //Sallie Q 11.18.2015//		made Link --- //Sallie Q 11.18.2015//
-	===== References =====	+	===== References =====</nodisp>

Kidney stones

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

01.03.2012		current
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	==== Epidemiological studies ====		==== Epidemiological studies ====

-	According to a 2011 systematic review performed by the Cochrane Collaboration, "Vitamin D3 combined with calcium significantly increased nephrolithiasis [kidney stones]."(({{pubmed>long:21735411}}))	+	According to a 2011 systematic review performed by the Cochrane Collaboration, "Vitamin D3 combined with calcium significantly increased nephrolithiasis [kidney stones]."(({{pmid>long:21735411}}))

-	A 1980 epidemiological study of lifeguards in Israel (who presumably were exposed to a great deal of sunshine) found that 11 of 45 (24%) had proven kidney stones, a rate twenty times the incidence in the general population.(({{pubmed>long:7424691}}))	+	A 1980 epidemiological study of lifeguards in Israel (who presumably were exposed to a great deal of sunshine) found that 11 of 45 (24%) had proven kidney stones, a rate twenty times the incidence in the general population.(({{pmid>long:7424691}}))


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	===== Evidence of infectious cause =====		===== Evidence of infectious cause =====

-	It is commonly accepted that stones composed of struvite are "derived from bacteria."(({{pubmed>long:10650513}}))	+	It is commonly accepted that stones composed of struvite are "derived from bacteria."(({{pmid>long:10650513}}))

-	According to researchers, most struvite (also referred to as "triple phosphate stones") were shown to be caused by //Proteus// or //Providencia// sub-species. In one study, //Proteus mirabilis// accounted for more than half of all urease-positive infections.(({{pubmed>long:10650513}})) Williams //et al//(({{pubmed>long:6472365}})) reported on 31 out of 39 patients with //Proteus// subspecies as the predominant urease-producing organisms. //Pseudomonas, Klebsiella, Providencia, Serratia// subspecies and //Staphylococci// accounted for the remaining cases.	+	According to researchers, most struvite (also referred to as "triple phosphate stones") were shown to be caused by //Proteus// or //Providencia// sub-species. In one study, //Proteus mirabilis// accounted for more than half of all urease-positive infections.(({{pmid>long:10650513}})) Williams //et al//(({{pmid>long:6472365}})) reported on 31 out of 39 patients with //Proteus// subspecies as the predominant urease-producing organisms. //Pseudomonas, Klebsiella, Providencia, Serratia// subspecies and //Staphylococci// accounted for the remaining cases.

-	Calcium oxalate stones are the most common form of kidney stones and there is emerging evidence they are caused by bacteria, specifically [[http://en.wikipedia.org/wiki/Nanobacterium\|nanobacteria]]. Certain small intracellular bacteria have been shown to be capable of forming calcium phosphate shells that serve as crystallization centers for kidney stones.(({{pubmed>long:12669155}})) Kajander //et al// note that, even in urine supersaturated by calcium oxalate and uric acid, kidney stone formation does not proceed unless there is a "nidi" (a central point or focus of bacterial growth in a living organism).(({{pubmed>long:12669155}}))	+	Calcium oxalate stones are the most common form of kidney stones and there is emerging evidence they are caused by bacteria, specifically [[https://en.wikipedia.org/wiki/Nanobacterium\|nanobacteria]]. Certain small intracellular bacteria have been shown to be capable of forming calcium phosphate shells that serve as crystallization centers for kidney stones.(({{pmid>long:12669155}})) Kajander //et al// note that, even in urine supersaturated by calcium oxalate and uric acid, kidney stone formation does not proceed unless there is a "nidi" (a central point or focus of bacterial growth in a living organism).(({{pmid>long:12669155}}))


	===== Incidence and prevalence =====		===== Incidence and prevalence =====

-	Kidney stones occur in up to 15% of the population. Between 0.1 and 0.4% of people form a kidney stone every year. The recurrence rate is high, reaching 52% within 10 years and 75% within 20 years.(({{pubmed>long:10756693}}))	+	Kidney stones occur in up to 15% of the population. Between 0.1 and 0.4% of people form a kidney stone every year. The recurrence rate is high, reaching 52% within 10 years and 75% within 20 years.(({{pmid>long:10756693}}))


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	sarcoidosis, psoriasis, insomnia, kidney stones		sarcoidosis, psoriasis, insomnia, kidney stones

-	Read the [[http://bacteriality.com/2007/08/10/interview1/\|interview]]	+	Read the [[https://bacteriality.com/2007/08/10/interview1/\|interview]]

	<html></div></div>		<html></div></div>
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-	{{tag>diseases}}	+	{{tag>disease}}


		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

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-	===== References =====	+	===== References =====</nodisp>

Learning difficulties (ADHD, ADD, dyslexia)

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

02.20.2019		current
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	===== Dyslexia =====		===== Dyslexia =====

-	Developmental dyslexia (DD) is a specific and persistent disability affecting the acquisition of written language. Prevalence is estimated to be between 5% and 17% of school-aged children; it therefore represents a major public health issue. (({{pubmed>long:23622168}}))	+	Developmental dyslexia (DD) is a specific and persistent disability affecting the acquisition of written language. Prevalence is estimated to be between 5% and 17% of school-aged children; it therefore represents a major public health issue. (({{pmid>long:23622168}}))

-	Reading disorders and dyslexia. (({{pubmed>long:27496059}}))	+	Reading disorders and dyslexia. (({{pmid>long:27496059}}))
	<blockquote>There are two distinct forms of reading disorder in children: dyslexia (a difficulty in learning to translate print into speech) and reading comprehension impairment. Both forms of reading problem appear to be predominantly caused by deficits in underlying oral language skills.</blockquote>		<blockquote>There are two distinct forms of reading disorder in children: dyslexia (a difficulty in learning to translate print into speech) and reading comprehension impairment. Both forms of reading problem appear to be predominantly caused by deficits in underlying oral language skills.</blockquote>


-	Developmental dyslexia (({{pubmed>long:25594880}}))	+	Developmental dyslexia (({{pmid>long:25594880}}))
	<blockquote> At the brain level, dyslexia is associated with aberrant structure and function, particularly in left hemisphere reading/language networks. The neurocognitive influences on dyslexia are also multifactorial and involve phonological processing deficits as well as weaknesses in other oral language skills and processing speed.		<blockquote> At the brain level, dyslexia is associated with aberrant structure and function, particularly in left hemisphere reading/language networks. The neurocognitive influences on dyslexia are also multifactorial and involve phonological processing deficits as well as weaknesses in other oral language skills and processing speed.

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		+	===== Perceptive difficulties =====
		+
		+	It is advisable to have children assessed occasionally for visual and hearing status. A child's hearing difficulty, if not picked up, can have a disproportionate effect on their life prospects.


	===== ADHD research =====		===== ADHD research =====

-	Shortened Sleep Duration Causes Sleepiness, Inattention, and Oppositionality in Adolescents With ADHD: Findings From a Crossover Sleep Restriction/Extension Study. (({{pubmed>long:30768404}}))	+	Shortened Sleep Duration Causes Sleepiness, Inattention, and Oppositionality in Adolescents With ADHD: Findings From a Crossover Sleep Restriction/Extension Study. (({{pmid>long:30768404}}))

	<blockquote>This study provides the first evidence that sleep duration is a causal contributor to daytime behaviors in adolescents with ADHD. Sleep may be an important target for intervention in adolescents with ADHD.		<blockquote>This study provides the first evidence that sleep duration is a causal contributor to daytime behaviors in adolescents with ADHD. Sleep may be an important target for intervention in adolescents with ADHD.
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-	The myeloarchitecture of impulsivity: premature responding in youth is associated with decreased myelination of ventral putamen. (({{pubmed>long:30770890}}))	+	The myeloarchitecture of impulsivity: premature responding in youth is associated with decreased myelination of ventral putamen. (({{pmid>long:30770890}}))

	<blockquote>Impulsivity has been suggested as a neurocognitive endophenotype conferring risk across a number of neuropsychiatric conditions, including substance and behavioural addictions, eating disorders, and attention deficit/hyperactivity disorder.		<blockquote>Impulsivity has been suggested as a neurocognitive endophenotype conferring risk across a number of neuropsychiatric conditions, including substance and behavioural addictions, eating disorders, and attention deficit/hyperactivity disorder.
Line 45:		Line 48:


-	Latent ERP components of cognitive dysfunctions in ADHD and schizophrenia. (({{pubmed>long:30769271}}))	+	Latent ERP components of cognitive dysfunctions in ADHD and schizophrenia. (({{pmid>long:30769271}}))


-	Sex Differences in Comorbidity Patterns of Attention-Deficit/Hyperactivity Disorder. (({{pubmed>long:30768399}}))	+	Sex Differences in Comorbidity Patterns of Attention-Deficit/Hyperactivity Disorder. (({{pmid>long:30768399}}))
	<blockquote>This study indicates that the association between ADHD and several comorbid disorders is stronger in females than in males.		<blockquote>This study indicates that the association between ADHD and several comorbid disorders is stronger in females than in males.
	</blockquote>		</blockquote>

-	Clinical developmental, neuropsychological, and social-emotional features of Turner syndrome. (({{pubmed>long:000}}))	+	Clinical developmental, neuropsychological, and social-emotional features of Turner syndrome. (({{pmid>long:000}}))
	<blockquote>TS is associated with an increased risk for difficulties with visual-spatial reasoning, visual-spatial memory, attention, executive functioning, motor, and math skills. Additionally, increased rates of social difficulties, anxiety, and depression are observed.		<blockquote>TS is associated with an increased risk for difficulties with visual-spatial reasoning, visual-spatial memory, attention, executive functioning, motor, and math skills. Additionally, increased rates of social difficulties, anxiety, and depression are observed.
	</blockquote>		</blockquote>

-	Towards a fuller assessment of benefits to children's health of reducing air pollution and mitigating climate change due to fossil fuel combustion. (({{pubmed>long:30771627}}))	+	Towards a fuller assessment of benefits to children's health of reducing air pollution and mitigating climate change due to fossil fuel combustion. (({{pmid>long:30771627}}))

	<blockquote>Various policies to reduce emissions have been implemented to reduce air pollution and mitigate climate change, with sizeable estimated health and economic benefits. However, only a few adverse outcomes in children have been considered, resulting in an undercounting of the benefits to this vulnerable population.		<blockquote>Various policies to reduce emissions have been implemented to reduce air pollution and mitigate climate change, with sizeable estimated health and economic benefits. However, only a few adverse outcomes in children have been considered, resulting in an undercounting of the benefits to this vulnerable population.
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	autism, ADHD, depression, severe anxiety, chronic fatigue syndrome (CFS)		autism, ADHD, depression, severe anxiety, chronic fatigue syndrome (CFS)

-	Read the [[http://bacteriality.com/2008/03/15/interview18/\|interview]]	+	Read the [[https://bacteriality.com/2008/03/15/interview18/\|interview]]

	<html></div></div></html>		<html></div></div></html>
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	rheumatoid arthritis, dyslexia		rheumatoid arthritis, dyslexia

-	Read the [[http://bacteriality.com/2007/09/01/interview2/\|interview]]	+	Read the [[https://bacteriality.com/2007/09/01/interview2/\|interview]]

	<html></div></div>		<html></div></div>
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		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

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-	===== References =====	+	===== References =====</nodisp>

Systemic lupus erythematosus (SLE)

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

02.09.2019		current
Line 6:		Line 6:


-	[[http://www.mayoclinic.org/diseases-conditions/lupus/basics/definition/con-20019676\|Mayo Clinic overview]]	+	[[https://www.mayoclinic.org/diseases-conditions/lupus/basics/definition/con-20019676\|Mayo Clinic overview]]

	===== Evidence of infectious cause =====		===== Evidence of infectious cause =====
	__		__
-	Amyloid-DNA Composites of Bacterial Biofilms Stimulate Autoimmunity.__ (({{pubmed>long:26084027}}))	+	Amyloid-DNA Composites of Bacterial Biofilms Stimulate Autoimmunity.__ (({{pmid>long:26084027}}))

	We found that a component of bacterial biofilms, the amyloid protein curli, irreversibly formed fibers with bacterial DNA during biofilm formation. This interaction accelerated amyloid polymerization and created potent immunogenic complexes that activated immune cells, including dendritic cells, to produce cytokines such as type I interferons, which are pathogenic in systemic lupus erythematosus (SLE).		We found that a component of bacterial biofilms, the amyloid protein curli, irreversibly formed fibers with bacterial DNA during biofilm formation. This interaction accelerated amyloid polymerization and created potent immunogenic complexes that activated immune cells, including dendritic cells, to produce cytokines such as type I interferons, which are pathogenic in systemic lupus erythematosus (SLE).

-	__Familial aggregation of lupus and autoimmunity in an unusual multiplex pedigree.__ (({{pubmed>long:10405936}}))	+	__Familial aggregation of lupus and autoimmunity in an unusual multiplex pedigree.__ (({{pmid>long:10405936}}))

	OBJECTIVE: To evaluate an unusual pedigree with 8 members diagnosed with systemic lupus erythematosus (SLE)		OBJECTIVE: To evaluate an unusual pedigree with 8 members diagnosed with systemic lupus erythematosus (SLE)
Line 26:		Line 26:


-	<blockquote>Now, researchers at Temple University School of Medicine (TUSM) have shown that bacterial communities that form biofilms play a role in the development of the autoimmune disease systemic lupus erythematosus -- a discovery that may provide important clues about several autoimmune ailments. (({{pubmed>long:26084027}})) </blockquote>	+	<blockquote>Now, researchers at Temple University School of Medicine (TUSM) have shown that bacterial communities that form biofilms play a role in the development of the autoimmune disease systemic lupus erythematosus -- a discovery that may provide important clues about several autoimmune ailments. (({{pmid>long:26084027}})) </blockquote>

	===== Diagnosis and Management =====		===== Diagnosis and Management =====

-	Predictors of flare include rising anti-dsDNA antibody titres, proteinuria and CRP and B lymphocyte stimulator levels(({{pubmed>long:28013206}}))	+	Predictors of flare include rising anti-dsDNA antibody titres, proteinuria and CRP and B lymphocyte stimulator levels(({{pmid>long:28013206}}))

-	Do classic blood biomarkers of JSLE identify active lupus nephritis? ...Binary logistic regression modeling demonstrated a combination of ESR, C3, white cell count, neutrophils, lymphocytes and IgG to be best for the identification of active LN(({{pubmed>long:28385126}}))	+	Do classic blood biomarkers of JSLE identify active lupus nephritis? ...Binary logistic regression modeling demonstrated a combination of ESR, C3, white cell count, neutrophils, lymphocytes and IgG to be best for the identification of active LN(({{pmid>long:28385126}}))

-	Potential Immune Biomarkers in Diagnosis and Clinical Management for Systemic Lupus Erythematosus.(({{pubmed>long:30581353}}))	+	Potential Immune Biomarkers in Diagnosis and Clinical Management for Systemic Lupus Erythematosus.(({{pmid>long:30581353}}))

-	Monitoring disease activity in systemic lupus erythematosus with single-molecule array digital ELISA quantification of serum interferon-α.(({{pubmed>long:30507062}}))	+	Monitoring disease activity in systemic lupus erythematosus with single-molecule array digital ELISA quantification of serum interferon-α.(({{pmid>long:30507062}}))

-	Effects of 12-week Aerobic Exercise on Arterial Stiffness, Inflammation, and Cardiorespiratory Fitness in Women with Systemic LUPUS Erythematosus: Non-Randomized Controlled Trial. (({{pubmed>long:30477218}}))	+	Effects of 12-week Aerobic Exercise on Arterial Stiffness, Inflammation, and Cardiorespiratory Fitness in Women with Systemic LUPUS Erythematosus: Non-Randomized Controlled Trial. (({{pmid>long:30477218}}))


Line 45:		Line 45:
	Does minocycline have side effects or cause lupus?		Does minocycline have side effects or cause lupus?

-	http://pediatrics.aappublications.org/cgi/content/extract/101/5/926	+	https://pediatrics.aappublications.org/cgi/content/extract/101/5/926

	The reports that Minocycline can induce lupus are laughable. Exactly how does a complex immune disease arise from the actions of a bacteriostatic antibiotic? Such a suggestion is ridiculous. The same goes for the suggestion that minocycline induces autoimmune hepatitis. Show us the beef, please - the molecular mechanisms.		The reports that Minocycline can induce lupus are laughable. Exactly how does a complex immune disease arise from the actions of a bacteriostatic antibiotic? Such a suggestion is ridiculous. The same goes for the suggestion that minocycline induces autoimmune hepatitis. Show us the beef, please - the molecular mechanisms.
Line 64:		Line 64:
	==== See also ====		==== See also ====

-	[[https://rarediseases.org/rare-diseases/mixed-connective-tissue-disease-mctd/\|Mixed Connective Tissue Disease]] MCTD patients have rheumatic overlap syndrome plus anti-RNP antibodies. (({{pubmed>long:25736140}})) (({{pubmed>long:27353506}}))	+	[[https://rarediseases.org/rare-diseases/mixed-connective-tissue-disease-mctd/\|Mixed Connective Tissue Disease]] MCTD patients have rheumatic overlap syndrome plus anti-RNP antibodies. (({{pmid>long:25736140}})) (({{pmid>long:27353506}}))


Line 70:		Line 70:

	<blockquote> BACKGROUND: Excessive activity of dendritic cells (DCs) is postulated as a central disease mechanism in Systemic Lupus Erythematosus (SLE). Vitamin D is known to reduce responsiveness of healthy donor DCs to the stimulatory effects of Type I IFN. As vitamin D deficiency is reportedly common in SLE, we hypothesized that vitamin D might play a regulatory role in the IFNalpha amplification loop in SLE. Our goals were to investigate the relationship between vitamin D levels and disease activity in SLE patients and to investigate the effects of vitamin D on DC activation and expression of IFNalpha-regulated genes in vitro.		<blockquote> BACKGROUND: Excessive activity of dendritic cells (DCs) is postulated as a central disease mechanism in Systemic Lupus Erythematosus (SLE). Vitamin D is known to reduce responsiveness of healthy donor DCs to the stimulatory effects of Type I IFN. As vitamin D deficiency is reportedly common in SLE, we hypothesized that vitamin D might play a regulatory role in the IFNalpha amplification loop in SLE. Our goals were to investigate the relationship between vitamin D levels and disease activity in SLE patients and to investigate the effects of vitamin D on DC activation and expression of IFNalpha-regulated genes in vitro.
-	(({{pubmed>long:20169063}}))	+	(({{pmid>long:20169063}}))
	</blockquote>		</blockquote>

Line 85:		Line 85:

	RESULTS: Hypertension, triglycerides and insulin resistance (determined by homeostasis model assessment of insulin resistance) and C-reactive protein (CRP) were increased in SLE (P < 0.01) while smoking, LDL, high density lipoprotein (HDL) did not differ between groups. Low levels of anti-PC IgM (lowest tertile) were more common in SLE patients than in controls (P = 0.0022). IMT and cIMa did not differ significantly between groups. However, plaques were more often found in SLE patients (P = 0.029). Age, LDL and IgM anti-PC (lowest tertile) were independently associated with plaque occurrence in SLE. Further, in the left carotid arteries echoluscent plaques (grade 1) were more prevalent in SLE as compared to controls (P < 0.016).		RESULTS: Hypertension, triglycerides and insulin resistance (determined by homeostasis model assessment of insulin resistance) and C-reactive protein (CRP) were increased in SLE (P < 0.01) while smoking, LDL, high density lipoprotein (HDL) did not differ between groups. Low levels of anti-PC IgM (lowest tertile) were more common in SLE patients than in controls (P = 0.0022). IMT and cIMa did not differ significantly between groups. However, plaques were more often found in SLE patients (P = 0.029). Age, LDL and IgM anti-PC (lowest tertile) were independently associated with plaque occurrence in SLE. Further, in the left carotid arteries echoluscent plaques (grade 1) were more prevalent in SLE as compared to controls (P < 0.016).
-	CONCLUSIONS: Plaque occurrence in the carotid arteries is increased in SLE and is independently associated with age, LDL and low anti-PC levels. Vulnerable plaques were more common in SLE. Anti-PC could be a novel risk marker also with a therapeutic potential in SLE. (({{pubmed>long:21092251}}))	+	CONCLUSIONS: Plaque occurrence in the carotid arteries is increased in SLE and is independently associated with age, LDL and low anti-PC levels. Vulnerable plaques were more common in SLE. Anti-PC could be a novel risk marker also with a therapeutic potential in SLE. (({{pmid>long:21092251}}))
	</blockquote>		</blockquote>

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-	Staph is commonly found on the skin or in the nose and can cause infections ranging from pneumonia to food poisoning. But skin infections are the most common, experts say, and are more likely to occur if you have a cut or scratch, or have contact with a person or surface that has staph bacteria. //Dr Chowdhary's studies// (({{pubmed>long:18793002}})) (({{pubmed>long:22798666}})) (({{pubmed>long:22859356}})) (({{pubmed>long:25369985}})) (({{pubmed>long:27520797}})) (({{pubmed>long:27365370}}))	+	Staph is commonly found on the skin or in the nose and can cause infections ranging from pneumonia to food poisoning. But skin infections are the most common, experts say, and are more likely to occur if you have a cut or scratch, or have contact with a person or surface that has staph bacteria. //Dr Chowdhary's studies// (({{pmid>long:18793002}})) (({{pmid>long:22798666}})) (({{pmid>long:22859356}})) (({{pmid>long:25369985}})) (({{pmid>long:27520797}})) (({{pmid>long:27365370}}))
	</blockquote>		</blockquote>

-	This Perspectives article discusses important questions about the use of ANA testing in both the clinical and research settings. (({{pubmed>long:28541299}}))	+	This Perspectives article discusses important questions about the use of ANA testing in both the clinical and research settings. (({{pmid>long:28541299}}))


-	This may indicate the importance of application of the test in a targeted way. (({{pubmed>long:27221374}}))	+	This may indicate the importance of application of the test in a targeted way. (({{pmid>long:27221374}}))

-	===== Recent Research =====	+	===== Research =====

	<blockquote>Ultraviolet (UV) light is an important environmental trigger for systemic lupus erythematosus (SLE) patients, yet the mechanisms by which UV light impacts disease are not fully known. This review covers evidence in both human and murine systems for the impacts of UV light on DNA damage, apoptosis, autoantigen exposure, cytokine production, inflammatory cell recruitment, and systemic flare induction. In addition, the role of the circadian clock is discussed. Evidence is compared in healthy individuals and SLE patients as well as in wild-type and lupus-prone mice. Further research is needed into the effects of UV light on cutaneous and systemic immune responses to understand how to prevent UV-light mediated lupus flares.		<blockquote>Ultraviolet (UV) light is an important environmental trigger for systemic lupus erythematosus (SLE) patients, yet the mechanisms by which UV light impacts disease are not fully known. This review covers evidence in both human and murine systems for the impacts of UV light on DNA damage, apoptosis, autoantigen exposure, cytokine production, inflammatory cell recruitment, and systemic flare induction. In addition, the role of the circadian clock is discussed. Evidence is compared in healthy individuals and SLE patients as well as in wild-type and lupus-prone mice. Further research is needed into the effects of UV light on cutaneous and systemic immune responses to understand how to prevent UV-light mediated lupus flares.

-	UV exposure induces DNA damage, which can result in the formation of dimeric photoproducts involving neighboring pyrimidine bases (11–13). UV irradiation can also cause an accumulation of reactive oxygen species (ROS) in keratinocytes that results in oxidative damage to DNA, lipids, and proteins and can ultimately induce apoptosis (11, 13–15). Of importance, the oxidative damage to DNA bases can lead to formation of 8-hydroxyguanosine (8-OHG) which has been shown to be immunogenic in patients with lupus erythematosus (LE) and abundantly present in UV-induced LE lesions (16–18). (({{pubmed>long:30405625}})) </blockquote>	+	UV exposure induces DNA damage, which can result in the formation of dimeric photoproducts involving neighboring pyrimidine bases (11–13). UV irradiation can also cause an accumulation of reactive oxygen species (ROS) in keratinocytes that results in oxidative damage to DNA, lipids, and proteins and can ultimately induce apoptosis (11, 13–15). Of importance, the oxidative damage to DNA bases can lead to formation of 8-hydroxyguanosine (8-OHG) which has been shown to be immunogenic in patients with lupus erythematosus (LE) and abundantly present in UV-induced LE lesions (16–18). (({{pmid>long:30405625}})) </blockquote>

-	When Chest Pain Reveals More: A Case of Hydrochlorothiazide-Induced Systemic Lupus Erythematosus. (({{pubmed>long:30613100}}))	+	When Chest Pain Reveals More: A Case of Hydrochlorothiazide-Induced Systemic Lupus Erythematosus. (({{pmid>long:30613100}}))

-	Curli-Containing Enteric Biofilms Inside and Out: Matrix Composition, Immune Recognition, and Disease Implications. (({{pubmed>long:30305312}}))	+	Curli-Containing Enteric Biofilms Inside and Out: Matrix Composition, Immune Recognition, and Disease Implications. (({{pmid>long:30305312}}))

	Furthermore, curli (and extracellular DNA) of enteric biofilms potentiate the autoimmune disease systemic lupus erythematosus (SLE) and promote the fibrillization of the pathogenic amyloid α-synuclein, which is implicated in Parkinson's disease. Homologues of curli-encoding genes are found in four additional bacterial phyla, suggesting that the biomedical implications involved with enteric biofilms are applicable to numerous bacterial species.		Furthermore, curli (and extracellular DNA) of enteric biofilms potentiate the autoimmune disease systemic lupus erythematosus (SLE) and promote the fibrillization of the pathogenic amyloid α-synuclein, which is implicated in Parkinson's disease. Homologues of curli-encoding genes are found in four additional bacterial phyla, suggesting that the biomedical implications involved with enteric biofilms are applicable to numerous bacterial species.

-	Calcium and vitamin D supplement intake may increase arterial stiffness in systemic lupus erythematosus patients. (({{pubmed>long:30628012}}))	+	Calcium and vitamin D supplement intake may increase arterial stiffness in systemic lupus erythematosus patients. (({{pmid>long:30628012}}))
		+
		+	Patients receiving the highest dose of olmesartan (40 and 80 mg) had an inward carotid remodeling and were shifted toward a lower elastic modulus at a given circumferential wall stress, indicating an improvement in the intrinsic elastic properties of the carotid artery wall material. These data suggest that 40 and 80 mg olmesartan were able to significantly remodel and destiffen the arterial wall material during long-term treatment, partly independently of blood pressure, compared with 20 mg. (({{pmid>long:25001274}}))


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	lupus, Sjogren’s Syndrome		lupus, Sjogren’s Syndrome

-	Read the [[http://bacteriality.com/2008/07/02/interview23/\|interview]]	+	Read the [[https://bacteriality.com/2008/07/02/interview23/\|interview]]

	<html></div></div>		<html></div></div>
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		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

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	* legacy content		* legacy content
-	* http://www.marshallprotocol.com/view_topic.php?id=10933&forum_id=32&jump_to=132470#p132470 f118	+	* https://www.marshallprotocol.com/view_topic.php?id=10933&forum_id=32&jump_to=132470#p132470 f118


	broken link		broken link
-	see also [[http://www.neuroscientistnews.com/research-news/research-team-finds-bacterial-biofilms-may-play-role-lupus-ms-other-auto-immune\|neuroscientistnews]]	+	see also [[https://www.neuroscientistnews.com/research-news/research-team-finds-bacterial-biofilms-may-play-role-lupus-ms-other-auto-immune\|neuroscientistnews]]
-	===== References =====	+	===== References =====</nodisp>

Chronic Lyme disease

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

09.13.2022		current
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	<blockquote>Lyme disease is considered to be caused by //Borrelia// species of bacteria but slowly evidence is accumulating which suggests that Lyme disease is a far more complex condition than //Borreliosis// alone. This hypothesis suggests that it may be more appropriate to regard Lyme disease as a tick borne disease complex. Over recent years numerous different microbes have been found in ticks which are known to be zoonotic and can coinfect the human host. The hypothesis suggests that multiple coinfections are invariably present in the clinical syndromes associated with Lyme disease and it is suggested that these act synergistically in complex ways.		<blockquote>Lyme disease is considered to be caused by //Borrelia// species of bacteria but slowly evidence is accumulating which suggests that Lyme disease is a far more complex condition than //Borreliosis// alone. This hypothesis suggests that it may be more appropriate to regard Lyme disease as a tick borne disease complex. Over recent years numerous different microbes have been found in ticks which are known to be zoonotic and can coinfect the human host. The hypothesis suggests that multiple coinfections are invariably present in the clinical syndromes associated with Lyme disease and it is suggested that these act synergistically in complex ways.

-	//D.C. Owen// (({{pubmed>long:16814477}}))	+	//D.C. Owen// (({{pmid>long:16814477}}))
-	//D.C. Owen// (({{pbmid>long:16814477}}))	+
	</blockquote>		</blockquote>

	Since first being recognized as a disease in 1981, Lyme has been widely assumed to be caused by a single infectious agent: //Borrelia//. In fact, the very reason the diagnosis of chronic Lyme is so controversial is that blood tests of people with Lyme-like symptoms infrequently show ongoing //Borrelia// infection. The assumption that one and only species (or genus) of microbe could cause a given symptom presentation is the antiquated legacy of Koch's postulates. More recent research suggests that the symptoms of chronic Lyme are caused my many microbes.		Since first being recognized as a disease in 1981, Lyme has been widely assumed to be caused by a single infectious agent: //Borrelia//. In fact, the very reason the diagnosis of chronic Lyme is so controversial is that blood tests of people with Lyme-like symptoms infrequently show ongoing //Borrelia// infection. The assumption that one and only species (or genus) of microbe could cause a given symptom presentation is the antiquated legacy of Koch's postulates. More recent research suggests that the symptoms of chronic Lyme are caused my many microbes.

-	W. Ian Lipkin's team sampled 286 adult ticks from the two counties in New York State where Lyme disease is endemic, looking for the prevalence of polymicrobial infection with //Borrelia burgdorferi, Anaplasma phagocytophilum, Babesia microti, Borrelia miyamotoi,// and Powassan virus.(({{pubmed>long:19725770}})) Seventy-one percent of the ticks harbored at least one organism; 30% had a polymicrobial infection. Infections with three microbes were detected in 5% of the ticks. One tick was infected with four organisms.	+	W. Ian Lipkin's team sampled 286 adult ticks from the two counties in New York State where Lyme disease is endemic, looking for the prevalence of polymicrobial infection with //Borrelia burgdorferi, Anaplasma phagocytophilum, Babesia microti, Borrelia miyamotoi,// and Powassan virus.(({{pmid>long:19725770}})) Seventy-one percent of the ticks harbored at least one organism; 30% had a polymicrobial infection. Infections with three microbes were detected in 5% of the ticks. One tick was infected with four organisms.

-	We collected data from an online survey of 200 of our patients, which evaluated the efficacy of dapsone (diaminodiphenyl sulfone, ie, DDS) combined with other antibiotics and agents that disrupt biofilms for the treatment of chronic Lyme disease/post-treatment Lyme disease syndrome (PTLDS). We also collected aggregate data from direct retrospective chart review, including laboratory testing for Lyme, other infections, and associated tick-borne coinfections. (({{pubmed>long:30863136}}))	+	We collected data from an online survey of 200 of our patients, which evaluated the efficacy of dapsone (diaminodiphenyl sulfone, ie, DDS) combined with other antibiotics and agents that disrupt biofilms for the treatment of chronic Lyme disease/post-treatment Lyme disease syndrome (PTLDS). We also collected aggregate data from direct retrospective chart review, including laboratory testing for Lyme, other infections, and associated tick-borne coinfections. (({{pmid>long:30863136}}))

	=== Australian ticks ===		=== Australian ticks ===

-	Human Tick-Borne Diseases in Australia. (({{pubmed>long:30746341}}))	+	Human Tick-Borne Diseases in Australia. (({{pmid>long:30746341}}))

	==== Borrelia and the VDR ====		==== Borrelia and the VDR ====
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	<relatedarticle> [[home:pathogenesis:vitamind:metabolism\|Metabolism of vitamin D and the Vitamin D Receptor]] </article>		<relatedarticle> [[home:pathogenesis:vitamind:metabolism\|Metabolism of vitamin D and the Vitamin D Receptor]] </article>

-	In the arms race of host–microbe co-evolution, successful microbial pathogens have evolved ingenious ways to evade host immune responses.(({{pubmed>long:21350579}}))	+	In the arms race of host–microbe co-evolution, successful microbial pathogens have evolved ingenious ways to evade host immune responses.(({{pmid>long:21350579}}))

	<blockquote>Studies have indicated that the dysregulation of VDR may lead to exaggerated inflammatory responses, raising the possibility that defects in Vitamin D and VDR signaling transduction may be linked to bacterial infection and chronic inflammation. Further characterization of Vitamin D/VDR will help elucidate the pathogenesis of various human diseases and in the design of new approaches for prevention and treatment.		<blockquote>Studies have indicated that the dysregulation of VDR may lead to exaggerated inflammatory responses, raising the possibility that defects in Vitamin D and VDR signaling transduction may be linked to bacterial infection and chronic inflammation. Further characterization of Vitamin D/VDR will help elucidate the pathogenesis of various human diseases and in the design of new approaches for prevention and treatment.

-	//Jun Sun// (({{pubmed>long:20639756}}))</blockquote>	+	//Jun Sun// (({{pmid>long:20639756}}))</blockquote>

-	Since the VDR is at the heart of the innate immune system, bacteria can survive by discovering how to disable it through a variety of different actions. Actions accumulate and are more powerful than individual actions. In keeping with evolutionary theory, a growing number of substances and species have been shown to downregulate the activity of the VDR, one of which is //Borrelia burgdorferi//. Live //Borrelia burgdorferi// reduced VDR expression in monocytes (phagocytes) by 50 times, and lysates ("dead" //Borrelia//) reduced it by 8 times(({{pubmed>long:19461888}}))	+	Since the VDR is at the heart of the innate immune system, bacteria can survive by discovering how to disable it through a variety of different actions. Actions accumulate and are more powerful than individual actions. In keeping with evolutionary theory, a growing number of substances and species have been shown to downregulate the activity of the VDR, one of which is //Borrelia burgdorferi//. Live //Borrelia burgdorferi// reduced VDR expression in monocytes (phagocytes) by 50 times, and lysates ("dead" //Borrelia//) reduced it by 8 times(({{pmid>long:19461888}}))

	Olmesartan is the main medication used by the Marshall Protocol and is believed to act as a VDR agonist, counteracting //Borrellia//'s effect on the Receptor and reversing the disease process.		Olmesartan is the main medication used by the Marshall Protocol and is believed to act as a VDR agonist, counteracting //Borrellia//'s effect on the Receptor and reversing the disease process.
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	==== Autoantibodies ====		==== Autoantibodies ====

-	Greco //et al.// claimed to find a variety of autoantibodies including antiphospholipid antibodies in patients with chronic Lyme disease.(({{pubmed>long:21729977}})) Autoantibodies have long been tied to persistent infections.	+	Greco //et al.// claimed to find a variety of autoantibodies including antiphospholipid antibodies in patients with chronic Lyme disease.(({{pmid>long:21729977}})) Autoantibodies have long been tied to persistent infections.

	===== Ticks, what to do when bitten =====		===== Ticks, what to do when bitten =====
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	===== Research =====		===== Research =====

-	Many antimicrobial agents (antibiotics, antivirals, antifungals, anthelmintics or antiparasitics) used for treating other infections were found to have better activity than the current Lyme antibiotics. These include antibacterials such as rifamycins (3-formal-rifamycin, rifaximin, rifamycin SV), thiostrepton, quinolone drugs (sarafloxacin, clinafloxacin, tosufloxacin), and cell wall inhibitors carbenicillin, tazobactam, aztreonam; antifungal agents such as fluconazole, mepartricin, bifonazole, climbazole, oxiconazole, nystatin; antiviral agents zanamivir, nevirapine, tilorone; antimalarial agents artemisinin, methylene blue, and quidaldine blue; antihelmintic and antiparasitic agents toltrazuril, tartar emetic, potassium antimonyl tartrate trihydrate, oxantel, closantel, hycanthone, pyrimethamine, and tetramisole. Interestingly, drugs used for treating other non-infectious conditions including verteporfin, oltipraz, pyroglutamic acid, pidolic acid, and dextrorphan tartrate, that act on the glutathione/γ-glutamyl pathway involved in protection against free radical damage, and also the antidepressant drug indatraline, were found to have high activity against stationary phase B. burgdorferi. (({{pubmed>long: 27025631}}))	+	Many antimicrobial agents (antibiotics, antivirals, antifungals, anthelmintics or antiparasitics) used for treating other infections were found to have better activity than the current Lyme antibiotics. These include antibacterials such as rifamycins (3-formal-rifamycin, rifaximin, rifamycin SV), thiostrepton, quinolone drugs (sarafloxacin, clinafloxacin, tosufloxacin), and cell wall inhibitors carbenicillin, tazobactam, aztreonam; antifungal agents such as fluconazole, mepartricin, bifonazole, climbazole, oxiconazole, nystatin; antiviral agents zanamivir, nevirapine, tilorone; antimalarial agents artemisinin, methylene blue, and quidaldine blue; antihelmintic and antiparasitic agents toltrazuril, tartar emetic, potassium antimonyl tartrate trihydrate, oxantel, closantel, hycanthone, pyrimethamine, and tetramisole. Interestingly, drugs used for treating other non-infectious conditions including verteporfin, oltipraz, pyroglutamic acid, pidolic acid, and dextrorphan tartrate, that act on the glutathione/γ-glutamyl pathway involved in protection against free radical damage, and also the antidepressant drug indatraline, were found to have high activity against stationary phase B. burgdorferi. (({{pmid>long: 27025631}}))

	===== Read more =====		===== Read more =====
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	* [[https://www.medscape.com/viewarticle/586226\|Chronic Lyme Disease and the "Axis of Evil"]] – A 2009 //Future Microbiology// paper written from the perspective of ILADS and LLMDs.		* [[https://www.medscape.com/viewarticle/586226\|Chronic Lyme Disease and the "Axis of Evil"]] – A 2009 //Future Microbiology// paper written from the perspective of ILADS and LLMDs.

