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Diabetes, Type II

http://www.ncbi.nlm.nih.gov/pubmed/19225551

egg consumption and diabetes1

Diabet Med. 2009 Feb;26(2):149-52. Serological evidence of infections and Type 2 diabetes: the MultiEthnic Study of Atherosclerosis. Lutsey PL, Pankow JS, Bertoni AG, Szklo M, Folsom AR.

Division of Epidemiology and Community Health, University of Minnesota, Minneapolis, MN, USA. lutsey@umn.edu Abstract AIMS: Prospective studies have identified chronic inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue. as a risk factor for Type 2 diabetes. However, it is not known whether infection by specific pathogens or having a greater 'pathogen burden' is associated with diabetes. The aim of this study was to examine the cross-sectional relation of seropositivity to five pathogens (Chlamydia pneumoniae, cytomegalovirus, Helicobacter pylori, hepatitis A virus, herpes simplex virus) and prevalent diabetes. METHODS: Baseline data from a random sample of MultiEthnic Study of Atherosclerosis (MESA) participants (n = 1000; age 45-84 years) were used. Diabetes was defined by American Diabetes Association 2003 criteria, and 'pathogen burden' by the number of pathogens (0-5) for which an individual was seropositive. Logistic regression was used to test differences in diabetes prevalence by seropositivity. Linear regression was used to explore associations between pathogen seropositivity and the inflammation markers C-reactive protein, interleukin-6 and fibrinogen. RESULTS: Diabetes prevalence was 12.7%, whereas seropositivity for C. pnuemoniae was 76%, cytomegalovirus 77%, H. pylori 45%, hepatitis A 58% and herpes simplex virus 85%. Seventy-two percent were seropositive for three or more pathogens. In crude analyses, the prevalence of diabetes was higher among those with a pathogen burden of three or more, and with seropositivity to cytomegalovirus, H. pylori, hepatitis A and herpes simplex virus. After adjustment for demographic covariates (particularly race), all associations became non-significant. Pathogen seropositivity was also not related to inflammation marker levels. CONCLUSIONS: Following demographic adjustments, no associations were observed between infection by several pathogens and diabetes status, suggesting no aetiological role for them in the occurrence of diabetes.

PMID: 19236617

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>;

Nestle Nutr Workshop Ser Clin Perform Programme. 2006;11:139-50; discussion 150-3. Links The accelerator hypothesis: a unifying explanation for type-1 and type-2 diabetes.

Wilkin TJ. Department of Medicine, Postgraduate Medical School, Derriford Hospital, Plymouth, UK. Despite 30 years of research, the cause of type-1 diabetes remains unknown. Meanwhile, its incidence has risen three-fold, its clinical features have become increasingly difficult to distinguish from type-2 diabetes and the contribution of genes to its pathogenesis has changed. The accelerator hypothesis argues that type-1 and type-2 diabetes are the same disorder of insulin resistance set against different genetic backgrounds. It identifies three processes which variably accelerate beta cell loss: constitution, insulin resistance and the immune response to it. None of the accelerators leads to diabetes in the absence of weight gain, a trend which the hypothesis deems central to the rising incidence of all diabetes in the industrially developed and developing world. Weight gain causes an increase in insulin resistance, which results in the weakening of glucose control. The rising blood glucose accelerates beta cell apoptosis (glucotoxicity) and, by increasing beta cell immunogenicity, further accelerates apoptosis in a subset genetically predisposed to an intense immune response. Rather than overlap between the two types of diabetes, the accelerator hypothesis envisages overlay–one a subset of the other. Body mass is central to the development and rising incidence of all diabetes. Only tempo distinguishes type 1 from type 2. The control of weight gain, and with it insulin resistance, could be the means of preventing both by slowing their progression. PMID: 16820737

Evidence of infectious cause

60. Rayfield EJ, Kelly KJ, Yoon JW. Rubella virus-in- duced diabetes in the hamster. Diabetes. 1986;35:1278-1281. 61. Menser MA, Forrest JM, Bransby RD. Rubella in- fection and diabetes mellitus. Lancet. 1978;1:57-60. 62. Ramsingh AI, Chapman N, Tracy S. Coxsackieviruses and diabetes. Bioessays. 1997;19:793-800.

