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--- home:diseases:aging [11.28.2018] – [summary of Olmesartan research on aging] sallieq
+++ home:diseases:aging [09.14.2022] (current) – external edit 127.0.0.1
@@ Line 2: / Line 2: @@
 ====== Aging (senescence) ======
-<relatedarticle> [[home:protocol:olmesartan:aging|Summary of research on aging and Olmesartan]] </article>
+<relatedarticle> [[home:food:aim_health:aging|Summary of research on aging and Olmesartan]] </article>
-The biological basis of aging (also known as senescence) is the subject of debate. A number of theories suggest aging is inevitable, the product of "wear and tear" or a result of some evolutionary necessity. For example, Skulachev argues that aging performs a specific biological function, with the turnover in new members of a species promoting greater evolutionary fitness.(({{pubmed>long:9467841}})) One of the longstanding problems of such theories is that they fail to account for dramatically different lifespans, or for the fact that chronic diseases are identical in presentation to diseases of the aging. We have a lot to learn about 'diseases of the aging'.
+The biological basis of aging (also known as senescence) is the subject of debate. A number of theories suggest aging is inevitable, the product of "wear and tear" or a result of some evolutionary necessity. For example, Skulachev argues that aging performs a specific biological function, with the turnover in new members of a species promoting greater evolutionary fitness.(({{pmid>long:9467841}})) One of the longstanding problems of such theories is that they fail to account for dramatically different lifespans, or for the fact that chronic diseases are identical in presentation to diseases of the aging. We have a lot to learn about 'diseases of the aging'.
  [[https://immunityageing.biomedcentral.com/articles/10.1186/1742-4933-3-12/comments|Recovery from some of the diseases of aging]]
-Health of the hypothalamus may be a controlling factor as demonstrated in a mouse study by Yalin Zhang et al <blockquote> Mechanistically, hypothalamic stem/progenitor cells contributed greatly to exosomal microRNAs (miRNAs) in the cerebrospinal fluid, and these exosomal miRNAs declined during ageing, whereas central treatment with healthy hypothalamic stem/progenitor cell-secreted exosomes led to the slowing of ageing.  [[http://www.nature.com/nature/journal/vaop/ncurrent/full/nature23282.html|Hypothalamic stem cells control ageing speed partly through exosomal miRNAs]]
+Inflammation, But Not Telomere Length, Predicts Successful Ageing at Extreme Old Age: A Longitudinal Study of Semi-supercentenarians.    (({{pmid>long:26629551}}))
+Health of the hypothalamus may be a controlling factor as demonstrated in a mouse study by Yalin Zhang et al <blockquote> Mechanistically, hypothalamic stem/progenitor cells contributed greatly to exosomal microRNAs (miRNAs) in the cerebrospinal fluid, and these exosomal miRNAs declined during ageing, whereas central treatment with healthy hypothalamic stem/progenitor cell-secreted exosomes led to the slowing of ageing.  [[https://www.nature.com/nature/journal/vaop/ncurrent/full/nature23282.html|Hypothalamic stem cells control ageing speed partly through exosomal miRNAs]]
 </blockquote>
@@ Line 32: / Line 34: @@
   * **Cellular theory** – According to this theory, the normal body has a finite potential to replicate and maintain functional capacity (Hayflick limit).
+==== Breaking up defunct cells ====
+[[https://www.ebiomedicine.com/article/S2352-3964(18)30629-7/fulltext|Article in Press
+Senolytics in idiopathic pulmonary fibrosis]]
+<blockquote>
+ Selectively ablating senescent cells using dasatinib plus quercetin (DQ) alleviates IPF-related dysfunction in bleomycin-administered mice.