-	* SPECT scans are abnormal in chronic Lyme patients – According to a 2012 study, 75% of brain SPECT scans are abnormal in patients with chronic Lyme disease.(({{pubmed>long:22889796}}))	+	* SPECT scans are abnormal in chronic Lyme patients – According to a 2012 study, 75% of brain SPECT scans are abnormal in patients with chronic Lyme disease.(({{pmid>long:22889796}}))


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	While there is general agreement on the optimal treatment for early Lyme disease, there is considerable controversy over the existence, prevalence, diagnostic criteria, and treatment of chronic Lyme disease.		While there is general agreement on the optimal treatment for early Lyme disease, there is considerable controversy over the existence, prevalence, diagnostic criteria, and treatment of chronic Lyme disease.

-	Over the past decade, two opposing camps have emerged in the battle over Lyme. One camp is represented by the International Lyme and Associated Diseases Society (ILADS), which argues that Lyme disease is not rare because its spread is facilitated by rodents, deer and birds, and can be found in an unpredictable distribution around the world accompanied by other tick-borne coinfections that may complicate the clinical presentation. According to the ILADS, tick bites often go unnoticed and commercial laboratory testing for Lyme disease is inaccurate. Consequently, the disease is often not recognized and may persist in a large number of patients, requiring prolonged antibiotic therapy to eradicate persistent infection with the evasive Lyme spirochete.(({{pubmed>long:19072179}}))	+	Over the past decade, two opposing camps have emerged in the battle over Lyme. One camp is represented by the International Lyme and Associated Diseases Society (ILADS), which argues that Lyme disease is not rare because its spread is facilitated by rodents, deer and birds, and can be found in an unpredictable distribution around the world accompanied by other tick-borne coinfections that may complicate the clinical presentation. According to the ILADS, tick bites often go unnoticed and commercial laboratory testing for Lyme disease is inaccurate. Consequently, the disease is often not recognized and may persist in a large number of patients, requiring prolonged antibiotic therapy to eradicate persistent infection with the evasive Lyme spirochete.(({{pmid>long:19072179}}))

-	The opposing camp is represented by the Infectious Diseases Society of America (IDSA), which maintains that Lyme disease is a rare illness localized to well-defined areas of the world. According to the IDSA, the disease is "hard to catch and easy to cure" because the infection is rarely encountered, easily diagnosed in its early stage by distinctive clinical features and in more advanced stages by accurate commercial laboratory tests, and effectively treated with a short course of antibiotics over 2-4 weeks. Chronic infection with the Lyme spirochete, //Borrelia burgdorferi//, is rare or nonexistent, and the concept of chronic Lyme disease rests on "faith-based" opinion rather than "evidence-based" science.(({{pubmed>long:19072179}}))	+	The opposing camp is represented by the Infectious Diseases Society of America (IDSA), which maintains that Lyme disease is a rare illness localized to well-defined areas of the world. According to the IDSA, the disease is "hard to catch and easy to cure" because the infection is rarely encountered, easily diagnosed in its early stage by distinctive clinical features and in more advanced stages by accurate commercial laboratory tests, and effectively treated with a short course of antibiotics over 2-4 weeks. Chronic infection with the Lyme spirochete, //Borrelia burgdorferi//, is rare or nonexistent, and the concept of chronic Lyme disease rests on "faith-based" opinion rather than "evidence-based" science.(({{pmid>long:19072179}}))

-	This mainstream view is exemplified by a 2007 review in the //New England Journal of Medicine//, which noted the diagnosis of chronic Lyme disease is used by a few physicians despite a lack of "reproducible or convincing scientific evidence", leading the authors to describe this diagnosis as "the latest in a series of syndromes that have been postulated in an attempt to attribute medically unexplained symptoms to particular infections."(({{pubmed>long:17914043}}))	+	This mainstream view is exemplified by a 2007 review in the //New England Journal of Medicine//, which noted the diagnosis of chronic Lyme disease is used by a few physicians despite a lack of "reproducible or convincing scientific evidence", leading the authors to describe this diagnosis as "the latest in a series of syndromes that have been postulated in an attempt to attribute medically unexplained symptoms to particular infections."(({{pmid>long:17914043}}))

	<blockquote>Chronic Lyme disease is the most recent in a continuing series of "medically unexplained symptoms" syndromes. These syndromes, such as fibromyalgia, chronic fatigue syndrome, and multiple chemical sensitivity, meet the need for a societally and morally acceptable explanation for ill-defined symptoms in the absence of objective physical and laboratory findings. We describe factors involved in the psychopathogenesis of chronic Lyme disease and focus on the confusion and insecurity these patients feel, which gives rise to an inability to adequately formulate and articulate their health concerns and to deal adequately with their medical needs, a state of disorganization termed aporia.		<blockquote>Chronic Lyme disease is the most recent in a continuing series of "medically unexplained symptoms" syndromes. These syndromes, such as fibromyalgia, chronic fatigue syndrome, and multiple chemical sensitivity, meet the need for a societally and morally acceptable explanation for ill-defined symptoms in the absence of objective physical and laboratory findings. We describe factors involved in the psychopathogenesis of chronic Lyme disease and focus on the confusion and insecurity these patients feel, which gives rise to an inability to adequately formulate and articulate their health concerns and to deal adequately with their medical needs, a state of disorganization termed aporia.

-	//L.H. Sigal// (({{pubmed>long:12194894}})) </blockquote>	+	//L.H. Sigal// (({{pmid>long:12194894}})) </blockquote>

	Groups of patients, patient advocates, and the small number of physicians who support the concept of chronic Lyme disease have organized to lobby for recognition of this diagnosis, as well as to argue for insurance coverage of long-term antibiotic therapy, which most insurers deny, as it is at odds with the guidelines of the major medical organizations.		Groups of patients, patient advocates, and the small number of physicians who support the concept of chronic Lyme disease have organized to lobby for recognition of this diagnosis, as well as to argue for insurance coverage of long-term antibiotic therapy, which most insurers deny, as it is at odds with the guidelines of the major medical organizations.
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	* [[home:othertreatments:rife\|Rife]] – There is no scientific evidence that the use of a Rife device has the intended effect on infectious bacteria. Instead, most patients using Rife are likely administering themselves nothing more than an expensive placebo.		* [[home:othertreatments:rife\|Rife]] – There is no scientific evidence that the use of a Rife device has the intended effect on infectious bacteria. Instead, most patients using Rife are likely administering themselves nothing more than an expensive placebo.

-	Selective Essential Oils from Spice or Culinary Herbs Have High Activity against Stationary Phase and Biofilm Borrelia burgdorferi. Some highly active essential oils were found to have excellent anti-biofilm ability (({{pubmed>long: 29075628}}))	+	Selective Essential Oils from Spice or Culinary Herbs Have High Activity against Stationary Phase and Biofilm Borrelia burgdorferi. Some highly active essential oils were found to have excellent anti-biofilm ability (({{pmid>long: 29075628}}))

	=== Disulfiram ===		=== Disulfiram ===
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	[[https://clinicaltrials.gov/ct2/show/NCT03891667\|Study to examine the safety of disulfiram among patients with post-treatment Lyme disease Sx]]		[[https://clinicaltrials.gov/ct2/show/NCT03891667\|Study to examine the safety of disulfiram among patients with post-treatment Lyme disease Sx]]

-	Screening to identify potent candidate drugs that can target the Borrelia persisters.(({{pubmed>long:27103785}}))	+	Screening to identify potent candidate drugs that can target the Borrelia persisters.(({{pmid>long:27103785}}))

-	Not suitable for children (({{pubmed>long:6470872}})), (({{pubmed>long:9093309}}))	+	Not suitable for children (({{pmid>long:6470872}})), (({{pmid>long:9093309}}))

-	may be possible for some adolescents (({{pubmed>long:27613346}}))	+	may be possible for some adolescents (({{pmid>long:27613346}}))

	=== ===		=== ===
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	Those affected by persistent Lyme disease, who are unable to follow the Marshall Protocol, could ask a medical practitioner about use of 3 antibiotic drugs in combination, as single drugs and 2-drug combinations appear to be ineffective with some PTLDS Borrelia biofilm.		Those affected by persistent Lyme disease, who are unable to follow the Marshall Protocol, could ask a medical practitioner about use of 3 antibiotic drugs in combination, as single drugs and 2-drug combinations appear to be ineffective with some PTLDS Borrelia biofilm.

-	the combination of different antiborrelial agents with synergistic effect seems to be a meaningful alternative and should be included in future studies in vitro as well as in vivo.(({{pubmed>long: 12073540}}))	+	the combination of different antiborrelial agents with synergistic effect seems to be a meaningful alternative and should be included in future studies in vitro as well as in vivo.(({{pmid>long: 12073540}}))

-	Borrelia burgdorferi persisters in vitro: eradication achieved by using daptomycin, cefoperazone and doxycycline. (({{pubmed>long: 25806811}}))	+	Borrelia burgdorferi persisters in vitro: eradication achieved by using daptomycin, cefoperazone and doxycycline. (({{pmid>long: 25806811}}))

-	Sulpha drugs and their combinations(({{pubmed>long:28327498}}))	+	Sulpha drugs and their combinations(({{pmid>long:28327498}}))

	{{tag>diseases}}		{{tag>diseases}}
		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

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	\|Diagnosis \|Diagnosed clinically based on symptoms, objective physical findings – such as erythema migrans (bulls eye rash), facial palsy or arthritis – or a history of possible exposure to infected ticks, as well as blood tests. Living in a tick-endemic area increases the likelihood of a Lyme diagnosis. \|For those with a negative test for //Borrelia//, getting a diagnosis of chronic Lyme depends largely on whether the doctor is "Lyme literate", that is if he/she even acknowledges the existence of chronic Lyme. \|		\|Diagnosis \|Diagnosed clinically based on symptoms, objective physical findings – such as erythema migrans (bulls eye rash), facial palsy or arthritis – or a history of possible exposure to infected ticks, as well as blood tests. Living in a tick-endemic area increases the likelihood of a Lyme diagnosis. \|For those with a negative test for //Borrelia//, getting a diagnosis of chronic Lyme depends largely on whether the doctor is "Lyme literate", that is if he/she even acknowledges the existence of chronic Lyme. \|
	\|Controversy over legitimacy of diagnosis \|Some disagreement over validity of tests, but controversy is relatively minimal. \|Diagnosis is most controversially applied to patients with nonspecific symptoms (e.g., fatigue), who show no objective evidence they have been infected with Lyme disease in the past, since the standard diagnostic tests for infection are negative. Most physicians [[#chronic_controversy_over_chronic_lyme_disease\|do not accept]] chronic Lyme as a legitimate diagnosis. \|		\|Controversy over legitimacy of diagnosis \|Some disagreement over validity of tests, but controversy is relatively minimal. \|Diagnosis is most controversially applied to patients with nonspecific symptoms (e.g., fatigue), who show no objective evidence they have been infected with Lyme disease in the past, since the standard diagnostic tests for infection are negative. Most physicians [[#chronic_controversy_over_chronic_lyme_disease\|do not accept]] chronic Lyme as a legitimate diagnosis. \|
-	\|Treatment \|Widely believed to be "readily curable." Conventional approach according to 2008 Infectious Diseases Society of America guidelines(({{pubmed>long:18452688}})) – antibiotics of choice are doxycycline (in adults), amoxicillin (in children), erythromycin (for pregnant women) and ceftriaxone \|"Lyme-literate" MDs often prescribe high-dose, often intravenous antibiotics such as Rocephin \|	+	\|Treatment \|Widely believed to be "readily curable." Conventional approach according to 2008 Infectious Diseases Society of America guidelines(({{pmid>long:18452688}})) – antibiotics of choice are doxycycline (in adults), amoxicillin (in children), erythromycin (for pregnant women) and ceftriaxone \|"Lyme-literate" MDs often prescribe high-dose, often intravenous antibiotics such as Rocephin \|


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	* [[home:othertreatments:rife\|Rife]] – There is no scientific evidence that the use of a Rife device has the intended effect on infectious bacteria. Instead, most patients using Rife are likely administering themselves nothing more than an expensive placebo.		* [[home:othertreatments:rife\|Rife]] – There is no scientific evidence that the use of a Rife device has the intended effect on infectious bacteria. Instead, most patients using Rife are likely administering themselves nothing more than an expensive placebo.

-	Selective Essential Oils from Spice or Culinary Herbs Have High Activity against Stationary Phase and Biofilm Borrelia burgdorferi. Some highly active essential oils were found to have excellent anti-biofilm ability (({{pubmed>long: 29075628}}))	+	Selective Essential Oils from Spice or Culinary Herbs Have High Activity against Stationary Phase and Biofilm Borrelia burgdorferi. Some highly active essential oils were found to have excellent anti-biofilm ability (({{pmid>long: 29075628}}))

	=== Disulfiram ===		=== Disulfiram ===
Line 457:		Line 457:
	[[https://clinicaltrials.gov/ct2/show/NCT03891667\|Study to examine the safety of disulfiram among patients with post-treatment Lyme disease Sx]]		[[https://clinicaltrials.gov/ct2/show/NCT03891667\|Study to examine the safety of disulfiram among patients with post-treatment Lyme disease Sx]]

-	Screening to identify potent candidate drugs that can target the Borrelia persisters.(({{pubmed>long:27103785}}))	+	Screening to identify potent candidate drugs that can target the Borrelia persisters.(({{pmid>long:27103785}}))

-	Not suitable for children (({{pubmed>long:6470872}})), (({{pubmed>long:9093309}}))	+	Not suitable for children (({{pmid>long:6470872}})), (({{pmid>long:9093309}}))

-	May be for adolescents (({{pubmed>long:27613346}}))	+	May be for adolescents (({{pmid>long:27613346}}))

	=== ===		=== ===
Line 489:		Line 489:
	Those affected by persistent Lyme disease, who are unable to follow the Marshall Protocol, could ask a medical practitioner about use of 3 antibiotic drugs in combination		Those affected by persistent Lyme disease, who are unable to follow the Marshall Protocol, could ask a medical practitioner about use of 3 antibiotic drugs in combination

-	the combination of different antiborrelial agents with synergistic effect seems to be a meaningful alternative and should be included in future studies in vitro as well as in vivo.(({{pubmed>long: 12073540}}))	+	the combination of different antiborrelial agents with synergistic effect seems to be a meaningful alternative and should be included in future studies in vitro as well as in vivo.(({{pmid>long: 12073540}}))

-	Borrelia burgdorferi persisters in vitro: eradication achieved by using daptomycin, cefoperazone and doxycycline. (({{pubmed>long: 25806811}}))	+	Borrelia burgdorferi persisters in vitro: eradication achieved by using daptomycin, cefoperazone and doxycycline. (({{pmid>long: 25806811}}))

-	Sulpha drugs and their combinations(({{pubmed>long:28327498}}))	+	Sulpha drugs and their combinations(({{pmid>long:28327498}}))

	===== References =====		===== References =====
		+	</nodisp>

Multiple chemical sensitivity (MCS)

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

10.19.2018		current
Line 5:		Line 5:

	Not unlike other poorly defined illnesses, many doctors believe hypersensitivity to chemicals is a psychological illness. But, the medical profession's track record for correctly identifying what is and is not a psychological illness is poor. That said, the exact pathophysiology of the disease is unclear. Given the size of the human microbiome and its ability to dysregulate the immune response, microbes, especially microbes in the gut, undoubtedly play a role in MCS.		Not unlike other poorly defined illnesses, many doctors believe hypersensitivity to chemicals is a psychological illness. But, the medical profession's track record for correctly identifying what is and is not a psychological illness is poor. That said, the exact pathophysiology of the disease is unclear. Given the size of the human microbiome and its ability to dysregulate the immune response, microbes, especially microbes in the gut, undoubtedly play a role in MCS.
		+
		+	Three types of overlap occur among the disease states chronic fatigue syndrome (CFS), fibromyalgia (FM), multiple chemical sensitivity (MCS) and posttraumatic stress disorder (PTSD). They share common symptoms. (({{pmid>long:11461161}}))

	A number of Marshall Protocol patients have reported improvement in their chemical sensitivities since starting the treatment.		A number of Marshall Protocol patients have reported improvement in their chemical sensitivities since starting the treatment.
Line 12:		Line 14:
	===== Prevalence =====		===== Prevalence =====

-	A 2012 paper in //Annals of Family Medicine// reports a study finding that 1 in 5 patients in a family practice doctor's waiting room are likely to be suffering from chemical intolerance.(({{pubmed>long:22778124}}))	+	A 2012 paper in //Annals of Family Medicine// reports a study finding that 1 in 5 patients in a family practice doctor's waiting room are likely to be suffering from chemical intolerance.(({{pmid>long:22778124}}))


Line 129:		Line 131:
	chronic fatigue syndrome (CFS), multiple chemical sensitivities		chronic fatigue syndrome (CFS), multiple chemical sensitivities

-	Read the [[http://bacteriality.com/2008/05/23/interview20/\|interview]]	+	Read the [[https://bacteriality.com/2008/05/23/interview20/\|interview]]

	<html></div></div>		<html></div></div>
Line 143:		Line 145:
	chronic borreliosis ("Lyme"), multiple chemical sensitivities, chronic spinal inflammation, peripheral neuropathy		chronic borreliosis ("Lyme"), multiple chemical sensitivities, chronic spinal inflammation, peripheral neuropathy

-	Read the [[http://bacteriality.com/2007/12/28/interview14/\|interview]]	+	Read the [[https://bacteriality.com/2007/12/28/interview14/\|interview]]

	<html></div></div>		<html></div></div>
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		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

-	===== References =====	+	===== References =====</nodisp>

Members & Diagnoses

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

Multiple sclerosis

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

02.07.2019		current
Line 6:		Line 6:


-	[[http://www.mayoclinic.org/diseases-conditions/multiple-sclerosis/home/ovc-20131882\|Mayo Clinic overview]]	+	[[https://www.mayoclinic.org/diseases-conditions/multiple-sclerosis/home/ovc-20131882\|Mayo Clinic overview]]


	==== Triggers and associations ====		==== Triggers and associations ====

-	- Exposure of the eyes to near-horizon sunshine may be a trigger for multiple sclerosis.(({{pubmed>long:19906495}}))	+	- Exposure of the eyes to near-horizon sunshine may be a trigger for multiple sclerosis.(({{pmid>long:19906495}}))

	BACKGROUND: Multiple sclerosis (MS) incidence is higher among those who live at high latitudes before adulthood. This is usually attributed to lower levels of Vitamin D, caused by lower UV levels. However direct damage of the optic nerve by near-horizon sunshine is a possible alternative explanation.		BACKGROUND: Multiple sclerosis (MS) incidence is higher among those who live at high latitudes before adulthood. This is usually attributed to lower levels of Vitamin D, caused by lower UV levels. However direct damage of the optic nerve by near-horizon sunshine is a possible alternative explanation.
Line 29:		Line 29:

	Multiple sclerosis etiology – an Epstein Barr hypothesis.		Multiple sclerosis etiology – an Epstein Barr hypothesis.
-	(({{pubmed>long:2833683}}))	+	(({{pmid>long:2833683}}))

	The pathogenesis of multiple sclerosis: reconsideration of		The pathogenesis of multiple sclerosis: reconsideration of
-	the role of viral agents and defence mechanisms. (({{pubmed>long:8803938}}))	+	the role of viral agents and defence mechanisms. (({{pmid>long:8803938}}))


Line 41:		Line 41:

	Anti-tumor necrosis factor		Anti-tumor necrosis factor
-	treatment restores the gut barrier in Crohn’s disease. (({{pubmed>long:12190167}}))	+	treatment restores the gut barrier in Crohn’s disease. (({{pmid>long:12190167}}))

-	Changes in gastrointestinal permeability in celiac disease. (({{pubmed>long:10207217}}))	+	Changes in gastrointestinal permeability in celiac disease. (({{pmid>long:10207217}}))

	Increased intestinal permeability as a cause of ﬂuctuating postprandial		Increased intestinal permeability as a cause of ﬂuctuating postprandial
-	blood glucose levels in Type 1 diabetic patients. (({{pubmed>long:12713453}}))	+	blood glucose levels in Type 1 diabetic patients. (({{pmid>long:12713453}}))

	Role of the intestinal tight junction modulator zonulin in the		Role of the intestinal tight junction modulator zonulin in the
-	pathogenesis of type I diabetes in BB diabetic-prone rats. (({{pubmed>long:15710870}}))	+	pathogenesis of type I diabetes in BB diabetic-prone rats. (({{pmid>long:15710870}}))


Line 59:		Line 59:


-	Multiple sclerosis or Lyme disease? a diagnosis problem of exclusion.(({{pubmed>long:2388492}}))	+	Multiple sclerosis or Lyme disease? a diagnosis problem of exclusion.(({{pmid>long:2388492}}))

-	Non-MS autoimmune demyelination.(({{pubmed>long:18928881}}))	+	Non-MS autoimmune demyelination.(({{pmid>long:18928881}}))

-	Multiple sclerosis: an infectious syndrome involving Chlamydophila pneumoniae. (({{pubmed>long:16996738}}))	+	Multiple sclerosis: an infectious syndrome involving Chlamydophila pneumoniae. (({{pmid>long:16996738}}))

-	Multiple sclerosis associated with Chlamydia pneumoniae infection of the CNS.(({{pubmed>long:9484408}}))	+	Multiple sclerosis associated with Chlamydia pneumoniae infection of the CNS.(({{pmid>long:9484408}}))

-	Chlamydia pneumoniae infection of the central nervous system in multiple sclerosis.(({{pubmed>long:10401775}}))	+	Chlamydia pneumoniae infection of the central nervous system in multiple sclerosis.(({{pmid>long:10401775}}))

-	Chlamydia pneumoniae infection of microglial cells in vitro: a model of microbial infection for neurological disease.(({{pubmed>long:16772424}}))	+	Chlamydia pneumoniae infection of microglial cells in vitro: a model of microbial infection for neurological disease.(({{pmid>long:16772424}}))

-	Association between Multiple Sclerosis and Cystic Structures in Cerebrospinal Fluid (({{pubmed>long:11787831}}))	+	Association between Multiple Sclerosis and Cystic Structures in Cerebrospinal Fluid (({{pmid>long:11787831}}))

-	Multifocal central nervous system lesions --multiple sclerosis or neuroborreliosis?(({{pubmed>long:16909774}}))	+	Multifocal central nervous system lesions --multiple sclerosis or neuroborreliosis?(({{pmid>long:16909774}}))

-	MR imaging assessment of brain and cervical cord damage in patients with neuroborreliosis.(({{pubmed>long:16611786}}))	+	MR imaging assessment of brain and cervical cord damage in patients with neuroborreliosis.(({{pmid>long:16611786}}))




-	Multiple sclerosis: infectious hypothesis. (({{pubmed>long:11603624}}))	+	Multiple sclerosis: infectious hypothesis. (({{pmid>long:11603624}}))
-	Role of viruses in etiology and pathogenesis of multiple sclerosis. (({{pubmed>long:11450311}}))	+	Role of viruses in etiology and pathogenesis of multiple sclerosis. (({{pmid>long:11450311}}))
-	Infection and the etiology and pathogenesis of multiple sclerosis. (({{pubmed>long:11898529}}))	+	Infection and the etiology and pathogenesis of multiple sclerosis. (({{pmid>long:11898529}}))


	Part I: the role of infection.		Part I: the role of infection.
-	Although genetic susceptibility explains the clustering of multiple sclerosis (MS) cases within families and the sharp decline in risk with increasing genetic distance, it cannot fully explain the geographic variations in MS frequency and the changes in risk that occur with migration. Epidemiological data provide some support for the "hygiene hypothesis," but with the additional proviso for a key role of Epstein-Barr virus (EBV) in determining MS risk. We show that whereas EBV stands out as the only infectious agent that can explain many of the key features of MS epidemiology, by itself the link between EBV and MS cannot explain the decline in risk among migrants from high to low MS prevalence areas. This decline implies that either EBV strains in low-risk areas have less propensity to cause MS, or that other infectious or noninfectious factors modify the host response to EBV or otherwise contribute to determine MS risk. (({{pubmed>long:17444504}}))	+	Although genetic susceptibility explains the clustering of multiple sclerosis (MS) cases within families and the sharp decline in risk with increasing genetic distance, it cannot fully explain the geographic variations in MS frequency and the changes in risk that occur with migration. Epidemiological data provide some support for the "hygiene hypothesis," but with the additional proviso for a key role of Epstein-Barr virus (EBV) in determining MS risk. We show that whereas EBV stands out as the only infectious agent that can explain many of the key features of MS epidemiology, by itself the link between EBV and MS cannot explain the decline in risk among migrants from high to low MS prevalence areas. This decline implies that either EBV strains in low-risk areas have less propensity to cause MS, or that other infectious or noninfectious factors modify the host response to EBV or otherwise contribute to determine MS risk. (({{pmid>long:17444504}}))

-	Correlation of mollicutes and their viruses with multiple sclerosis and other demyelinating diseases.(({{pubmed>long:12606251}}))	+	Correlation of mollicutes and their viruses with multiple sclerosis and other demyelinating diseases.(({{pmid>long:12606251}}))

-	The MSMV hypothesis: measles virus and multiple sclerosis, etiology and treatment. (({{pubmed>long:18703291}}))	+	The MSMV hypothesis: measles virus and multiple sclerosis, etiology and treatment. (({{pmid>long:18703291}}))

-	Epidemiology and etiology of multiple sclerosis.(({{pubmed>long:15893675}}))	+	Epidemiology and etiology of multiple sclerosis.(({{pmid>long:15893675}}))


	Detection of EBV-infected B-cells in patients' brain raises the possibility that intrathecal B-cell abnormalities and T-cell-mediated immunopathology in MS are the consequence of a persistently dysregulated EBV infection.		Detection of EBV-infected B-cells in patients' brain raises the possibility that intrathecal B-cell abnormalities and T-cell-mediated immunopathology in MS are the consequence of a persistently dysregulated EBV infection.
-	(({{pubmed>long:19359987}}))	+	(({{pmid>long:19359987}}))


Line 104:		Line 104:

	This review encompasses the clinical and pathological findings that pertain to the CNS infection in humans and includes experimental data from animal models that illuminate how these microbes enter the CNS. Recent experimental data showing that L. monocytogenes can invade the CNS by more than one mechanism make it a useful model for discussing the various routes for neuroinvasion used by intracellular bacterial pathogens.		This review encompasses the clinical and pathological findings that pertain to the CNS infection in humans and includes experimental data from animal models that illuminate how these microbes enter the CNS. Recent experimental data showing that L. monocytogenes can invade the CNS by more than one mechanism make it a useful model for discussing the various routes for neuroinvasion used by intracellular bacterial pathogens.
-	(({{pubmed>long:15084504}}))	+	(({{pmid>long:15084504}}))

	===== Of further interest =====		===== Of further interest =====

	By shedding light on the involvement of EBV in MS, these findings will pave the way to disease prevention and increase the therapeutic index of future treatments.		By shedding light on the involvement of EBV in MS, these findings will pave the way to disease prevention and increase the therapeutic index of future treatments.
-	(({{pubmed>long:19359987}}))	+	(({{pmid>long:19359987}}))

-	In a collaborative GWAS involving 9772 cases of European descent collected by 23 research groups working in 15 different countries, we have replicated almost all of the previously suggested associations and identified at least a further 29 novel susceptibility loci. Within the MHC we have refined the identity of the DRB1 risk alleles and confirmed that variation in the HLA-A gene underlies the independent protective effect attributable to the Class I region. Immunologically relevant genes are significantly over-represented amongst those mapping close to the identified loci and particularly implicate T helper cell differentiation in the pathogenesis of multiple sclerosis. (({{pubmed>long:21833088}}))	+	In a collaborative GWAS involving 9772 cases of European descent collected by 23 research groups working in 15 different countries, we have replicated almost all of the previously suggested associations and identified at least a further 29 novel susceptibility loci. Within the MHC we have refined the identity of the DRB1 risk alleles and confirmed that variation in the HLA-A gene underlies the independent protective effect attributable to the Class I region. Immunologically relevant genes are significantly over-represented amongst those mapping close to the identified loci and particularly implicate T helper cell differentiation in the pathogenesis of multiple sclerosis. (({{pmid>long:21833088}}))

-	Antibiotic Use (({{pubmed>long:21920946}}))	+	Antibiotic Use (({{pmid>long:21920946}}))


Line 120:		Line 120:


-	{{http://www.guardian.co.uk/science/2011/dec/28/vitamin-d-ms-medical-research?newsfeed=true\|bureaucratic blight on medical research}}	+	{{https://www.guardian.co.uk/science/2011/dec/28/vitamin-d-ms-medical-research?newsfeed=true\|bureaucratic blight on medical research}}


Line 138:		Line 138:


-	Occupational exposure to UV light and mortality from multiple sclerosis(({{pubmed>long:19197935}}))	+	Occupational exposure to UV light and mortality from multiple sclerosis(({{pmid>long:19197935}}))

	<blockquote>		<blockquote>

-	"Cholecalciferol plus calcium suppresses abnormal PBMC reactivity in patients with multiple sclerosis."(({{pubmed>long:21697250}}))	+	"Cholecalciferol plus calcium suppresses abnormal PBMC reactivity in patients with multiple sclerosis."(({{pmid>long:21697250}}))

	Forty-nine patients were matched (for age, sex, disease duration, disease-modifying drug, and disability) and enrolled (treated n = 25; control n = 24). Four patients were lost to follow-up (n = 2 from each group).		Forty-nine patients were matched (for age, sex, disease duration, disease-modifying drug, and disability) and enrolled (treated n = 25; control n = 24). Four patients were lost to follow-up (n = 2 from each group).
Line 151:		Line 151:


-	[{{ home:diseases:multiple_sclerosis_incidence_world_map.jpg\|MS is rare in China.	+	[{{home:diseases:multiple_sclerosis_incidence_world_map.jpg\|MS is rare in China.
-	Low prevalence in Russia, although it varies by ethnic region.	+	Low prevalence in Russia, although it varies by ethnic region.}}] map from msrc.co.uk
-	**map from msrc.co.u}}]	+


Line 160:		Line 159:


-	==== Myelin sheath ====	+	===== Myelin sheath =====


Line 190:		Line 189:


-	2018 This review focuses on four main themes influencing current understanding of thermoregulatory dysfunction in MS (({{pubmed>long:30459034}}))	+	2018 This review focuses on four main themes influencing current understanding of thermoregulatory dysfunction in MS (({{pmid>long:30459034}}))

	2019 [[https://www.cell.com/neuron/fulltext/S0896-6273(18)31123-1?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0896627318311231%3Fshowall%3Dtrue\|from Misgeld, Kerschensteiner. et al]]		2019 [[https://www.cell.com/neuron/fulltext/S0896-6273(18)31123-1?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0896627318311231%3Fshowall%3Dtrue\|from Misgeld, Kerschensteiner. et al]]
Line 198:		Line 197:
	• Calcium influx from the extracellular space drives axon degeneration		• Calcium influx from the extracellular space drives axon degeneration
	• Nanoscale ruptures allow entry of calcium across the axonal plasma membrane		• Nanoscale ruptures allow entry of calcium across the axonal plasma membrane
		+
	===== Member experience =====		===== Member experience =====

Line 231:		Line 231:

	First: Greg Blaney some years ago...		First: Greg Blaney some years ago...
-	[[http://AutoimmunityResearch.org/transcripts/ICA2008_Transcript_GregBlaney.pdf\|Two MS cases]]	+	[[https://AutoimmunityResearch.org/transcripts/ICA2008_Transcript_GregBlaney.pdf\|Two MS cases]]

	Next: Dr Roswitha Goetze-Pelka, on MS patient in 2011:		Next: Dr Roswitha Goetze-Pelka, on MS patient in 2011:
-	[[http://autoimmunityresearch.org/transcripts/Singapore_ACA2011_Goetze-Pelka.pdf\|Case history by neurologist]]	+	[[https://autoimmunityresearch.org/transcripts/Singapore_ACA2011_Goetze-Pelka.pdf\|Case history by neurologist]]

-	Our simplified article in [[http://autoimmunityresearch.org/preprints/Proal_2013_CurrentOpinion-Preprint.pdf\|Current Opinion in Rheumatology 2013]]	+	Our simplified article in [[https://autoimmunityresearch.org/preprints/Proal_2013_CurrentOpinion-Preprint.pdf\|Current Opinion in Rheumatology 2013]]

	{{tag>disease }}		{{tag>disease }}
Line 242:		Line 242:


		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

	removed FAILED LINK --- //Sallie Q 01.18.2019//		removed FAILED LINK --- //Sallie Q 01.18.2019//
-	{{http://www.wired.com/wiredscience/2010/04/multiple-sclerosis-twinmystery/\|MS study deepens twin mystery}}	+	{{https://www.wired.com/wiredscience/2010/04/multiple-sclerosis-twinmystery/\|MS study deepens twin mystery}}


Line 258:		Line 259:
	<blockquote>High-dose vitamin D also was not associated with a significant difference in change in total volume of T2 lesions, with median changes of −330 mm3 compared with a change of −95 mm3 for low-dose vitamin D (P=0.6), the investigators reported in the October 25 issue of Neurology.		<blockquote>High-dose vitamin D also was not associated with a significant difference in change in total volume of T2 lesions, with median changes of −330 mm3 compared with a change of −95 mm3 for low-dose vitamin D (P=0.6), the investigators reported in the October 25 issue of Neurology.

-	[[http://www.medpagetoday.com/clinical-context/MultipleSclerosis/29235\|High-Dose Vitamin D No Help in MS]]	+	[[https://www.medpagetoday.com/clinical-context/MultipleSclerosis/29235\|High-Dose Vitamin D No Help in MS]]

	2011. "A randomized trial of high-dose vitamin D2 in relapsing-remitting multiple sclerosis."		2011. "A randomized trial of high-dose vitamin D2 in relapsing-remitting multiple sclerosis."

-	OBJECTIVE: Higher latitude, lower ultraviolet exposure, and lower serum 25-hydroxyvitamin D (25OHD) correlate with higher multiple sclerosis (MS) prevalence, relapse rate, and mortality. We therefore evaluated the effects of high-dose vitamin D2 (D2) in MS. METHODS: Adults with clinically active relapsing-remitting MS (RRMS) were randomized to 6 months' double-blind placebo-controlled high-dose vitamin D2, 6,000 IU capsules, dose adjusted empirically aiming for a serum 25OHD 130-175 nM. All received daily low-dose (1,000 IU) D2 to prevent deficiency. Brain MRIs were performed at baseline, 4, 5, and 6 months. Primary endpoints were the cumulative number of new gadolinium-enhancing lesions and change in the total volume of T2 lesions. Secondary endpoints were Expanded Disability Status Scale (EDSS) score and relapses. RESULTS: Twenty-three people were randomized, of whom 19 were on established interferon or glatiramer acetate (Copaxone) treatment. Median 25OHD rose from 54 to 69 nM (low-dose D2) vs 59 to 120 nM (high-dose D2) (p = 0.002). No significant treatment differences were detected in the primary MRI endpoints. Exit EDSS, after adjustment for entry EDSS, was higher following high-dose D2 than following low-dose D2 (p = 0.05). There were 4 relapses with high-dose D2 vs none with low-dose D2 (p = 0.04). CONCLUSION: We did not find a therapeutic advantage in RRMS for high-dose D2 over low-dose D2 supplementation. Classification of evidence: This study provides Class I evidence that high-dose vitamin D2 (targeting 25OHD 130-175 nM), compared to low-dose supplementation (1,000 IU/d), was not effective in reducing MRI lesions in patients with RRMS. (({{pubmed>long:22025459}}))	+	OBJECTIVE: Higher latitude, lower ultraviolet exposure, and lower serum 25-hydroxyvitamin D (25OHD) correlate with higher multiple sclerosis (MS) prevalence, relapse rate, and mortality. We therefore evaluated the effects of high-dose vitamin D2 (D2) in MS. METHODS: Adults with clinically active relapsing-remitting MS (RRMS) were randomized to 6 months' double-blind placebo-controlled high-dose vitamin D2, 6,000 IU capsules, dose adjusted empirically aiming for a serum 25OHD 130-175 nM. All received daily low-dose (1,000 IU) D2 to prevent deficiency. Brain MRIs were performed at baseline, 4, 5, and 6 months. Primary endpoints were the cumulative number of new gadolinium-enhancing lesions and change in the total volume of T2 lesions. Secondary endpoints were Expanded Disability Status Scale (EDSS) score and relapses. RESULTS: Twenty-three people were randomized, of whom 19 were on established interferon or glatiramer acetate (Copaxone) treatment. Median 25OHD rose from 54 to 69 nM (low-dose D2) vs 59 to 120 nM (high-dose D2) (p = 0.002). No significant treatment differences were detected in the primary MRI endpoints. Exit EDSS, after adjustment for entry EDSS, was higher following high-dose D2 than following low-dose D2 (p = 0.05). There were 4 relapses with high-dose D2 vs none with low-dose D2 (p = 0.04). CONCLUSION: We did not find a therapeutic advantage in RRMS for high-dose D2 over low-dose D2 supplementation. Classification of evidence: This study provides Class I evidence that high-dose vitamin D2 (targeting 25OHD 130-175 nM), compared to low-dose supplementation (1,000 IU/d), was not effective in reducing MRI lesions in patients with RRMS. (({{pmid>long:22025459}}))


Line 277:		Line 278:


-	May 2005: Interesting new abstract about MS as an infection (({{pubmed>long:15893675}}))	+	May 2005: Interesting new abstract about MS as an infection (({{pmid>long:15893675}}))


Line 408:		Line 409:

	Here is an example of the type of study which had initially side-tracked me into thinking viruses might play a part in MS		Here is an example of the type of study which had initially side-tracked me into thinking viruses might play a part in MS
-	http://www.primezone.com/newsroom/news.html?d=87395	+	https://www.primezone.com/newsroom/news.html?d=87395

	But what these scientists are forgetting is that a monkey is not a human. Animal models have failed to predict human autoimmune disease time after time. So, while this study sounds very persuasive, it will fail to be replicated in man.		But what these scientists are forgetting is that a monkey is not a human. Animal models have failed to predict human autoimmune disease time after time. So, while this study sounds very persuasive, it will fail to be replicated in man.
Line 423:		Line 424:

	Here is a paper on cytokine profiles in MS		Here is a paper on cytokine profiles in MS
-	http://tinyurl.com/5pa9n	+	https://tinyurl.com/5pa9n

	They concluded that the Th1 profile is predominant, except during pregnancy. That conclusion was erroneous, in my opinion, for the reasons I stated here		They concluded that the Th1 profile is predominant, except during pregnancy. That conclusion was erroneous, in my opinion, for the reasons I stated here
-	http://tinyurl.com/6f6qr	+	https://tinyurl.com/6f6qr

	however their raw data seem reliable, and it indicates Th1 is dominant.		however their raw data seem reliable, and it indicates Th1 is dominant.
Line 461:		Line 462:

	Proc Natl Acad Sci U S A. 2010 Apr 6;107(14):6418-23. Epub 2010 Mar 22.		Proc Natl Acad Sci U S A. 2010 Apr 6;107(14):6418-23. Epub 2010 Mar 22.
-	UV radiation suppresses experimental autoimmune encephalomyelitis independent of vitamin D production.(({{pubmed>long:20308557}}))	+	UV radiation suppresses experimental autoimmune encephalomyelitis independent of vitamin D production.(({{pmid>long:20308557}}))
	Becklund BR, Severson KS, Vang SV, DeLuca HF.		Becklund BR, Severson KS, Vang SV, DeLuca HF.
	Department of Biochemistry, University of Wisconsin, Madison, WI 53706, USA.		Department of Biochemistry, University of Wisconsin, Madison, WI 53706, USA.
Line 468:		Line 469:
	Abstract		Abstract
	Although the exact cause of multiple sclerosis (MS) is unknown, a number of genetic and environmental factors are thought to influence MS susceptibility. One potential environmental factor is sunlight and the subsequent production of vitamin D. A number of studies have correlated decreased exposure to UV radiation (UVR) and low serum 25-hydroxyvitamin D(3) [25(OH)D(3)] levels with an increased risk for developing MS. Furthermore, both UVR and the active form of vitamin D, 1alpha,25-dihydroxyvitamin D(3), suppress disease in the experimental autoimmune encephalomyelitis (EAE) animal model of MS. These observations led to the hypothesis that UVR likely suppresses disease through the increased production of vitamin D. However, UVR can suppress the immune system independent of vitamin D. Therefore, it is unclear whether UVR, vitamin D, or both are necessary for the putative decrease in MS susceptibility. We have probed the ability of UVR to suppress disease in the EAE model of MS and assessed the effect of UVR on serum 25(OH)D(3) and calcium levels. Our results indicate that continuous treatment with UVR dramatically suppresses clinical signs of EAE. Interestingly, disease suppression occurs with only a modest, transient increase in serum 25(OH)D(3) levels. Further analysis demonstrated that the levels of 25(OH)D(3) obtained upon UVR treatment were insufficient to suppress EAE independent of UVR treatment. These results suggest that UVR is likely suppressing disease independent of vitamin D production, and that vitamin D supplementation alone may not replace the ability of sunlight to reduce MS susceptibility.		Although the exact cause of multiple sclerosis (MS) is unknown, a number of genetic and environmental factors are thought to influence MS susceptibility. One potential environmental factor is sunlight and the subsequent production of vitamin D. A number of studies have correlated decreased exposure to UV radiation (UVR) and low serum 25-hydroxyvitamin D(3) [25(OH)D(3)] levels with an increased risk for developing MS. Furthermore, both UVR and the active form of vitamin D, 1alpha,25-dihydroxyvitamin D(3), suppress disease in the experimental autoimmune encephalomyelitis (EAE) animal model of MS. These observations led to the hypothesis that UVR likely suppresses disease through the increased production of vitamin D. However, UVR can suppress the immune system independent of vitamin D. Therefore, it is unclear whether UVR, vitamin D, or both are necessary for the putative decrease in MS susceptibility. We have probed the ability of UVR to suppress disease in the EAE model of MS and assessed the effect of UVR on serum 25(OH)D(3) and calcium levels. Our results indicate that continuous treatment with UVR dramatically suppresses clinical signs of EAE. Interestingly, disease suppression occurs with only a modest, transient increase in serum 25(OH)D(3) levels. Further analysis demonstrated that the levels of 25(OH)D(3) obtained upon UVR treatment were insufficient to suppress EAE independent of UVR treatment. These results suggest that UVR is likely suppressing disease independent of vitamin D production, and that vitamin D supplementation alone may not replace the ability of sunlight to reduce MS susceptibility.
-	PMID: 20308557 (({{pubmed>long:11111111}}))	+	PMID: 20308557 (({{pmid>long:11111111}}))
	</blockquote>		</blockquote>

Line 480:		Line 481:
	From: Varia		From: Varia
	Date: 2010-07-07 15:47:41		Date: 2010-07-07 15:47:41
-	Reply: http://www.curemyth1.org/reply.php?topic_id=2490	+	Reply: https://www.curemyth1.org/reply.php?topic_id=2490


Line 498:		Line 499:
	Phillyguy: Probably explains one of the reasons why the incidence of autoimmune disease is lower in developing countries and infectious disease is higher. Interestingly, VDR generally increases the expression ofTregs, IL-10 and TGFbeta and represses IFNg and IL-12.		Phillyguy: Probably explains one of the reasons why the incidence of autoimmune disease is lower in developing countries and infectious disease is higher. Interestingly, VDR generally increases the expression ofTregs, IL-10 and TGFbeta and represses IFNg and IL-12.