Burden of Infection and Insulin Resistance in Healthy Middle-Aged Men

Helicobacter pylori Infection Significantly Increases Insulin Resistance in the Asymptomatic Japanese Population

 	
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Author(s): Gunji T (Gunji, Toshiaki)2, Matsuhashi N (Matsuhashi, Nobuyuki)1, Sato H (Sato, Hajime)3, Fujibayashi K (Fujibayashi, Kazutoshi)2, Okumura M (Okumura, Mitsue)2, Sasabe N (Sasabe, Noriko)2, Urabe A (Urabe, Akio)2 Source: HELICOBACTER Volume: 14 Issue: 5 Pages: 144-150 Published: OCT 2009 Times Cited: 1 References: 44 Citation Map Abstract: Background: Helicobacter pylori infection has been shown to contribute to atherosclerosis and cardiovascular diseases. Insulin resistance is the pathophysiologic background of the clinical features of atherosclerosis and cardiovascular diseases. We examined the association between H. pylori infection and insulin resistance in a large Japanese population. Materials and Methods: Fifteen hundred ninety-eight consecutive asymptomatic subjects that underwent a complete medical survey in our institute between May 2007 and July 2008 were recruited. Cases under medication for hypertension, hyperlipidemia, diabetes mellitus, hyperuricemia, or cardiovascular diseases were excluded from the study. Cases suffering from chronic renal or liver failure were also excluded. The homeostasis model assessment of insulin resistance (HOMA-IR) score was used to quantitatively estimate insulin resistance. Visceral and subcutaneous adipose tissues (SAT) were measured by computed tomography. The association between H. pylori serostatus and HOMA-IR score was investigated by multivariate regression analysis. Results: A total of 988 men and 119 women were eventually eligible for this cross-sectional survey. Helicobacter pylori seropositivity was significantly higher in 99 cases with insulin resistance (HOMA-IR >= 2.5) compared with 1008 cases without insulin resistance (HOMA-IR < 2.5) (39.4 vs 28.7%, p = .027). There was a significant association between H. pylori serostatus and HOMA-IR score by multiple linear regression analysis (coefficients = 0.152, 95% CI = 0.058-0.246, p = .001), after adjusting for sex, age, body mass index, waist girth, visceral and subcutaneous adipose tissues, smoking status, alcohol consumption, dietary habits, and physical activity. Conclusions: Helicobacter pylori infection significantly and independently contributed to promoting insulin resistance in a large asymptomatic population.

Notes and comments

===== Symptoms ===== ===== Management ===== ===== Other treatments ===== ===== Tests ===== ===== Diagnosis ===== ===== Epidemiology ===== ===== Types ===== ===== Evidence of infectious cause===== ===== Role of vitamin D metabolism ===== ===== Politics ===== ===== Patient interviews ===== ===== Presentations and publications=====

  • s174:

Parathyroid Hormone and Th1 inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue.

1,25-DPrimary biologically active vitamin D hormone. Activates the vitamin D nuclear receptor. Produced by hydroxylation of 25-D. Also known as 1,25-dihydroxycholecalciferol, 1,25-hydroxyvitamin D and calcitirol. spreads from the site of the inflammation (where it is acting as a cytokineAny of various protein molecules secreted by cells of the immune system that serve to regulate the immune system.) through the bloodstream (acting as a hormone)… 1,25-D directly controls the Parathyroid Hormone (PTH) and thence the Thyroid hormones as well as a number of other metabolic pathways, so it is pretty powerful feedback to the body systems, and when the bacteria interrupt that feedback path everything goes unstable (that's how a control-systems engineer might describe it).”

..Trevor..

s177, s178:

Infectious cause of diabetes

Minocycline reduces proinflammatory cytokine expression, microglial activation, and caspase-3 activation in a rodent model of diabetic retinopathy.

The association of metabolic syndrome and Chlamydia pneumoniae, Helicobacter pylori, cytomegalovirus, and herpes simplex virus type 1: the Persian Gulf Healthy Heart Study.

Diabetes clusters suggest infectious cause

Thu Jul 13, 2005

NEW YORK (Reuters Health) - Results of a new study support the notion that common infections may trigger type 1 diabetes in children and young adults.

Specifically, UK researchers uncovered evidence of clustering among young diabetes patients.

A relative high number of cases in a small area and within a limited period – space-time clustering –is “consistent” with an environmental component in disease development, “possibly linked to infections,” Dr. Richard J. Q. McNally, of the University of Newcastle upon Tyne, and colleagues explain in the journal Diabetologia.