+Our first-in-humans open-label pilot supports study feasibility and provides initial evidence that senolytics may alleviate physical dysfunction in IPF  (({{pmid>long:30616998}})).</blockquote>
 ===== Diseases of the aging are chronic diseases =====
@@ Line 46: / Line 55: @@
 <blockquote>Aging is a super-category. We’ve gradually lumped together more and more symptoms under the category of natural aging. Many of these symptoms are the same as those caused by diseases that surely have an infectious cause. In that sense, you could view much of what we now call aging as an incapacitating illness that leads to a decrease in function. We know that inflammation and the interaction of the immune system with pathogens can destroy tissue. So it’s not surprising that the tissues of a person who harbors a lot of pathogens would age earlier and alter their biological structure earlier in life. I do believe it is inevitable that people will eventually die of old age, but I suspect that this should generally happen when they are 80-100 years old. But we are increasingly seeing signs of aging-related diseases in people who are much younger.
-//**Paul Ewald**, [[http://bacteriality.com/2008/02/11/ewald/|Bacteriality interview]]//</blockquote>
+//**Paul Ewald**, [[https://bacteriality.com/2008/02/11/ewald/|Bacteriality interview]]//</blockquote>
@@ Line 52: / Line 61: @@
 ===== Infection and decline in immune function =====
-A typical feature of aging is a chronic, low-grade inflammation characterized by a general increase in the production of pro-inflammatory cytokines and inflammatory markers.(({{pubmed>long:20388071}})) There is even a term for it: inflammaging. According to Franchesci: "A large part of the aging phenotype, including immunosenescence, is explained by an imbalance between inflammatory and anti-inflammatory networks, which results in the low grade chronic pro-inflammatory status we proposed to call inflammaging."(({{pubmed>long:17116321}}))
+A typical feature of aging is a chronic, low-grade inflammation characterized by a general increase in the production of pro-inflammatory cytokines and inflammatory markers.(({{pmid>long:20388071}})) There is even a term for it: inflammaging. According to Franchesci: "A large part of the aging phenotype, including immunosenescence, is explained by an imbalance between inflammatory and anti-inflammatory networks, which results in the low grade chronic pro-inflammatory status we proposed to call inflammaging."(({{pmid>long:17116321}}))
+Aging deeply affects (or is affected by!) the human microbiota's homeostasis with the host's immune system:(({{pmid>long: 20498852}})) (({{pmid>long:22283774}}))
+  * **autoimmune** – As people age, their risk for developing an "autoimmune" condition also increases.(({{pmid>long:1822969}})) The article on [[home:alternate:autoimmunity|autoimmune conditions]] discusses why so-called “autoantibodies” are merely antibodies generated in response to pathogenic bacterial cells that have been destroyed as a result of an active immune response.
+  * **macrophage function** – Macrophages, which act as "pathogen sensors", lose the ability to initiate an inflammatory response as people age.(({{pmid>long:15268749}})) Microbes use a variety of methods to infect macrophages. For example, //Neisseria meningitidis// prevents macrophage apoptosis via genes encoding nitric oxide detoxification and a porin, PorB.(({{pmid>long:16369030}}))
+<blockquote>This theory is based on the fact that genes affecting host organism longevity are represented by subpopulations: genes of host eukaryotic cells, commensal microbiota, and non-living genetic elements. ........... we propose that lifespan and aging are defined by the accumulation of alterations over all genes of macroorganism and microbiome and the non-living genetic elements associated with them. (({{pmid>long:29978435}}))  </blockquote>
-Aging deeply affects (or is affected by!) the human microbiota's homeostasis with the host's immune system:(({{pubmed>long: 20498852}})) (({{pubmed>long:22283774}}))
-  * **macrophage function** – Macrophages, which act as "pathogen sensors", lose the ability to initiate an inflammatory response as people age.(({{pubmed>long:15268749}})) Microbes use a variety of methods to infect macrophages. For example, //Neisseria meningitidis// prevents macrophage apoptosis via genes encoding nitric oxide detoxification and a porin, PorB.(({{pubmed>long:16369030}}))
-  * **autoimmune** – As people age, their risk for developing an "autoimmune" condition also increases.(({{pubmed>long:1822969}})) The article on [[home:alternate:autoimmunity|autoimmune conditions]] discusses why so-called “autoantibodies” are merely antibodies generated in response to pathogenic bacterial cells that have been destroyed as a result of an active immune response.
 Could the chronic inflammation associated with aging be caused by pathogens? Given the crudeness of tools now used to measure microbes and the ubiquity of the human microbiota, this seems like a reasonable if not inevitable conclusion as the early studies have begun to suggest.