-	(({{pubmed>long:11111111}}))	+	(({{pmid>long:11111111}}))
	PMID: 21277637 </blockquote>		PMID: 21277637 </blockquote>

Line 510:		Line 511:
	Abstract		Abstract
	It has recently been suggested that, rather than being an autoimmune disease, multiple sclerosis (MS) is an example of a neurocristopathy, a pathological process resulting from a faulty development of the neural crest. Whilst several characteristics of the disease suggest a neurocristopathy, other aetiological factors require consideration, including hygiene-related factors that alter the immune responses to common pathogens resulting in an eclipse of immune reactivity that could protect against MS, the possible role of human endogenous retroviruses (HERVs) in pathogenesis and autoimmune phenomena, HLA polymorphism, vitamin D levels before and after birth and immune repair mechanisms. A postulated aetiological factor in MS, associated with altered vitamin D metabolism and abnormal HERV expression, is a long-lasting disturbed redox regulation in the biosynthesis of a melanoma-like melanin pigment. Although intensive further studies on melanin pigments in nerve tissue in MS are required, the known properties of a pathological form of such pigments in melanoma could explain a number of observations in MS, including the impact of light, UV-light, and vitamin D, and could explain the clinical manifestations of MS on the basis of an oscillating process of oxidative charge and discharge of the pigments and a threshold phenomenon with a change of the quasi-catalytic function of the pigment from destroying reactive oxygen radicals or species to transforming them to more harmful long-persisting highly reactive species. Taken together with the consequences of an adaptive process in partly demyelinated neurons, resulting in an increase in number of mitochondria, and the impact of stressful life events, these conditions are necessary and sufficient to explain the disease process of MS with its spatial (plaques) and temporal (attacks and remissions) characteristics. This suggested unifying concept of the pathogenesis of MS may open perspectives for prevention, diagnosis and therapy. In particular, prevention may be achieved by vaccinating against Epstein-Barr virus in early childhood.		It has recently been suggested that, rather than being an autoimmune disease, multiple sclerosis (MS) is an example of a neurocristopathy, a pathological process resulting from a faulty development of the neural crest. Whilst several characteristics of the disease suggest a neurocristopathy, other aetiological factors require consideration, including hygiene-related factors that alter the immune responses to common pathogens resulting in an eclipse of immune reactivity that could protect against MS, the possible role of human endogenous retroviruses (HERVs) in pathogenesis and autoimmune phenomena, HLA polymorphism, vitamin D levels before and after birth and immune repair mechanisms. A postulated aetiological factor in MS, associated with altered vitamin D metabolism and abnormal HERV expression, is a long-lasting disturbed redox regulation in the biosynthesis of a melanoma-like melanin pigment. Although intensive further studies on melanin pigments in nerve tissue in MS are required, the known properties of a pathological form of such pigments in melanoma could explain a number of observations in MS, including the impact of light, UV-light, and vitamin D, and could explain the clinical manifestations of MS on the basis of an oscillating process of oxidative charge and discharge of the pigments and a threshold phenomenon with a change of the quasi-catalytic function of the pigment from destroying reactive oxygen radicals or species to transforming them to more harmful long-persisting highly reactive species. Taken together with the consequences of an adaptive process in partly demyelinated neurons, resulting in an increase in number of mitochondria, and the impact of stressful life events, these conditions are necessary and sufficient to explain the disease process of MS with its spatial (plaques) and temporal (attacks and remissions) characteristics. This suggested unifying concept of the pathogenesis of MS may open perspectives for prevention, diagnosis and therapy. In particular, prevention may be achieved by vaccinating against Epstein-Barr virus in early childhood.
-	(({{pubmed>long:11111111}}))	+	(({{pmid>long:11111111}}))
	PMID: 21547536 [</blockquote>		PMID: 21547536 [</blockquote>

Line 521:		Line 522:
	In an astonishing new study published in Nature today, researchers at the Max Planck Institute of Neurobiology in Martinsried in Munich, Germany say they have found evidence that suggests multiple sclerosis (MS) is triggered by natural intestinal flora, the so-called friendly bacteria that reside in the gut. They found genetically engineered mice with normal gut bacteria developed brain inflammation similar to MS in humans. They say the bacteria first activated the immune T-cells, then the B-cells, which resulted in an attack on the myelin layer in the brain. The same could happen in humans with a corresponding genetic predisposition, they say.		In an astonishing new study published in Nature today, researchers at the Max Planck Institute of Neurobiology in Martinsried in Munich, Germany say they have found evidence that suggests multiple sclerosis (MS) is triggered by natural intestinal flora, the so-called friendly bacteria that reside in the gut. They found genetically engineered mice with normal gut bacteria developed brain inflammation similar to MS in humans. They say the bacteria first activated the immune T-cells, then the B-cells, which resulted in an attack on the myelin layer in the brain. The same could happen in humans with a corresponding genetic predisposition, they say.

-	http://www.medicalnewstoday.com/articles/236776.php	+	https://www.medicalnewstoday.com/articles/236776.php


Line 530:		Line 531:
	Department of Neuroimmunology, Max Planck Institute of Neurobiology, 82152 Martinsried, Germany.		Department of Neuroimmunology, Max Planck Institute of Neurobiology, 82152 Martinsried, Germany.
	Abstract		Abstract
-	Active multiple sclerosis lesions show inflammatory changes suggestive of a combined attack by autoreactive T and B lymphocytes against brain white matter. These pathogenic immune cells derive from progenitors that are normal, innocuous components of the healthy immune repertoire but become autoaggressive upon pathological activation. The stimuli triggering this autoimmune conversion have been commonly attributed to environmental factors, in particular microbial infection. However, using the relapsing-remitting mouse model of spontaneously developing experimental autoimmune encephalomyelitis, here we show that the commensal gut flora-in the absence of pathogenic agents-is essential in triggering immune processes, leading to a relapsing-remitting autoimmune disease driven by myelin-specific CD4(+) T cells. We show further that recruitment and activation of autoantibody-producing B cells from the endogenous immune repertoire depends on availability of the target autoantigen, myelin oligodendrocyte glycoprotein (MOG), and commensal microbiota. Our observations identify a sequence of events triggering organ-specific autoimmune disease and these processes may offer novel therapeutic targets. (({{pubmed>long:11111111}}))	+	Active multiple sclerosis lesions show inflammatory changes suggestive of a combined attack by autoreactive T and B lymphocytes against brain white matter. These pathogenic immune cells derive from progenitors that are normal, innocuous components of the healthy immune repertoire but become autoaggressive upon pathological activation. The stimuli triggering this autoimmune conversion have been commonly attributed to environmental factors, in particular microbial infection. However, using the relapsing-remitting mouse model of spontaneously developing experimental autoimmune encephalomyelitis, here we show that the commensal gut flora-in the absence of pathogenic agents-is essential in triggering immune processes, leading to a relapsing-remitting autoimmune disease driven by myelin-specific CD4(+) T cells. We show further that recruitment and activation of autoantibody-producing B cells from the endogenous immune repertoire depends on availability of the target autoantigen, myelin oligodendrocyte glycoprotein (MOG), and commensal microbiota. Our observations identify a sequence of events triggering organ-specific autoimmune disease and these processes may offer novel therapeutic targets. (({{pmid>long:11111111}}))
	PMID: 22031325		PMID: 22031325
	</blockquote></blockquote>		</blockquote></blockquote>
Line 574:		Line 575:
	<blockquote>New autoantibody found in MS		<blockquote>New autoantibody found in MS

-	http://www.sciencedaily.com/releases/2012/07/120712101549.htm?utm_source=feedburner&utm_medium=email&utm_campaign=Feed%3A+sciencedaily%2Fmind_brain%2Fmultiple_sclerosis+%28ScienceDaily%3A+Mind+%26+Brain+News+--+Multiple+Sclerosis%29	+	https://www.sciencedaily.com/releases/2012/07/120712101549.htm?utm_source=feedburner&utm_medium=email&utm_campaign=Feed%3A+sciencedaily%2Fmind_brain%2Fmultiple_sclerosis+%28ScienceDaily%3A+Mind+%26+Brain+News+--+Multiple+Sclerosis%29

	</blockquote>		</blockquote>
Line 580:		Line 581:


-	- Review Finds Marijuana May Help MS Patients - http://bit.ly/7ksqMT	+	- Review Finds Marijuana May Help MS Patients - https://bit.ly/7ksqMT

	<blockquote>		<blockquote>
Line 628:		Line 629:


-	===== References =====	+	===== References =====</nodisp>

Obesity

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

01.10.2020		current
Line 21:		Line 21:
	{{section>:home:alternate:environment#poor_diet_and_a_lack_of_exercise&noheader&firstseconly}}		{{section>:home:alternate:environment#poor_diet_and_a_lack_of_exercise&noheader&firstseconly}}

-	(({{pubmed>long:19901833}}))	+	(({{pmid>long:19901833}}))
-	(({{pubmed>long:14594792}}))	+	(({{pmid>long:14594792}}))
-	(({{pubmed>long:17652652}}))	+	(({{pmid>long:17652652}}))
-	(({{pubmed>long:17183312}}))	+	(({{pmid>long:17183312}}))
-	(({{pubmed>long:20804522}}))	+	(({{pmid>long:20804522}}))

	Restoration of the gastrointestinal mucosal barrier may include dietary changes, treatment of dysbiosis, digestive supports, and anti-inflammatory therapies.		Restoration of the gastrointestinal mucosal barrier may include dietary changes, treatment of dysbiosis, digestive supports, and anti-inflammatory therapies.
Line 35:		Line 35:
	===== Evidence of infectious cause =====		===== Evidence of infectious cause =====

-	The increase (percentage points) in obesity and overweight in adults was faster than in children (0.77 vs. 0.46–0.49), and in women than in men (0.91 vs. 0.65). If these trends continue, by 2030, 86.3% adults will be overweight or obese; and 51.1%, obese. Black women (96.9%) and Mexican-American men (91.1%) would be the most affected. By 2048, all American adults would become overweight or obese, while black women will reach that state by 2034. In children, the prevalence of overweight (BMI 95th percentile, 30%) will nearly double by 2030. Total health-care costs attributable to obesity/overweight would double every decade to 860.7–956.9 billion US dollars by 2030, accounting for 16–18% of total US health-care costs. We continue to move away from the Healthy People 2010 objectives. Timely, dramatic, and effective development and implementation of corrective programs/policies are needed to avoid the otherwise inevitable health and societal consequences implied by our projections.(({{pubmed>long:18719634}}))	+	The increase (percentage points) in obesity and overweight in adults was faster than in children (0.77 vs. 0.46–0.49), and in women than in men (0.91 vs. 0.65). If these trends continue, by 2030, 86.3% adults will be overweight or obese; and 51.1%, obese. Black women (96.9%) and Mexican-American men (91.1%) would be the most affected. By 2048, all American adults would become overweight or obese, while black women will reach that state by 2034. In children, the prevalence of overweight (BMI 95th percentile, 30%) will nearly double by 2030. Total health-care costs attributable to obesity/overweight would double every decade to 860.7–956.9 billion US dollars by 2030, accounting for 16–18% of total US health-care costs. We continue to move away from the Healthy People 2010 objectives. Timely, dramatic, and effective development and implementation of corrective programs/policies are needed to avoid the otherwise inevitable health and societal consequences implied by our projections.(({{pmid>long:18719634}}))


Line 44:		Line 44:
	RESULTS: Reductions in Clostridium histolyticum and E. rectale-C. coccoides proportions significantly correlated with weight and BMI z-score reductions in the whole adolescent population. Proportions of C. histolyticum, C. lituseburense and E. rectale-C. coccoides dropped significantly whereas those of the Bacteroides-Prevotella group increased after the intervention in those adolescents who lost more than 4 kg. Total fecal energy was almost significantly reduced in the same group of adolescents but not in the group that lost less than 2.5 kg. IgA-coating bacterial proportions also decreased significantly in participants who lost more than 6 kg after the intervention, paralleled to reductions in C. histolyticum and E. rectale-C. coccoides populations. E. rectale-C. coccoides proportions also correlated with weight loss and BMI z-score reduction in participants whose weight loss exceeded 4 kg.		RESULTS: Reductions in Clostridium histolyticum and E. rectale-C. coccoides proportions significantly correlated with weight and BMI z-score reductions in the whole adolescent population. Proportions of C. histolyticum, C. lituseburense and E. rectale-C. coccoides dropped significantly whereas those of the Bacteroides-Prevotella group increased after the intervention in those adolescents who lost more than 4 kg. Total fecal energy was almost significantly reduced in the same group of adolescents but not in the group that lost less than 2.5 kg. IgA-coating bacterial proportions also decreased significantly in participants who lost more than 6 kg after the intervention, paralleled to reductions in C. histolyticum and E. rectale-C. coccoides populations. E. rectale-C. coccoides proportions also correlated with weight loss and BMI z-score reduction in participants whose weight loss exceeded 4 kg.

-	CONCLUSIONS: Specific gut bacteria and an associated IgA response were related to body weight changes in adolescents under lifestyle intervention. These results suggest interactions between diet, gut microbiota and host metabolism and immunity in obesity.(({{pubmed>long:19050675}}))	+	CONCLUSIONS: Specific gut bacteria and an associated IgA response were related to body weight changes in adolescents under lifestyle intervention. These results suggest interactions between diet, gut microbiota and host metabolism and immunity in obesity.(({{pmid>long:19050675}}))

	Some studies are indicating that immune cells and molecules are important for regulating metabolism—and are dysregulated in obesity.		Some studies are indicating that immune cells and molecules are important for regulating metabolism—and are dysregulated in obesity.

-	[[http://microbeminded.com/2017/12/15/cholesterol-fat-and-human-metabolism-a-microbiome-based-paradigm-shift/\|Microbe Minded: cholesterol, fat & human metabolism]]	+	[[https://microbeminded.com/2017/12/15/cholesterol-fat-and-human-metabolism-a-microbiome-based-paradigm-shift/\|Microbe Minded: cholesterol, fat & human metabolism]]

	[[home:food:real_foods\|Know your rice and lose weight]]		[[home:food:real_foods\|Know your rice and lose weight]]
Line 63:		Line 63:
	Obesity has a clear but not yet precisely defined effect on the immune response through a variety of immune mediators, which leads to susceptibility to infections.		Obesity has a clear but not yet precisely defined effect on the immune response through a variety of immune mediators, which leads to susceptibility to infections.

-	The available data suggest that obese people are more likely than people of normal weight to develop infections of various types including postoperative infections and other nosocomial infections, as well to develop serious complications of common infections. (({{pubmed>long:16790384}}))	+	The available data suggest that obese people are more likely than people of normal weight to develop infections of various types including postoperative infections and other nosocomial infections, as well to develop serious complications of common infections. (({{pmid>long:16790384}}))


-	Although excess visceral fat is associated with noninfectious inflammation, it is not clear whether visceral fat is simply associated with or actually causes metabolic disease in humans. To evaluate the hypothesis that visceral fat promotes systemic inflammation by secreting inflammatory adipokines into the portal circulation that drains visceral fat, we determined adipokine arteriovenous concentration differences across visceral fat, by obtaining portal vein and radial artery blood samples, in 25 extremely obese subjects (mean +/- SD BMI 54.7 +/- 12.6 kg/m(2)) during gastric bypass surgery at Barnes-Jewish Hospital in St. Louis, Missouri. Mean plasma interleukin (IL)-6 concentration was approximately 50% greater in the portal vein than in the radial artery in obese subjects (P = 0.007). Portal vein IL-6 concentration correlated directly with systemic C-reactive protein concentrations (r = 0.544, P = 0.005). Mean plasma leptin concentration was approximately 20% lower in the portal vein than in the radial artery in obese subjects (P = 0.0002). Plasma tumor necrosis factor-alpha, resistin, macrophage chemoattractant protein-1, and adiponectin concentrations were similar in the portal vein and radial artery in obese subjects. These data suggest that visceral fat is an important site for IL-6 secretion and provide a potential mechanistic link between visceral fat and systemic inflammation in people with abdominal obesity.(({{pubmed>long:17287468}}))	+	Although excess visceral fat is associated with noninfectious inflammation, it is not clear whether visceral fat is simply associated with or actually causes metabolic disease in humans. To evaluate the hypothesis that visceral fat promotes systemic inflammation by secreting inflammatory adipokines into the portal circulation that drains visceral fat, we determined adipokine arteriovenous concentration differences across visceral fat, by obtaining portal vein and radial artery blood samples, in 25 extremely obese subjects (mean +/- SD BMI 54.7 +/- 12.6 kg/m(2)) during gastric bypass surgery at Barnes-Jewish Hospital in St. Louis, Missouri. Mean plasma interleukin (IL)-6 concentration was approximately 50% greater in the portal vein than in the radial artery in obese subjects (P = 0.007). Portal vein IL-6 concentration correlated directly with systemic C-reactive protein concentrations (r = 0.544, P = 0.005). Mean plasma leptin concentration was approximately 20% lower in the portal vein than in the radial artery in obese subjects (P = 0.0002). Plasma tumor necrosis factor-alpha, resistin, macrophage chemoattractant protein-1, and adiponectin concentrations were similar in the portal vein and radial artery in obese subjects. These data suggest that visceral fat is an important site for IL-6 secretion and provide a potential mechanistic link between visceral fat and systemic inflammation in people with abdominal obesity.(({{pmid>long:17287468}}))


Line 75:		Line 75:

	Abstract		Abstract
-	Vascular dysfunction is a major complication of metabolic disorders such as diabetes and obesity. The current studies were undertaken to determine whether inflammatory responses are activated in the vasculature of mice with diet-induced obesity, and if so, whether Toll-Like Receptor-4 (TLR4), a key mediator of innate immunity, contributes to these responses. Mice lacking TLR4 (TLR4(-/-)) and wild-type (WT) controls were fed either a low fat (LF) control diet or a diet high in saturated fat (HF) for 8 weeks. In response to HF feeding, both genotypes displayed similar increases of body weight, body fat content, and serum insulin and free fatty acid (FFA) levels compared with mice on a LF diet. In lysates of thoracic aorta from WT mice maintained on a HF diet, markers of vascular inflammation both upstream (IKKbeta activity) and downstream of the transcriptional regulator, NF-kappaB (ICAM protein and IL-6 mRNA expression), were increased and this effect was associated with cellular insulin resistance and impaired insulin stimulation of eNOS. In contrast, vascular inflammation and impaired insulin responsiveness were not evident in aortic samples taken from TLR4(-/-) mice fed the same HF diet, despite comparable increases of body fat mass. Incubation of either aortic explants from WT mice or cultured human microvascular endothelial cells with the saturated FFA, palmitate (100 micromol/L), similarly activated IKKbeta, inhibited insulin signal transduction and blocked insulin-stimulated NO production. Each of these effects was subsequently shown to be dependent on both TLR4 and NF-kappaB activation. These findings identify the TLR4 signaling pathway as a key mediator of the deleterious effects of palmitate on endothelial NO signaling, and are the first to document a key role for TLR4 in the mechanism whereby diet-induced obesity induces vascular inflammation and insulin resistance.(({{pubmed>long:17478729}}))	+	Vascular dysfunction is a major complication of metabolic disorders such as diabetes and obesity. The current studies were undertaken to determine whether inflammatory responses are activated in the vasculature of mice with diet-induced obesity, and if so, whether Toll-Like Receptor-4 (TLR4), a key mediator of innate immunity, contributes to these responses. Mice lacking TLR4 (TLR4(-/-)) and wild-type (WT) controls were fed either a low fat (LF) control diet or a diet high in saturated fat (HF) for 8 weeks. In response to HF feeding, both genotypes displayed similar increases of body weight, body fat content, and serum insulin and free fatty acid (FFA) levels compared with mice on a LF diet. In lysates of thoracic aorta from WT mice maintained on a HF diet, markers of vascular inflammation both upstream (IKKbeta activity) and downstream of the transcriptional regulator, NF-kappaB (ICAM protein and IL-6 mRNA expression), were increased and this effect was associated with cellular insulin resistance and impaired insulin stimulation of eNOS. In contrast, vascular inflammation and impaired insulin responsiveness were not evident in aortic samples taken from TLR4(-/-) mice fed the same HF diet, despite comparable increases of body fat mass. Incubation of either aortic explants from WT mice or cultured human microvascular endothelial cells with the saturated FFA, palmitate (100 micromol/L), similarly activated IKKbeta, inhibited insulin signal transduction and blocked insulin-stimulated NO production. Each of these effects was subsequently shown to be dependent on both TLR4 and NF-kappaB activation. These findings identify the TLR4 signaling pathway as a key mediator of the deleterious effects of palmitate on endothelial NO signaling, and are the first to document a key role for TLR4 in the mechanism whereby diet-induced obesity induces vascular inflammation and insulin resistance.(({{pmid>long:17478729}}))


	and in March 2007		and in March 2007
-	Lipopolysaccharide activates an innate immune system response in human adipose tissue in obesity and type 2 diabetes. (({{pubmed>long:17090751}}))	+	Lipopolysaccharide activates an innate immune system response in human adipose tissue in obesity and type 2 diabetes. (({{pmid>long:17090751}}))


Line 102:		Line 102:

	In summary, our results suggest that T2DM is associated with increased endotoxemia, with AT able to initiate an innate immune response. Thus, increased adiposity may increase proinflammatory cytokines and therefore contribute to the pathogenic risk of T2DM.		In summary, our results suggest that T2DM is associated with increased endotoxemia, with AT able to initiate an innate immune response. Thus, increased adiposity may increase proinflammatory cytokines and therefore contribute to the pathogenic risk of T2DM.
-	(({{pubmed>long:17090751}}))	+	(({{pmid>long:17090751}}))


Line 121:		Line 121:
	Pediatrics, Sept. 2010		Pediatrics, Sept. 2010

-	see also {{http://children.webmd.com/news/20080814/ear-infections-may-increase-obesity-risk\|Ear infections}}	+	see also {{https://children.webmd.com/news/20080814/ear-infections-may-increase-obesity-risk\|Ear infections}}



-	Fecal microbiota composition in children may predict overweight.(({{pubmed>long:18326589}}))	+	Fecal microbiota composition in children may predict overweight.(({{pmid>long:18326589}}))

	===== Research =====		===== Research =====

-	Cellular and molecular players in adipose tissue inflammation in the development of obesity-induced insulin resistance. (({{pubmed>long:23707515}}))	+	Cellular and molecular players in adipose tissue inflammation in the development of obesity-induced insulin resistance. (({{pmid>long:23707515}}))

-	Adenosine is an endogenous metabolite that is released from all tissues and cells including liver, pancreas, muscle and fat, particularly under stress, intense exercise, or during cell damage. (({{pubmed>long:23460239}}))	+	Adenosine is an endogenous metabolite that is released from all tissues and cells including liver, pancreas, muscle and fat, particularly under stress, intense exercise, or during cell damage. (({{pmid>long:23460239}}))

-	Here, we report that adenosine level in the cerebrospinal fluid, and hypothalamic expression of A1R, are increased in the diet-induced obesity (DIO) mouse. We find that mice with overexpression of A1R in the neurons of paraventricular nucleus (PVN) of the hypothalamus are hyperphagic, have glucose intolerance and high body weight. Central or peripheral administration of caffeine reduces the body weight of DIO mice by the suppression of appetite and increasing of energy expenditure. We also show that caffeine excites oxytocin expressing neurons, and blockade of the action of oxytocin significantly attenuates the effect of caffeine on energy balance. (({{pubmed>long:28654087}}))	+	Here, we report that adenosine level in the cerebrospinal fluid, and hypothalamic expression of A1R, are increased in the diet-induced obesity (DIO) mouse. We find that mice with overexpression of A1R in the neurons of paraventricular nucleus (PVN) of the hypothalamus are hyperphagic, have glucose intolerance and high body weight. Central or peripheral administration of caffeine reduces the body weight of DIO mice by the suppression of appetite and increasing of energy expenditure. We also show that caffeine excites oxytocin expressing neurons, and blockade of the action of oxytocin significantly attenuates the effect of caffeine on energy balance. (({{pmid>long:28654087}}))

-	Higher zonulin levels are associated with higher waist circumference, diastolic blood pressure, fasting glucose, and increased risk of metabolic diseases (({{pubmed>long:28282855}}))	+	Higher zonulin levels are associated with higher waist circumference, diastolic blood pressure, fasting glucose, and increased risk of metabolic diseases (({{pmid>long:28282855}}))

-	'Western'-style diets, high in fat/sugar, low in fibre, decrease beneficial Firmicutes that metabolise dietary plant-derived polysaccharides to SCFAs and increase mucosa-associated Proteobacteria (including enteric pathogens). (({{pubmed>long:26011307}}))	+	'Western'-style diets, high in fat/sugar, low in fibre, decrease beneficial Firmicutes that metabolise dietary plant-derived polysaccharides to SCFAs and increase mucosa-associated Proteobacteria (including enteric pathogens). (({{pmid>long:26011307}}))

-	This was of particular interest to us because other research has shown that having more Bacteroidetes may be beneficial because the higher that proportion is, the individual tends to be leaner. With higher Firmicutes, that individual tends to be more obese," Holscher said. "We don't know if there is any causality for weight loss, but studies have shown that having a higher fiber diet is protective against obesity. (({{pubmed>long: 25414978}})) (({{pubmed>long:25527750}}))	+	This was of particular interest to us because other research has shown that having more Bacteroidetes may be beneficial because the higher that proportion is, the individual tends to be leaner. With higher Firmicutes, that individual tends to be more obese," Holscher said. "We don't know if there is any causality for weight loss, but studies have shown that having a higher fiber diet is protective against obesity. (({{pmid>long: 25414978}})) (({{pmid>long:25527750}}))


Line 151:		Line 151:


-	(({{pubmed>long:31911661}}))	+	(({{pmid>long:31911661}}))

	[[https://www.sciencealert.com/your-gut-bacteria-appear-to-be-controlling-your-appetite\|Bacteria in the gut produce appetite-suppressing proteins about 20 minutes after a meal]]		[[https://www.sciencealert.com/your-gut-bacteria-appear-to-be-controlling-your-appetite\|Bacteria in the gut produce appetite-suppressing proteins about 20 minutes after a meal]]
Line 158:		Line 158:
	===== Learn More =====		===== Learn More =====

-	[[http://arstechnica.com/science/2014/12/immune-cells-tweak-the-bodys-metabolism-to-help-control-obesity/\|Immune cells tweak the body’s metabolism to help control obesity]]	+	[[https://arstechnica.com/science/2014/12/immune-cells-tweak-the-bodys-metabolism-to-help-control-obesity/\|Immune cells tweak the body’s metabolism to help control obesity]]


-	[[http://www.foodsmatter.com/es/health_risks/articles/goldsworthy-biological-effects-04-12.pdf\|biological effects]]	+	[[https://www.foodsmatter.com/es/health_risks/articles/goldsworthy-biological-effects-04-12.pdf\|biological effects]]

	{{tag>diseases }}		{{tag>diseases }}
		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

-	(({{pubmed>long:000}}))	+

	not sure why I placed this https://www.marshallprotocol.com/forum11/16602-2.html		not sure why I placed this https://www.marshallprotocol.com/forum11/16602-2.html
	so took it out pending working on what was i thinking		so took it out pending working on what was i thinking

-	removed broken link {{http://www.apa.org/releases/earinfectionC08.html\|Ear infection}}	+	removed broken link {{https://www.apa.org/releases/earinfectionC08.html\|Ear infection}}

	<DiseaseHierarchy>		<DiseaseHierarchy>
Line 185:		Line 186:

	"Fat people harbour 'fat' microbes"		"Fat people harbour 'fat' microbes"
-	http://www.bioedonline.org/news/news.cfm?art=3017	+	https://www.bioedonline.org/news/news.cfm?art=3017
	and		and
	"An obesity-associated gut microbiome with increased capacity for energy harvest"		"An obesity-associated gut microbiome with increased capacity for energy harvest"
-	http://tinyurl.com/2rfrzp PMID: 17183312	+	https://tinyurl.com/2rfrzp PMID: 17183312

	Well, this week I had an abstract accepted for presentation at an upcoming conference, Metagenomics 2007, and as the moderators were browsing through the conference website, Janet noticed that Jeffrey Gordon had spoken at the same conference last year, and that the video of that presentation was still online.		Well, this week I had an abstract accepted for presentation at an upcoming conference, Metagenomics 2007, and as the moderators were browsing through the conference website, Janet noticed that Jeffrey Gordon had spoken at the same conference last year, and that the video of that presentation was still online.
Line 196:		Line 197:

	The video "It's So Nice to Have a Few Trillion Friends: Exploring the Structure and Functions of Our Human Gut Microbiota and Microbiome, Jeffrey I. Gordon, Washington University of St. Louis"		The video "It's So Nice to Have a Few Trillion Friends: Exploring the Structure and Functions of Our Human Gut Microbiota and Microbiome, Jeffrey I. Gordon, Washington University of St. Louis"
-	is at http://rpvss.ucsd.edu:8080/ramgen/calit2/metagenomics/gordon.rm	+	is at https://rpvss.ucsd.edu:8080/ramgen/calit2/metagenomics/gordon.rm

	This is a "MUST SEE" video. Please put aside 32 minutes of your time to watch it. You will come away with a new appreciation for the bacteria which live in symbiosis with Homo sapiens.		This is a "MUST SEE" video. Please put aside 32 minutes of your time to watch it. You will come away with a new appreciation for the bacteria which live in symbiosis with Homo sapiens.

	And as an added bonus, there is a video where W. Ford Doolittle, of Dalhousie University (Canada), argues against the concept of Bacterial species altogether. Another 'must see.'		And as an added bonus, there is a video where W. Ford Doolittle, of Dalhousie University (Canada), argues against the concept of Bacterial species altogether. Another 'must see.'
-	http://rpvss.ucsd.edu:8080/ramgen/calit2/metagenomics/doolittle.rm	+	https://rpvss.ucsd.edu:8080/ramgen/calit2/metagenomics/doolittle.rm

	Note particularly the "agreement to disagree" during the question and answer session of this latter video. This frank exchange of scientific concepts is something I sorely miss when I am in Clinical Medicine circles, where the instinct is to suppress any thought which conflicts with what one supposes to be 'the consensus'.		Note particularly the "agreement to disagree" during the question and answer session of this latter video. This frank exchange of scientific concepts is something I sorely miss when I am in Clinical Medicine circles, where the instinct is to suppress any thought which conflicts with what one supposes to be 'the consensus'.
Line 240:		Line 241:
	Here is an interesting article which points really well to macrophage-centric immune changes in obesity:		Here is an interesting article which points really well to macrophage-centric immune changes in obesity:
	"New method finds networks of genes behind obesity"		"New method finds networks of genes behind obesity"
-	http://www.reuters.com/article/healthNews/idUSN1645889420080316	+	https://www.reuters.com/article/healthNews/idUSN1645889420080316

	Schadt's team, writing in two studies published in the journal Nature, said the diseases of obesity appear to originate in the immune system. "The network is enriched for genes that are involved in macrophages," Schadt said.		Schadt's team, writing in two studies published in the journal Nature, said the diseases of obesity appear to originate in the immune system. "The network is enriched for genes that are involved in macrophages," Schadt said.