The team used data from a population-based register in Yorkshire to look for evidence of space-time clustering of diabetes among subjects younger than age 30.

Included in the analysis were two data sets of patients diagnosed with type 1 diabetes: 3019 children up to 14 years of age who resided in Yorkshire between 1978 and 2002; and 989 patients between 15 and 29 years who resided in West Yorkshire between 1991 and 2002.

In the first group, significant space-time clustering, based on place and time of diagnosis, was confirmed for the children between 10 and 14 years old. In the second group, space-time clustering was observed for those between 15 and 19 years old.

“These findings suggest that infections may precipitate type 1 diabetes in a limited number of susceptible people,” McNally commented to Reuters Health. “Other environmental factors are also likely to be involved.”

Although the findings suggest an environmental cause, the investigators note that the study cannot confirm if the environmental effects are direct or if they merely unmask latent diabetes.

SOURCE: Diabetologia, July 2006.

BCG vaccine and diabetes

It is well documented, over several decades, that the BCG vaccine causes Sarcoidosis, eg “Juvenile sarcoidosis after BCG vaccination (2006)” http://www.ncbi.nlm.nih.gov/pubmed/12734491

“Juvenile sarcoidosis after BCG vaccination (1989)” http://www.ncbi.nlm.nih.gov/pubmed/2602688

“Incidence of Intrathoracic Sarcoidosis among young adults participating in a trial of Tuberculosis vaccines (1965)” http://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 http://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..

See also Infections linked to Type 1 diabetes

Last edited on Mon Mar 17th, 2008 15:22 by

Barb: Dx Inflammatory Disease Endocrine Imbalance 2003| 24+ years not Dx| MP Aug04| ABC of MP| MP Search| Aussie Barb Research Team

Joined: Thu Jul 22nd, 2004 Location: Australia Posts: 19485 Status: Offline

Posted: Tue Jun 14th, 2005 15:36 

(filelink) Diabetes and the Marshall ProtocolA curative medical treatment for chronic inflammatory disease. Based on the Marshall Pathogenesis.

I have no data whether the damage causing Type 1 diabetes can be reversed. Certainly it will take a long time for the body's normal insulin production to start up again. ..Trevor..

How much resolution of your type I diabetes you will achieve on the MP is impossible to say since this is relatively uncharted territory. You will want to follow your doctors recommendations for monitoring your blood sugar levels.

Immunopathology may reveal inflammation in delicate tissues that are commonly damaged by high blood sugar and high insulin levels. Therefore, your doctor may want to monitor your kidney function, liver enzymes and eye inflammation. He will know what tests to order. You can expect some exacerbation of inflamed tissues and may see some labwork temporarily elevated. Adjusting the MP medications to reduce the Herx reactions will keep the inflammation under control.

See BENICAR AMELIORATES INSULIN RESISTANCE

Here is good news for those who are looking for recovery from Type 1 Diabetes: Insulin cells persist in long-standing diabetes by Megan Rauscher

I have suspected that recovery was possible right from my early days studying Diabetes in the early 80s, and it is nice to see studies which confirm my suspicion ..Trevor..

We are confident that benicar, plus the 1,2 and 3 abx combos we now have available, will get all of the species, or at least enough to get a patient to 'cure.' But different folks have different species dominant, and will need slightly different abx combos as they progress through the MP.

..Trevor..

s176:

Member's with diabetes

Interview with Chris Eastlund, a long-time MPer who has now essentially recovered from diabetes, sarcoidosis, and irritable bowel syndrome thanks to the MP.

captkirk: Bree: summary of improvements: A1C, weight, hearing etc

44 years of Diabetes Debbie Y

rc45guy: Type1 Diabetes Jan89, insulin pump, improvements.

Reported lapse in Benicar blockade results in ocular hemorrhage

-I was on prednisone for two years before starting the MP. Before I was on prednisone, I had little to no retinopathy. In the timespan of those two years on prednisone, I went from little to severe.

I had a hemmorhage in my right eye about 6wks ago. I was very lax in taking my Benicar over a period of 2 days (like twice a day, 16h apart), and on the 2nd day I got the hemmorhage.

It wasn't a conscious risk, I was 4h away from the hotel and my wife didn't have her normal purse carrying it. A total mistake on my part - not making that one again!