-<blockquote>At present, a study on gut microbiota composition shows that three main modifications occur in faecal microbiota from old frail subjects: a 26-fold reduction in the number of lactobacilli (which stimulate immune functions and help the nutrient absorption), a 3-fold reduction in the number of bacteriodes (which digest polysaccarides, some species are opportunist pathogens) and a 7-fold increase in the number of enterobacteriacee (potentially pathogens)(({{pubmed>long:16204576}})). Differences in faecal microbiota were also found in a study on people of different countries and ages, including aged and long-lived people(({{pubmed>long:16461645}})).
+<blockquote>At present, a study on gut microbiota composition shows that three main modifications occur in faecal microbiota from old frail subjects: a 26-fold reduction in the number of lactobacilli (which stimulate immune functions and help the nutrient absorption), a 3-fold reduction in the number of bacteriodes (which digest polysaccarides, some species are opportunist pathogens) and a 7-fold increase in the number of enterobacteriacee (potentially pathogens)(({{pmid>long:16204576}})). Differences in faecal microbiota were also found in a study on people of different countries and ages, including aged and long-lived people(({{pmid>long:16461645}})).
+//**E. Cevenini**//(({{pmid>long:20388071}}))</blockquote>
-//**E. Cevenini**//(({{pubmed>long:20388071}}))</blockquote>
@@ Line 71: / Line 87: @@
+===== Research into effects of Olmesartan =====
+[[home:food:aim_health:aging|Protective effects of Olmesartan]]
 ===== Role of vitamin D metabolism =====
@@ Line 80: / Line 99: @@
 <blockquote>Overall, VDR KO mice showed several aging related phenotypes, including poorer survival, early alopecia, thickened skin, enlarged sebaceous glands and development of epidermal cysts.... Unlike the wildtype controls, VDR KO mice lose their ability to swim after 6 months of age. Expression of all the genes was lower in old VDR KO mice, but only NF-kappaB, Fgf-23, p53 and IGF1R were significantly lower. Since the phenotype of aged VDR knockout mice is similar to mouse models with hypervitaminosis D(3), our study suggests that VDR genetic ablation promotes premature aging in mice, and that vitamin D(3) homeostasis regulates physiological aging.
-//**T. Keisala** et al.//(({{pubmed>long:19500727}}))</blockquote>
+//**T. Keisala** et al.//(({{pmid>long:19500727}}))</blockquote>
-  * **Vitamin D restriction reduces signs of aging in certain mice** – The Klotho-insufficient (klotho) mouse exhibits a syndrome that resembles human aging including retarded growth, osteoporosis, atherosclerosis, ectopic calcification, immunological deficiency, skin and general organ atrophy, hypogonadism and short lifespan.(({{pubmed>long:19444937}})) This syndrome is mitigated – in one researcher's words, "rescued" – when mice have their vitamin D restricted.(({{pubmed>long:21276773}})) Interestingly, while murine research is a mainstay of the community of researchers and patients interested in longevity, this line of research has not led for calls to restrict vitamin D in the name of health.
+  * **Vitamin D restriction reduces signs of aging in certain mice** – The Klotho-insufficient (klotho) mouse exhibits a syndrome that resembles human aging including retarded growth, osteoporosis, atherosclerosis, ectopic calcification, immunological deficiency, skin and general organ atrophy, hypogonadism and short lifespan.(({{pmid>long:19444937}})) This syndrome is mitigated – in one researcher's words, "rescued" – when mice have their vitamin D restricted.(({{pmid>long:21276773}})) Interestingly, while murine research is a mainstay of the community of researchers and patients interested in longevity, this line of research has not led for calls to restrict vitamin D in the name of health.
 ===== Falls and Fractures =====
@@ Line 112: / Line 131: @@
+===== Recent research =====
-===== Read more =====
+Cell membranes are primarily made up of two types of lipids — phospholipids and glycolipids. Inside cells, these lipids bind to a molecule called CD1d that transports them to the surface. Once there, phospholipids stimulate phospholipid-reactive T cells, and glycolipids stimulate a different type of T cell called iNKTs.