-	http://www.reuters.com/article/healthNews/idUSN1645889420080316	+	https://www.reuters.com/article/healthNews/idUSN1645889420080316

	..Trevor..		..Trevor..
Line 506:		Line 507:

	<blockquote>Balamurugan, R., G. George, et al. (2010). "Quantitative differences in intestinal Faecalibacterium prausnitzii in obese Indian children." Br J Nutr 103(3): 335-338.		<blockquote>Balamurugan, R., G. George, et al. (2010). "Quantitative differences in intestinal Faecalibacterium prausnitzii in obese Indian children." Br J Nutr 103(3): 335-338.
-	(({{pubmed>long:19849869}}))	+	(({{pmid>long:19849869}}))

	Gut bacteria contribute to energy conservation in man through their ability to ferment unabsorbed carbohydrate. The present study examined the composition of predominant faecal microbiota in obese and non-obese children. The participants (n 28) aged 11-14 years provided fresh faecal samples and completed a dietary survey consisting of 24 h diet recall and a FFQ of commonly used foods taken over the previous 3 months. Faecal bacteria were quantitated by real-time PCR using primers targeted at 16S rDNA. Of the participants, fifteen (seven female) were obese, with median BMI-for-age at the 99th percentile (range 97 to>99) while thirteen participants (seven female) were normal weight, with median BMI-for age being at the 50th percentile (range 1-85). Consumption of energy, carbohydrates, fat and protein was not significantly different between the obese and non-obese participants. There was no significant difference between the two groups in faecal levels of Bacteroides-Prevotella, Bifidobacterium species, Lactobacillus acidophilus group or Eubacterium rectale. Levels of Faecalibacterium prausnitzii were significantly higher in obese children than in non-obese participants (P = 0.0253). We concluded that the finding of increased numbers of F. prausnitzii in the faeces of obese children in south India adds to the growing information on alterations in faecal microbiota in obesity.		Gut bacteria contribute to energy conservation in man through their ability to ferment unabsorbed carbohydrate. The present study examined the composition of predominant faecal microbiota in obese and non-obese children. The participants (n 28) aged 11-14 years provided fresh faecal samples and completed a dietary survey consisting of 24 h diet recall and a FFQ of commonly used foods taken over the previous 3 months. Faecal bacteria were quantitated by real-time PCR using primers targeted at 16S rDNA. Of the participants, fifteen (seven female) were obese, with median BMI-for-age at the 99th percentile (range 97 to>99) while thirteen participants (seven female) were normal weight, with median BMI-for age being at the 50th percentile (range 1-85). Consumption of energy, carbohydrates, fat and protein was not significantly different between the obese and non-obese participants. There was no significant difference between the two groups in faecal levels of Bacteroides-Prevotella, Bifidobacterium species, Lactobacillus acidophilus group or Eubacterium rectale. Levels of Faecalibacterium prausnitzii were significantly higher in obese children than in non-obese participants (P = 0.0253). We concluded that the finding of increased numbers of F. prausnitzii in the faeces of obese children in south India adds to the growing information on alterations in faecal microbiota in obesity.
Line 512:		Line 513:

	<blockquote>		<blockquote>
-	The Human Visceral Fat Depot Has a Unique Inflammatory Profile(({{pubmed>long:20186138}}))	+	The Human Visceral Fat Depot Has a Unique Inflammatory Profile(({{pmid>long:20186138}}))

	Obesity can be considered as a low-grade inflammatory condition, strongly linked to adverse metabolic outcomes. Obesity-associated adipose tissue inflammation is characterized by infiltration of macrophages and increased cytokine and chemokine production. The distribution of adipose tissue impacts the outcomes of obesity, with the accumulation of fat in visceral adipose tissue (VAT) and deep subcutaneous adipose tissue (SAT), but not superficial SAT, being linked to insulin resistance. We hypothesized that the inflammatory gene expression in deep SAT and VAT is higher than in superficial SAT. A total of 17 apparently healthy women (BMI: 29.3±5.5 kg/m2) were included in the study. Body fat (dual-energy X-ray absorptiometry) and distribution (computed tomography) were measured, and insulin sensitivity, blood lipids, and blood pressure were determined. Inflammation-related differences in gene expression (real-time PCR) from VAT, superficial and deep SAT biopsies were analyzed using univariate and multivariate data analyses. Using multivariate discrimination analysis, VAT appeared as a distinct depot in adipose tissue inflammation, while the SAT depots had a similar pattern, with respect to gene expression. A significantly elevated (P < 0.01) expression of the CC chemokine receptor 2 (CCR2) and macrophage migration inhibitory factor (MIF) in VAT contributed strongly to the discrimination. In conclusion, the human adipose tissue depots have unique inflammatory patterns, with CCR2 and MIF distinguishing between VAT and the SAT depots.</blockquote>		Obesity can be considered as a low-grade inflammatory condition, strongly linked to adverse metabolic outcomes. Obesity-associated adipose tissue inflammation is characterized by infiltration of macrophages and increased cytokine and chemokine production. The distribution of adipose tissue impacts the outcomes of obesity, with the accumulation of fat in visceral adipose tissue (VAT) and deep subcutaneous adipose tissue (SAT), but not superficial SAT, being linked to insulin resistance. We hypothesized that the inflammatory gene expression in deep SAT and VAT is higher than in superficial SAT. A total of 17 apparently healthy women (BMI: 29.3±5.5 kg/m2) were included in the study. Body fat (dual-energy X-ray absorptiometry) and distribution (computed tomography) were measured, and insulin sensitivity, blood lipids, and blood pressure were determined. Inflammation-related differences in gene expression (real-time PCR) from VAT, superficial and deep SAT biopsies were analyzed using univariate and multivariate data analyses. Using multivariate discrimination analysis, VAT appeared as a distinct depot in adipose tissue inflammation, while the SAT depots had a similar pattern, with respect to gene expression. A significantly elevated (P < 0.01) expression of the CC chemokine receptor 2 (CCR2) and macrophage migration inhibitory factor (MIF) in VAT contributed strongly to the discrimination. In conclusion, the human adipose tissue depots have unique inflammatory patterns, with CCR2 and MIF distinguishing between VAT and the SAT depots.</blockquote>
Line 530:		Line 531:

	<blockquote>Diabetes. 2007 Jul;56(7):1761-72. Epub 2007 Apr 24.		<blockquote>Diabetes. 2007 Jul;56(7):1761-72. Epub 2007 Apr 24.
-	Metabolic endotoxemia initiates obesity and insulin resistance.(({{pubmed>long:17456850}}))	+	Metabolic endotoxemia initiates obesity and insulin resistance.(({{pmid>long:17456850}}))

	Cani PD, Amar J, Iglesias MA, Poggi M, Knauf C, Bastelica D, Neyrinck AM, Fava F, Tuohy KM, Chabo C, Waget A, Delmée E, Cousin B, Sulpice T, Chamontin B, Ferrières J, Tanti JF, Gibson GR, Casteilla L, Delzenne NM, Alessi MC, Burcelin R.		Cani PD, Amar J, Iglesias MA, Poggi M, Knauf C, Bastelica D, Neyrinck AM, Fava F, Tuohy KM, Chabo C, Waget A, Delmée E, Cousin B, Sulpice T, Chamontin B, Ferrières J, Tanti JF, Gibson GR, Casteilla L, Delzenne NM, Alessi MC, Burcelin R.
Line 543:		Line 544:

	<blockquote>Proc Natl Acad Sci U S A. 2007 Jan 16;104(3):979-84. Epub 2007 Jan 8.		<blockquote>Proc Natl Acad Sci U S A. 2007 Jan 16;104(3):979-84. Epub 2007 Jan 8.
-	Mechanisms underlying the resistance to diet-induced obesity in germ-free mice.(({{pubmed>long:17210919}}))	+	Mechanisms underlying the resistance to diet-induced obesity in germ-free mice.(({{pmid>long:17210919}}))

	Bäckhed F, Manchester JK, Semenkovich CF, Gordon JI.		Bäckhed F, Manchester JK, Semenkovich CF, Gordon JI.
Line 556:		Line 557:


-	http://www.wlshelp.com/news/intestinal-bacteria-can-contribute-to-obesity/#more-226	+	https://www.wlshelp.com/news/intestinal-bacteria-can-contribute-to-obesity/#more-226

-	http://www.eurekalert.org/pub_releases/2010-03/eu-ibd030110.php	+	https://www.eurekalert.org/pub_releases/2010-03/eu-ibd030110.php

	Good find, Donna. This goes beyond the earlier work with Gordon's group and links obesity to different species within the Firmicutes and Bacteroidetes and to a specific immune dysfunction (TLR5 deficiency).		Good find, Donna. This goes beyond the earlier work with Gordon's group and links obesity to different species within the Firmicutes and Bacteroidetes and to a specific immune dysfunction (TLR5 deficiency).
Line 592:		Line 593:

	<blockquote>Obese People Have 'Severe Brain Degeneration		<blockquote>Obese People Have 'Severe Brain Degeneration
-	http://www.livescience.com/10582-obese-people-severe-brain-degeneration.html</blockquote>	+	https://www.livescience.com/10582-obese-people-severe-brain-degeneration.html</blockquote>

	<blockquote>		<blockquote>
Line 628:		Line 629:
	X-OriginalArrivalTime: 05 Oct 2011 11:42:53.0219 (UTC) FILETIME=[EAD40730:01CC8353]		X-OriginalArrivalTime: 05 Oct 2011 11:42:53.0219 (UTC) FILETIME=[EAD40730:01CC8353]

-	http://www.sciencedaily.com/releases/2011/10/111004123600.htm	+	https://www.sciencedaily.com/releases/2011/10/111004123600.htm

	</blockquote>		</blockquote>
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	</blockquote>		</blockquote>
-	===== References =====	+	===== References =====</nodisp>

Obsessive compulsive disorder (OCD)

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

02.17.2019		current
Line 13:		Line 13:


-	The identification of clinical features associated with PANDAS should assist in delineating risks for this subtype of obsessive-compulsive disorder/tics (({{pubmed>long:21868033}}))	+	The identification of clinical features associated with PANDAS should assist in delineating risks for this subtype of obsessive-compulsive disorder/tics (({{pmid>long:21868033}}))


Line 22:		Line 22:
	This report provides phenotypic descriptions of three youth with PANDAS as well as their genetically identical siblings (in two cases of twins and one case of triplets). These cases highlight the potential for environmental influences for discordant presentations in genetically identical siblings.		This report provides phenotypic descriptions of three youth with PANDAS as well as their genetically identical siblings (in two cases of twins and one case of triplets). These cases highlight the potential for environmental influences for discordant presentations in genetically identical siblings.

-	Despite identical genetics, presentations showed marked variation across siblings (from a full PANDAS presentation to asymptomatic). Further research into environmentally driven influences such as postinfectious molecular mimicry and epigenetic factors that may influence the manifestation of these pediatric neuropsychiatric disorders will promote our understanding of their prevention and treatment. (({{pubmed>long:21486169}}))	+	Despite identical genetics, presentations showed marked variation across siblings (from a full PANDAS presentation to asymptomatic). Further research into environmentally driven influences such as postinfectious molecular mimicry and epigenetic factors that may influence the manifestation of these pediatric neuropsychiatric disorders will promote our understanding of their prevention and treatment. (({{pmid>long:21486169}}))


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	===== Experience of Patients =====		===== Experience of Patients =====
		+
		+	<relatedarticle> [[home:symptoms:neurological:managing\|Managing symptoms]] </article>


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	Interview with Julia Grier - sarcoidosis, OCD		Interview with Julia Grier - sarcoidosis, OCD
-	================================

-	Phobias and OCD help available in the UK	+
		+	__Phobias and OCD help__ available in the UK

	I think you've spoken to my twin sister Jean (also on the MP). I have been on the MP now for about 4 months. I developed Obsessive Compulsive Disorder last July after my doctor gave me three antibiotics for CFS. I could never have imagined the effect on my brain and the obsessive thoughts and handwashing rituals that resulted. I would never have understood the link between bacteria and the brain if it weren't for the MP and information from my doctor. It makes a lot of sense though.		I think you've spoken to my twin sister Jean (also on the MP). I have been on the MP now for about 4 months. I developed Obsessive Compulsive Disorder last July after my doctor gave me three antibiotics for CFS. I could never have imagined the effect on my brain and the obsessive thoughts and handwashing rituals that resulted. I would never have understood the link between bacteria and the brain if it weren't for the MP and information from my doctor. It makes a lot of sense though.
Line 64:		Line 66:
	In support of a humoral immune mechanism, clinical improvement often follows plasmapheresis or intravenous immunoglobulin. We recently described a PANDAS mouse model wherein repetitive behaviors correlate with peripheral anti-CNS antibodies and immune deposits in brain following streptococcal immunization. These antibodies are directed against group A beta-hemolytic streptococcus matrix (M) protein and cross-react with molecular targets complement C4 protein and alpha-2-macroglobulin in brain. Here we show additional deficits in motor coordination, learning/memory and social interaction in PANDAS mice, replicating more complex aspects of human disease.		In support of a humoral immune mechanism, clinical improvement often follows plasmapheresis or intravenous immunoglobulin. We recently described a PANDAS mouse model wherein repetitive behaviors correlate with peripheral anti-CNS antibodies and immune deposits in brain following streptococcal immunization. These antibodies are directed against group A beta-hemolytic streptococcus matrix (M) protein and cross-react with molecular targets complement C4 protein and alpha-2-macroglobulin in brain. Here we show additional deficits in motor coordination, learning/memory and social interaction in PANDAS mice, replicating more complex aspects of human disease.

-	Furthermore, we demonstrate for the first time that humoral immunity is necessary and sufficient to induce the syndrome through experiments wherein naive mice are transfused with immunoglobulin G (IgG) from PANDAS mice. Depletion of IgG from donor sera abrogates behavior changes. These functional disturbances link to the autoimmunity-related IgG1 subclass but are not attributable to differences in cytokine profiles. The mode of disrupting blood-brain barrier integrity differentially affects the ultimate CNS distribution of these antibodies and is shown to be an additional important determinant of neuropsychiatric outcomes. This work provides insights into PANDAS pathogenesis and may lead to new strategies for identification and treatment of children at risk for autoimmune brain disorders. (({{pubmed>long:19668249}}))	+	Furthermore, we demonstrate for the first time that humoral immunity is necessary and sufficient to induce the syndrome through experiments wherein naive mice are transfused with immunoglobulin G (IgG) from PANDAS mice. Depletion of IgG from donor sera abrogates behavior changes. These functional disturbances link to the autoimmunity-related IgG1 subclass but are not attributable to differences in cytokine profiles. The mode of disrupting blood-brain barrier integrity differentially affects the ultimate CNS distribution of these antibodies and is shown to be an additional important determinant of neuropsychiatric outcomes. This work provides insights into PANDAS pathogenesis and may lead to new strategies for identification and treatment of children at risk for autoimmune brain disorders. (({{pmid>long:19668249}}))

-	See also Orbitofrontal-Cortex-Lesioned Rats: Possible Involvement of the Serotonergic System. (({{pubmed>long:20072118}}))	+	See also Orbitofrontal-Cortex-Lesioned Rats: Possible Involvement of the Serotonergic System. (({{pmid>long:20072118}}))


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		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

Line 81:		Line 84:


-	* Obsessive compulsive disorder and childhood infections like strep – A 2010 team of researchers developed a new animal model to show how exposure to strep affects the brain and leads to a number of physical and mental ailments. According to one of the collaborators, Daphna Joel, "It's almost impossible to show how strep can lead to OCD in humans ― almost all of us, even very young children, have been exposed to the bacterium at one time or another. But childhood seems to provide a distinct window of opportunity for the disorder to take root through strep infection. This work was presented at a [[http://www.sciencedaily.com/releases/2010/10/101020131712.htm\|2010 meeting]] and is expected to be published at the beginning of 2011.	+	* Obsessive compulsive disorder and childhood infections like strep – A 2010 team of researchers developed a new animal model to show how exposure to strep affects the brain and leads to a number of physical and mental ailments. According to one of the collaborators, Daphna Joel, "It's almost impossible to show how strep can lead to OCD in humans ― almost all of us, even very young children, have been exposed to the bacterium at one time or another. But childhood seems to provide a distinct window of opportunity for the disorder to take root through strep infection. This work was presented at a [[https://www.sciencedaily.com/releases/2010/10/101020131712.htm\|2010 meeting]] and is expected to be published at the beginning of 2011.


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	* legacy content		* legacy content
-	* http://www.marshallprotocol.com/view_topic.php?id=4243&forum_id=37&jump_to=54060#p54060 s64	+	* https://www.marshallprotocol.com/view_topic.php?id=4243&forum_id=37&jump_to=54060#p54060 s64


Line 104:		Line 107:
	School of Psychological Sciences, Tel Aviv University, Tel Aviv, Israel.		School of Psychological Sciences, Tel Aviv University, Tel Aviv, Israel.
	Abstract		Abstract
-	Group A streptococcal (GAS) infections and autoimmunity are associated with the onset of a spectrum of neuropsychiatric disorders in children, with the prototypical disorder being Sydenham chorea (SC). Our aim was to develop an animal model that resembled the behavioral, pharmacological, and immunological abnormalities of SC and other streptococcal-related neuropsychiatric disorders. Male Lewis rats exposed to GAS antigen exhibited motor symptoms (impaired food manipulation and beam walking) and compulsive behavior (increased induced-grooming). These symptoms were alleviated by the D2 blocker haloperidol and the selective serotonin reuptake inhibitor paroxetine, respectively, drugs that are used to treat motor symptoms and compulsions in streptococcal-related neuropsychiatric disorders. Streptococcal exposure resulted in antibody deposition in the striatum, thalamus, and frontal cortex, and concomitant alterations in dopamine and glutamate levels in cortex and basal ganglia, consistent with the known pathophysiology of SC and related neuropsychiatric disorders. Autoantibodies (IgG) of GAS rats reacted with tubulin and caused elevated calcium/calmodulin-dependent protein kinase II signaling in SK-N-SH neuronal cells, as previously found with sera from SC and related neuropsychiatric disorders. Our new animal model translates directly to human disease and led us to discover autoantibodies targeted against dopamine D1 and D2 receptors in the rat model as well as in SC and other streptococcal-related neuropsychiatric disorders. (({{pubmed>long:22534626}}))	+	Group A streptococcal (GAS) infections and autoimmunity are associated with the onset of a spectrum of neuropsychiatric disorders in children, with the prototypical disorder being Sydenham chorea (SC). Our aim was to develop an animal model that resembled the behavioral, pharmacological, and immunological abnormalities of SC and other streptococcal-related neuropsychiatric disorders. Male Lewis rats exposed to GAS antigen exhibited motor symptoms (impaired food manipulation and beam walking) and compulsive behavior (increased induced-grooming). These symptoms were alleviated by the D2 blocker haloperidol and the selective serotonin reuptake inhibitor paroxetine, respectively, drugs that are used to treat motor symptoms and compulsions in streptococcal-related neuropsychiatric disorders. Streptococcal exposure resulted in antibody deposition in the striatum, thalamus, and frontal cortex, and concomitant alterations in dopamine and glutamate levels in cortex and basal ganglia, consistent with the known pathophysiology of SC and related neuropsychiatric disorders. Autoantibodies (IgG) of GAS rats reacted with tubulin and caused elevated calcium/calmodulin-dependent protein kinase II signaling in SK-N-SH neuronal cells, as previously found with sera from SC and related neuropsychiatric disorders. Our new animal model translates directly to human disease and led us to discover autoantibodies targeted against dopamine D1 and D2 receptors in the rat model as well as in SC and other streptococcal-related neuropsychiatric disorders. (({{pmid>long:22534626}}))

	</blockquote>		</blockquote>


-	===== References =====	+	===== References =====</nodisp>

Osteoarthritis

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

01.11.2019		current
Line 8:		Line 8:


-	Usefulness of broad-range PCR for the diagnosis of osteoarticular infections.(({{pubmed>long:18525362}}))	+	Usefulness of broad-range PCR for the diagnosis of osteoarticular infections.(({{pmid>long:18525362}}))
	===== Evidence of infectious cause =====		===== Evidence of infectious cause =====

	Since studies are now showing that tetracycline can slow down the OA process, this suggests that this process is impacted by bacteria. I suspect that lost cartilage will not be replaced but that eliminating CWD bacteria might halt the degenerative process.		Since studies are now showing that tetracycline can slow down the OA process, this suggests that this process is impacted by bacteria. I suspect that lost cartilage will not be replaced but that eliminating CWD bacteria might halt the degenerative process.

-	<blockquote>The almost universal use of methotrexate and the rapid development of potent biologic agents have eclipsed the potential usage of TETs for RA. Ironically, it is in osteoarthritis, where there has only been one clinical trial which essentially failed, that the best potential exists for use of an MMP-inhibiting TET. (({{pubmed>long:21723947}}))</blockquote>	+	<blockquote>The almost universal use of methotrexate and the rapid development of potent biologic agents have eclipsed the potential usage of TETs for RA. Ironically, it is in osteoarthritis, where there has only been one clinical trial which essentially failed, that the best potential exists for use of an MMP-inhibiting TET. (({{pmid>long:21723947}}))</blockquote>



	===== Accepted knowledge =====		===== Accepted knowledge =====
-	[[http://www.medicinenet.com/osteoarthritis/article.htm\|This osteoarthritis (degenerative arthritis) website]] states:	+	[[https://www.medicinenet.com/osteoarthritis/article.htm\|This osteoarthritis (degenerative arthritis) website]] states:

	<blockquote>Research scientists have found that doxycycline, a tetracycline drug, has been shown to slow the progression of cartilage degeneration in the knees of patients with osteoarthritis. This effect seems to be a result of the drug's effect on enzymes that destroy cartilage rather than on their properties as antibiotics. More studies are needed to determine the significance of this interesting work.</blockquote>		<blockquote>Research scientists have found that doxycycline, a tetracycline drug, has been shown to slow the progression of cartilage degeneration in the knees of patients with osteoarthritis. This effect seems to be a result of the drug's effect on enzymes that destroy cartilage rather than on their properties as antibiotics. More studies are needed to determine the significance of this interesting work.</blockquote>
Line 42:		Line 42:
	===== Management =====		===== Management =====

-	Is aquatic exercise more effective than land-based exercise for knee osteoarthritis? (({{pubmed>long:30593178}}))	+	Is aquatic exercise more effective than land-based exercise for knee osteoarthritis? (({{pmid>long:30593178}}))

	===== Research =====		===== Research =====

-	Why does hyaline cartilage fail to repair? (({{pubmed>long:30605736}}))	+	Why does hyaline cartilage fail to repair? (({{pmid>long:30605736}}))

-	a comprehensive review on recent literature describing signal pathways in the hypertrophy of MSCs-derived in vitro differentiated chondrocytes and chondrocytes, with an emphasis on the crosstalk between these pathways. (({{pubmed>long:26287176}}))	+	a comprehensive review on recent literature describing signal pathways in the hypertrophy of MSCs-derived in vitro differentiated chondrocytes and chondrocytes, with an emphasis on the crosstalk between these pathways. (({{pmid>long:26287176}}))

-	Cytokines such as IL-1 and TNF-alpha produced by activated synoviocytes, mononuclear cells or by articular cartilage itself significantly up-regulate metalloproteinases (MMP) gene expression. Cytokines also blunt chondrocyte compensatory synthesis pathways required to restore the integrity of the degraded extrecellular matrix (ECM). Moreover, in OA synovium, a relative deficit in the production of natural antagonists of the IL-1 receptor (IL-1Ra) has been demonstrated, and could possibly be related to an excess production of nitric oxide in OA tissues. (({{pubmed>long:12082286}}))	+	Cytokines such as IL-1 and TNF-alpha produced by activated synoviocytes, mononuclear cells or by articular cartilage itself significantly up-regulate metalloproteinases (MMP) gene expression. Cytokines also blunt chondrocyte compensatory synthesis pathways required to restore the integrity of the degraded extrecellular matrix (ECM). Moreover, in OA synovium, a relative deficit in the production of natural antagonists of the IL-1 receptor (IL-1Ra) has been demonstrated, and could possibly be related to an excess production of nitric oxide in OA tissues. (({{pmid>long:12082286}}))

-	Altogether, our data show that tetracyclines have no inhibitory potential on any proteoglycanolytic activities within mild or moderately affected human OA cartilage at therapeutic achievable plasma levels. (({{pubmed>long:20069635}}))	+	Altogether, our data show that tetracyclines have no inhibitory potential on any proteoglycanolytic activities within mild or moderately affected human OA cartilage at therapeutic achievable plasma levels. (({{pmid>long:20069635}}))

-	Biomarkers of early stage osteoarthritis, rheumatoid arthritis and musculoskeletal health. <blockquote>We detected CP in the plasma of healthy subjects and surprisingly found that CP was increased in both patients with eOA and eRA whereas anti-CCP antibodies were predominantly present in eRA. A 4-class diagnostic algorithm combining plasma/serum CP, anti-CCP antibody and hydroxyproline applied to a cohort gave specific and sensitive detection and discrimination of eOA, eRA, other non-RA inflammatory joint diseases and good skeletal health.(({{pubmed>long:25788417}}))</blockquote>	+	Biomarkers of early stage osteoarthritis, rheumatoid arthritis and musculoskeletal health. <blockquote>We detected CP in the plasma of healthy subjects and surprisingly found that CP was increased in both patients with eOA and eRA whereas anti-CCP antibodies were predominantly present in eRA. A 4-class diagnostic algorithm combining plasma/serum CP, anti-CCP antibody and hydroxyproline applied to a cohort gave specific and sensitive detection and discrimination of eOA, eRA, other non-RA inflammatory joint diseases and good skeletal health.(({{pmid>long:25788417}}))</blockquote>

	After adjusting for all the covariates, the relative odds (95% confidence interval) of developing definite knee OA per increment of 1 SD (20.7 ng/mL) in winter season 25(OH)D was 1.57 (1.10-2.27), whereas for summer season sera the corresponding rate was 0.53 (0.28-1.00).		After adjusting for all the covariates, the relative odds (95% confidence interval) of developing definite knee OA per increment of 1 SD (20.7 ng/mL) in winter season 25(OH)D was 1.57 (1.10-2.27), whereas for summer season sera the corresponding rate was 0.53 (0.28-1.00).
-	CONCLUSION: The results do not support the hypothesis that a low level of serum 25(OH)D contributes to the development of OA. (({{pubmed>long:22043944}}))	+	CONCLUSION: The results do not support the hypothesis that a low level of serum 25(OH)D contributes to the development of OA. (({{pmid>long:22043944}}))

	{{tag>disease }}		{{tag>disease }}
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		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

		+	Somewhere I think I have seen the idea that microbes multipy with ease in damged tissu... if only i knew where (sigh) --- //Sallie Q 02.17.2019//
		+
		+
		+	//broken link//
	broken promise ??		broken promise ??
	The Promise of a Tetracycline Antibiotic for Treating Osteoarthritis		The Promise of a Tetracycline Antibiotic for Treating Osteoarthritis
-	[[http://www.soundmedicine.iu.edu/segment.php4?seg=104\|An Antibiotic to Slow Osteoarthritis]]	+	[[https://www.soundmedicine.iu.edu/segment.php4?seg=104\|An Antibiotic to Slow Osteoarthritis]]

	<DiseaseHierarchy>		<DiseaseHierarchy>
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	* legacy content		* legacy content
-	* http://www.marshallprotocol.com/view_topic.php?id=3220&forum_id=37&jump_to=45630#p45630 s249	+	* https://www.marshallprotocol.com/view_topic.php?id=3220&forum_id=37&jump_to=45630#p45630 s249

		+	https://www.webmd.com/osteoarthritis/news/20101108/vitamin-d-fails-osteoarthritis-test?ecd=wnl_art_111910

-	http://www.webmd.com/osteoarthritis/news/20101108/vitamin-d-fails-osteoarthritis-test?ecd=wnl_art_111910

		+	===== References =====</nodisp>

-	===== References =====

Osteoporosis and osteopenia

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

02.02.2020		current
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	* minimizing intake of caffeine		* minimizing intake of caffeine
	* refraining from excess alcohol or sodium consumption		* refraining from excess alcohol or sodium consumption
-	* limiting smoking (({{pubmed>long:8363002}}))	+	* limiting smoking (({{pmid>long:8363002}}))
	* weaning from drugs, which lead to bone loss including:		* weaning from drugs, which lead to bone loss including:
	* [[home:othertreatments::corticosteroids\|corticosteroids]]		* [[home:othertreatments::corticosteroids\|corticosteroids]]
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-	* high levels of 1,25-D affect osteoclast activity – When functioning properly, the Vitamin D Receptor contributes to bone health in an underecognized way distinct from other classical calcium regulating hormones.(({{pubmed>long:20813899}})) However, proper functioning becomes disrupted when, according to the Marshall Pathogenesis, pathogenic microbes create proteins that bind and block the Vitamin D Receptor, preventing it from expressing many essential components required for health. These include the estrogen receptors, upon which the bone matrix is dependent. The bone matrix is dependent on estrogen homeostasis (estrogen is important to stimulate osteoblast activity).(({{pubmed>long:12682916}})) This model of disease is partially validated by the fact that drugs such as [[home:othertreatments:antitnf\|TNF-alpha inhibitors]], which prevent inflammation, often lead to //temporary// increases in bone mass in patients with osteoporosis. Stimulated osteoclasts dissolve bone material, causing it to be reabsorbed into the bloodstream. This leads to bone loss as well as calcium being deposited in the soft tissues of the body, including those in the lungs, breasts and the kidneys (where it forms kidney stones).	+	* high levels of 1,25-D affect osteoclast activity – When functioning properly, the Vitamin D Receptor contributes to bone health in an underecognized way distinct from other classical calcium regulating hormones.(({{pmid>long:20813899}})) However, proper functioning becomes disrupted when, according to the Marshall Pathogenesis, pathogenic microbes create proteins that bind and block the Vitamin D Receptor, preventing it from expressing many essential components required for health. These include the estrogen receptors, upon which the bone matrix is dependent. The bone matrix is dependent on estrogen homeostasis (estrogen is important to stimulate osteoblast activity).(({{pmid>long:12682916}})) This model of disease is partially validated by the fact that drugs such as [[home:othertreatments:antitnf\|TNF-alpha inhibitors]], which prevent inflammation, often lead to //temporary// increases in bone mass in patients with osteoporosis. Stimulated osteoclasts dissolve bone material, causing it to be reabsorbed into the bloodstream. This leads to bone loss as well as calcium being deposited in the soft tissues of the body, including those in the lungs, breasts and the kidneys (where it forms kidney stones).
-	* osteoporotic bone has lower levels of expression //of// VDR – A recent study evaluating expression of (rather than by) the VDR in platelets in osteoporotic bone versus healthy subjects.(({{pubmed>long:22801440}})) The authors found:	+	* osteoporotic bone has lower levels of expression //of// VDR – A recent study evaluating expression of (rather than by) the VDR in platelets in osteoporotic bone versus healthy subjects.(({{pmid>long:22801440}})) The authors found:
	* lower levels of VDR in all patients,		* lower levels of VDR in all patients,
	* number of VDRs was positively correlated with bone density, and		* number of VDRs was positively correlated with bone density, and
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	<html><!--		<html><!--
-	In addition, if the VDR is blocked, the enzyme CYP24 is not transcribed. Since CYP24 is needed to keep levels of 1,25-D in check, the level of 1,25-D becomes greatly elevated in individuals without the active enzyme. The cytokine release stimulated by Th1 pathogens activates the pathway which causes increased production of CYP27B1, the enzyme that converts 25-D into 1,25-D. As more conversion occurs, the level of 1,25-D in the body rises.(({{pubmed>long:18200565}})) As 1,25-D rises above a certain range - approximately 43 pg/ml - elevated levels of 1,25-D stimulate bone osteoclasts, cells that remove minerals from the bone.(({{pubmed>long:10782361}})) (({{pubmed>long:10363752}}))	+	In addition, if the VDR is blocked, the enzyme CYP24 is not transcribed. Since CYP24 is needed to keep levels of 1,25-D in check, the level of 1,25-D becomes greatly elevated in individuals without the active enzyme. The cytokine release stimulated by Th1 pathogens activates the pathway which causes increased production of CYP27B1, the enzyme that converts 25-D into 1,25-D. As more conversion occurs, the level of 1,25-D in the body rises.(({{pmid>long:18200565}})) As 1,25-D rises above a certain range - approximately 43 pg/ml - elevated levels of 1,25-D stimulate bone osteoclasts, cells that remove minerals from the bone.(({{pmid>long:10782361}})) (({{pmid>long:10363752}}))
	-->		-->
	</html>		</html>
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	===== Other treatments =====		===== Other treatments =====

-	Calcitonin (({{pubmed>long: 30725954}}))	+	Calcitonin (({{pmid>long: 30725954}}))

	<blockquote>Salmon calcitonin (after this referred to as “calcitonin”) is an analog of human calcitonin used in the treatment of postmenopausal osteoporosis, Paget disease of bone, and hypercalcemia. Its clinical importance derives from its ability to inhibit osteoclasts and increase renal excretion of calcium.		<blockquote>Salmon calcitonin (after this referred to as “calcitonin”) is an analog of human calcitonin used in the treatment of postmenopausal osteoporosis, Paget disease of bone, and hypercalcemia. Its clinical importance derives from its ability to inhibit osteoclasts and increase renal excretion of calcium.
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	</blockquote>		</blockquote>

		+
		+
		+	==== Boron ====
		+
		+	[[https://www.educate-yourself.org/cn/boraxconspiracy03jul12.shtml\|boron deficiency is common in western diets]]
		+
		+	<blockquote>Boron deficiency causes greatly increased amounts of calcium and magnesium to be lost with the urine. A borax supplement will reduce the daily loss of calcium by nearly 50%. As this calcium comes mainly from resorbed bone and teeth, boron deficiency may be the most important factor in causing osteoporosis and tooth decay.</blockquote>


	==== Cannabinoids ====		==== Cannabinoids ====

-	An optimal correlation of cannabinoid dose, duration, moment of action, and affinity can lead to an increased bone regeneration capacity (({{pubmed>long:30702341}}))	+	An optimal correlation of cannabinoid dose, duration, moment of action, and affinity can lead to an increased bone regeneration capacity (({{pmid>long:30702341}}))

-	Heavy cannabis use is associated with low bone mineral density, low BMI, high bone turnover, and an increased risk of fracture. (({{pubmed>long:27593602}})) [[https://www.amjmed.com/article/S0002-9343(17)30392-3/fulltext\|Response by H W Daniell, M.D.]]	+	Heavy cannabis use is associated with low bone mineral density, low BMI, high bone turnover, and an increased risk of fracture. (({{pmid>long:27593602}})) [[https://www.amjmed.com/article/S0002-9343(17)30392-3/fulltext\|Response by H W Daniell, M.D.]]


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	[[https://www.amjmed.com/article/S0002-9343(17)30613-7/fulltext\|Reply: Sophocleous et al]]		[[https://www.amjmed.com/article/S0002-9343(17)30613-7/fulltext\|Reply: Sophocleous et al]]

-	Cannabinoids induce incomplete maturation of cultured human leukemia cells. (({{pubmed>long:3037549}}))	+	Cannabinoids induce incomplete maturation of cultured human leukemia cells. (({{pmid>long:3037549}}))
		+
		+	The psychoactive component of marijuana, delta9-tetrahydrocannabinol (THC) suppresses different functions of immunocytes, including the antimicrobicidal activity of macrophages. (({{pmid>long:10733093}}))
		+
		+	the first observations of GcMAF effects on the transcriptionomics of the endocannabinoid system and expression of CB2R protein. These data point to a potential nexus between endocannabinoids, vitamin D and its transporter proteins, and the immune dysregulations observed with autism. (({{pmid>long: 24739187}}))

-	The psychoactive component of marijuana, delta9-tetrahydrocannabinol (THC) suppresses different functions of immunocytes, including the antimicrobicidal activity of macrophages. (({{pubmed>long:10733093}}))

-	the first observations of GcMAF effects on the transcriptionomics of the endocannabinoid system and expression of CB2R protein. These data point to a potential nexus between endocannabinoids, vitamin D and its transporter proteins, and the immune dysregulations observed with autism. (({{pubmed>long: 24739187}}))

	==== Calcium supplementation ====		==== Calcium supplementation ====
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	==== TNF-alpha drugs ====		==== TNF-alpha drugs ====

-	Multiple research teams have found that drugs which inhibit production of TNF-alpha lead to a short-term increase in patients’ spine and femoral bone mineral density. (({{pubmed>long:16263785}}))	+	Multiple research teams have found that drugs which inhibit production of TNF-alpha lead to a short-term increase in patients’ spine and femoral bone mineral density. (({{pmid>long:16263785}}))

	It should be noted that [[home:othertreatments:antitnf\|TNF-alpha blocking drugs]] do not provide a permanent solution to osteoporosis, since Th1 pathogens will continue to spread as the drug is administered. Also, TNF-alpha blocking medications are known to have serious side effects. However, the research is of interest since it confirms the importance of Th1 inflammation in osteoporosis.		It should be noted that [[home:othertreatments:antitnf\|TNF-alpha blocking drugs]] do not provide a permanent solution to osteoporosis, since Th1 pathogens will continue to spread as the drug is administered. Also, TNF-alpha blocking medications are known to have serious side effects. However, the research is of interest since it confirms the importance of Th1 inflammation in osteoporosis.
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	==== Vitamin D supplementation ====		==== Vitamin D supplementation ====

-	Some clinicians encourage patients with inadequate bone density to supplement with vitamin D and calcium. (({{pubmed>long:30293909}})) While [[home:food:calcium\|calcium]] has been shown to be somewhat helpful in certain patient cohorts, both controlled trials and molecular evidence do not support supplementation with vitamin D to reverse bone loss as, over the long term, it only exacerbates the disease process.	+	Some clinicians encourage patients with inadequate bone density to supplement with vitamin D and calcium. (({{pmid>long:30293909}})) While [[home:food:calcium\|calcium]] has been shown to be somewhat helpful in certain patient cohorts, both controlled trials and molecular evidence do not support supplementation with vitamin D to reverse bone loss as, over the long term, it only exacerbates the disease process.