-I am a MPer in phase 3 who is on an insulin pump and have had diabetes type 1 for 46 years. My blood sugar levels have consistently dropped on the day I take my Z and for a few days after. Several things have changed since being on the MP: I can feel my hypoglycemia more now where before MP I could not feel any signs of hypoglycemia due to longstanding diabetes, at times I have had unexplained high glucose levels for no reason other than an IP event and taking extra Benicar straightened it out, my A1C has lowered to normal when it had not been for awhile, I have had no diabetic problems with my eyes since on antibiotics and Benicar, I have had no diabetic problems with infections and or healing. Taking the antibiotics and Benicar, along with the proper diabetic diet, checking glucose levels regularly and recording them and having regular A1C levels checked, have helped my diabetes status and has allowed me to see the effects from the MP meds. ~debbie y

s175:

Tests to monitor diabetes

Please see Suggested tests to monitor your progress on the MP.

You will want to monitor serum glucose levels at home. Doc will test HbA1C periodically.

s181:

Pancreatic transplants have high failure rate

I just attended a conference on Autoimmune Clinical Research and one of the papers was on Diabetes Type 1. It was reporting failures of pancreatic transplants, as they lost the ability to generate insulin after about 7 months.

The speaker was very insistent that this was due to an unknown cause, as they specifically looked to make sure (by biopsy) that there was no organ rejection. When they showed the biopsy slides with monocytes invading the new pancreas I knew we had a winner here

The monocytes had started to infiltrate the new pancreas by about 7 months, which is a very similar time to that it takes for granuloma to start to form in lungs transplanted into Sarc patients (granuloma are 90% monocytes). Glycogen was still being accreted by the islet cells, but the insulin secretion had already shut down.

..Trevor..

s180:

Eye problems are common in diabetics

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

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

Retinopathy

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 ).

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

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).

There is no effective treatment for Diabetic Retinopathy, so I would doubt that it “could be prevented with early detection.” I would like to see real data to back up that assertion

Peripheral blood vessels are profoundly affected during Th1 disease, usually by increased vascular permeability, but I am not sure how that translates to the retina. Blood flow takes a while to return to normal, maybe 3-5 years, depending on how sick you were in the first place.

The disease mechanisms are complex, I wouldn't even venture to fully characterize them. Blood flow is a very small part of it, as the changes that influence blood flow are the critical factors.

Dr. Trevor Marshall, Ph.D

See Pubmed: a common antibiotic called minocyclineBacteriostatic antibiotic used by Marshall Protocol patients. may slow or prevent diabetic retinopathy

Members' experiences

-I am a type 1 diabetic on MP, on an insulin pump. I have had DM for 46 years. Since being on MP, I have not experienced any negative issues with my diabetes. In fact, my A1C has improved, my eyes show no signs of retinopathy and I am checked every 6 months - she even took photos of my retinas they were so perfect! ~debbie y

As was sorting through the genes transcribed by the VDRThe Vitamin D Receptor. A nuclear receptor located throughout the body that plays a key role in the innate immune response. I noticed that several of them were involved with retinal structure. I suspect the improvements in your eyes are not just due to reduced inflammation, but also increased transcription of these retinal structure proteins. ..Trevor..

Adequate eye protection is essential

See Protecting Your Eyes

-I started wearing my Bolle 100s around the house, and stayed inside until I get my 2% NoIRsSpecial sunglasses worn by Marshall Protocol patients to block light. 207s. WOW - just by wearing the Bolle's inside, the spots in my eyes went down about 80% in about 8hrs! After 4-5 days of wearing Bolle's inside, I'd say my spots are about 10%-20% of what they were (yay!). I just recv'd my 207s so now I can go outside. btw, Trevor said it was essential that I wear Bolle's inside and 2%'s outside, especially because of my retinopathy. ~rc45guy

Numerous anecdotal reports confirm the effects of increased and decreased light on the eyes of patients with Th1 inflammation.

See also:

Eye Inflammation

Eye inflammation, vision, and bacteria

Testimonials to the need to wear adequate eye protection.

Patient interviews

Chris Eastlund

diabetes, sarcoidosis, irritable bowel syndrome

Read the interview


Interviews of patients with other diseases are also available.

Read more:

Notes and comments

===== Symptoms ===== ===== Management ===== ===== Other treatments ===== ===== Tests ===== ===== Diagnosis ===== ===== Epidemiology ===== ===== Types ===== ===== Evidence of infectious cause===== ===== Role of vitamin D metabolism ===== ===== Politics ===== ===== Patient interviews ===== ===== Presentations and publications=====

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Last modified: 07.10.2010
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