-  * **Declining testosterone levels in men not part of normal aging, study finds** – A [[http://www.eurekalert.org/pub_releases/2012-06/tes-dtl062212.php|2012 study]] found that declining testosterone levels are not an inevitable part of the aging process, as many people think. Men who had declines in testosterone were more likely to be those who became obese, had stopped smoking or were depressed at either clinic visit.
+On their way to the cell’s surface, phospholipids more easily attach themselves to CD1d molecules, making it more difficult for glycolipids to attach to CD1d. Because of this, it is harder for glycolipids to make it to the surface of the cell. This means that iNKTs cannot be as easily stimulated by glycolipids.
+Scientists believe iNKT cells are necessary because they appear to protect cells against the progression of certain cancers and autoimmune diseases. However, iNKT cells are extremely active and can cause alcoholic hepatitis or other types of liver diseases if they are overstimulated. The phospholipid’s ability to more easily bind to CD1d molecules than glycolipids keeps a balance between the two cell types and maintains homeostasis in the immune system.   (({{pmid>long:30508304}}))
+===== Read more =====
-==== summary of Olmesartan research on aging ====
+  * **Declining testosterone levels in men not part of normal aging, study finds** – A [[https://www.eurekalert.org/pub_releases/2012-06/tes-dtl062212.php|2012 study]] found that declining testosterone levels are not an inevitable part of the aging process, as many people think. Men who had declines in testosterone were more likely to be those who became obese, had stopped smoking or were depressed at either clinic visit.
+  * [[https://immunityageing.biomedcentral.com/articles/10.1186/1742-4933-3-12/comments|We have a lot to learn about 'diseases of the aging']]
-[[home:food:aim_health:aging|Geriatric protective effects of Olmesartan]]
-=== Examples of some of the documented protective effects of ARBs ===
- include the ability to:
-  * decrease the incidence and progression of  Alzheimer's disease and dementia  9)
-  * prevent migraines10)
-  * inhibit liver fibrosis and aid liver healing11)
-  * reduce insulin resistance in rats12)
-  * protect the mitochondria from age-associated damage from oxidation13)
-  * reduce liver fibrosis14)
-  * treatment of anxiety and stress-related disorders15)
-  * reduce oxidative damage16) and limit aging 17) 18).
-)
-Use of angiotensin receptor blockers and risk of dementia in a predominantly male population: prospective cohort analysis.
-Li NC, Lee A, Whitmer RA, Kivipelto M, Lawler E, Kazis LE, Wolozin B
-BMJ340pb5465(2010 Jan 12)
-)
-Prophylactic treatment of migraine with an angiotensin II receptor blocker: a randomized controlled trial.
-Tronvik E, Stovner LJ, Helde G, Sand T, Bovim G
-JAMA289p65-9(2003 Jan 1)
-)
-An angiotensin II type 1 receptor antagonist, olmesartan medoxomil, improves experimental liver fibrosis by suppression of proliferation and collagen synthesis in activated hepatic stellate cells.
-Kurikawa N, Suga M, Kuroda S, Yamada K, Ishikawa H
-Br J Pharmacol139p1085-94(2003 Jul)
-)
-Olmesartan medoxomil, an angiotensin II receptor blocker ameliorates insulin resistance and decreases triglyceride production in fructose-fed rats.
-Okada K, Hirano T, Ran J, Adachi M
-Hypertens Res27p293-9(2004 Apr)
-)
-Enalapril and losartan attenuate mitochondrial dysfunction in aged rats.
-de Cavanagh EM, Piotrkowski B, Basso N, Stella I, Inserra F, Ferder L, Fraga CG
-FASEB J17p1096-8(2003 Jun)
-)
-Angiotensin II activates I kappaB kinase phosphorylation of RelA at Ser 536 to promote myofibroblast survival and liver fibrosis.
-Oakley F, Teoh V, Ching-A-Sue G, Bataller R, Colmenero J, Jonsson JR, Eliopoulos AG, Watson MR, Manas D, Mann DA
-Gastroenterology136p2334-2344.e1(2009 Jun)
-)
-Anti-stress and anti-anxiety effects of centrally acting angiotensin II AT1 receptor antagonists.