-	<blockquote>Calcium supplements have been widely used by older men and women. However, in little more than a decade, authoritative recommendations have changed from encouraging the widespread use of calcium supplements to stating that they should not be used for primary prevention of fractures. This substantial shift in recommendations has occurred as a result of accumulated evidence of marginal antifracture efficacy, and important adverse effects from large randomized controlled trials of calcium or coadministered calcium and vitamin D supplements. In this review, we discuss this evidence, with a particular focus on increased cardiovascular risk with calcium supplements, which we first described 5 years ago. Calcium supplements with or without vitamin D marginally reduce total fractures but do not prevent hip fractures in community-dwelling individuals. They also cause kidney stones, acute gastrointestinal events, and increase the risk of myocardial infarction and stroke. //Bolland MJ, Grey A, and Reid IR// 2013 (({{pubmed>long:25114781}}))</blockquote>	+	<blockquote>Calcium supplements have been widely used by older men and women. However, in little more than a decade, authoritative recommendations have changed from encouraging the widespread use of calcium supplements to stating that they should not be used for primary prevention of fractures. This substantial shift in recommendations has occurred as a result of accumulated evidence of marginal antifracture efficacy, and important adverse effects from large randomized controlled trials of calcium or coadministered calcium and vitamin D supplements. In this review, we discuss this evidence, with a particular focus on increased cardiovascular risk with calcium supplements, which we first described 5 years ago. Calcium supplements with or without vitamin D marginally reduce total fractures but do not prevent hip fractures in community-dwelling individuals. They also cause kidney stones, acute gastrointestinal events, and increase the risk of myocardial infarction and stroke. //Bolland MJ, Grey A, and Reid IR// 2013 (({{pmid>long:25114781}}))</blockquote>

-	<blockquote>Web of industry, advocacy, and academia in the management of osteoporosis [[http://www.bmj.com/content/351/bmj.h3170\| BMJ 2015;351:h3170 ]]	+	<blockquote>Web of industry, advocacy, and academia in the management of osteoporosis [[https://www.bmj.com/content/351/bmj.h3170\| BMJ 2015;351:h3170 ]]

	"Calcium and vitamin D supplementation continue to be recommended to prevent and treat osteoporosis despite evidence of lack of benefit, say Andrew Grey and Mark Bolland. They examine why change is difficult and call for advocacy organisations, academics, and specialist societies to abandon industry ties" </blockquote>		"Calcium and vitamin D supplementation continue to be recommended to prevent and treat osteoporosis despite evidence of lack of benefit, say Andrew Grey and Mark Bolland. They examine why change is difficult and call for advocacy organisations, academics, and specialist societies to abandon industry ties" </blockquote>
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	^Author/Year ^Study Design ^Findings ^		^Author/Year ^Study Design ^Findings ^
-	\|Steven R. Cummings, MD; Douglas P. Kiel, MD, MPH; Dennis M. Black, PhD, 2016 (({{pubmed>long:26746474}}))\|Two “high” doses (60 000 IU of vitamin D3 per month or 24 000 IU vitamin D3 plus 300 mg of calcifediol per month) achieved a serum 25-hydroxyvitamin D (25[OH]D) level of 30 ng/mL in 80% of participants, a level that has been recommended as best for reducing the risk of fractures \|compared with a dose of 24 000 IU of vitamin D3 per month (equivalent to 800 IU per day), the higher doses had no effect on lower extremity physical performance and increased the risk of falls.\|	+	\|Steven R. Cummings, MD; Douglas P. Kiel, MD, MPH; Dennis M. Black, PhD, 2016 (({{pmid>long:26746474}}))\|Two “high” doses (60 000 IU of vitamin D3 per month or 24 000 IU vitamin D3 plus 300 mg of calcifediol per month) achieved a serum 25-hydroxyvitamin D (25[OH]D) level of 30 ng/mL in 80% of participants, a level that has been recommended as best for reducing the risk of fractures \|compared with a dose of 24 000 IU of vitamin D3 per month (equivalent to 800 IU per day), the higher doses had no effect on lower extremity physical performance and increased the risk of falls.\|
-	\|Karen E. Hansen, MD, MS; R. Erin Johnson, BS; Kaitlin R. Chambers, BS et al., 2015 (({{pubmed>long:26237520}}))\|randomized, double-blind, placebo-controlled clinical trial from May 1, 2010, through July 31, 2013, and final visit on August 8, 2014. A total of 230 postmenopausal women 75 years or younger with baseline 25(OH)D levels of 14 through 27 ng/mL and no osteoporosis were studied. \|“We found that compared with placebo, high-dose cholecalciferol had a very small effect on calcium absorption (1%) that did not translate into meaningful changes in lumbar spine, mean total-hip, femoral neck, or total-body BMD, trabecular bone score, TUG score, STS test score, muscle mass, number of falls, or number of fallers. ”\|	+	\|Karen E. Hansen, MD, MS; R. Erin Johnson, BS; Kaitlin R. Chambers, BS et al., 2015 (({{pmid>long:26237520}}))\|randomized, double-blind, placebo-controlled clinical trial from May 1, 2010, through July 31, 2013, and final visit on August 8, 2014. A total of 230 postmenopausal women 75 years or younger with baseline 25(OH)D levels of 14 through 27 ng/mL and no osteoporosis were studied. \|“We found that compared with placebo, high-dose cholecalciferol had a very small effect on calcium absorption (1%) that did not translate into meaningful changes in lumbar spine, mean total-hip, femoral neck, or total-body BMD, trabecular bone score, TUG score, STS test score, muscle mass, number of falls, or number of fallers. ”\|
-	\|J Christopher Gallagher,Prachi S Jindal, Lynette M Smith, 2014 (({{pubmed>long:24166866}}))\| A total of 198 white and African American women, aged 25 to 45 years, with serum 25OHD <20 ng/mL, were randomized in a double-blind study to vitamin D3 400, 800, 1600, 2400 IU, or placebo. A calcium supplement was given to increase mean calcium intake at baseline from 706 mg/d to 1031 mg/d. Calcium absorption was measured at baseline and after 12 months using a single isotope method with radiocalcium45 and 100 mg of calcium. Mean baseline serum 25OHD was 13.4 ng/mL (33.5 nmol/L) and increased to 40 ng/mL (100 nmol/L) on the highest dose of 2400 IU.\| " There is no need to recommend vitamin D for increasing calcium absorption in normal subjects. Very efficient calcium absorption at very low levels of serum 25OHD explains why people do not develop osteomalacia provided that dietary intakes of calcium and phosphorus are adequate."\|	+	\|J Christopher Gallagher,Prachi S Jindal, Lynette M Smith, 2014 (({{pmid>long:24166866}}))\| A total of 198 white and African American women, aged 25 to 45 years, with serum 25OHD <20 ng/mL, were randomized in a double-blind study to vitamin D3 400, 800, 1600, 2400 IU, or placebo. A calcium supplement was given to increase mean calcium intake at baseline from 706 mg/d to 1031 mg/d. Calcium absorption was measured at baseline and after 12 months using a single isotope method with radiocalcium45 and 100 mg of calcium. Mean baseline serum 25OHD was 13.4 ng/mL (33.5 nmol/L) and increased to 40 ng/mL (100 nmol/L) on the highest dose of 2400 IU.\| " There is no need to recommend vitamin D for increasing calcium absorption in normal subjects. Very efficient calcium absorption at very low levels of serum 25OHD explains why people do not develop osteomalacia provided that dietary intakes of calcium and phosphorus are adequate."\|
-	\|Gallagher JC1, Yalamanchili V, Smith LM., 2012(({{pubmed>long:22855333}})) \| a randomized double-blind placebo-controlled trial at Creighton University Medical Center, Omaha, NE. included 163 postmenopausal Caucasian women with insufficiency, defined as a serum 25OHD below 20 ng/ml (50 nmol/liter).\| There was no evidence of a threshold for reduced calcium absorption in the serum 25OHD range of 10-66 ng/ml. The results challenge assumptions about the value of adding vitamin D to increase calcium absorption except when serum 25OHD is less than 10 ng/ml.\|	+	\|Gallagher JC1, Yalamanchili V, Smith LM., 2012(({{pmid>long:22855333}})) \| a randomized double-blind placebo-controlled trial at Creighton University Medical Center, Omaha, NE. included 163 postmenopausal Caucasian women with insufficiency, defined as a serum 25OHD below 20 ng/ml (50 nmol/liter).\| There was no evidence of a threshold for reduced calcium absorption in the serum 25OHD range of 10-66 ng/ml. The results challenge assumptions about the value of adding vitamin D to increase calcium absorption except when serum 25OHD is less than 10 ng/ml.\|
-	\|Brunner //et al.//, 2008(({{pubmed>long:18755319}})) \|The largest randomized double-blind placebo-controlled study (the most valid study design possible) on vitamin D and calcium to date. More than 33,000 50-79 year old women at 40 centers participated.\| "Calcium and vitamin D do not protect against decline of physical functioning in older women."\|	+	\|Brunner //et al.//, 2008(({{pmid>long:18755319}})) \|The largest randomized double-blind placebo-controlled study (the most valid study design possible) on vitamin D and calcium to date. More than 33,000 50-79 year old women at 40 centers participated.\| "Calcium and vitamin D do not protect against decline of physical functioning in older women."\|
-	\|Tang //et al.//, 2007 (({{pubmed>long:17720017}})) \|The largest meta-analysis of calcium and vitamin D trials in people over 50. combined the results of 29 randomized trials in which researchers had given participants supplements of calcium and vitamin D. \|Although the team did find a small reduction in fracture risk (12%) correlated with calcium supplementation, they state, "Addition of vitamin D supplementation was not shown to offer additional risk reduction over and above the use of calcium alone."\|	+	\|Tang //et al.//, 2007 (({{pmid>long:17720017}})) \|The largest meta-analysis of calcium and vitamin D trials in people over 50. combined the results of 29 randomized trials in which researchers had given participants supplements of calcium and vitamin D. \|Although the team did find a small reduction in fracture risk (12%) correlated with calcium supplementation, they state, "Addition of vitamin D supplementation was not shown to offer additional risk reduction over and above the use of calcium alone."\|
-	\|Porthouse //et al.//, 2005(({{pubmed>long:15860827}})) \|Randomized controlled trial of 3,314 women, 70+ years old who were at risk for hip fractures because of decreased bone mass. The women supplemented with 1000 mg of calcium and 800 IU of vitamin D over a period of 24-62 months. \|There was no measurable change in the bone quality of any of the women. Researchers found “no evidence that calcium and vitamin D supplementation reduce the risk of clinical fractures in women with one or more risk factors for hip fracture.”(({{pubmed>long:15860827}})) (Other well-designed studies on elderly women at risk for fractures have come to identical conclusions.(({{pubmed>long:15885294}})) (({{pubmed>long:10999778}})) (({{pubmed>long:16481635}}))) \|	+	\|Porthouse //et al.//, 2005(({{pmid>long:15860827}})) \|Randomized controlled trial of 3,314 women, 70+ years old who were at risk for hip fractures because of decreased bone mass. The women supplemented with 1000 mg of calcium and 800 IU of vitamin D over a period of 24-62 months. \|There was no measurable change in the bone quality of any of the women. Researchers found “no evidence that calcium and vitamin D supplementation reduce the risk of clinical fractures in women with one or more risk factors for hip fracture.”(({{pmid>long:15860827}})) (Other well-designed studies on elderly women at risk for fractures have come to identical conclusions.(({{pmid>long:15885294}})) (({{pmid>long:10999778}})) (({{pmid>long:16481635}}))) \|
-	\|Sanders KM1, Stuart AL, Williamson EJ, Simpson JA, Kotowicz MA, Young D, Nicholson GC. 2010(({{pubmed>long:20460620}})) \|A double-blind, placebo-controlled trial of 2256 community-dwelling women, aged 70 years or older, considered to be at high risk of fracture were recruited from June 2003 to June 2005 and were randomly assigned to receive cholecalciferol or placebo each autumn to winter for 3 to 5 years. The study concluded in 2008.\| "CONCLUSION: Among older community-dwelling women, annual oral administration of high-dose cholecalciferol resulted in an increased risk of falls and fractures."\|	+	\|Sanders KM1, Stuart AL, Williamson EJ, Simpson JA, Kotowicz MA, Young D, Nicholson GC. 2010(({{pmid>long:20460620}})) \|A double-blind, placebo-controlled trial of 2256 community-dwelling women, aged 70 years or older, considered to be at high risk of fracture were recruited from June 2003 to June 2005 and were randomly assigned to receive cholecalciferol or placebo each autumn to winter for 3 to 5 years. The study concluded in 2008.\| "CONCLUSION: Among older community-dwelling women, annual oral administration of high-dose cholecalciferol resulted in an increased risk of falls and fractures."\|


	A number of recent studies examining calcium and vitamin D supplementation are compromised by a flaw in methodology: the authors mistakenly attribute positive increases in bone density to both calcium and vitamin D. Studies which separately measure the positive or sometimes equivocal effect of calcium from that of vitamin D tend to show that vitamin D has no positive effect on bone health.		A number of recent studies examining calcium and vitamin D supplementation are compromised by a flaw in methodology: the authors mistakenly attribute positive increases in bone density to both calcium and vitamin D. Studies which separately measure the positive or sometimes equivocal effect of calcium from that of vitamin D tend to show that vitamin D has no positive effect on bone health.

-	For example, one study found that calcium supplementation (750 mg) improved bone density over a four-year period, whereas vitamin D supplementation (600 IU) had no effect. In fact, the effect of calcium on bone loss was blunted in subjects with the highest levels of vitamin D, causing the team to point out the danger of over-supplementation of the elderly with vitamin D if they have an adequate calcium intake.(({{pubmed>long:10999778}}))	+	For example, one study found that calcium supplementation (750 mg) improved bone density over a four-year period, whereas vitamin D supplementation (600 IU) had no effect. In fact, the effect of calcium on bone loss was blunted in subjects with the highest levels of vitamin D, causing the team to point out the danger of over-supplementation of the elderly with vitamin D if they have an adequate calcium intake.(({{pmid>long:10999778}}))

	In the case of studies showing a neutral effect of vitamin D and calcium supplementation, it’s quite possible that calcium did have a positive effect on the bone mass of the study subjects. One likely explanation is that the positive effects of calcium were offset by the negative effects of VDR blockage and elevated 1,25-D caused by consumption of the vitamin D supplements.		In the case of studies showing a neutral effect of vitamin D and calcium supplementation, it’s quite possible that calcium did have a positive effect on the bone mass of the study subjects. One likely explanation is that the positive effects of calcium were offset by the negative effects of VDR blockage and elevated 1,25-D caused by consumption of the vitamin D supplements.
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	<blockquote>Occult vitamin D intoxication was detected in patients who were using dietary supplements that contained an unadvertised high level of vitamin D. Resolution of vitamin D intoxication was associated with a rebound in bone mineral density.		<blockquote>Occult vitamin D intoxication was detected in patients who were using dietary supplements that contained an unadvertised high level of vitamin D. Resolution of vitamin D intoxication was associated with a rebound in bone mineral density.

-	//J.S. Adams, et al.// (({{pubmed>long:10215562}})) </blockquote>	+	//J.S. Adams, et al.// (({{pmid>long:10215562}})) </blockquote>

	Adams's study is particularly valuable because their three-year follow-up phase, which is significantly longer than some, showed that the increase in bone mineral density persisted after initial recovery.		Adams's study is particularly valuable because their three-year follow-up phase, which is significantly longer than some, showed that the increase in bone mineral density persisted after initial recovery.

-	Similarly, researchers at the University of Science and Technology in Norway published a study that measured the forearm bone mineral density of 3,042 Norwegian women, aged 50 to 70 years old. They found that those women who had not taken cod liver oil (a substance that contains high levels of vitamin D) during childhood had higher bone mineral density compared to those who had ingested cod liver oil.(({{pubmed>long:18033763}})) Since the study compared childhood intake of vitamin D to bone density at least 4-5 decades after ingestion, it is a good example of how only those studies which track vitamin D intake over long periods of time, namely decades, are likely to pick up on the harm the secosteroid causes in the long term.	+	Similarly, researchers at the University of Science and Technology in Norway published a study that measured the forearm bone mineral density of 3,042 Norwegian women, aged 50 to 70 years old. They found that those women who had not taken cod liver oil (a substance that contains high levels of vitamin D) during childhood had higher bone mineral density compared to those who had ingested cod liver oil.(({{pmid>long:18033763}})) Since the study compared childhood intake of vitamin D to bone density at least 4-5 decades after ingestion, it is a good example of how only those studies which track vitamin D intake over long periods of time, namely decades, are likely to pick up on the harm the secosteroid causes in the long term.

-	Yet another example came in a 2010 double-blind, placebo-controlled trial of 2256 community-dwelling women, aged 70 years or older, considered to be at high risk of fracture. Over the course of three to five years, every year subjects were given 500,000 IU of cholecalciferol or placebo. Women in the vitamin D group were significantly more likely to experience falls or fractures.(({{pubmed>long:20460620}}))	+	Yet another example came in a 2010 double-blind, placebo-controlled trial of 2256 community-dwelling women, aged 70 years or older, considered to be at high risk of fracture. Over the course of three to five years, every year subjects were given 500,000 IU of cholecalciferol or placebo. Women in the vitamin D group were significantly more likely to experience falls or fractures.(({{pmid>long:20460620}}))

	=== Molecular evidence against vitamin D supplementation ===		=== Molecular evidence against vitamin D supplementation ===

-	Contrary to most received wisdom, vitamin D does not enhance the absorption of calcium. As Aloia showed there is no relationship whatsoever between 25-D levels and calcium absorption.(({{pubmed>long:20660223}})) 25-D is a simple secosteroid which does not affect the genes responsible for calcium absorption. Further, there is no evidence to suggest that additional vitamin D leads to a more active Vitamin D Receptor.	+	Contrary to most received wisdom, vitamin D does not enhance the absorption of calcium. As Aloia showed there is no relationship whatsoever between 25-D levels and calcium absorption.(({{pmid>long:20660223}})) 25-D is a simple secosteroid which does not affect the genes responsible for calcium absorption. Further, there is no evidence to suggest that additional vitamin D leads to a more active Vitamin D Receptor.

-	By way of contrast, the Vitamin D Receptor is a receptor that transcribes thousands of genes,(({{pubmed>long:16002434}})) some of which do affect the metabolism of calcium.	+	By way of contrast, the Vitamin D Receptor is a receptor that transcribes thousands of genes,(({{pmid>long:16002434}})) some of which do affect the metabolism of calcium.

	<blockquote>		<blockquote>
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	===== Evidence of infectious cause =====		===== Evidence of infectious cause =====

-	* certain antibiotics help strengthen bones – NIH animal studies have shown that minocycline, an [[home:mp\|MP antibiotic]], increased bone density, "stimulated bone formation substantially" and slowed bone resorption. (({{pubmed>long:9972125}}))	+	* certain antibiotics help strengthen bones – NIH animal studies have shown that minocycline, an [[home:mp\|MP antibiotic]], increased bone density, "stimulated bone formation substantially" and slowed bone resorption. (({{pmid>long:9972125}}))
-	* connection with disparate diseases – the NIH connects several Th1 diseases with higher risk of osteoporosis, including rheumatoid arthritis, inflammatory bowel disease, lupus, celiac disease (({{pubmed>long:25971649}})), and anorexia nervosa (({{pubmed>long:31765843}})) ,	+	* connection with disparate diseases – the NIH connects several Th1 diseases with higher risk of osteoporosis, including rheumatoid arthritis, inflammatory bowel disease, lupus, celiac disease (({{pmid>long:25971649}})), and anorexia nervosa (({{pmid>long:31765843}})) ,


Line 243:		Line 252:
	===== Recent Research =====		===== Recent Research =====

-	//Zhao JG, Zeng XT, Wang J, Liu L. in// Association Between Calcium or Vitamin D Supplementation and Fracture Incidence in Community-Dwelling Older Adults: A Systematic Review and Meta-analysis. (({{pubmed>long:29279934}}))	+	//Zhao JG, Zeng XT, Wang J, Liu L. in// Association Between Calcium or Vitamin D Supplementation and Fracture Incidence in Community-Dwelling Older Adults: A Systematic Review and Meta-analysis. (({{pmid>long:29279934}}))

	<blockquote>Results:		<blockquote>Results:
Line 253:		Line 262:


-	//Bolland MJ, Grey A and Avenell A. in// Effects of vitamin D supplementation on musculoskeletal health: a systematic review, meta-analysis, and trial sequential analysis. (({{pubmed>long:30293909}}))	+	//Bolland MJ, Grey A and Avenell A. in// Effects of vitamin D supplementation on musculoskeletal health: a systematic review, meta-analysis, and trial sequential analysis. (({{pmid>long:30293909}}))


Line 266:		Line 275:
	<blockquote>Assessment of the genetic and clinical determinants of fracture risk: genome wide association and mendelian randomisation study.		<blockquote>Assessment of the genetic and clinical determinants of fracture risk: genome wide association and mendelian randomisation study.

-	This large scale GWAS meta-analysis for fracture identified 15 genetic determinants of fracture, all of which also influenced bone mineral density. Among the clinical risk factors for fracture assessed, only bone mineral density showed a major causal effect on fracture. Genetic predisposition to lower levels of vitamin D and estimated calcium intake from dairy sources were not associated with fracture risk. (({{pubmed>long:30158200}}))</blockquote>	+	This large scale GWAS meta-analysis for fracture identified 15 genetic determinants of fracture, all of which also influenced bone mineral density. Among the clinical risk factors for fracture assessed, only bone mineral density showed a major causal effect on fracture. Genetic predisposition to lower levels of vitamin D and estimated calcium intake from dairy sources were not associated with fracture risk. (({{pmid>long:30158200}}))</blockquote>


	{{tag>disease}}		{{tag>disease}}
		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

Line 277:		Line 287:

	* To do - create new article for secondary hyperparathyroidism.		* To do - create new article for secondary hyperparathyroidism.
-	* To begin with, patients with chronic disease may obtain less of a benefit from calcium supplements since the calcium metabolism of patients suffering from chronic disease is different from that of healthy individuals.(({{pubmed>long:8386185}}))	+	* To begin with, patients with chronic disease may obtain less of a benefit from calcium supplements since the calcium metabolism of patients suffering from chronic disease is different from that of healthy individuals.(({{pmid>long:8386185}}))
	* Legacy content		* Legacy content
	* f166		* f166
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	* f97		* f97

-	http://www.docguide.com/diabetes-mellitus-has-protective-effect-bone-density-even-elderly-female-nursing-home-patients-prese	+	https://www.docguide.com/diabetes-mellitus-has-protective-effect-bone-density-even-elderly-female-nursing-home-patients-prese

	I removed this. I'm not too sure how this quote was helping. It is unprofessional, IMO. --- //Paul Albert 06.07.2010//		I removed this. I'm not too sure how this quote was helping. It is unprofessional, IMO. --- //Paul Albert 06.07.2010//
Line 308:		Line 318:
	All the intricate central processing takes place in the hypothalamus, a small yet complex region of the brain that links the nervous and hormone systems.		All the intricate central processing takes place in the hypothalamus, a small yet complex region of the brain that links the nervous and hormone systems.

-	From: [[http://www.physorg.com/news180708867.html\|We now know that the brain controls the formation of bone]]	+	From: [[https://www.physorg.com/news180708867.html\|We now know that the brain controls the formation of bone]]
	</blockquote>		</blockquote>

Line 325:		Line 335:

	<blockquote>Another study is out, this one showing that Vitamin D doesn't boost bone strength in aging men. Most of the previous studies have looked only at women:		<blockquote>Another study is out, this one showing that Vitamin D doesn't boost bone strength in aging men. Most of the previous studies have looked only at women:
-	http://jcem.endojournals.org/cgi/content/abstract/jc.2010-2284v1	+	https://jcem.endojournals.org/cgi/content/abstract/jc.2010-2284v1

	So why do we continue to 'fortify' our milk? Apparently it is because of people like this:Despite the findings, people still need to get enough calcium and vitamin D to reduce the risk of osteoporosis, or bone thinning, said Dr. Mone Zaidi, an osteoporosis researcher at the Mount Sinai School of Medicine in New York, who was not involved in the study.		So why do we continue to 'fortify' our milk? Apparently it is because of people like this:Despite the findings, people still need to get enough calcium and vitamin D to reduce the risk of osteoporosis, or bone thinning, said Dr. Mone Zaidi, an osteoporosis researcher at the Mount Sinai School of Medicine in New York, who was not involved in the study.
-	http://www.reuters.com/article/idUSTRE70Q8V020110127	+	https://www.reuters.com/article/idUSTRE70Q8V020110127

	IMO Vitamin D will turn out to be the biggest, and most costly, mistake that Medicine has ever made. Worse than Thalidomide. Worse than FenFen. It is just a matter of time until the people taking high doses of Vitamin D find that not only is it harming them, but they cannot even wean from this steroid.		IMO Vitamin D will turn out to be the biggest, and most costly, mistake that Medicine has ever made. Worse than Thalidomide. Worse than FenFen. It is just a matter of time until the people taking high doses of Vitamin D find that not only is it harming them, but they cannot even wean from this steroid.
Line 347:		Line 357:
	CONCLUSIONS: In a prospective study of the elderly, diet, including consumption of dairy products, alcohol and vitamin D, did not appear to play a major role in hip fracture incidence. There is however, weak and statistically non-significant evidence that vegetable and fish consumption and intake of polyunsaturated lipids may have a beneficial, whereas saturated lipid intake a detrimental effect.		CONCLUSIONS: In a prospective study of the elderly, diet, including consumption of dairy products, alcohol and vitamin D, did not appear to play a major role in hip fracture incidence. There is however, weak and statistically non-significant evidence that vegetable and fish consumption and intake of polyunsaturated lipids may have a beneficial, whereas saturated lipid intake a detrimental effect.
	PMID: 20948558</blockquote>		PMID: 20948558</blockquote>
-	===== References =====	+	===== References =====</nodisp>

Parkinson's disease

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

Periodontal disease and gingivitis

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

Peripheral neuropathy

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

02.18.2019		current
Line 6:		Line 6:


-	[[http://www.mayoclinic.org/diseases-conditions/peripheral-neuropathy/home/ovc-20204944\|Mayo Clinic overview]]	+	[[https://www.mayoclinic.org/diseases-conditions/peripheral-neuropathy/home/ovc-20204944\|Mayo Clinic overview]]


Line 12:		Line 12:


-	The Peripheral Neuropathy Research Registry (PNRR) is a prospective cohort of peripheral neuropathy (PN) patients focused on idiopathic axonal peripheral neuropathy. (({{pubmed>long:30629307}}))	+	The Peripheral Neuropathy Research Registry (PNRR) is a prospective cohort of peripheral neuropathy (PN) patients focused on idiopathic axonal peripheral neuropathy. (({{pmid>long:30629307}}))

-	Peripheral Neuropathy and Nerve Compression Syndromes in Burns. (({{pubmed>long:28888304}}))	+	Peripheral Neuropathy and Nerve Compression Syndromes in Burns. (({{pmid>long:28888304}}))

-	B vitamins and chemotherapy-induced peripheral neuropathy. (({{pubmed>long:28983799}}))	+	B vitamins and chemotherapy-induced peripheral neuropathy. (({{pmid>long:28983799}}))
	===== Evidence of infectious cause =====		===== Evidence of infectious cause =====

-	<blockquote>[[http://www.medscape.com/viewarticle/712640\|Inflammatory Peripheral Neuropathies Prevalent in Poultry and Swine Farmers]]	+	<blockquote>[[https://www.medscape.com/viewarticle/712640\|Inflammatory Peripheral Neuropathies Prevalent in Poultry and Swine Farmers]]

	November 18, 2009 (Philadelphia, Pennsylvania) — Symptoms associated with inflammatory peripheral neuropathies are significantly higher in farm workers exposed to poultry and swine, researchers reported here at the American Public Health Association 137th Annual Meeting.		November 18, 2009 (Philadelphia, Pennsylvania) — Symptoms associated with inflammatory peripheral neuropathies are significantly higher in farm workers exposed to poultry and swine, researchers reported here at the American Public Health Association 137th Annual Meeting.
Line 57:		Line 57:
	===== Management =====		===== Management =====

-	A Practical Approach to Diagnosis and Symptom Management. (({{pubmed>long:26141332}}))	+	A Practical Approach to Diagnosis and Symptom Management. (({{pmid>long:26141332}}))

	==== Caution ====		==== Caution ====
Line 72:		Line 72:

	<blockquote>Itching much better, but having a lot pf peripheral neuropathy in feet and hands, especially at night, when hands go numb and feet burn and prickle. Most annoying. Not sure if this is IP //Kas 2013//</blockquote>		<blockquote>Itching much better, but having a lot pf peripheral neuropathy in feet and hands, especially at night, when hands go numb and feet burn and prickle. Most annoying. Not sure if this is IP //Kas 2013//</blockquote>
		+
		+	<blockquote>Stabbing pains in my eye, various parts of my head, a feeling of an ant crawling over my skin; I never asked the doctor, but guess this is neuropathy. It is much reduced during my continued use of Olmesartan, but not completely so. The fleeting stabs have mostly resolved. //Sallie//</blockquote>


Line 136:		Line 138:
	chronic borreliosis ("Lyme"), multiple chemical sensitivities, chronic spinal inflammation, peripheral neuropathy		chronic borreliosis ("Lyme"), multiple chemical sensitivities, chronic spinal inflammation, peripheral neuropathy

-	Read the [[http://bacteriality.com/2007/12/28/interview14/\|interview]]	+	Read the [[https://bacteriality.com/2007/12/28/interview14/\|interview]]

	<html></div></div>		<html></div></div>
Line 159:		Line 161:


		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

Line 181:		Line 184:
	</blockquote>		</blockquote>

-	===== References =====	+	===== References =====</nodisp>

Pernicious anemia

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

01.11.2019		current
Line 6:		Line 6:


-	[[http://www.mayoclinic.org/diseases-conditions/anemia/symptoms-causes/syc-20351360\|Mayo Clinic overview]]	+	[[https://www.mayoclinic.org/diseases-conditions/anemia/symptoms-causes/syc-20351360\|Mayo Clinic overview]]

	Normal human gastric juice contains an "intrinsic factor" that, given simultaneously with vitamin B12 causes erythropoiesis (production of red blood cells).		Normal human gastric juice contains an "intrinsic factor" that, given simultaneously with vitamin B12 causes erythropoiesis (production of red blood cells).
Line 24:		Line 24:
	Breastfed infants of strict vegetarian mothers also are at risk for pernicious anemia. These infants can develop anemia within months of being born.		Breastfed infants of strict vegetarian mothers also are at risk for pernicious anemia. These infants can develop anemia within months of being born.

-	Gastric parietal cells produce two essential biologics: intrinsic factor and HCl acid. Pernicious anemia is a consequence of intrinsic factor loss and neutralizing intrinsic factor antibody that impairs cobalamin absorption. (({{pubmed>long:27538411}}))	+	Gastric parietal cells produce two essential biologics: intrinsic factor and HCl acid. Pernicious anemia is a consequence of intrinsic factor loss and neutralizing intrinsic factor antibody that impairs cobalamin absorption. (({{pmid>long:27538411}}))

-	[[https://www.ncbi.nlm.nih.gov/pubmed/28164751\|Aspects in Diagnosis.]] (({{pubmed>long:28164751}}))	+	[[https://www.ncbi.nlm.nih.gov/pubmed/28164751\|Aspects in Diagnosis.]] (({{pmid>long:28164751}}))

-	Large intakes of folic acid may delay the diagnosis of vitamin B-12 deficiency, which could lead to irreversible neuropathy. (({{pubmed>long:17921401}}))	+	Large intakes of folic acid may delay the diagnosis of vitamin B-12 deficiency, which could lead to irreversible neuropathy. (({{pmid>long:17921401}}))

-	This review discusses the usefulness and limitations of current biomarkers of B12 status in newborn screening, infant and adult diagnostics, the algorithms utilized to diagnose B12 deficiency and unusual findings of vitamin B12 status in various human disorders. (({{pubmed>long:27446930}}))	+	This review discusses the usefulness and limitations of current biomarkers of B12 status in newborn screening, infant and adult diagnostics, the algorithms utilized to diagnose B12 deficiency and unusual findings of vitamin B12 status in various human disorders. (({{pmid>long:27446930}}))


Line 36:		Line 36:
	==== Laboratory findings ====		==== Laboratory findings ====

-	[[http://www.discoverymedicine.com/Thein-H-Oo/2017/09/challenging-clinical-presentations-of-pernicious-anemia/\|Differing presentations]]	+	[[https://www.discoverymedicine.com/Thein-H-Oo/2017/09/challenging-clinical-presentations-of-pernicious-anemia/\|Differing presentations]]


Line 55:		Line 55:
	A high level of blood serum homocysteine (known as "homocysteinemia") is associated with pernicious anemia. Because supplementation of the B vitamins lower levels of homocysteine, one common intervention for altering this risk factor is to supplement patients at risk for cardiovascular disease with folic acid (B<sub>9</sub>), pyridoxine (B<sub>6</sub>), and cyanocobalamin (B<sub>12</sub>). In fact, interventions designed to lower levels of homocysteine with high-dose supplementation of the B vitamins have been equivocal, in some cases, seeming to exacerbate disease.		A high level of blood serum homocysteine (known as "homocysteinemia") is associated with pernicious anemia. Because supplementation of the B vitamins lower levels of homocysteine, one common intervention for altering this risk factor is to supplement patients at risk for cardiovascular disease with folic acid (B<sub>9</sub>), pyridoxine (B<sub>6</sub>), and cyanocobalamin (B<sub>12</sub>). In fact, interventions designed to lower levels of homocysteine with high-dose supplementation of the B vitamins have been equivocal, in some cases, seeming to exacerbate disease.

-	* A 2010 study by House //et al.// has shown substantial adverse outcomes associated with high-dose B vitamins in patients with advanced diabetic nephropathy.(({{pubmed>long:20424250}})) These side effects included myocardial infarction, stroke, revascularization, and all-cause mortality. According to [[http://www.medscape.com/viewarticle/731177\|one commentator]], unless other explanations come to light in further analyses of the study, these findings make repetition of a similar trial in this high-risk patient group unethical.	+	* A 2010 study by House //et al.// has shown substantial adverse outcomes associated with high-dose B vitamins in patients with advanced diabetic nephropathy.(({{pmid>long:20424250}})) These side effects included myocardial infarction, stroke, revascularization, and all-cause mortality. According to [[https://www.medscape.com/viewarticle/731177\|one commentator]], unless other explanations come to light in further analyses of the study, these findings make repetition of a similar trial in this high-risk patient group unethical.
-	* The Heart Outcomes Prevention Evaluation (HOPE-2) study, involved 5,522 patients with vascular disease or diabetes mellitus and found no effect of high-dose B6, B9 and B12 cosupplementation on death from cardiovascular disease, whereas the risk of stroke was decreased and the risk of unstable angina requiring hospitalization was increased.(({{pubmed>long:16531613}}))	+	* The Heart Outcomes Prevention Evaluation (HOPE-2) study, involved 5,522 patients with vascular disease or diabetes mellitus and found no effect of high-dose B6, B9 and B12 cosupplementation on death from cardiovascular disease, whereas the risk of stroke was decreased and the risk of unstable angina requiring hospitalization was increased.(({{pmid>long:16531613}}))

-	Marino //et al.// showed that eradication of //Helicobacter pylori// associated with gastritis reduced abnormally high levels of homocysteine.(({{pubmed>long:17005765}}))	+	Marino //et al.// showed that eradication of //Helicobacter pylori// associated with gastritis reduced abnormally high levels of homocysteine.(({{pmid>long:17005765}}))


Line 64:		Line 64:


-	Methylcobalamin and cyanocobalamin supplementation differ in their effects on gut bacteria (({{pubmed>long:30505299}}))	+	Methylcobalamin and cyanocobalamin supplementation differ in their effects on gut bacteria (({{pmid>long:30505299}}))


Line 89:		Line 89:
	===== Management =====		===== Management =====

-	Given that the B vitamins probably interfere with immune response to microbes, MP patients should as far as possible avoid taking supplemental doses of vitamin B12, provided appropriate tests for B12 deficiency are made with no finding of profoundly low B12. (({{pubmed>long:17921401}}))	+	Given that the B vitamins probably interfere with immune response to microbes, MP patients should as far as possible avoid taking supplemental doses of vitamin B12, provided appropriate tests for B12 deficiency are made with no finding of profoundly low B12. (({{pmid>long:17921401}}))

	==== Caution ====		==== Caution ====

-	Myeloneuropathy is caused by inactivation of vitamin B12 by nitrous oxide. This syndrome can also be seen in patients with borderline vitamin B12 deficiency who have recently been anesthetized with nitrous oxide. (({{pubmed>long:9613506}}))	+	Myeloneuropathy is caused by inactivation of vitamin B12 by nitrous oxide. This syndrome can also be seen in patients with borderline vitamin B12 deficiency who have recently been anesthetized with nitrous oxide. (({{pmid>long:9613506}}))



-	{{tag>disease arrange}}	+	{{tag>disease }}

		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

Line 118:		Line 119:

	Lots of discussion about PA and B12 deficiency here:		Lots of discussion about PA and B12 deficiency here:
-	http://curemyth1.org/view_topic.php?id=2626&forum_id=2	+	https://curemyth1.org/view_topic.php?id=2626&forum_id=2


-	Lots of content here: http://www.curemyth1.org/forum2/2626.html	+	Lots of content here: https://www.curemyth1.org/forum2/2626.html



-	===== References =====	+	===== References =====</nodisp>

Psoriasis

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

01.01.2019		current
Line 23:		Line 23:
	===== Evidence of infectious cause =====		===== Evidence of infectious cause =====

-	* cell wall deficient bacteria – In a 2009 study, Wang investigated the carriage rate of cell wall deficient bacteria in the tonsil or pharynx of psoriasis patients. Cell wall deficient bacteria, a term often used interchangeably with l-form, were isolated from 74.2% of psoriasis patients, 23.5% of chronic tonsillitis patients and only 6.3% of controls.(({{pubmed>long:20137493}}))	+	* cell wall deficient bacteria – In a 2009 study, Wang investigated the carriage rate of cell wall deficient bacteria in the tonsil or pharynx of psoriasis patients. Cell wall deficient bacteria, a term often used interchangeably with l-form, were isolated from 74.2% of psoriasis patients, 23.5% of chronic tonsillitis patients and only 6.3% of controls.(({{pmid>long:20137493}}))
-	* differences in microbiota between psoriasis and normal skin – A 2008 study of psoriatic skin not only found 84 novel species never before known to persist in skin, but also double the proportion of microbes from the //Firmicutes// phylum in psoriatic patients, as compared to healthy controls.(({{pubmed>long:18648509}})) In contrast, Fahlén's study analyzed 10 psoriatic patients using pyrosequencing,(({{pubmed>long:22065152}})) finding no difference in levels of Firmicutes but confirmed lower levels of //Propionibacterium//. The discrepancies between these two studies illustrate the importance of focusing on the [[home:pathogenesis:microbiota#effect_of_bacteria_on_their_human_host\|activity of microbes]] and as well as the competence of the immune response.	+	* differences in microbiota between psoriasis and normal skin – A 2008 study of psoriatic skin not only found 84 novel species never before known to persist in skin, but also double the proportion of microbes from the //Firmicutes// phylum in psoriatic patients, as compared to healthy controls.(({{pmid>long:18648509}})) In contrast, Fahlén's study analyzed 10 psoriatic patients using pyrosequencing,(({{pmid>long:22065152}})) finding no difference in levels of Firmicutes but confirmed lower levels of //Propionibacterium//. The discrepancies between these two studies illustrate the importance of focusing on the [[home:pathogenesis:microbiota#effect_of_bacteria_on_their_human_host\|activity of microbes]] and as well as the competence of the immune response.
-	* bacterial DNA in blood of psoriatic patients – Peripheral blood samples from 20 patients with psoriasis and from 16 control subjects were studied for the presence of bacteria by PCR using universal 16S ribosomal DNA primers and specific primers for S. pyogenes. Sequence analysis of amplified 16S rRNA sequences was used to determine taxonomic identity. Ribosomal bacterial DNA was detected in the blood of all 20 patients with psoriasis, but in none of the controls.(({{pubmed>long:20607546}}))	+	* bacterial DNA in blood of psoriatic patients – Peripheral blood samples from 20 patients with psoriasis and from 16 control subjects were studied for the presence of bacteria by PCR using universal 16S ribosomal DNA primers and specific primers for S. pyogenes. Sequence analysis of amplified 16S rRNA sequences was used to determine taxonomic identity. Ribosomal bacterial DNA was detected in the blood of all 20 patients with psoriasis, but in none of the controls.(({{pmid>long:20607546}}))


Line 38:		Line 38:

	* corticosteroids – For even short periods of time, steroid use can become genuinely addictive. Research shows that any kind of short-term symptomatic improvement from corticosteroid use does not last, and that over the longer term, use of the drugs entales a litany of side effects. For their own safety, patients on the Marshall Protocol (MP) must [[home:othertreatments:corticosteroids:weaningoffsteroids\|wean off]] of them as opposed to discontinuing them outright.		* corticosteroids – For even short periods of time, steroid use can become genuinely addictive. Research shows that any kind of short-term symptomatic improvement from corticosteroid use does not last, and that over the longer term, use of the drugs entales a litany of side effects. For their own safety, patients on the Marshall Protocol (MP) must [[home:othertreatments:corticosteroids:weaningoffsteroids\|wean off]] of them as opposed to discontinuing them outright.
-	* TNF-alpha inhibitors – Tumor necrosis factor-alpha or TNF-alpha is a cytokine critical for effective immune surveillance.(({{pubmed>long:16331857}})) TNF-alpha inhibitors, also known as TNF blockers, anti-TNF drugs or TNF-alpha antagonists, are drugs which interfere with the body's production of TNF-alpha.(({{pubmed>long: 18387510}})) Anti-TNF drugs are expensive, ineffective at treating chronic disease and have a number of adverse effects such as increase risk of serious infection such as mycobacterial infection.(({{pubmed>long:16705109}})) (({{pubmed>long:12614731}}))	+	* TNF-alpha inhibitors – Tumor necrosis factor-alpha or TNF-alpha is a cytokine critical for effective immune surveillance.(({{pmid>long:16331857}})) TNF-alpha inhibitors, also known as TNF blockers, anti-TNF drugs or TNF-alpha antagonists, are drugs which interfere with the body's production of TNF-alpha.(({{pmid>long: 18387510}})) Anti-TNF drugs are expensive, ineffective at treating chronic disease and have a number of adverse effects such as increase risk of serious infection such as mycobacterial infection.(({{pmid>long:16705109}})) (({{pmid>long:12614731}}))
	* methotrexate – Methotrexate (MTX) is an antibiotic that interferes with bacteria's ability to synthesize folate. It is used to treat diseases with rapid cell growth such as cancer and some autoimmune diseases, particularly the rheumatic diseases. A superior alternative to MTX is the Marshall Protocol antibiotic, Bactrim DS.		* methotrexate – Methotrexate (MTX) is an antibiotic that interferes with bacteria's ability to synthesize folate. It is used to treat diseases with rapid cell growth such as cancer and some autoimmune diseases, particularly the rheumatic diseases. A superior alternative to MTX is the Marshall Protocol antibiotic, Bactrim DS.
-	* [[home:othertreatments:sunshine\|light therapy]] – Phototherapy suppresses immunity which can lead to the progression of other infections such as human papilloma virus (HPV). A 2010 study used a nested polymerase chain reaction, to analyze skin biopsies taken a from 20 psoriasis patients under phototherapy (UVB) and 20 untreated psoriatic patients. The authors were able to detect viruses in 60% of the treatment but in none of the controls.(({{pubmed>long:20415738}})) In reality, light therapy does nothing to resolve underlying disease state and can actually delay progress for MP patients. Certainly prolonged light exposure has been shown to increase skin melanoma – the World Health Organization now categorizes tanning beds under the highest cancer risk category.(({{pubmed>long:19655431}})) MP patients who have completed the treatment have been able to attest to the fact that sunshine is not necessary for good health or happiness.	+	* [[home:othertreatments:sunshine\|light therapy]] – Phototherapy suppresses immunity which can lead to the progression of other infections such as human papilloma virus (HPV). A 2010 study used a nested polymerase chain reaction, to analyze skin biopsies taken a from 20 psoriasis patients under phototherapy (UVB) and 20 untreated psoriatic patients. The authors were able to detect viruses in 60% of the treatment but in none of the controls.(({{pmid>long:20415738}})) In reality, light therapy does nothing to resolve underlying disease state and can actually delay progress for MP patients. Certainly prolonged light exposure has been shown to increase skin melanoma – the World Health Organization now categorizes tanning beds under the highest cancer risk category.(({{pmid>long:19655431}})) MP patients who have completed the treatment have been able to attest to the fact that sunshine is not necessary for good health or happiness.