-Saavedra JM, Ando H, Armando I, Baiardi G, Bregonzio C, Juorio A, Macova M
-Regul Pept128p227-38(2005 Jun 30)
-)
-Effect of olmesartan on oxidative stress in hypertensive patients: mechanistic support to clinical trials derived evidence.
-Cal LA, Maso LD, Caielli P, Pagnin E, Fusaro M, Davis PA, Pessina AC
-Blood Press20p376-82(2011 Dec)
-)
-Angiotensin receptors as determinants of life span.
-Cassis P, Conti S, Remuzzi G, Benigni A
-Pflugers Arch459p325-32(2010 Jan)
-)
-Role of renin-angiotensin system in inflammation, immunity and aging.
-Capettini LS, Montecucco F, Mach F, Stergiopulos N, Santos RA, da Silva RF
-Curr Pharm Des18p963-70(2012)
-)
-Optimal therapeutic strategy for treating patients with hypertension and atherosclerosis: focus on olmesartan medoxomil.
-Mason RP
-Vasc Health Risk Manag7p405-16(2011)
-== Olmesartan and other ARBs have been used ==
- to block various bad effects of Angiotensin II, including heart failure. In this regard, olmesartan has been shown to:
-  * protect the heart from damage from inflammation in myocarditis20)
-  * ameliorate acute experimental autoimmune myocarditis, in rats, suppressing cytotoxic myocardial injury 21)
-  * prevent acute left ventricular dysfunction22)
-  * lower C-reactive protein, one of the acute phase proteins that increase during systemic inflammation23)
-  * act as an antiarrhythmic24)
-  * block the production of Angiotensin II, thus improving mortality rates in heart failure patients25)
-)
-Effect of the angiotensin II receptor blocker olmesartan on the development of murine acute myocarditis caused by coxsackievirus B3.
-Seko Y
-Clin Sci (Lond)110p379-86(2006 Mar)
-)
-Olmesartan, a novel AT1 antagonist, suppresses cytotoxic myocardial injury in autoimmune heart failure.
-Yuan Z, Nimata M, Okabe TA, Shioji K, Hasegawa K, Kita T, Kishimoto C
-Am J Physiol Heart Circ Physiol289pH1147-52(2005 Sep)
-)
-Unequal effects of renin-angiotensin system inhibitors in acute cardiac dysfunction induced by isoproterenol.
-Ohta T, Hasebe N, Tsuji S, Izawa K, Jin YT, Kido S, Natori S, Sato M, Kikuchi K
-Am J Physiol Heart Circ Physiol287pH2914-21(2004 Dec)
-)
-C-reactive protein (CRP)-lowering agents.
-Prasad K
-Cardiovasc Drug Rev24p33-50(2006 Spring)
-)
-Targeting the renin-angiotensin-aldosterone system in atrial fibrillation: from pathophysiology to clinical trials.
-Boos CJ, Lip GY
-J Hum Hypertens19p855-9(2005 Nov)
-)
-Angiotensin II in the failing heart. Short communication.
-Schulz R, Heusch G
-Kidney Blood Press Res28p349-52(2005)
-)
-Angiotensin-converting-enzyme inhibition in stable coronary artery disease.
-Braunwald E, Domanski MJ, Fowler SE, Geller NL, Gersh BJ, Hsia J, Pfeffer MA, Rice MM, Rosenberg YD, Rouleau JL
-N Engl J Med351p2058-68(2004 Nov 11)
-)
-Systematic review: comparative effectiveness of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers for treating essential hypertension.
-Matchar DB, McCrory DC, Orlando LA, Patel MR, Patel UD, Patwardhan MB, Powers B, Samsa GP, Gray RN
-Ann Intern Med148p16-29(2008 Jan 1)
-In August 2002, Trevor Marshall and Frances  Marshall published a NetPrint about valsartan (Diovan), in which they reported that the once daily dosing of the ARB caused psychedelic dreams and psychotic events in two sarcoidosis patients. On the theory that these symptoms were caused by changes in plasma concentration, the frequency of the dosing of ARB was increased, which ended up reducing symptoms of disease including psychedelic dreams. This early insight into ARBs anti-inflammatory effects led Marshall to conclude that for an ARB to provide symptomatic relief, it was necessary to use more frequent dosing than typical. Professor Marshall would later go on to recommend frequent dosing of another ARB, olmesartan.
-== Olmesartan has also been shown to ==
-  * prevent or delay left ventricular remodeling and hypertrophy in patients with type 2 diabetes 29)
-  * reduce the volume of atherosclerotic plaques30) 31)
-  * mildly reduce the risk of stroke in people at high risk for strokes (cerebrovascular events).32)
-  * significantly remodel and destiffen the arterial wall material during long-term treatment 33).
-Prevention of electrocardiographic left ventricular remodeling by the angiotensin receptor blocker olmesartan in patients with type 2 diabetes.
-Raff U, Ott C, Ruilope LM, Menne J, Haller H, Schmieder RE
-J Hypertens32p2267-76; discussion 2276(2014 Nov)
-)
-Carotid intima-media thickness and plaque volume changes following 2-year angiotensin II-receptor blockade. The Multicentre Olmesartan atherosclerosis Regression Evaluation (MORE) study.
-Stumpe KO, Agabiti-Rosei E, Zielinski T, Schremmer D, Scholze J, Laeis P, Schwandt P, Ludwig M
-Ther Adv Cardiovasc Dis1p97-106(2007 Dec)
-)
-Impact of olmesartan on progression of coronary atherosclerosis a serial volumetric intravascular ultrasound analysis from the OLIVUS (impact of OLmesarten on progression of coronary atherosclerosis: evaluation by intravascular ultrasound) trial.
-Hirohata A, Yamamoto K, Miyoshi T, Hatanaka K, Hirohata S, Yamawaki H, Komatsubara I, Murakami M, Hirose E, Sato S, Ohkawa K, Ishizawa M, Yamaji H, Kawamura H, Kusachi S, Murakami T, Hina K, Ohe T
-J Am Coll Cardiol55p976-82(2010 Mar 9)
-)
-A systematic review of angiotensin receptor blockers in preventing stroke.
-Lu GC, Cheng JW, Zhu KM, Ma XJ, Shen FM, Su DF
-Stroke40p3876-8(2009 Dec)
-)
-Dose-dependent arterial destiffening and inward remodeling after olmesartan in hypertensives with metabolic syndrome.
-Laurent S, Boutouyrie P
-Hypertension64p709-16(2014 Oct)
-== A number of studies have found ==
- that olmesartan and other ARBs possess various ways of protecting the kidneys from the effects of inflammation and cytokine damage.
-  * in circadian rhythms between HR and MAP in CKD. Synchronization between the two rhythms was progressively lost as renal function deteriorated, and Olmesartan partly restored the synchronization 34)
-  * in hypertensive patients with CKD, olmesartan add-on therapy improves the ambulatory BP profile via a preferential reduction in nighttime BP with concomitant renal injury inhibition 35)
-  * results suggest olmesartan can help decrease plasma AGE levels in patients on HD 36)
-  * renal protective effects of olmesartan may be better than those of other ARBs 37)
-  * olmesartan may uniquely increase urinary ACE2 level, which could offer additional renoprotective effects 38)
-)
-Angiotensin receptor blockers regulate the synchronization of circadian rhythms in heart rate and blood pressure.
-Sato R, Mizuno M, Miura T, Kato Y, Watanabe S, Fuwa D, Ogiyama Y, Tomonari T, Ota K, Ichikawa T, Shirasawa Y, Ito A, Yoshida A, Fukuda M, Kimura G
-J Hypertens31p1233-8(2013 Jun)
-)
-The angiotensin II type 1 receptor blocker olmesartan preferentially improves nocturnal hypertension and proteinuria in chronic kidney disease.
-Yanagi M, Tamura K, Fujikawa T, Wakui H, Kanaoka T, Ohsawa M, Azushima K, Maeda A, Kobori H, Umemura S
-Hypertens Res36p262-9(2013 Mar)
-)
-Olmesartan medoxomil is associated with decreased plasma AGEs, pentosidine, and N-(epsilon)-carboxymethyl-lysine levels in hemodialysis patients.