	===== Research =====		===== Research =====

-	<blockquote>	+	<blockquote>Antimicrobial peptides (AMPs) are strongly expressed in lesional skin in psoriasis and play an important role as proinflammatory "alarmins" in this chronic skin disease. Vitamin D analogs like calcipotriol have antipsoriatic effects and might mediate this effect by changing AMP expression. In this study, keratinocytes in lesional psoriatic plaques showed decreased expression of the AMPs beta-defensin (HBD) 2 and HBD3 after topical treatment with calcipotriol. At the same time, calcipotriol normalized the proinflammatory cytokine milieu and decreased interleukin (IL)-17A, IL-17F and IL-8 transcript abundance in lesional psoriatic skin. In contrast, cathelicidin antimicrobial peptide expression was increased by calcipotriol while psoriasin expression remained unchanged. In cultured human epidermal keratinocytes the effect of different vitamin D analogs on the expression of AMPs was further analyzed. All vitamin D analogs tested blocked IL-17A induced HBD2 expression by increasing IkappaB-alpha protein and inhibition of NF-kappaB signaling. At the same time vitamin D analogs induced cathelicidin through activation of the vitamin D receptor and MEK/ERK signaling. These studies suggest that vitamin D analogs differentially alter AMP expression in lesional psoriatic skin and cultured keratinocytes. Balancing AMP "alarmin" expression might be a novel goal in treatment of chronic inflammatory skin diseases. (({{pmid>long:19623255}}))
-	Not sure where this should go. Here? Psoriasis? Innate immunity? MOVING >Psoriasis	+
-		+
-	PLoS One. 2009 Jul 22;4(7):e6340.	+
-	Vitamin D analogs differentially control antimicrobial peptide/"alarmin" expression in psoriasis.	+
-		+
-	Peric M, Koglin S, Dombrowski Y, Gross K, Bradac E, Büchau A, Steinmeyer A, Zügel U, Ruzicka T, Schauber J.	+
-	Department of Dermatology and Allergology, Ludwig-Maximilians-University, Munich, Germany.	+
-	Abstract	+
-	Antimicrobial peptides (AMPs) are strongly expressed in lesional skin in psoriasis and play an important role as proinflammatory "alarmins" in this chronic skin disease. Vitamin D analogs like calcipotriol have antipsoriatic effects and might mediate this effect by changing AMP expression. In this study, keratinocytes in lesional psoriatic plaques showed decreased expression of the AMPs beta-defensin (HBD) 2 and HBD3 after topical treatment with calcipotriol. At the same time, calcipotriol normalized the proinflammatory cytokine milieu and decreased interleukin (IL)-17A, IL-17F and IL-8 transcript abundance in lesional psoriatic skin. In contrast, cathelicidin antimicrobial peptide expression was increased by calcipotriol while psoriasin expression remained unchanged. In cultured human epidermal keratinocytes the effect of different vitamin D analogs on the expression of AMPs was further analyzed. All vitamin D analogs tested blocked IL-17A induced HBD2 expression by increasing IkappaB-alpha protein and inhibition of NF-kappaB signaling. At the same time vitamin D analogs induced cathelicidin through activation of the vitamin D receptor and MEK/ERK signaling. These studies suggest that vitamin D analogs differentially alter AMP expression in lesional psoriatic skin and cultured keratinocytes. Balancing AMP "alarmin" expression might be a novel goal in treatment of chronic inflammatory skin diseases. (({{pubmed>long:19623255}}))	+
	</blockquote>		</blockquote>

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	sarcoidosis, psoriasis, insomnia, kidney stones		sarcoidosis, psoriasis, insomnia, kidney stones

-	Read the [[http://bacteriality.com/2007/08/10/interview1/\|interview]]	+	Read the [[https://bacteriality.com/2007/08/10/interview1/\|interview]]

	<html></div></div>		<html></div></div>
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	{{tag>disease}}		{{tag>disease}}

		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

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-	===== References =====	+	===== References =====</nodisp>

Raynaud's phenomenon

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

01.27.2019		current
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-	[[http://www.nhlbi.nih.gov/health/dci/Diseases/raynaud/ray_what.html\|NHLBI information on Raynaud's]]	+	[[https://www.nhlbi.nih.gov/health/dci/Diseases/raynaud/ray_what.html\|NHLBI information on Raynaud's]]

-	[[http://www.mayoclinic.com/health/raynauds-disease/DS00433\|Mayo Clinic information]]	+	[[https://www.mayoclinic.com/health/raynauds-disease/DS00433\|Mayo Clinic information]]

	===== Affected areas =====		===== Affected areas =====
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	Raynaud's usually affects the fingers and toes, but the ears, nose, lips or nipples may also be affected. People with this disorder are intolerant of cold. Exposure to cold or even strong emotions causes a brief interruption of the flow of blood to extremities such as the hands or feet due to spasmodic contractions of blood vessels. Affected areas will feel cold, numb, tingly or throb painfully for minutes, sometimes hours until the episode passes. In severe episodes, the pain may extend up the hand into the lower arm.		Raynaud's usually affects the fingers and toes, but the ears, nose, lips or nipples may also be affected. People with this disorder are intolerant of cold. Exposure to cold or even strong emotions causes a brief interruption of the flow of blood to extremities such as the hands or feet due to spasmodic contractions of blood vessels. Affected areas will feel cold, numb, tingly or throb painfully for minutes, sometimes hours until the episode passes. In severe episodes, the pain may extend up the hand into the lower arm.

-	When an attack occurs, if you look closely, you may see the skin [[http://www.humanillnesses.com/original/images/hdc_0001_0003_0_img0216.jpg\|turn white]] when the blood flow is interrupted. Then the skin may [[http://www.sclero.org/medical/symptoms/photos/raynauds/judith-t/1-palms-up-468.jpg\|turn blue]] while blood vessels dilate. When the flow of blood returns, the area may turn pink or red and then eventually return to normal color. Sometimes the affected skin will turn only white and red during an attack.	+	When an attack occurs, if you look closely, you may see the skin [[https://www.humanillnesses.com/original/images/hdc_0001_0003_0_img0216.jpg\|turn white]] when the blood flow is interrupted. Then the skin may [[https://www.sclero.org/medical/symptoms/photos/raynauds/judith-t/1-palms-up-468.jpg\|turn blue]] while blood vessels dilate. When the flow of blood returns, the area may turn pink or red and then eventually return to normal color. Sometimes the affected skin will turn only white and red during an attack.

	When Raynaud's occurs without any underlying disease, it can be caused from repetitive trauma such as working with vibrating tools that damage nerves and blood vessels.		When Raynaud's occurs without any underlying disease, it can be caused from repetitive trauma such as working with vibrating tools that damage nerves and blood vessels.
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	===== Patient reports =====		===== Patient reports =====

-		+	<blockquote>For a few weeks now, I've been noticing that my Raynaud's-type problems have diminished to the point of having (almost) completely vanished! I'm no longer as cold in the extremeties (fingers and toes) as I used to be! I often bike to work. It's been in the 30's Farenheit in the last couple of weeks or so in the mornings when I bike in so I wear the same gloves I have in past years. When the temperature used to be in the 40's before and I had the same gloves on, my fingers would be ice-cold - so would my toes. Now, in the 30's, my fingers and toes are just fine with the same gloves and shoes. I also find I dno't need to wear slippers in the house anymore. I went winter camping a couple of times with a friend over the last few years and my toes would always be ice-cold while he had no problem. Now I know why. //Rico: 5 months on MP, 2006//</blockquote>
-		+
-	<blockquote>For a few weeks now, I've been noticing that my Raynaud's-type problems have diminished to the point of having (almost) completely vanished! I'm no longer as cold in the extremeties (fingers and toes) as I used to be! I often bike to work. It's been in the 30's Farenheit in the last couple of weeks or so in the mornings when I bike in so I wear the same gloves I have in past years. When the temperature used to be in the 40's before and I had the same gloves on, my fingers would be ice-cold - so would my toes. Now, in the 30's, my fingers and toes are just fine with the same gloves and shoes. I also find I dno't need to wear slippers in the house anymore. I went winter camping a couple of times with a friend over the last few years and my toes would always be ice-cold while he had no problem. Now I know why. //5 months on MP Rico 2006//</blockquote>	+

	Rico now writes "although I had made some progress with that a few years back, it's much worse now. Not severely, but worse than it was." //hmmm//		Rico now writes "although I had made some progress with that a few years back, it's much worse now. Not severely, but worse than it was." //hmmm//
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	<blockquote>My Raynaud's is still retreating. I've had my 4th dose of Mino and at the moment I'm typing sans gloves....again. It is a very pleasant sensation. I am having very few herxes now. Quite the turnaround from this time last week. I am having just some minor aches and pains and slight word retrieval issues, but my light sensitivity seems to be decreasing. I just ordered the DVD's and I am hoping to spread them around. I know like this is working.		<blockquote>My Raynaud's is still retreating. I've had my 4th dose of Mino and at the moment I'm typing sans gloves....again. It is a very pleasant sensation. I am having very few herxes now. Quite the turnaround from this time last week. I am having just some minor aches and pains and slight word retrieval issues, but my light sensitivity seems to be decreasing. I just ordered the DVD's and I am hoping to spread them around. I know like this is working.

-	The Raynaud's aspect is particularly interesting to me because some of my friends who are on 200 mg of Mino bid (as I used to be!)say that the raynaud's is the last symptom to go. 2008 Elijuh 2 months on MP</blockquote>	+	The Raynaud's aspect is particularly interesting to me because some of my friends who are on 200 mg of Mino bid (as I used to be!)say that the raynaud's is the last symptom to go. //Elijuh: 2 months on MP, 2008//</blockquote>

-	<blockquote>Finger ulcers, a very common problem for 7 years after using a heavy in-line sander for a month, day in and day out, and triggered regularly by any form of chilling of limbs or body (Raynaud's comes to mind, but my dermatologist wouldn't go there) and that move very rapidly to bleeding cuts in something much less than an hour, went away almost immediately after starting the MP, except for one or two instances that had to be IP, as there was no chilling involved. It has not returned this cold season yet, even tho I have chilled my fingers to an icy severe pain breaking up frozen hamburger. //Cynthia S 1 yr anniversary post//</blockquote>	+	<blockquote>Finger ulcers, a very common problem for 7 years after using a heavy in-line sander for a month, day in and day out, and triggered regularly by any form of chilling of limbs or body (Raynaud's comes to mind, but my dermatologist wouldn't go there) and that move very rapidly to bleeding cuts in something much less than an hour, went away almost immediately after starting the MP, except for one or two instances that had to be IP, as there was no chilling involved. It has not returned this cold season yet, even tho I have chilled my fingers to an icy severe pain breaking up frozen hamburger. //Cynthia S: 1 yr anniversary post//</blockquote>


	Juliette starts MP 2006 with SYMPTOMS: Raynaud's (10 yrs), peripheral neuropathy, migrating joint pain, food sensitivities, menstrual irregularities, swollen lymph nodes, photosensitivity		Juliette starts MP 2006 with SYMPTOMS: Raynaud's (10 yrs), peripheral neuropathy, migrating joint pain, food sensitivities, menstrual irregularities, swollen lymph nodes, photosensitivity
-	<blockquote> It's crazy cold here and my fingers are not blue! Usually at this time of year, the cold feels like it grips my veins and makes them go into spasms- leaving my fingers white, then blue. This has happened for at least 15 years. My body temperature regulation has improved tenfold! Juliette Jan 25th, 2014</blockquote>	+	<blockquote> It's crazy cold here and my fingers are not blue! Usually at this time of year, the cold feels like it grips my veins and makes them go into spasms- leaving my fingers white, then blue. This has happened for at least 15 years. My body temperature regulation has improved tenfold! //Juliette: Jan 25th, 2014//</blockquote>


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	Andreea, it is quite common to have many symptoms resolve in the first 1-3 years on MP,// what we think of as the 'low hanging fruit' that renewing immune activity has gone after//, followed 2 to 5 years later by intense immunopathology as immune activity really gets to work in difficult areas. Hopefully in the early stages, one learns to manage herx, because for most people management becomes quite a challenge. With heart issues, a reminder not to overdo anything just because of early gains.		Andreea, it is quite common to have many symptoms resolve in the first 1-3 years on MP,// what we think of as the 'low hanging fruit' that renewing immune activity has gone after//, followed 2 to 5 years later by intense immunopathology as immune activity really gets to work in difficult areas. Hopefully in the early stages, one learns to manage herx, because for most people management becomes quite a challenge. With heart issues, a reminder not to overdo anything just because of early gains.
		+
		+	<blockquote>My mood issues are better than ever. I'm back on C and no mood issues so far. My teeth are hurting again and my ears are ringing very loudly. I had almost no Raynaud's issues this winter. //Jon Paul Jones: 3 yrs on MP, 2012//</blockquote>

	{{tag>disease }}		{{tag>disease }}
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		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

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	* legacy content		* legacy content
-	* http://www.marshallprotocol.com/forum37/7418.html s373	+	* https://www.marshallprotocol.com/forum37/7418.html s373

		+	===== References =====</nodisp>

-	===== References =====

Reactive arthritis (Reiter's syndrome)

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

02.17.2019		current
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-	[[http://www.mayoclinic.org/diseases-conditions/reactive-arthritis/basics/definition/con-20020872\|Mayo Clinic overview]]	+	[[https://www.mayoclinic.org/diseases-conditions/reactive-arthritis/basics/definition/con-20020872\|Mayo Clinic overview]]

	===== Evidence of infectious cause =====		===== Evidence of infectious cause =====
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	<blockquote>		<blockquote>
-	Reactive arthritis (ReA), an inflammatory arthritic condition that is commonly associated with Chlamydia infections, represents a significant health burden, yet is poorly understood. The enigma of this disease is reflected in its problematic name and in its ill-defined pathogenesis. The existence of persistent pathogens in the arthritic joint is acknowledged, but their relevance remains elusive. Progress is being made in understanding the underlying mechanisms of ReA, whereby an imbalance between type 1 and type 2 immune responses seems to be critical in determining susceptibility to disease. Such an imbalance occurs prior to the initiation of an adaptive immune response, suggesting that innate cellular and molecular mechanisms in ReA should be prioritized as fruitful areas for investigation. (({{pubmed>long:22105240}}))	+	Reactive arthritis (ReA), an inflammatory arthritic condition that is commonly associated with Chlamydia infections, represents a significant health burden, yet is poorly understood. The enigma of this disease is reflected in its problematic name and in its ill-defined pathogenesis. The existence of persistent pathogens in the arthritic joint is acknowledged, but their relevance remains elusive. Progress is being made in understanding the underlying mechanisms of ReA, whereby an imbalance between type 1 and type 2 immune responses seems to be critical in determining susceptibility to disease. Such an imbalance occurs prior to the initiation of an adaptive immune response, suggesting that innate cellular and molecular mechanisms in ReA should be prioritized as fruitful areas for investigation. (({{pmid>long:22105240}}))
	</blockquote>		</blockquote>


-	Combination antibiotics for Chlamydia-induced arthritis: breakthrough to a cure? (({{pubmed>long:20155826}}))	+	Combination antibiotics for Chlamydia-induced arthritis: breakthrough to a cure? (({{pmid>long:20155826}}))

	Editorial		Editorial
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-	"Combination antibiotics as a treatment for chronic Chlamydia-induced reactive arthritis." (({{pubmed>long:20155838}}))	+	"Combination antibiotics as a treatment for chronic Chlamydia-induced reactive arthritis." (({{pmid>long:20155838}}))

	BACKGROUND:: Chlamydia trachomatis (Ct) and Chlamydophila (Chlamydia) pneumoniae (Cpn) are known triggers of reactive arthritis (ReA). These chlamydial species exist in a persistent metabolically active infection state in the synovium suggesting that persistent chlamydiae may be susceptible to antimicrobial agents. The goal of this study was to investigate whether a six-month course of combination antibiotics is an effective therapy for patients with chronic Chlamydia-induced ReA.		BACKGROUND:: Chlamydia trachomatis (Ct) and Chlamydophila (Chlamydia) pneumoniae (Cpn) are known triggers of reactive arthritis (ReA). These chlamydial species exist in a persistent metabolically active infection state in the synovium suggesting that persistent chlamydiae may be susceptible to antimicrobial agents. The goal of this study was to investigate whether a six-month course of combination antibiotics is an effective therapy for patients with chronic Chlamydia-induced ReA.
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	CONCLUSION:: These data suggest that a 6-month course of combination antibiotics is an effective therapy for chronic Chlamydia-induced ReA.		CONCLUSION:: These data suggest that a 6-month course of combination antibiotics is an effective therapy for chronic Chlamydia-induced ReA.

-	===== Diary of a patient 2005-2012, with follow up posts =====	+	===== Diary of a patient 2005-2012 =====

	My diagnosis was Reiter's Syndrome (10 yrs) was on methotrexate and cortizone,until i found Dr Browns protocol,now on arthrexin and sulphasalazine,My diet contains quite a lot of dairy,variety of breads rye and white,pastas and meat.		My diagnosis was Reiter's Syndrome (10 yrs) was on methotrexate and cortizone,until i found Dr Browns protocol,now on arthrexin and sulphasalazine,My diet contains quite a lot of dairy,variety of breads rye and white,pastas and meat.
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		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

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	{{:home:diseases:screen_shot_2010-10-27_at_5.20.03_pm.png\|}}		{{:home:diseases:screen_shot_2010-10-27_at_5.20.03_pm.png\|}}

-	===== References =====	+	===== References =====</nodisp>

Restless leg syndrome

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

04.08.2020		current
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-	[[http://www.mayoclinic.org/diseases-conditions/restless-legs-syndrome/basics/definition/con-20031101\|Mayo Clinic overview]]	+	[[https://www.mayoclinic.org/diseases-conditions/restless-legs-syndrome/basics/definition/con-20031101\|Mayo Clinic overview]]

-	[[http://www.nhlbi.nih.gov/health/health-topics/topics/rls\|NIH Link]]	+	[[https://www.nhlbi.nih.gov/health/health-topics/topics/rls\|NIH Link]]


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-	Some doctors prescribe [[http://en.wikipedia.org/wiki/Pramipexole\|Mirapex (pramipexole)]] for restless leg syndrome.	+	Some doctors prescribe [[https://en.wikipedia.org/wiki/Pramipexole\|Mirapex (pramipexole)]] for restless leg syndrome.


	===== Evidence of infectious cause =====		===== Evidence of infectious cause =====

-	Restless Legs Syndrome and Sleep-Related Movement Disorders. (({{pubmed>long: 28777173}}))	+	Restless Legs Syndrome and Sleep-Related Movement Disorders. (({{pmid>long: 28777173}}))

	as the MP has progressed I'm finding I get restless limbs less often :) It even went away for a couple of months and now comes back sometimes, but less frequently. ~//RichardM//		as the MP has progressed I'm finding I get restless limbs less often :) It even went away for a couple of months and now comes back sometimes, but less frequently. ~//RichardM//
	===== Recent research =====		===== Recent research =====

-	Restless legs syndrome (({{pubmed>long: 26118915}}))	+	Restless legs syndrome (({{pmid>long: 26118915}}))

		+	Restless Legs Syndrome: clinical features, diagnosis and a practical approach to management. (({{pmid>long: 29097554}}))

-	Restless Legs Syndrome: clinical features, diagnosis and a practical approach to management. (({{pubmed>long: 29097554}}))	+	Emerging Concepts of the Pathophysiology and Adverse Outcomes of RLS (({{pmid>long: 32247713}}))

-	[[https://www.ncbi.nlm.nih.gov/pubmed/32247713\|emerging Concepts of the Pathophysiology and Adverse Outcomes of RLS]]emerging Concepts of the Pathophysiology and Adverse Outcomes of RLS.[/url] (({{pubmed>long: 32247713}}))	+	Relationship between lesion location and post-stroke RLS (({{pmid>long:32229419}}))

-	[url=https://www.ncbi.nlm.nih.gov/pubmed/32229419]].relationship between lesion location and post-stroke RLS.[/url] (({{pubmed>long:32229419}}))	+	Fe deficiency and sleep (({{pmid>long: 32224451}}))

-	[url=https://www.ncbi.nlm.nih.gov/pubmed/32215360]..[/url] (({{pubmed>long:32215360}}))	+	RLS following the use of ziprasidone: a case report (({{pmid>long:32215360}}))

-	[url=https://www.ncbi.nlm.nih.gov/pubmed/32224451].Fe deficiency and sleep.[/url] (({{pubmed>long: 32224451}}))	+	The MMF07 foot massage device and heat therapy may be effective (({{pmid>long:32240228}}))

-	[url=https://www.ncbi.nlm.nih.gov/pubmed/32215360].RLS following the use of ziprasidone: a case report.[/url] (({{pubmed>long:32215360}}))	+	Prevalence of symptomatic insomnia & prevalence of RLS higher among patients with rheumatic diseases (({{pmid>long:32197267}}))

-	[url=https://www.ncbi.nlm.nih.gov/pubmed/32240228].the MMF07 foot massage device and heat therapy may be effective.[/url] (({{pubmed>long:32240228}}))	+	Repetitive transcranial magnetic stimulation (rTMS) in patients with sleep disorders (({{pmid>long:3217318}}))

-	[url=https://www.ncbi.nlm.nih.gov/pubmed/32197267].prevalence of symptomatic insomnia & prevalence of RLS higher among patients with rheumatic diseases.[/url] (({{pubmed>long:32197267}}))	+	Looking for other causes (({{pmid>long: 32200395}}))

-	[url=https://www.ncbi.nlm.nih.gov/pubmed/32173186].repetitive transcranial magnetic stimulation (rTMS) in patients with sleep disorders.[/url] (({{pubmed>long:3217318}}))	+
-		+
-	[url=https://www.ncbi.nlm.nih.gov/pubmed/32200395].looking for other causes.[/url] (({{pubmed>long: 32200395}}))	+
-		+
-	(({{pubmed>long:888}}))	+
	===== Patient interviews =====		===== Patient interviews =====

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	sarcoidosis, cat scratch fever, restless leg syndrome		sarcoidosis, cat scratch fever, restless leg syndrome

-	Read the [[http://bacteriality.com/2007/11/19/interview13/\|interview]]	+	Read the [[https://bacteriality.com/2007/11/19/interview13/\|interview]]

	<html></div></div>		<html></div></div>
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		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

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-	===== References =====	+	===== References =====</nodisp>

Arthritis

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

07.10.2019		current
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	=====Management =====		=====Management =====

-	Managing Rheumatoid Arthritis with Dietary Interventions (({{pubmed>long:29167795}}))	+	Managing Rheumatoid Arthritis with Dietary Interventions (({{pmid>long:29167795}}))

	==== Pain medications ====		==== Pain medications ====
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	===== Evidence of infectious cause =====		===== Evidence of infectious cause =====

-	Scher's and Abramson's 2011 review "The microbiome and rheumatoid arthritis" offers a variety of evidence pointing to a key role of microbes in RA.(({{pubmed>long:21862983}}))	+	Scher's and Abramson's 2011 review "The microbiome and rheumatoid arthritis" offers a variety of evidence pointing to a key role of microbes in RA.(({{pmid>long:21862983}}))


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	<relatedarticle> [[home:alternate:autoimmunity\|Autoimmune theory of disease]] </article>		<relatedarticle> [[home:alternate:autoimmunity\|Autoimmune theory of disease]] </article>

-	An increasing number of studies are providing support for the view that “autoantibodies” can be generated in response to the persistent presence of a pathogenic microbiota. While high titers of rheumatoid factor (RF) are associated with severe rheumatoid arthritis, they also appear in a number of other diseases including viral, bacterial, and parasitic infections.(({{pubmed>long:9198668}})) Maturation of RF can be initiated by chronic infections.(({{pubmed>long:8898963}}))	+	An increasing number of studies are providing support for the view that “autoantibodies” can be generated in response to the persistent presence of a pathogenic microbiota. While high titers of rheumatoid factor (RF) are associated with severe rheumatoid arthritis, they also appear in a number of other diseases including viral, bacterial, and parasitic infections.(({{pmid>long:9198668}})) Maturation of RF can be initiated by chronic infections.(({{pmid>long:8898963}}))


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	==== Development during IRIS ====		==== Development during IRIS ====

-	During IRIS, HIV/AIDS patients experience the worsening or onset of systemic inflammatory clinical signs and symptoms following treatment with highly active antiretroviral therapy (HAART). This syndrome results when HAART allows for partial recovery of the immune response. This causes renewed and exuberant host immunological responses towards opportunistic infectious agents, agents that the host accumulated during prior periods of immunosuppression.(({{pubmed>long:20507930}}))	+	During immune reconstitution inflammatory syndrome, HIV/AIDS patients experience the worsening or onset of systemic inflammatory clinical signs and symptoms following treatment with highly active antiretroviral therapy (HAART). This syndrome results when HAART allows for partial recovery of the immune response. This causes renewed and exuberant host immunological responses towards opportunistic infectious agents, agents that the host accumulated during prior periods of immunosuppression.(({{pmid>long:20507930}}))

-	A number of well-known readily cultured pathogens have been conclusively linked to IRIS: the herpes viruses, cytomegalovirus, hepatitis B and C, //M. tuberculosis//, //Mycobacterium avium// complex and //Cryptococcus neoformans//.(({{pubmed>long:17488505}})) However, many more microbes likely contribute to the reaction since AIDS clinicians do not yet have access to the metagenomic tools. Certainly, the existence of IRIS in culture-negative HAART patients suggests that more microbes may be present than the few that have already been isolated.(({{pubmed>long:19365271}}))	+	A number of well-known readily cultured pathogens have been conclusively linked to IRIS: the herpes viruses, cytomegalovirus, hepatitis B and C, //M. tuberculosis//, //Mycobacterium avium// complex and //Cryptococcus neoformans//.(({{pmid>long:17488505}})) However, many more microbes likely contribute to the reaction since AIDS clinicians do not yet have access to the metagenomic tools. Certainly, the existence of IRIS in culture-negative HAART patients suggests that more microbes may be present than the few that have already been isolated.(({{pmid>long:19365271}}))

-	Interestingly, patients experiencing IRIS often "develop" autoimmune conditions as a manifestation of immune restoration including rheumatoid arthritis,(({{pubmed>long:12194745}})) This suggests that patients with RA accumulated microbes that are directly involved in the pathogenesis of this disease state.	+	Interestingly, patients experiencing IRIS often "develop" autoimmune conditions as a manifestation of immune restoration including rheumatoid arthritis,(({{pmid>long:12194745}})) This suggests that patients with RA accumulated microbes that are directly involved in the pathogenesis of this disease state.

	==== Other evidence ====		==== Other evidence ====

-	* Gut-joint axis – One excellent example gut–joint axis hypothesis is represented by classic Whipple disease, in which the presence of a single bacterium in the small intestine, //Tropheryma whipplei//, is sufficient for the development of joint inflammation in predisposed individuals.(({{pubmed>long:21461659}})) A 2008 comparison of the composition of intestinal microbiota of 101 patients with early rheumatoid arthritis with those diagnosed with fibromyalgia. In comparison to patients with fibromyalgia patients, RA patients had significantly less //Bifidobacteria// and bacteria of the //Bacteroides-Porphyromonas-Prevotella// group, //Bacteroides fragilis// subgroup, and //Eubacterium rectale//--//Clostridium coccoides// group.(({{pubmed>long:18528968}}))	+	* Gut-joint axis – One excellent example gut–joint axis hypothesis is represented by classic Whipple disease, in which the presence of a single bacterium in the small intestine, //Tropheryma whipplei//, is sufficient for the development of joint inflammation in predisposed individuals.(({{pmid>long:21461659}})) A 2008 comparison of the composition of intestinal microbiota of 101 patients with early rheumatoid arthritis with those diagnosed with fibromyalgia. In comparison to patients with fibromyalgia patients, RA patients had significantly less //Bifidobacteria// and bacteria of the //Bacteroides-Porphyromonas-Prevotella// group, //Bacteroides fragilis// subgroup, and //Eubacterium rectale//--//Clostridium coccoides// group.(({{pmid>long:18528968}}))
-	* Presence of microbes in the synovium – Several reports have associated RA with bacterial overgrowth and deposition of resultant immune complexes in the synovial fluid.(({{pubmed>long:2670259}}))	+	* Presence of microbes in the synovium – Several reports have associated RA with bacterial overgrowth and deposition of resultant immune complexes in the synovial fluid.(({{pmid>long:2670259}}))
-	* Periodontal disease comorbidity – Patients with RA often exhibit periodontal disease, which is associated with pathogens like //Porphyromonas gingivalis//. A 2010 study showed that //P. gingivalis// promotes early and later stages of apoptosis of primary human chondrocytes, which might contribute to the joint damage seen in the pathogenesis of RA.(({{pubmed>long:20582408}}))	+	* Periodontal disease comorbidity – Patients with RA often exhibit periodontal disease, which is associated with pathogens like //Porphyromonas gingivalis//. A 2010 study showed that //P. gingivalis// promotes early and later stages of apoptosis of primary human chondrocytes, which might contribute to the joint damage seen in the pathogenesis of RA.(({{pmid>long:20582408}}))


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	<mainarticle> [[home:pathogenesis:vitamind:metabolism\|Metabolism of vitamin D and the Vitamin D Receptor]] </article>		<mainarticle> [[home:pathogenesis:vitamind:metabolism\|Metabolism of vitamin D and the Vitamin D Receptor]] </article>

-	Consistent with the Marshall Pathogenesis, patients with RA tend to have higher than normal levels of 1,25-D. Mawer //et al.// found that 1,25-D levels were particularly elevated in the synovial fluid surrounding the joints of patients with rheumatoid arthritis (RA).(({{pubmed>long:1950677}})) In this study, median serum levels of 1,25-D at baseline was not elevated in the RA patients — only 24 pg/ml. Thus, the extrarenal synthesis of 1,25-D was not obvious from the routine blood test for 1,25-D. There is no reason to think that the metabolism of other diseases is any different. Mice without functional Vitamin D Receptor signaling develop arthritic symptoms.(({{pubmed>long:22064970}}))	+	Consistent with the Marshall Pathogenesis, patients with RA tend to have higher than normal levels of 1,25-D. Mawer //et al.// found that 1,25-D levels were particularly elevated in the synovial fluid surrounding the joints of patients with rheumatoid arthritis (RA).(({{pmid>long:1950677}})) In this study, median serum levels of 1,25-D at baseline was not elevated in the RA patients — only 24 pg/ml. Thus, the extrarenal synthesis of 1,25-D was not obvious from the routine blood test for 1,25-D. There is no reason to think that the metabolism of other diseases is any different. Mice without functional Vitamin D Receptor signaling develop arthritic symptoms.(({{pmid>long:22064970}}))


-	1,25-dihydroxyvitamin D3 (1,25(OH)2D3), has potent anti-inflammatory effects on T-cells. However the efficacy of vitamin-D in an inflammatory setting is unclear. [[http://ard.bmj.com/content/75/Suppl_1/A29.1?utm_source=TrendMD&utm_medium=cpc&utm_campaign=ARD_TrendMD-1\|D 1,25]]	+	1,25-dihydroxyvitamin D3 (1,25(OH)2D3), has potent anti-inflammatory effects on T-cells. However the efficacy of vitamin-D in an inflammatory setting is unclear. [[https://ard.bmj.com/content/75/Suppl_1/A29.1?utm_source=TrendMD&utm_medium=cpc&utm_campaign=ARD_TrendMD-1\|D 1,25]]


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	<mainarticle> [[home:alternate:genetic_predisposition\|Genetic predisposition to disease]] </article>		<mainarticle> [[home:alternate:genetic_predisposition\|Genetic predisposition to disease]] </article>

-	Evidence as to how human genes contribute to the development of RA has been weak. Genome-wide associations studies explain only 16% of disease variance.(({{pubmed>long:10643697}})) Moreover, the prevalence of RA concordance in monozygotic twins in European studies is ≤15%,(({{pubmed>long:3820198}})) (({{pubmed>long:8402000}})) and it is unclear whether this level actually exceeds the risk of developing RA that exists in the general population.(({{pubmed>long:11823356}}))	+	Evidence as to how human genes contribute to the development of RA has been weak. Genome-wide associations studies explain only 16% of disease variance.(({{pmid>long:10643697}})) Moreover, the prevalence of RA concordance in monozygotic twins in European studies is ≤15%,(({{pmid>long:3820198}})) (({{pmid>long:8402000}})) and it is unclear whether this level actually exceeds the risk of developing RA that exists in the general population.(({{pmid>long:11823356}}))


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-	//Proal, et al., "Immunostimulation in the era of the metagenome"//(({{pubmed>long:21278764}}))</blockquote>	+	//Proal, et al., "Immunostimulation in the era of the metagenome"//(({{pmid>long:21278764}}))</blockquote>


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-	//Proal, et al., "Immunostimulation in the era of the metagenome"//(({{pubmed>long:21278764}}))</blockquote>	+	//Proal, et al., "Immunostimulation in the era of the metagenome"//(({{pmid>long:21278764}}))</blockquote>

	===== Data =====		===== Data =====
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	sarcoidosis, rheumatoid arthritis		sarcoidosis, rheumatoid arthritis

-	Read the [[http://bacteriality.com/2008/06/03/interview21/\|interview]]	+	Read the [[https://bacteriality.com/2008/06/03/interview21/\|interview]]

	<html></div></div></html>		<html></div></div></html>
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	rheumatoid arthritis, dyslexia		rheumatoid arthritis, dyslexia

-	Read the [[http://bacteriality.com/2007/09/01/interview2/\|interview]]	+	Read the [[https://bacteriality.com/2007/09/01/interview2/\|interview]]

	<html></div></div>		<html></div></div>
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	===== Childhood =====		===== Childhood =====

-	Do infections trigger juvenile idiopathic arthritis? (({{pubmed>long:000}}))	+	Do infections trigger juvenile idiopathic arthritis? (({{pmid>long:000}}))

	===== Gout =====		===== Gout =====
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	I drink about an extra 2.2 L (outside of meals) of water daily and I haven't had a major flare since doing so.		I drink about an extra 2.2 L (outside of meals) of water daily and I haven't had a major flare since doing so.

-	I recently heard that phytic acid is able to inhibit the enzyme xanthine oxidase that causes a build up of uric acid(({{pubmed>long:14738912}})). The supplement IP6 Gold is a good source of phytic acid but I have not tried it though. I am concerned that this supplement might be immunosuppressive as it works like Allopurinol which also blocks xanthine oxidase - we know that Allopurinol to be immunosuppressive.	+	I recently heard that phytic acid is able to inhibit the enzyme xanthine oxidase that causes a build up of uric acid(({{pmid>long:14738912}})). The supplement IP6 Gold is a good source of phytic acid but I have not tried it though. I am concerned that this supplement might be immunosuppressive as it works like Allopurinol which also blocks xanthine oxidase - we know that Allopurinol to be immunosuppressive.
	//David//</blockquote>		//David//</blockquote>

-	Herein, we report a positive relationship between serum UA and acute-phase reactants, such as high-sensitivity C-reactive protein, fibrinogen, ferritin, complement C3, and erythrocyte sedimentation rate, in a cohort of 2731 nondiabetic adults. The relationship remains significant after adjustment for several confounders, including age, sex, adiposity, anti-hypertensive treatments or diuretics use. To confirm the existence of a causal relationship, we examined the effect of UA on the expression of inflammatory biomarkers in human hepatoma HepG2 cells and characterized the signaling pathway by which UA acts. .......The effect of UA was completely blocked by the antioxidant N-acetylcysteine. (({{pubmed>long:28408375}}))	+	Herein, we report a positive relationship between serum UA and acute-phase reactants, such as high-sensitivity C-reactive protein, fibrinogen, ferritin, complement C3, and erythrocyte sedimentation rate, in a cohort of 2731 nondiabetic adults. The relationship remains significant after adjustment for several confounders, including age, sex, adiposity, anti-hypertensive treatments or diuretics use. To confirm the existence of a causal relationship, we examined the effect of UA on the expression of inflammatory biomarkers in human hepatoma HepG2 cells and characterized the signaling pathway by which UA acts. .......The effect of UA was completely blocked by the antioxidant N-acetylcysteine. (({{pmid>long:28408375}}))


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		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

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	If we ever have an article on JIA:		If we ever have an article on JIA:
-	<blockquote>Do infections trigger juvenile idiopathic arthritis?(({{pubmed>long:20012631}}))	+	<blockquote>Do infections trigger juvenile idiopathic arthritis?(({{pmid>long:20012631}}))

	Aslan M, Kasapcopur O, Yasar H, Polat E, Saribas S, Cakan H, Dirican A, Torun MM, Arısoy N, Kocazeybek B.		Aslan M, Kasapcopur O, Yasar H, Polat E, Saribas S, Cakan H, Dirican A, Torun MM, Arısoy N, Kocazeybek B.
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	Rheumatology International, published online before print December 13, 2009.		Rheumatology International, published online before print December 13, 2009.

-	http://dx.doi.org/10.1007/s00296-009-1253-4	+	https://dx.doi.org/10.1007/s00296-009-1253-4

	Abstract		Abstract
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	jejuni come forward and seen common in JIA cases. We also suggest that the pre-diagnosis of microorganisms, which can play a role as primarily or by intervening in the etiopathogenesis of JIA and adding specific antimicrobial therapy to the standard JIA therapy, it is possible to perform new, extended, especially molecular based serial case studies.		jejuni come forward and seen common in JIA cases. We also suggest that the pre-diagnosis of microorganisms, which can play a role as primarily or by intervening in the etiopathogenesis of JIA and adding specific antimicrobial therapy to the standard JIA therapy, it is possible to perform new, extended, especially molecular based serial case studies.

-	http://dx.doi.org/10.1007/s00296-009-1253-4	+	https://dx.doi.org/10.1007/s00296-009-1253-4
	</blockquote>		</blockquote>

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-	===== References =====	+	===== References =====</nodisp>

Rickets (osteomalacia)

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

Sarcoidosis

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:47 +0000

08.12.2019		current
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	====== Anemia ======		====== Anemia ======

-	<relatedarticles> [[home:diseases:cfs\|Chronic fatigue syndrome]], [[home:diseases:pernicious_anemia\|Pernicious anemia]]</article>	+	<relatedarticles> [[home:diseases:cfs\|Chronic fatigue syndrome]], [[home:othertreatments:othertreatments\|Thyroid hormone and mineral supplementation]], [[home:diseases:pernicious_anemia\|Pernicious anemia]]</article>

-	Anemia of chronic disease, also referred to as anemia of inflammatory response, is a common condition seen in chronic illness.(({{pubmed>long:7719246}})) Anemia is not due to iron deficiency, nor will it be helped by iron supplements. In fact, iron supplements are counterproductive because iron is "crucial" to the survival and multiplication of pathogens.(({{pubmed>long:21414421}}))	+	Anemia of chronic disease, also referred to as anemia of inflammatory response, is a common condition seen in chronic illness.(({{pmid>long:7719246}})) Anemia is not due to iron deficiency, nor will it be helped by iron supplements. In fact, iron supplements are counterproductive because iron is "crucial" to the survival and multiplication of pathogens.(({{pmid>long:21414421}}))

	Standard measures of iron status, such as ferritin, total iron-binding capacity, and serum iron are directly affected by chronic disease. In contrast, soluble transferrin receptor (sTfR) is elevated in iron deficiency but is not appreciably affected by chronic disease.		Standard measures of iron status, such as ferritin, total iron-binding capacity, and serum iron are directly affected by chronic disease. In contrast, soluble transferrin receptor (sTfR) is elevated in iron deficiency but is not appreciably affected by chronic disease.
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	<blockquote>Excessive and misplaced iron promotes an array of neurodegenerative and endocrine diseases as well as cardiomyopathy, arthropathy, neoplasia and infection. Vertebrates maintain an iron withholding defense system designed to prevent accumulation of redox-active (free) iron in sensitive sites and to sequester the metal in innocuous packages.		<blockquote>Excessive and misplaced iron promotes an array of neurodegenerative and endocrine diseases as well as cardiomyopathy, arthropathy, neoplasia and infection. Vertebrates maintain an iron withholding defense system designed to prevent accumulation of redox-active (free) iron in sensitive sites and to sequester the metal in innocuous packages.

-	//Eugene D. Weinberg, "Iron Withholding: A Defense Against Disease"//(({{pubmed>long:18487852}}))</blockquote>	+	//Eugene D. Weinberg, "Iron Withholding: A Defense Against Disease"//(({{pmid>long:18487852}}))</blockquote>


-	The low levels of blood cells characteristic of anemia of chronic disease (ACD) are relatively common among autoimmune conditions(({{pubmed>long:18695181}})) and obesity.(({{pubmed>long:17766530}})) A related hallmark of ACD is increased uptake and retention of iron within cells.(({{pubmed>long:15758012}})) For many physicians, ACD should be treated as a cause of illness, but the condition serves to protect the host against further infection including those that may drive autoimmune processes. In their //New England Journal of Medicine// review, Weiss and Goodnough write that despite treatment guidelines, “anemia of chronic disease remains underrecognized and undertreated.” Anemia should be actively managed, they put forth, because the condition “has been associated with a relatively poor prognosis” and is associated with suboptimal oxygen delivery.(({{pubmed>long:15758012}}))	+	The low levels of blood cells characteristic of anemia of chronic disease (ACD) are relatively common among autoimmune conditions(({{pmid>long:18695181}})) and obesity.(({{pmid>long:17766530}})) A related hallmark of ACD is increased uptake and retention of iron within cells.(({{pmid>long:15758012}})) For many physicians, ACD should be treated as a cause of illness, but the condition serves to protect the host against further infection including those that may drive autoimmune processes. In their //New England Journal of Medicine// review, Weiss and Goodnough write that despite treatment guidelines, “anemia of chronic disease remains underrecognized and undertreated.” Anemia should be actively managed, they put forth, because the condition “has been associated with a relatively poor prognosis” and is associated with suboptimal oxygen delivery.(({{pmid>long:15758012}}))

-	However, Zarychanski and Houston state ACD is fundamentally an adaptive physiologic response which benefits the patient during times of infection(({{pubmed>long:18695181}})) with Baker and Ghio offering a similar argument.(({{pubmed>long:19628641}})) As a nutrient that is essential for the function of many microbes, increased iron availability promotes microbial growth.(({{pubmed>long:1560730}})) For example, //Mycobacteria// synthesize molecules that have several times higher affinity for iron than their host counterparts, they also synthesize molecules for efficient storage of excess iron.(({{pubmed>long: 21414421}})) Further, moderation of iron inside a host is a threat to mycobacterial persistence.	+	However, Zarychanski and Houston state ACD is fundamentally an adaptive physiologic response which benefits the patient during times of infection(({{pmid>long:18695181}})) with Baker and Ghio offering a similar argument.(({{pmid>long:19628641}})) As a nutrient that is essential for the function of many microbes, increased iron availability promotes microbial growth.(({{pmid>long:1560730}})) For example, //Mycobacteria// synthesize molecules that have several times higher affinity for iron than their host counterparts, they also synthesize molecules for efficient storage of excess iron.(({{pmid>long: 21414421}})) Further, moderation of iron inside a host is a threat to mycobacterial persistence.

-	Further, the ability of a particular species of bacteria to glean iron from its host is often a good indicator of its virulence. It is logical then that the body sequesters iron in response to an infection: Kemna et al. showed that injecting human volunteers with lipopolysaccharides, a component of the cell walls of gram-negative bacteria, leads to a significant decrease in serum iron.(({{pubmed>long:15886319}})) In iron-deficient conditions, blood plasma is moderately effective at inhibiting bacterial growth.(({{pubmed>long:1560730}})) (({{pubmed>long:15372409}})) (({{pubmed>long:1748112}}))	+	Further, the ability of a particular species of bacteria to glean iron from its host is often a good indicator of its virulence. It is logical then that the body sequesters iron in response to an infection: Kemna et al. showed that injecting human volunteers with lipopolysaccharides, a component of the cell walls of gram-negative bacteria, leads to a significant decrease in serum iron.(({{pmid>long:15886319}})) In iron-deficient conditions, blood plasma is moderately effective at inhibiting bacterial growth.(({{pmid>long:1560730}})) (({{pmid>long:15372409}})) (({{pmid>long:1748112}}))

	It might otherwise seem reasonable for a clinician to directly manage ACD using iron supplements or other antianemic therapies: fatigue and shortness of breath can be very unpleasant. However, administering this type of short-time palliation may lead to poorer outcomes. The possibility that ACD is an adaptive response by the host to microbes raises the specter that artificially resolving anemia subverts the immune response allowing microbes to spread by subverting the immune response and consequently allowing microbial infections to proliferate, thus, making the question of what ultimately causes autoimmune diseases all the more urgent.		It might otherwise seem reasonable for a clinician to directly manage ACD using iron supplements or other antianemic therapies: fatigue and shortness of breath can be very unpleasant. However, administering this type of short-time palliation may lead to poorer outcomes. The possibility that ACD is an adaptive response by the host to microbes raises the specter that artificially resolving anemia subverts the immune response allowing microbes to spread by subverting the immune response and consequently allowing microbial infections to proliferate, thus, making the question of what ultimately causes autoimmune diseases all the more urgent.
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	===== Tests =====		===== Tests =====

-	* serum ferritin – The protein in the blood that stores iron for later use by the body. Serum ferritin is also an acute phase reactant and will rise rapidly in the face of inflammation. May be high in anemia of chronic disease, especially if the liver is involved. Macrophages, a type of phagocyte, are the cells responsible for accreting ferritin. Described further [[http://www.labtestsonline.org/understanding/analytes/ferritin/test.html\|here]].	+	* serum ferritin – The protein in the blood that stores iron for later use by the body. Serum ferritin is also an acute phase reactant and will rise rapidly in the face of inflammation. May be high in anemia of chronic disease, especially if the liver is involved. Macrophages, a type of phagocyte, are the cells responsible for accreting ferritin. Described further [[https://www.labtestsonline.org/understanding/analytes/ferritin/test.html\|here]].
-	* serum iron – The amount of iron being carried by transferrin in the blood plasma. On its own, serum iron provides no useful information. Serum iron has a diurnal variation that can be as much as 30% within a single individual. It is sensitive to the day's dietary iron intake and is affected by all the confounding diseases listed above. A low serum iron picked up as an incidental finding has a very low specificity for iron deficiency. Described further [[http://www.labtestsonline.org/understanding/analytes/serum_iron/test.html\|here]].	+	* serum iron – The amount of iron being carried by transferrin in the blood plasma. On its own, serum iron provides no useful information. Serum iron has a diurnal variation that can be as much as 30% within a single individual. It is sensitive to the day's dietary iron intake and is affected by all the confounding diseases listed above. A low serum iron picked up as an incidental finding has a very low specificity for iron deficiency. Described further [[https://www.labtestsonline.org/understanding/analytes/serum_iron/test.html\|here]].
-	* total iron binding capacity (TIBC) – Shows if there is the "right amount" of iron in the blood. TIBC helps measure the ability of transferrin to carry iron in the blood. TIBC is typically measured along with serum iron to evaluate people suspected of having either iron deficiency or iron overload. The iron concentration divided by TIBC gives the transferrin saturation, which is a more useful indicator of iron status than iron or TIBC alone. The TIBC test measures the amount of iron that the blood would carry if the transferrin were fully saturated. Since transferrin is produced by the liver, the TIBC can be used to monitor liver function and nutrition. Described further [[http://www.labtestsonline.org/understanding/analytes/tibc/test.html\|here]].	+	* total iron binding capacity (TIBC) – Shows if there is the "right amount" of iron in the blood. TIBC helps measure the ability of transferrin to carry iron in the blood. TIBC is typically measured along with serum iron to evaluate people suspected of having either iron deficiency or iron overload. The iron concentration divided by TIBC gives the transferrin saturation, which is a more useful indicator of iron status than iron or TIBC alone. The TIBC test measures the amount of iron that the blood would carry if the transferrin were fully saturated. Since transferrin is produced by the liver, the TIBC can be used to monitor liver function and nutrition. Described further [[https://www.labtestsonline.org/understanding/analytes/tibc/test.html\|here]].
	* soluble transferrin receptor (sTfR) – Relatively new test. While standard measures of iron status such as ferritin, total iron-binding capacity, and serum iron are directly affected by chronic disease sTfR is elevated in iron deficiency but is not appreciably affected by chronic disease. A good way to verify anemia of chronic desease because it is not affected by inflammation. Should be considered for anemic patients whose differential diagnosis includes iron deficiency and anemia of inflammatory disease.		* soluble transferrin receptor (sTfR) – Relatively new test. While standard measures of iron status such as ferritin, total iron-binding capacity, and serum iron are directly affected by chronic disease sTfR is elevated in iron deficiency but is not appreciably affected by chronic disease. A good way to verify anemia of chronic desease because it is not affected by inflammation. Should be considered for anemic patients whose differential diagnosis includes iron deficiency and anemia of inflammatory disease.
	* hemoglobin (HGB) – The iron-containing oxygen-transport metalloprotein in the red blood cells of all vertebrates. The effect of locking up iron stores is to reduce the ability of the bone marrow to produce red blood cells. These cells require iron for their massive amounts of hemoglobin which allow them to transport oxygen.		* hemoglobin (HGB) – The iron-containing oxygen-transport metalloprotein in the red blood cells of all vertebrates. The effect of locking up iron stores is to reduce the ability of the bone marrow to produce red blood cells. These cells require iron for their massive amounts of hemoglobin which allow them to transport oxygen.
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	Doctors using these drugs are advised "to maintain the lowest hemoglobin level consistent with avoiding the need for transfusions." It isn't necessary to maintain a normal HGB and HCT while patients are recovering on the MP.		Doctors using these drugs are advised "to maintain the lowest hemoglobin level consistent with avoiding the need for transfusions." It isn't necessary to maintain a normal HGB and HCT while patients are recovering on the MP.

-	A randomized controlled trial of critically ill patients showed erythropoiesis-stimulating agents did not reduce overall mortality.(({{pubmed>long:17804841}}))	+	A randomized controlled trial of critically ill patients showed erythropoiesis-stimulating agents did not reduce overall mortality.(({{pmid>long:17804841}}))


	===== Epidemiological studies =====		===== Epidemiological studies =====

-	In a 10 year follow up study from Chile, infants who already had high levels of hemoglobin proteins in their blood and were fed iron-fortified formula [[http://www.reuters.com/article/2011/11/12/us-iron-babies-idUSTRE7AB02820111112\|ended up with lower scores on tests of thinking and memory]] than those given low-iron formula.(({{pubmed>long:22064877}}))	+	In a 10 year follow up study from Chile, infants who already had high levels of hemoglobin proteins in their blood and were fed iron-fortified formula [[https://www.reuters.com/article/2011/11/12/us-iron-babies-idUSTRE7AB02820111112\|ended up with lower scores on tests of thinking and memory]] than those given low-iron formula.(({{pmid>long:22064877}}))


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	{{tag>diseases}}		{{tag>diseases}}

		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

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	* Legacy content		* Legacy content
-	* [[http://www.marshallprotocol.com/forum32/3479.html]]	+	* [[https://www.marshallprotocol.com/forum32/3479.html]]
-	* [[http://www.marshallprotocol.com/view_topic.php?id=10090&forum_id=39&jump_to=135337]]	+	* [[https://www.marshallprotocol.com/view_topic.php?id=10090&forum_id=39&jump_to=135337]]

	Given iron’s role as a key microbial nutrient, it may be that patients receiving blood plasma have significantly increased mortality as was reported in a randomized controlled trial(9971864) and why an		Given iron’s role as a key microbial nutrient, it may be that patients receiving blood plasma have significantly increased mortality as was reported in a randomized controlled trial(9971864) and why an
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-	According to the textbook "An Introduction to Human Disease: Pathology and Pathophysiology Correlations" by Leonard V. Crowley,[[http://books.google.com/books?id=vnT6enWTnZoC&pg=PA357&lpg=PA357&dq=bone+marrow+suppression&source=web&ots=TRxz3MI3Aw&sig=DKx-gUq6L5NAQpS4D6tC0C7CMjk&hl=en#v=onepage&q=bone%20marrow%20suppression&f=false\|Bone Marrow Suppression, Damage, or Infiltration]] "Many conditions may depress bone marrow functions. Chronic diseases of all types may impair hematopoiesis and lead to mild or moderate anemia, which is called the anemia of chronic disease. ... The most common cause of this type of anemia is chronic infection, but other chronic diseases and some malignant tumors may also be responsible."	+	According to the textbook "An Introduction to Human Disease: Pathology and Pathophysiology Correlations" by Leonard V. Crowley,[[https://books.google.com/books?id=vnT6enWTnZoC&pg=PA357&lpg=PA357&dq=bone+marrow+suppression&source=web&ots=TRxz3MI3Aw&sig=DKx-gUq6L5NAQpS4D6tC0C7CMjk&hl=en#v=onepage&q=bone%20marrow%20suppression&f=false\|Bone Marrow Suppression, Damage, or Infiltration]] "Many conditions may depress bone marrow functions. Chronic diseases of all types may impair hematopoiesis and lead to mild or moderate anemia, which is called the anemia of chronic disease. ... The most common cause of this type of anemia is chronic infection, but other chronic diseases and some malignant tumors may also be responsible."


	GI bleeding		GI bleeding

-	A simple outpatient two minute check of your stool for blood would rule out your doctor's concerns pertaining to bleeding into the gut.[[http://www.nlm.nih.gov/medlineplus/ency/article/007008.htm\|NIH: Fecal occult blood test]]	+	A simple outpatient two minute check of your stool for blood would rule out your doctor's concerns pertaining to bleeding into the gut.[[https://www.nlm.nih.gov/medlineplus/ency/article/007008.htm\|NIH: Fecal occult blood test]]


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	Lowering olmesartan might improve the RBC levels but at the cost increasing the anoxia and and impeding the healing in the kidneys.		Lowering olmesartan might improve the RBC levels but at the cost increasing the anoxia and and impeding the healing in the kidneys.

-	for reference links, see full [[http://marshallprotocol.com/view_topic.php?id=7525&forum_id=35&jump_to=227096#p227096\|post by Jigsaw]]</blockquote>	+	for reference links, see full [[https://marshallprotocol.com/view_topic.php?id=7525&forum_id=35&jump_to=227096#p227096\|post by Jigsaw]]</blockquote>
-	===== References =====	+	===== References =====</nodisp>

04.26.2020		current
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	====== HIV and AIDS ======		====== HIV and AIDS ======

-	[[https:home:pathogenesis:microbiota:interaction#viruses\|Effects of bacteria and viruses on their human host]] </article>	+	<relatedarticle> [[https:home:pathogenesis:microbiota:interaction#viruses\|Effects of bacteria and viruses on their human host]] </article>


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	<mainarticle> [[home:pathogenesis:vitamind:metabolism\|Metabolism of vitamin D and the Vitamin D Receptor]] </article>		<mainarticle> [[home:pathogenesis:vitamind:metabolism\|Metabolism of vitamin D and the Vitamin D Receptor]] </article>

-	HIV uses the VDR to recognize its own LTR promoter region in order to transcribe its own genome, thus taking over the VDR.(({{pubmed>long:17556530}}))	+	HIV uses the VDR to recognize its own LTR promoter region in order to transcribe its own genome, thus taking over the VDR.(({{pmid>long:17556530}}))

	{{section>:home:pathogenesis:vitamind:metabolism#hivaids&noheader&firstseconly}}		{{section>:home:pathogenesis:vitamind:metabolism#hivaids&noheader&firstseconly}}
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	There is no evidence that supplemental vitamin D helps HIV or AIDS patients.		There is no evidence that supplemental vitamin D helps HIV or AIDS patients.

-	<blockquote>Vitamin D supplementation is associated with reduced immune activation levels in HIV-1-infected patients on suppressive antiretroviral therapy. (({{pubmed>long:25493593}}))	+	<blockquote>Vitamin D supplementation is associated with reduced immune activation levels in HIV-1-infected patients on suppressive antiretroviral therapy. (({{pmid>long:25493593}}))

	Of note, we observed that patients with low vitamin D levels displayed a reduced CD4/CD8 ratio (P ¼ 0.03, Table 1), which is usually a sign of increased immune activation in HIV-infected patients receiving effective ART [16]. We also analyzed CD38 expression on the surface of memory CD8+ T cells as a robust marker of immune activation. Although there was substantial interindividual variability, patients with severe vitamin D deficiency displayed modest but statistically significant higher levels of CD38 expression, compared with individuals with normal vitamin D (P ¼ 0.04, Table 1).		Of note, we observed that patients with low vitamin D levels displayed a reduced CD4/CD8 ratio (P ¼ 0.03, Table 1), which is usually a sign of increased immune activation in HIV-infected patients receiving effective ART [16]. We also analyzed CD38 expression on the surface of memory CD8+ T cells as a robust marker of immune activation. Although there was substantial interindividual variability, patients with severe vitamin D deficiency displayed modest but statistically significant higher levels of CD38 expression, compared with individuals with normal vitamin D (P ¼ 0.04, Table 1).
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	Pathogens are able spread effectively in an immunocompromised environment. This means it's possible that AIDS patients pick up substantial pathogen loads. It is further possible that it is these Th1 pathogens, which kill patients. Viral co-infections (including Epstein-Barr virus, Human Herpes Virus 6, etc.) are found in all the diseases the Marshall Protocol treats, but the viruses are not believed to bethe proximate cause of disease.		Pathogens are able spread effectively in an immunocompromised environment. This means it's possible that AIDS patients pick up substantial pathogen loads. It is further possible that it is these Th1 pathogens, which kill patients. Viral co-infections (including Epstein-Barr virus, Human Herpes Virus 6, etc.) are found in all the diseases the Marshall Protocol treats, but the viruses are not believed to bethe proximate cause of disease.

-	Mycobacterium avium-intracellulare infection and immunoblastic sarcoma in a fatal case of AIDS. (({{pubmed>long: 3732865}}))	+	Mycobacterium avium-intracellulare infection and immunoblastic sarcoma in a fatal case of AIDS. (({{pmid>long: 3732865}}))

-	[[http://www.joimr.org/JOIMR-2007-5-1-Cantwell.pdf\|Do TB-type bacteria cause AIDS?]]	+	[[https://www.joimr.org/JOIMR-2007-5-1-Cantwell.pdf\|Do TB-type bacteria cause AIDS?]]

	===== CD38 =====		===== CD38 =====


-	CD38 plays a role in effective containment of mycobacteria within granulomata and polarization of Th1 immune responses against Mycobacterium avium. (({{pubmed>long:17533152}}))	+	CD38 plays a role in effective containment of mycobacteria within granulomata and polarization of Th1 immune responses against Mycobacterium avium. (({{pmid>long:17533152}}))

	...		...
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		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

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	his HIV-positive patients, even if they are not deficient.		his HIV-positive patients, even if they are not deficient.

-	http://www.medpagetoday.com/tbprint.cfm?tbid=22132	+	https://www.medpagetoday.com/tbprint.cfm?tbid=22132

	Indeed, a third study here confirmed the risk of bone loss among those with HIV.		Indeed, a third study here confirmed the risk of bone loss among those with HIV.
Line 300:		Line 301:

	* Legacy content		* Legacy content
-	* http://www.marshallprotocol.com/forum37/9768.html#p39531 s329	+	* https://www.marshallprotocol.com/forum37/9768.html#p39531 s329
-	* http://www.marshallprotocol.com/view_topic.php?id=4404&forum_id=28&jump_to=40327#p40327 s330	+	* https://www.marshallprotocol.com/view_topic.php?id=4404&forum_id=28&jump_to=40327#p40327 s330
-	* http://www.marshallprotocol.com/view_topic.php?id=4404&forum_id=28&jump_to=40685#p40685 s331	+	* https://www.marshallprotocol.com/view_topic.php?id=4404&forum_id=28&jump_to=40685#p40685 s331
-	* http://www.marshallprotocol.com/view_topic.php?id=4404&forum_id=28&jump_to=40688#p40688 s332	+	* https://www.marshallprotocol.com/view_topic.php?id=4404&forum_id=28&jump_to=40688#p40688 s332
-	* http://www.marshallprotocol.com/forum37/9768.html#p72952 s333	+	* https://www.marshallprotocol.com/forum37/9768.html#p72952 s333
-	* http://www.marshallprotocol.com/forum37/9768.html#p112657 s334	+	* https://www.marshallprotocol.com/forum37/9768.html#p112657 s334

-	http://content.karger.com/ProdukteDB/produkte.asp?Aktion=ShowAbstract&ArtikelNr=92475&Ausgabe=231692&ProduktNr=223834	+	https://content.karger.com/ProdukteDB/produkte.asp?Aktion=ShowAbstract&ArtikelNr=92475&Ausgabe=231692&ProduktNr=223834
		+
		+	===== References =====</nodisp>

-	===== References =====

07.14.2020		current
Line 5:		Line 5:
	==== All patient interviews ====		==== All patient interviews ====

-	//N.B.// Patient interviews no longer available	+	//N.B.// Patient interviews no longer available
	===== Attention Deficit =====		===== Attention Deficit =====

-	* [[http://bacteriality.com/2008/03/15/interview18/\|Interview with Doreen V. - autism, ADHD depression, severe anxiety, CFS]]	+	* [[https://bacteriality.com/2008/03/15/interview18/\|Interview with Doreen V. - autism, ADHD depression, severe anxiety, CFS]]


	===== Anxiety =====		===== Anxiety =====

-	* [[http://bacteriality.com/2008/03/15/interview18/\|Interview with Doreen V. - autism, ADHD depression, severe anxiety, CFS]]	+	* [[https://bacteriality.com/2008/03/15/interview18/\|Interview with Doreen V. - autism, ADHD depression, severe anxiety, CFS]]


	===== Arthritis =====		===== Arthritis =====

-	* [[http://bacteriality.com/2007/09/01/interview2/\|Interview with Ival Meyer - Arthritis, dyslexia]]	+	* [[https://bacteriality.com/2007/09/01/interview2/\|Interview with Ival Meyer - Arthritis, dyslexia]]

-	* [[http://bacteriality.com/2008/06/03/interview21/\|Interview with Roy P. - sarcoidosis, rheumatoid arthritis]]	+	* [[https://bacteriality.com/2008/06/03/interview21/\|Interview with Roy P. - sarcoidosis, rheumatoid arthritis]]


	===== Atrial fibrillation =====		===== Atrial fibrillation =====

-	* [[http://bacteriality.com/2008/01/18/interview15/\|Interview with Freddie Ash - Sarcoidosis of the heart, coronary artery disease, atrial fibrillation]]	+	* [[https://bacteriality.com/2008/01/18/interview15/\|Interview with Freddie Ash - Sarcoidosis of the heart, coronary artery disease, atrial fibrillation]]


	===== Autism =====		===== Autism =====

-	* [[http://bacteriality.com/2008/03/15/interview18/\|Interview with Doreen V. - autism, ADHD depression, severe anxiety, CFS]]	+	* [[https://bacteriality.com/2008/03/15/interview18/\|Interview with Doreen V. - autism, ADHD depression, severe anxiety, CFS]]


	===== Babesia =====		===== Babesia =====

-	* [[http://bacteriality.com/2007/09/22/interview3/\|Interview with Sue Andorn - Lyme, Babesia]]	+	* [[https://bacteriality.com/2007/09/22/interview3/\|Interview with Sue Andorn - Lyme, Babesia]]


	===== Bartonella (cat scratch disease) =====		===== Bartonella (cat scratch disease) =====

-	* [[http://bacteriality.com/2007/11/19/interview13/\|Interview with Sherry Cook - Sarcoidosis, Cat Scratch Fever, Restless Leg Syndrome]]	+	* [[https://bacteriality.com/2007/11/19/interview13/\|Interview with Sherry Cook - Sarcoidosis, Cat Scratch Fever, Restless Leg Syndrome]]


	===== Cancer =====		===== Cancer =====

-	* [[http://bacteriality.com/2008/07/18/interview24/\|Interview with Gene Johnson - sarcoidosis, bladder cancer]]	+	* [[https://bacteriality.com/2008/07/18/interview24/\|Interview with Gene Johnson - sarcoidosis, bladder cancer]]


	===== CFS (chronic fatigue syndrome) =====		===== CFS (chronic fatigue syndrome) =====

-	* [[http://bacteriality.com/2007/11/10/interview10/\|Interview with Paul Albert - CFS, depression, food sensitivities]]. [[http://www.marshallprotocol.com/view_user.php?id=41&posts=1\|Recent posts by PaulAlbert]].	+	* [[https://bacteriality.com/2007/11/10/interview10/\|Interview with Paul Albert - CFS, depression, food sensitivities]]. [[https://www.marshallprotocol.com/view_user.php?id=41&posts=1\|Recent posts by PaulAlbert]].

-	* [[http://bacteriality.com/2007/11/08/interview8/\|Interview with Carole Morgan - Sarcoidosis, fibromyalgia, CFS]]	+	* [[https://bacteriality.com/2007/11/08/interview8/\|Interview with Carole Morgan - Sarcoidosis, fibromyalgia, CFS]]

-	* [[http://bacteriality.com/2008/05/23/interview20/\|Interview with Peter de Jager: chronic fatigue syndrome, multiple chemical sensitivity]]	+	* [[https://bacteriality.com/2008/05/23/interview20/\|Interview with Peter de Jager: chronic fatigue syndrome, multiple chemical sensitivity]]


	===== Chronic spinal inflammation =====		===== Chronic spinal inflammation =====

-	* [[http://bacteriality.com/2007/12/28/interview14/\|Interview with P. Bear R.N. – Chronic Borreliosis (”Lyme”), MCS (multiple chemical sensitivities), Chronic Spinal Inflammation, Peripheral Neuropathy]]	+	* [[https://bacteriality.com/2007/12/28/interview14/\|Interview with P. Bear R.N. – Chronic Borreliosis (”Lyme”), MCS (multiple chemical sensitivities), Chronic Spinal Inflammation, Peripheral Neuropathy]]


	===== Coronary artery disease =====		===== Coronary artery disease =====

-	* [[http://bacteriality.com/2008/01/18/interview15/\|Interview with Freddie Ash - Sarcoidosis of the heart, coronary artery disease, atrial fibrillation]]	+	* [[https://bacteriality.com/2008/01/18/interview15/\|Interview with Freddie Ash - Sarcoidosis of the heart, coronary artery disease, atrial fibrillation]]

	===== Depression =====		===== Depression =====

-	* [[http://bacteriality.com/2007/11/10/interview10/\|Interview with Paul Albert - CFS, depression, food sensitivities]]. [[http://www.marshallprotocol.com/view_user.php?id=41&posts=1\|Recent posts by PaulAlbert]].	+	* [[https://bacteriality.com/2007/11/10/interview10/\|Interview with Paul Albert - CFS, depression, food sensitivities]]. [[https://www.marshallprotocol.com/view_user.php?id=41&posts=1\|Recent posts by PaulAlbert]].


	===== Diabetes =====		===== Diabetes =====

-	* [[http://bacteriality.com/2008/06/19/interview22/\|Interview with Chris Eastlund - diabetes, sarcoidosis, irritable bowel syndrome]]	+	* [[https://bacteriality.com/2008/06/19/interview22/\|Interview with Chris Eastlund - diabetes, sarcoidosis, irritable bowel syndrome]]


	===== Dyslexia =====		===== Dyslexia =====

-	* [[http://bacteriality.com/2007/09/01/interview2/\|Interview with Ival Meyer - Arthritis, dyslexia]]	+	* [[https://bacteriality.com/2007/09/01/interview2/\|Interview with Ival Meyer - Arthritis, dyslexia]]


	===== EMF sensitivities =====		===== EMF sensitivities =====

-	* [[http://www.marshallprotocol.com/view_user.php?id=12432&posts=1\|Recent posts by mvanwink5]]	+	* [[https://www.marshallprotocol.com/view_user.php?id=12432&posts=1\|Recent posts by mvanwink5]]

	===== Fibromyalgia =====		===== Fibromyalgia =====

-	* [[http://bacteriality.com/2007/11/08/interview8/\|Interview with Carole Morgan - Sarcoidosis, fibromyalgia, CFS]]	+	* [[https://bacteriality.com/2007/11/08/interview8/\|Interview with Carole Morgan - Sarcoidosis, fibromyalgia, CFS]]


	===== Food sensitivities =====		===== Food sensitivities =====

-	* [[http://bacteriality.com/2007/11/10/interview10/\|Interview with Paul Albert - CFS, depression, food sensitivities]]. [[http://www.marshallprotocol.com/view_user.php?id=41&posts=1\|Recent posts by PaulAlbert]].	+	* [[https://bacteriality.com/2007/11/10/interview10/\|Interview with Paul Albert - CFS, depression, food sensitivities]]. [[https://www.marshallprotocol.com/view_user.php?id=41&posts=1\|Recent posts by PaulAlbert]].


	===== Insomnia =====		===== Insomnia =====

-	* [[http://bacteriality.com/2007/08/10/interview1/\|Interview with Guss Wilkinson - Sarcoidosis, psoriasis, insomnia]]	+	* [[https://bacteriality.com/2007/08/10/interview1/\|Interview with Guss Wilkinson - Sarcoidosis, psoriasis, insomnia]]


	===== Irritable bowel syndrome =====		===== Irritable bowel syndrome =====

-	* [[http://bacteriality.com/2008/02/17/interview16/\|Interview with Melinda Stiles – Lyme, Irritable bowel syndrome/colitis, Radiculitis (inflammation of the nerve roots)]]	+	* [[https://bacteriality.com/2008/02/17/interview16/\|Interview with Melinda Stiles – Lyme, Irritable bowel syndrome/colitis, Radiculitis (inflammation of the nerve roots)]]

-	* [[http://bacteriality.com/2008/06/19/interview22/\|Interview with Chris Eastlund - diabetes, sarcoidosis, irritable bowel syndrome]]	+	* [[https://bacteriality.com/2008/06/19/interview22/\|Interview with Chris Eastlund - diabetes, sarcoidosis, irritable bowel syndrome]]


	===== Lupus =====		===== Lupus =====

-	* [[http://bacteriality.com/2008/07/02/interview23/\|Interview with Bonnie B - lupus, Sjogren’s Syndrome]]	+	* [[https://bacteriality.com/2008/07/02/interview23/\|Interview with Bonnie B - lupus, Sjogren’s Syndrome]]


	===== Lyme disease =====		===== Lyme disease =====

-	* [[http://bacteriality.com/2007/09/22/interview3/\|Interview with Sue Andorn - Lyme, Babesia]]	+	* [[https://bacteriality.com/2007/09/22/interview3/\|Interview with Sue Andorn - Lyme, Babesia]]

-	* [[http://bacteriality.com/2007/10/28/interview6/\|Interview with Robyn Russell - Lyme, myoclonus]]	+	* [[https://bacteriality.com/2007/10/28/interview6/\|Interview with Robyn Russell - Lyme, myoclonus]]

-	* [[http://bacteriality.com/2007/12/28/interview14/\|Interview with P. Bear R.N. – Chronic Borreliosis (”Lyme”), MCS (multiple chemical sensitivities), Chronic Spinal Inflammation, Peripheral Neuropathy]]	+	* [[https://bacteriality.com/2007/12/28/interview14/\|Interview with P. Bear R.N. – Chronic Borreliosis (”Lyme”), MCS (multiple chemical sensitivities), Chronic Spinal Inflammation, Peripheral Neuropathy]]

-	* [[http://bacteriality.com/2008/02/17/interview16/\|Interview with Melinda Stiles – Lyme, Irritable bowel syndrome/colitis, Radiculitis (inflammation of the nerve roots)]]	+	* [[https://bacteriality.com/2008/02/17/interview16/\|Interview with Melinda Stiles – Lyme, Irritable bowel syndrome/colitis, Radiculitis (inflammation of the nerve roots)]]

-	* [[http://bacteriality.com/2008/03/31/interview19/\|Interview with Ken L. - Post Treatment Lyme Disease Syndrome (PTLDS)]]	+	* [[https://bacteriality.com/2008/03/31/interview19/\|Interview with Ken L. - Post Treatment Lyme Disease Syndrome (PTLDS)]]

-	* [[http://www.marshallprotocol.com/view_user.php?id=4677&posts=1\|Recent posts by jcocain]] - Lyme	+	* [[https://www.marshallprotocol.com/view_user.php?id=4677&posts=1\|Recent posts by jcocain]] - Lyme


	===== MCS (multiple chemical sensitivities) =====		===== MCS (multiple chemical sensitivities) =====

-	* [[http://bacteriality.com/2007/12/28/interview14/\|Interview with P. Bear R.N. – Chronic Borreliosis (”Lyme”), MCS (multiple chemical sensitivities), Chronic Spinal Inflammation, Peripheral Neuropathy]]	+	* [[https://bacteriality.com/2007/12/28/interview14/\|Interview with P. Bear R.N. – Chronic Borreliosis (”Lyme”), MCS (multiple chemical sensitivities), Chronic Spinal Inflammation, Peripheral Neuropathy]]

-	* [[http://bacteriality.com/2008/05/23/interview20/\|Interview with Peter de Jager: chronic fatigue syndrome, multiple chemical sensitivity]]	+	* [[https://bacteriality.com/2008/05/23/interview20/\|Interview with Peter de Jager: chronic fatigue syndrome, multiple chemical sensitivity]]


	===== Myoclonus =====		===== Myoclonus =====

-	* [[http://bacteriality.com/2007/10/28/interview6/\|Interview with Robyn Russell - Lyme, myoclonus]]	+	* [[https://bacteriality.com/2007/10/28/interview6/\|Interview with Robyn Russell - Lyme, myoclonus]]


	===== OCD (obsessive compulsive disorder) =====		===== OCD (obsessive compulsive disorder) =====

-	* [[http://bacteriality.com/2007/11/10/interview9/\|Interview with Julia Grier — Sarcoidosis, OCD, uveitis]]	+	* [[https://bacteriality.com/2007/11/10/interview9/\|Interview with Julia Grier — Sarcoidosis, OCD, uveitis]]

	===== Peripheral Neuropathy =====		===== Peripheral Neuropathy =====

-	* [[http://bacteriality.com/2007/12/28/interview14/\|Interview with P. Bear R.N. – Chronic Borreliosis (”Lyme”), MCS (multiple chemical sensitivities), Chronic Spinal Inflammation, Peripheral Neuropathy]]	+	* [[https://bacteriality.com/2007/12/28/interview14/\|Interview with P. Bear R.N. – Chronic Borreliosis (”Lyme”), MCS (multiple chemical sensitivities), Chronic Spinal Inflammation, Peripheral Neuropathy]]


	===== Psoriasis =====		===== Psoriasis =====

-	* [[http://bacteriality.com/2007/08/10/interview1/\|Interview with Guss Wilkinson - Sarcoidosis, psoriasis, insomnia]]	+	* [[https://bacteriality.com/2007/08/10/interview1/\|Interview with Guss Wilkinson - Sarcoidosis, psoriasis, insomnia]]


	===== Radiculitis =====		===== Radiculitis =====

-	* [[http://bacteriality.com/2008/02/17/interview16/\|Interview with Melinda Stiles – Lyme, Irritable bowel syndrome/colitis, Radiculitis (inflammation of the nerve roots)]]	+	* [[https://bacteriality.com/2008/02/17/interview16/\|Interview with Melinda Stiles – Lyme, Irritable bowel syndrome/colitis, Radiculitis (inflammation of the nerve roots)]]


	===== Restless leg syndrome =====		===== Restless leg syndrome =====

-	* [[http://bacteriality.com/2007/11/19/interview13/\|Interview with Sherry Cook - Sarcoidosis, Cat Scratch Fever, Restless Leg Syndrome]]	+	* [[https://bacteriality.com/2007/11/19/interview13/\|Interview with Sherry Cook - Sarcoidosis, Cat Scratch Fever, Restless Leg Syndrome]]


	===== Sarcoidosis =====		===== Sarcoidosis =====

-	* [[http://bacteriality.com/2007/11/04/interview7/\|Interview with Shirley J. (Saj) - Sarcoidosis]]	+	* [[https://bacteriality.com/2007/11/04/interview7/\|Interview with Shirley J. (Saj) - Sarcoidosis]]

-	* [[http://bacteriality.com/2007/11/17/interview11/\|Interview with Mirek Wozga - sarcoidosis]]	+	* [[https://bacteriality.com/2007/11/17/interview11/\|Interview with Mirek Wozga - sarcoidosis]]

-	* [[http://bacteriality.com/2008/01/18/interview15/\|Interview with Freddie Ash - Sarcoidosis of the heart, coronary artery disease, atrial fibrillation]]	+	* [[https://bacteriality.com/2008/01/18/interview15/\|Interview with Freddie Ash - Sarcoidosis of the heart, coronary artery disease, atrial fibrillation]]

-	* [[http://bacteriality.com/2008/03/02/interview17/\|Interview with JST: Neurosarcoidosis, systemic sarcoidosis; spasticity, myasthenia, CNS dysfunction, joint pain, pulmonary, splenic and cardiac involvement]]	+	* [[https://bacteriality.com/2008/03/02/interview17/\|Interview with JST: Neurosarcoidosis, systemic sarcoidosis; spasticity, myasthenia, CNS dysfunction, joint pain, pulmonary, splenic and cardiac involvement]]

-	* [[http://bacteriality.com/2007/08/10/interview1/\|Interview with Guss Wilkinson - Sarcoidosis, psoriasis, insomnia]]	+	* [[https://bacteriality.com/2007/08/10/interview1/\|Interview with Guss Wilkinson - Sarcoidosis, psoriasis, insomnia]]

-	* [[http://bacteriality.com/2007/11/08/interview8/\|Interview with Carole Morgan - Sarcoidosis, fibromyalgia, CFS]]	+	* [[https://bacteriality.com/2007/11/08/interview8/\|Interview with Carole Morgan - Sarcoidosis, fibromyalgia, CFS]]

-	* [[http://bacteriality.com/2008/07/18/interview24/\|Interview with Gene Johnson - sarcoidosis, bladder cancer]]	+	* [[https://bacteriality.com/2008/07/18/interview24/\|Interview with Gene Johnson - sarcoidosis, bladder cancer]]

-	* [[http://bacteriality.com/2007/11/19/interview12/\|Interview with Leesa Shanahan - Sarcoidosis (Hedfort Syndrome), Uveitis]]	+	* [[https://bacteriality.com/2007/11/19/interview12/\|Interview with Leesa Shanahan - Sarcoidosis (Hedfort Syndrome), Uveitis]]

-	* [[http://bacteriality.com/2008/06/03/interview21/\|Interview with Roy P. - sarcoidosis, rheumatoid arthritis]]	+	* [[https://bacteriality.com/2008/06/03/interview21/\|Interview with Roy P. - sarcoidosis, rheumatoid arthritis]]

-	* [[http://bacteriality.com/2008/06/19/interview22/\|Interview with Chris Eastlund - diabetes, sarcoidosis, irritable bowel syndrome]]	+	* [[https://bacteriality.com/2008/06/19/interview22/\|Interview with Chris Eastlund - diabetes, sarcoidosis, irritable bowel syndrome]]

-	* [[http://www.marshallprotocol.com/view_user.php?id=10560&posts=1\|Recent posts by didierchretien]] - Sarcoidosis	+	* [[https://www.marshallprotocol.com/view_user.php?id=10560&posts=1\|Recent posts by didierchretien]] - Sarcoidosis


	===== Sjogren’s Syndrome =====		===== Sjogren’s Syndrome =====

-	* [[http://bacteriality.com/2008/07/02/interview23/\|Interview with Bonnie B - lupus, Sjogren’s Syndrome]]	+	* [[https://bacteriality.com/2008/07/02/interview23/\|Interview with Bonnie B - lupus, Sjogren’s Syndrome]]


	===== Uveitis =====		===== Uveitis =====

-	* [[http://bacteriality.com/2007/11/10/interview9/\|Interview with Julia Grier — Sarcoidosis, OCD, uveitis]]	+	* [[https://bacteriality.com/2007/11/10/interview9/\|Interview with Julia Grier — Sarcoidosis, OCD, uveitis]]

-	* [[http://bacteriality.com/2007/11/19/interview12/\|Interview with Leesa Shanahan - Sarcoidosis (Hedfort Syndrome), Uveitis]]	+	* [[https://bacteriality.com/2007/11/19/interview12/\|Interview with Leesa Shanahan - Sarcoidosis (Hedfort Syndrome), Uveitis]]


Line 204:		Line 204:


		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

Line 212:		Line 213:
	\\		\\
	TEMPLATES		TEMPLATES
-	* <nowiki>[[http://www.marshallprotocol.com/view_user.php?id=oooooo&posts=1\|Recent posts by ScreenNAME]] - DIAGNOSES</nowiki>	+	* <nowiki>[[https://www.marshallprotocol.com/view_user.php?id=oooooo&posts=1\|Recent posts by ScreenNAME]] - DIAGNOSES</nowiki>
	* <nowiki>[[interviewLINK\|InterviewTITLE]]</nowiki>		* <nowiki>[[interviewLINK\|InterviewTITLE]]</nowiki>
-	* <nowiki>[[interviewLINK\|InterviewTITLE]]. [[http://www.marshallprotocol.com/view_user.php?id=oooooo&posts=1\|Recent posts by ScreenNAME]]</nowiki>	+	* <nowiki>[[interviewLINK\|InterviewTITLE]]. [[https://www.marshallprotocol.com/view_user.php?id=oooooo&posts=1\|Recent posts by ScreenNAME]]</nowiki></nodisp>

02.17.2019		current
Line 3:		Line 3:
	====== Parkinson's disease ======		====== Parkinson's disease ======

-	[[http://www.mayoclinic.org/diseases-conditions/parkinsons-disease/basics/definition/con-20028488\|Mayo Clinic overview]]	+	[[https://www.mayoclinic.org/diseases-conditions/parkinsons-disease/basics/definition/con-20028488\|Mayo Clinic overview]]


Line 16:		Line 16:
	RESULTS: The probabilities of random occurrence (P values) in the 3 clusters were P = 7.9 x 10 (-7)for cluster 1, P = 2.6 x 10 (-7)for cluster 2, and P = 1.5 x 10 (-7)for cluster 3.		RESULTS: The probabilities of random occurrence (P values) in the 3 clusters were P = 7.9 x 10 (-7)for cluster 1, P = 2.6 x 10 (-7)for cluster 2, and P = 1.5 x 10 (-7)for cluster 3.

-	CONCLUSIONS: Our findings indicate an important role for environmental causation in Parkinson disease. A possible role exists for environmental factors such as viral infection and toxins in the light of current evidence. (({{pubmed>long:15262735}}))	+	CONCLUSIONS: Our findings indicate an important role for environmental causation in Parkinson disease. A possible role exists for environmental factors such as viral infection and toxins in the light of current evidence. (({{pmid>long:15262735}}))

	===== Gastrointestinal inflammation =====		===== Gastrointestinal inflammation =====
Line 22:		Line 22:
	<blockquote>		<blockquote>

-	Colonoscopy or flexible sigmoidoscopy may be used to predict Parkinson's (({{pubmed>long:22550057}})) (({{pubmed>long:26539989}})) (({{pubmed>long:26179554}}))	+	Colonoscopy or flexible sigmoidoscopy may be used to predict Parkinson's (({{pmid>long:22550057}})) (({{pmid>long:26539989}})) (({{pmid>long:26179554}}))

	</blockquote>		</blockquote>
Line 28:		Line 28:
	<blockquote>OBJECTIVE:An inflammation-driven model of PD has been proposed based on the endotoxin lipopolysaccaride (LPS), a potential source of inflammation in the gastrointestinal system linked to neurotoxicity. Systemic exposure to bacterial endotoxin (LPS) can be determined by measuring plasma LPS binding protein (LBP). We aimed to evaluate whether lipopolysaccharide binding protein (LBP) can be used to distinguish PD subjects from control subjects and to assess whether LBP levels correlate with PD disease severity.		<blockquote>OBJECTIVE:An inflammation-driven model of PD has been proposed based on the endotoxin lipopolysaccaride (LPS), a potential source of inflammation in the gastrointestinal system linked to neurotoxicity. Systemic exposure to bacterial endotoxin (LPS) can be determined by measuring plasma LPS binding protein (LBP). We aimed to evaluate whether lipopolysaccharide binding protein (LBP) can be used to distinguish PD subjects from control subjects and to assess whether LBP levels correlate with PD disease severity.

-	CONCLUSIONS: Our data suggests that LBP is one GI biomarker related to LPS induced neurotoxicity. However, there was significant variability in LBP levels within the PD and control groups, limiting its utility as a stand-alone biomarker. //Pal et al// Front Neurosci. 2015 Sep 1 (({{pubmed>long:26388718}}))</blockquote>	+	CONCLUSIONS: Our data suggests that LBP is one GI biomarker related to LPS induced neurotoxicity. However, there was significant variability in LBP levels within the PD and control groups, limiting its utility as a stand-alone biomarker. //Pal et al// Front Neurosci. 2015 Sep 1 (({{pmid>long:26388718}}))</blockquote>

	<blockquote>Strong epidemiologic evidence suggests that smokers and coffee drinkers have a lower risk of Parkinson's disease (PD). The explanation for this finding is still unknown, and the discussion has focused on two main hypotheses.		<blockquote>Strong epidemiologic evidence suggests that smokers and coffee drinkers have a lower risk of Parkinson's disease (PD). The explanation for this finding is still unknown, and the discussion has focused on two main hypotheses.

-	We propose an alternative third hypothesis, in which both cigarette and coffee consumption change the composition of the microbiota in the gut in a way that mitigates intestinal inflammation. //Derkinderen et al// Mov Disord. 2014 Jul 29 (({{pubmed>long:24753353}}))</blockquote>	+	We propose an alternative third hypothesis, in which both cigarette and coffee consumption change the composition of the microbiota in the gut in a way that mitigates intestinal inflammation. //Derkinderen et al// Mov Disord. 2014 Jul 29 (({{pmid>long:24753353}}))</blockquote>

	===== Neuropathology =====		===== Neuropathology =====
Line 56:		Line 56:
	<blockquote>Helicobacter. 2005 Aug;10(4):276-87.		<blockquote>Helicobacter. 2005 Aug;10(4):276-87.
	Role of chronic infection and inflammation in the gastrointestinal tract in the etiology and pathogenesis of idiopathic parkinsonism. Part 2: response of facets of clinical idiopathic parkinsonism to Helicobacter pylori eradication. A randomized, double-blind, placebo-controlled efficacy study.		Role of chronic infection and inflammation in the gastrointestinal tract in the etiology and pathogenesis of idiopathic parkinsonism. Part 2: response of facets of clinical idiopathic parkinsonism to Helicobacter pylori eradication. A randomized, double-blind, placebo-controlled efficacy study.
-	Bjarnason IT, Charlett A, Dobbs RJ, Dobbs SM, Ibrahim MA, Kerwin RW, Mahler RF, Oxlade NL, Peterson DW, Plant JM, Price AB, Weller C. (({{pubmed>long:16104942}}))</blockquote>	+	Bjarnason IT, Charlett A, Dobbs RJ, Dobbs SM, Ibrahim MA, Kerwin RW, Mahler RF, Oxlade NL, Peterson DW, Plant JM, Price AB, Weller C. (({{pmid>long:16104942}}))</blockquote>

	Section of Neuropharmacology, Institute of Psychiatry, London, UK.		Section of Neuropharmacology, Institute of Psychiatry, London, UK.
Line 84:		Line 84:
	<blockquote> Ulcer bacteria may contribute to development of Parkinson's disease		<blockquote> Ulcer bacteria may contribute to development of Parkinson's disease

-	http://www.eurekalert.org/pub_releases/2011-05/asfm-ubm051811.php	+	https://www.eurekalert.org/pub_releases/2011-05/asfm-ubm051811.php

	NEW ORLEANS, LA – May 22, 2011 -- The stomach bacteria responsible for ulcers could also play a role in the development of Parkinson's disease according to research presented today at the 111th General Meeting of the American Society for Microbiology.		NEW ORLEANS, LA – May 22, 2011 -- The stomach bacteria responsible for ulcers could also play a role in the development of Parkinson's disease according to research presented today at the 111th General Meeting of the American Society for Microbiology.
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	Studies in the Role of chronic infection and inflammation in the gastrointestinal tract in the etiology and pathogenesis of idiopathic parkinsonism. Dobbs RJ1, Dobbs SM, Weller C, Bjarnason IT, Oxlade NL, Charlett A et al		Studies in the Role of chronic infection and inflammation in the gastrointestinal tract in the etiology and pathogenesis of idiopathic parkinsonism. Dobbs RJ1, Dobbs SM, Weller C, Bjarnason IT, Oxlade NL, Charlett A et al

-	AIM: To consider the candidature of Helicobacter in parkinsonism with cachexia. (({{pubmed>long:16104942}}))	+	AIM: To consider the candidature of Helicobacter in parkinsonism with cachexia. (({{pmid>long:16104942}}))

-	AIM: Proof-of-principle that infection contributes to idiopathic parkinsonism. (({{pubmed>long:16104943}}))	+	AIM: Proof-of-principle that infection contributes to idiopathic parkinsonism. (({{pmid>long:16104943}}))

-	AIM: To explore the cross-sectional fit of parkinsonism as an extra-alimentary consequence of Helicobacter pylori, using the serum antibody profile. (({{pubmed>long:16104944}}))	+	AIM: To explore the cross-sectional fit of parkinsonism as an extra-alimentary consequence of Helicobacter pylori, using the serum antibody profile. (({{pmid>long:16104944}}))

-	Abstract: We challenge the concept of idiopathic parkinsonism (IP) as inevitably progressive neurodegeneration (({{pubmed>long:19250506}})) (({{pubmed>long:20633189}}))	+	Abstract: We challenge the concept of idiopathic parkinsonism (IP) as inevitably progressive neurodegeneration (({{pmid>long:19250506}})) (({{pmid>long:20633189}}))

	<blockquote>Med Hypotheses. 2010 May;74(5):895-7. Epub 2009 Dec 3.		<blockquote>Med Hypotheses. 2010 May;74(5):895-7. Epub 2009 Dec 3.
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	Abstract		Abstract

-	Antibiotic therapy to eradicate Helicobacter pylori, the causative agent of gastric and duodenal ulcers, has been suggested to improve L-DOPA bioavailability in Parkinson's and thereby improve patient symptomology. To date, there has been no proven mechanism to explain the purported benefit of treatment of H. pylori in the management of Parkinson's disease. I propose the hypothesis, and provide initial data, that the mechanism of action is due to direct utilization of L-DOPA by H. pylori to maintain its ecological niche within the gastrointestinal tract. In support of this hypothesis, data is presented which demonstrates for the first time the ability of L-DOPA to influence the in vitro growth of H. pylori in an iron-restricted minimal medium. H. pylori utilization of L-DOPA for its own growth requirement reduces the amount of per orally administered L-DOPA that would be available to the patient for the treatment of Parkinson's disease-related pathology. Neuroendocrine-mediated interactions with bacteria represent the emerging interdisciplinary field of microbial endocrinology. Thus, microbial endocrinology provides for a mechanism between L-DOPA and H. pylori with which to explain the purported benefit of H. pylori-directed antibiotic therapy to improve L-DOPA bioavailability in Parkinson's patients and thereby improve drug therapy management. Further, if other bacterial species within the gastrointestinal tract depend on the availability of L-DOPA or other similar neuroendocrine-based drugs for their survival, then the efficacy of such neuroendocrine-based drugs not restricted solely for the management of parkinsonian symptomology may also be adversely affected and may therefore justify the use of an antibiotic regimen to eradicate them. (({{pubmed>long:19962247}})) </blockquote>	+	Antibiotic therapy to eradicate Helicobacter pylori, the causative agent of gastric and duodenal ulcers, has been suggested to improve L-DOPA bioavailability in Parkinson's and thereby improve patient symptomology. To date, there has been no proven mechanism to explain the purported benefit of treatment of H. pylori in the management of Parkinson's disease. I propose the hypothesis, and provide initial data, that the mechanism of action is due to direct utilization of L-DOPA by H. pylori to maintain its ecological niche within the gastrointestinal tract. In support of this hypothesis, data is presented which demonstrates for the first time the ability of L-DOPA to influence the in vitro growth of H. pylori in an iron-restricted minimal medium. H. pylori utilization of L-DOPA for its own growth requirement reduces the amount of per orally administered L-DOPA that would be available to the patient for the treatment of Parkinson's disease-related pathology. Neuroendocrine-mediated interactions with bacteria represent the emerging interdisciplinary field of microbial endocrinology. Thus, microbial endocrinology provides for a mechanism between L-DOPA and H. pylori with which to explain the purported benefit of H. pylori-directed antibiotic therapy to improve L-DOPA bioavailability in Parkinson's patients and thereby improve drug therapy management. Further, if other bacterial species within the gastrointestinal tract depend on the availability of L-DOPA or other similar neuroendocrine-based drugs for their survival, then the efficacy of such neuroendocrine-based drugs not restricted solely for the management of parkinsonian symptomology may also be adversely affected and may therefore justify the use of an antibiotic regimen to eradicate them. (({{pmid>long:19962247}})) </blockquote>


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	<blockquote>I am a Parkinson's patient and on the MP since Sept 2008. I am currently halfway phase 3. The results in summary: The progression of the disease has not stopped (maybe slowed down?).		<blockquote>I am a Parkinson's patient and on the MP since Sept 2008. I am currently halfway phase 3. The results in summary: The progression of the disease has not stopped (maybe slowed down?).

-	I know one other person on the MP who thinks he has Parkinson's. He is also in phase 3 but not reporting on an MP site. I am reporting as EpoxyJan since Oct.2009 on the study site [[http://www.marshallprotocol.com/forum35/13482.html\|here]].	+	I know one other person on the MP who thinks he has Parkinson's. He is also in phase 3 but not reporting on an MP site. I am reporting as EpoxyJan since Oct.2009 on the study site [[https://www.marshallprotocol.com/forum35/13482.html\|here]].

	//EpoxyJan, MarshallProtocol.com//</blockquote>		//EpoxyJan, MarshallProtocol.com//</blockquote>

-	===== Recent research and further reading =====	+	===== Research and further reading =====

-	<blockquote>Towards this end, we used a published dataset to analyse bacteriophage composition and determine the phage/bacteria ratio in faecal samples from drug-naive PD patients and healthy participants. Our analyses revealed significant alterations in the representation of certain bacteriophages in the phagobiota of PD patients. (({{pubmed>long:30018338}})) </blockquote>	+	<blockquote>Towards this end, we used a published dataset to analyse bacteriophage composition and determine the phage/bacteria ratio in faecal samples from drug-naive PD patients and healthy participants. Our analyses revealed significant alterations in the representation of certain bacteriophages in the phagobiota of PD patients. (({{pmid>long:30018338}})) </blockquote>

-	<blockquote>In 1919, it was first recognized that loss of pigmentation in the substantia nigra of the midbrain is a feature (({{pubmed>long:29261972}})) </blockquote>	+	<blockquote>In 1919, it was first recognized that loss of pigmentation in the substantia nigra of the midbrain is a feature (({{pmid>long:29261972}})) </blockquote>

-	[[http://books.google.com/books?id=REICWr22YR8C&dq=Parkinson's:+another+look.+Is+Parkinson's+disease+caused+by+a+bacteria%3F&printsec=frontcover&source=bn&hl=en&ei=Khj-SZmdFaCltgegm62SDA&sa=X&oi=book_result&ct=result&resnum=4\|Parkinson's Another Look]]	+	The implication of tyrosine hydroxylase (TH), the enzyme that catalyzes the formation of L-3,4-dihydroxyphenylalanine, in the pathogenesis of PD at different levels makes it a promising candidate for developing efficient treatment based on correcting or bypassing the enzyme deficiency. (({{pmid>long:22483311}}))
		+
		+	[[https://books.google.com/books?id=REICWr22YR8C&dq=Parkinson's:+another+look.+Is+Parkinson's+disease+caused+by+a+bacteria%3F&printsec=frontcover&source=bn&hl=en&ei=Khj-SZmdFaCltgegm62SDA&sa=X&oi=book_result&ct=result&resnum=4\|Parkinson's Another Look]]

	{{tag>disease }}		{{tag>disease }}


		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

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	<blockquote>ASM Live 2011: Bacteria May Contribute to Development of Parkinsons Disease: A new mouse model suggests that the... bit.ly/iywhdJ</blockquote>		<blockquote>ASM Live 2011: Bacteria May Contribute to Development of Parkinsons Disease: A new mouse model suggests that the... bit.ly/iywhdJ</blockquote>
-	===== References =====	+	===== References =====</nodisp>

10.17.2018		current
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	===== Role of phosphorous =====		===== Role of phosphorous =====

-	In a 2007 study, Harvard Medical School researchers engineered mice without vitamin D receptors (VDRs). Since vitamin D can have no effect on the body unless it can bind to the VDR, the mice could use no vitamin D whatsoever in their bodies. The researchers found that if the mice were given a diet high in calcium and phosphorous they did not develop rickets and their bones were just as strong as normal mice with active Vitamin D Receptors.(({{pubmed>long:17332234}}))	+	In a 2007 study, Harvard Medical School researchers engineered mice without vitamin D receptors (VDRs). Since vitamin D can have no effect on the body unless it can bind to the VDR, the mice could use no vitamin D whatsoever in their bodies. The researchers found that if the mice were given a diet high in calcium and phosphorous they did not develop rickets and their bones were just as strong as normal mice with active Vitamin D Receptors.(({{pmid>long:17332234}}))


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-	A second study by the same research team at Harvard corrected rickets by replacing calcium and phosphate ions in the bloodstream of mice without Vitamin D Receptors, thereby confirming the results. The team concluded that rickets is not caused by a deficiency of vitamin D but instead results from hypophosphatemia, a condition where the level of phosphorous in the blood is too low.(({{pubmed>long:16831920}}))	+	A second study by the same research team at Harvard corrected rickets by replacing calcium and phosphate ions in the bloodstream of mice without Vitamin D Receptors, thereby confirming the results. The team concluded that rickets is not caused by a deficiency of vitamin D but instead results from hypophosphatemia, a condition where the level of phosphorous in the blood is too low.(({{pmid>long:16831920}}))

-	This work is also echoed by Schubert and De Luca who found that muscle weakness in hypophosphatemic rats could be corrected with supplementation of phosphorus, and that hypocalcemia together with vitamin D deficiency did not produce muscle weakness.(({{pubmed>long:20515645}}))	+	This work is also echoed by Schubert and De Luca who found that muscle weakness in hypophosphatemic rats could be corrected with supplementation of phosphorus, and that hypocalcemia together with vitamin D deficiency did not produce muscle weakness.(({{pmid>long:20515645}}))

	===== Role of calcium =====		===== Role of calcium =====

-	According to a 2000 paper by Goswami //et al.//, "Despite abundant sunlight, rickets and osteomalacia are prevalent in South Asian countries. The cause of this paradox is not clear."(({{pubmed>long:10919943}})) Interestingly, the paper goes on to say that subjects who are at risk for rickets had low dietary calcium consumption and significantly low calcium consumption.	+	According to a 2000 paper by Goswami //et al.//, "Despite abundant sunlight, rickets and osteomalacia are prevalent in South Asian countries. The cause of this paradox is not clear."(({{pmid>long:10919943}})) Interestingly, the paper goes on to say that subjects who are at risk for rickets had low dietary calcium consumption and significantly low calcium consumption.

	Along with phosphorous, low calcium plays a role in rickets. Diminished levels of calcium cause an increase in parathyroid hormone, which subsequently causes the body to excrete too much phosphorous. This causes the level of phosphate in the body to drop, leading to the altered bone formation seen in rickets.		Along with phosphorous, low calcium plays a role in rickets. Diminished levels of calcium cause an increase in parathyroid hormone, which subsequently causes the body to excrete too much phosphorous. This causes the level of phosphate in the body to drop, leading to the altered bone formation seen in rickets.
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	//Joyce Waterhouse, PhD// </blockquote>		//Joyce Waterhouse, PhD// </blockquote>

-	Other studies have confirmed that a low level of calcium can lead to rickets. One team assessed the absorption of calcium in 15 Nigerian children with active rickets. They found that all 15 children had resolution or improvement of rickets after six months of treatment with calcium supplements. (({{pubmed>long:15531695}}))	+	Other studies have confirmed that a low level of calcium can lead to rickets. One team assessed the absorption of calcium in 15 Nigerian children with active rickets. They found that all 15 children had resolution or improvement of rickets after six months of treatment with calcium supplements. (({{pmid>long:15531695}}))

-	This paper is acknowledged by the {{https://www.ars.usda.gov/research/publications/publication/?seqNo115=169216\|Children's Nutrition Research Center: Houston, TX}}	+	This paper is acknowledged by the [[https://www.ars.usda.gov/research/publications/publication/?seqNo115=169216\|Children's Nutrition Research Center: Houston, TX]]

	<blockquote>Interpretive Summary: Rickets in toddlers is a large problem in parts of Africa, especially Nigeria. It is not due to vitamin D deficiency but is caused by not having enough calcium in the diet. We wanted to know whether there was a problem with absorbing calcium in children in Nigeria. We measured how much calcium was absorbed in a group of children with rickets and compared that with how much was absorbed by children that did not have rickets. We found that children with rickets were able to absorb calcium normally. This means that it is probably another factor in the diet or an overall lack of calcium that causes the rickets rather than an inability of some children to absorb the calcium that is in their diet. </blockquote>		<blockquote>Interpretive Summary: Rickets in toddlers is a large problem in parts of Africa, especially Nigeria. It is not due to vitamin D deficiency but is caused by not having enough calcium in the diet. We wanted to know whether there was a problem with absorbing calcium in children in Nigeria. We measured how much calcium was absorbed in a group of children with rickets and compared that with how much was absorbed by children that did not have rickets. We found that children with rickets were able to absorb calcium normally. This means that it is probably another factor in the diet or an overall lack of calcium that causes the rickets rather than an inability of some children to absorb the calcium that is in their diet. </blockquote>
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	<blockquote>Persons with a 25(OH)D<sub>3</sub> concentration <20 nmol/L probably have rickets or osteomalacia.		<blockquote>Persons with a 25(OH)D<sub>3</sub> concentration <20 nmol/L probably have rickets or osteomalacia.

-	//Dr. Anthony Norman//(({{pubmed>long:18689389}}))	+	//Dr. Anthony Norman//(({{pmid>long:18689389}}))
	</blockquote>		</blockquote>

-	However, a randomized double-blind placebo-controlled trial at Creighton University Medical Center found no beneficial effect of vitamin D on calcium absorption in older women.(({{pubmed>long:22855333}}))	+	However, a randomized double-blind placebo-controlled trial at Creighton University Medical Center found no beneficial effect of vitamin D on calcium absorption in older women.(({{pmid>long:22855333}}))
	==== Marshall Protocol patients ====		==== Marshall Protocol patients ====

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	<blockquote>We did not see any cases of rickets in any of the 80 study participants; as such, there was no evidence that universal supplementation of vitamin D in breast-fed infants is either necessary or efficacious for rickets prevention in southern Louisiana.... This suggests that the current recommendations for universal vitamin D supplementation of breast-fed infants throughout the United States may need to be revised.		<blockquote>We did not see any cases of rickets in any of the 80 study participants; as such, there was no evidence that universal supplementation of vitamin D in breast-fed infants is either necessary or efficacious for rickets prevention in southern Louisiana.... This suggests that the current recommendations for universal vitamin D supplementation of breast-fed infants throughout the United States may need to be revised.

-	//Tulasi Ponnapakkam, PhD (({{pubmed>long:20724336}}))//</blockquote>	+	//Tulasi Ponnapakkam, PhD (({{pmid>long:20724336}}))//</blockquote>


	==== Nigerian children ====		==== Nigerian children ====

-	Thacher //et al// conducted a case-control study to determine factors associated with rickets in Nigerian children. The study compared 123 Nigerian children who had rickets with matched control subjects. Of the 134 subjects with rickets, only 46 subjects (37%) had 25-hydroxyvitamin D values <30 nmol/L (12 ng/mL).(({{pubmed>long:10969262}})) The team concluded:	+	Thacher //et al// conducted a case-control study to determine factors associated with rickets in Nigerian children. The study compared 123 Nigerian children who had rickets with matched control subjects. Of the 134 subjects with rickets, only 46 subjects (37%) had 25-hydroxyvitamin D values <30 nmol/L (12 ng/mL).(({{pmid>long:10969262}})) The team concluded:

	<blockquote>		<blockquote>
	Vitamin D deficiency appears unlikely to be the primary etiologic factor of rickets in African children. Moreover, low dietary calcium intake alone does not account for rickets. Insufficient dietary calcium probably interacts with genetic, hormonal, and other nutritional factors to cause rickets in susceptible children.		Vitamin D deficiency appears unlikely to be the primary etiologic factor of rickets in African children. Moreover, low dietary calcium intake alone does not account for rickets. Insufficient dietary calcium probably interacts with genetic, hormonal, and other nutritional factors to cause rickets in susceptible children.

-	//Thacher et al.// (({{pubmed>long:10969262}})) </blockquote>	+	//Thacher et al.// (({{pmid>long:10969262}})) </blockquote>


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	//Marie Demay, personal communication//</blockquote>		//Marie Demay, personal communication//</blockquote>

-	As a nod to this molecular evidence, the [[http://arsserv0.tamu.edu/research/publications/publications.htm?SEQ_NO_115=169216\|US Department of Agriculture]] has said, “Rickets in toddlers is a large problem in parts of Africa, especially Nigeria. It is not due to vitamin D deficiency but is caused by not having enough calcium in the diet.”	+	As a nod to this molecular evidence, the [[https://arsserv0.tamu.edu/research/publications/publications.htm?SEQ_NO_115=169216\|US Department of Agriculture]] has said, “Rickets in toddlers is a large problem in parts of Africa, especially Nigeria. It is not due to vitamin D deficiency but is caused by not having enough calcium in the diet.”


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	Robins (2009) notes that nearly half of all African Americans are classified as vitamin-D deficient and yet show no signs of calcium deficiency, which would be a logical result of vitamin D deficiency. Indeed, they “have a lower prevalence of osteoporosis, a lower incidence of fractures and a higher bone mineral density than white Americans, who generally exhibit a much more favourable vitamin D status.” He also cites a survey of 232 black (East African) immigrant children in Melbourne, Australia, among whom 87% had levels below 50 nmol/L and 44% below 25 nmol/L. None had rickets—the usual sign of vitamin-D deficiency in children (McGillivray et al., 2007).		Robins (2009) notes that nearly half of all African Americans are classified as vitamin-D deficient and yet show no signs of calcium deficiency, which would be a logical result of vitamin D deficiency. Indeed, they “have a lower prevalence of osteoporosis, a lower incidence of fractures and a higher bone mineral density than white Americans, who generally exhibit a much more favourable vitamin D status.” He also cites a survey of 232 black (East African) immigrant children in Melbourne, Australia, among whom 87% had levels below 50 nmol/L and 44% below 25 nmol/L. None had rickets—the usual sign of vitamin-D deficiency in children (McGillivray et al., 2007).

-	//Peter Frost, PhD, [[http://evoandproud.blogspot.com/2009/07/african-americans-and-vitamin-d.html\|African Americans and vitamin D]]// </blockquote>	+	//Peter Frost, PhD, [[https://evoandproud.blogspot.com/2009/07/african-americans-and-vitamin-d.html\|African Americans and vitamin D]]// </blockquote>

	===== Reexamining the cause of rickets =====		===== Reexamining the cause of rickets =====

-	The role of calcium is being reexamined in North America as well. DeLucia //et al.// emphasize that “Nutritional calcium deficiency may occur in North American infants and is not limited to the setting of developing countries.”(({{pubmed>long:12915633}})) Some attribute a recent small increase in rickets in North America to an increase in breast feeding, claiming that this is due to breast milk being low in vitamin D. However, breast feeding is also often accompanied by a diet low in calcium, particularly after weaning (e.g., juices rather than milk). Also, in recent years, more people have begun to avoid milk due to a greater awareness of lactose intolerance.	+	The role of calcium is being reexamined in North America as well. DeLucia //et al.// emphasize that “Nutritional calcium deficiency may occur in North American infants and is not limited to the setting of developing countries.”(({{pmid>long:12915633}})) Some attribute a recent small increase in rickets in North America to an increase in breast feeding, claiming that this is due to breast milk being low in vitamin D. However, breast feeding is also often accompanied by a diet low in calcium, particularly after weaning (e.g., juices rather than milk). Also, in recent years, more people have begun to avoid milk due to a greater awareness of lactose intolerance.

-	Trevor Marshall, PhD has suggested that rickets may be related to Th1 inflammation, as a number of patients on the [[home:protocol\|Marshall Protocol]] with [[home:pathogenesis:th1spectrum\|Th1 illnesses]] and their close relatives report having had rickets as children. Proponent of vitamin D supplementation claim that vitamin D added to the food supply was responsible for a historical decrease in rickets. But the history of rickets shows that a typical rickets case often had a history of smallpox, measles, or whooping cough.(({{pubmed>long:4862158}})) Plus, a 1997 study in Ethiopia found a high association between pneumonia and rickets.(({{pubmed>long:9269215}})) This provides more suggestive evidence that infection, either obvious and acute, or subtle and chronic, may play a role in the development of rickets and may exacerbate the effects of a low calcium diet.	+	Trevor Marshall, PhD has suggested that rickets may be related to Th1 inflammation, as a number of patients on the [[home:protocol\|Marshall Protocol]] with [[home:pathogenesis:th1spectrum\|Th1 illnesses]] and their close relatives report having had rickets as children. Proponent of vitamin D supplementation claim that vitamin D added to the food supply was responsible for a historical decrease in rickets. But the history of rickets shows that a typical rickets case often had a history of smallpox, measles, or whooping cough.(({{pmid>long:4862158}})) Plus, a 1997 study in Ethiopia found a high association between pneumonia and rickets.(({{pmid>long:9269215}})) This provides more suggestive evidence that infection, either obvious and acute, or subtle and chronic, may play a role in the development of rickets and may exacerbate the effects of a low calcium diet.


	===== Further reading =====		===== Further reading =====

-	* [[http://www.ncbi.nlm.nih.gov/pubmed/22837003\|ACE2 links amino acid malnutrition to microbial ecology and intestinal inflammation]] – In their 2012 //Nature// study, Hashimoto //et al.// provide a molecular explanation for how malnutrition promotes inflammation, "rogue" bacteria, and in the process diarrhea and other hallmarks of the condition.(({{pubmed>long:22837003}}))	+	* [[https://www.ncbi.nlm.nih.gov/pubmed/22837003\|ACE2 links amino acid malnutrition to microbial ecology and intestinal inflammation]] – In their 2012 //Nature// study, Hashimoto //et al.// provide a molecular explanation for how malnutrition promotes inflammation, "rogue" bacteria, and in the process diarrhea and other hallmarks of the condition.(({{pmid>long:22837003}}))



	{{tag>disease no_current_patients}}		{{tag>disease no_current_patients}}
		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

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	* include link to this article in the list of diseases		* include link to this article in the list of diseases
	* Legacy content		* Legacy content
-	* http://www.marshallprotocol.com/forum39/8687.html	+	* https://www.marshallprotocol.com/forum39/8687.html

	<blockquote>Marshall Protocol patients		<blockquote>Marshall Protocol patients
	In fact, many of the patients on the Marshall Protocol have been avoiding consumption of vitamin D – some of them for several years – to the point where most patients in later stages of the treatment have 25-D levels below the detectable threshold. Yet, there has not been a single reported case of rickets.</blockquote> The above should be removed as it gives no meaning in light of the fact that olmesartan is vitamin D, sort of.		In fact, many of the patients on the Marshall Protocol have been avoiding consumption of vitamin D – some of them for several years – to the point where most patients in later stages of the treatment have 25-D levels below the detectable threshold. Yet, there has not been a single reported case of rickets.</blockquote> The above should be removed as it gives no meaning in light of the fact that olmesartan is vitamin D, sort of.

-	===== References =====	+	===== References =====</nodisp>