-Honda H, Hosaka N, Aoshima Y, Hirai Y, Michihata T, Akizawa T
-Clin Exp Hypertens34p17-23(2012)
-)
-A possible role of antihypertensive polar renomedullary lipid (APRL) and prostaglandin E2 in the kidney in the antihypertensive action of pindolol.
-Matsudaira T, Kogo H, Satoh T
-Res Commun Chem Pathol Pharmacol49p65-9(1985 Jul)
-)
-Urinary angiotensin-converting enzyme 2 in hypertensive patients may be increased by olmesartan, an angiotensin II receptor blocker.
-Furuhashi M, Moniwa N, Mita T, Fuseya T, Ishimura S, Ohno K, Shibata S, Tanaka M, Watanabe Y, Akasaka H, Ohnishi H, Yoshida H, Takizawa H, Saitoh S, Ura N, Shimamoto K, Miura T
-Am J Hypertens28p15-21(2015 Jan)
-== Recent studies showed ==
-  * treatment with olmesartan inhibited bone loss 39)
-  * olmesartan protects endothelial cells against oxidative stress-mediated cellular injury 40)
-  * carotid IMT and BP decreased similarly with olmesartan and atenolol, but only olmesartan reduced the volume of larger atherosclerotic plaques 41)
-  * improvement of Plasma Biomarkers after switching stroke patients from other Angiotensin II Type I Receptor Blockers to Olmesartan 42)
-  * improvement of glycemic control & insulin resistance was only observed in olmesartan group 43)
-  * OLM substantially delayed the development of left ventricular remodeling in type 2 diabetes 44)
-  * prevention of microalbuminuria in patients with type 2 diabetes and hypertension 45).
-data suggest 40 & 80 mg olmesartan are able to significantly remodel & destiffen the arterial wall material during long-term treatment, partly independently of blood pressure, compared with 20 mg.
-[ https://hyper.ahajournals.org/content/early/2014/07/07/HYPERTENSIONAHA.114.03282.reprint ]
-)
-Effect of angiotensin II receptor blocker, olmesartan, on turnover of bone metabolism in bedridden elderly hypertensive women with disuse syndrome.
-Aoki M, Kawahata H, Sotobayashi D, Yu H, Moriguchi A, Nakagami H, Ogihara T, Morishita R
-Geriatr Gerontol Int15p1064-72(2015 Aug)
-)
-Olmesartan protects endothelial cells against oxidative stress-mediated cellular injury.
-Kadowaki D, Anraku M, Sakaya M, Hirata S, Maruyama T, Otagiri M
-Clin Exp Nephrol19p1007-14(2015 Dec)
-)
-Improvement of Plasma Biomarkers after Switching Stroke Patients from Other Angiotensin II Type I Receptor Blockers to Olmesartan.
-Tada Y, Yagi K, Uno M, Matsushita N, Kanematsu Y, Kuwayama K, Shimada K, Nishi K, Hirasawa M, Satomi J, Kitazato KT, Kageji T, Matsuura E, Nagahiro S
-J Stroke Cerebrovasc Dis24p1487-92(2015 Jul)
-)
-Antihypertensive and metabolic effects of high-dose olmesartan and telmisartan in type 2 diabetes patients with hypertension.
-Arao T, Okada Y, Mori H, Nishida K, Tanaka Y
-Endocr J60p563-70(2013)
-)
-Prevention of microalbuminuria in patients with type 2 diabetes and hypertension.
-Menne J, Izzo JL Jr, Ito S, Januszewicz A, Katayama S, Chatzykirkou C, Mimran A, Rabelink TJ, Ritz E, Ruilope LM, Rump LC, Viberti G, Haller H
-J Hypertens30p811-8; discussion 818(2012 Apr)
-)
-Porphyria cutanea tarda induced by olmesartan.
-Mas-Vidal A, Coto-Segura P, García-Varona A, Santos-Juanes J
-J Eur Acad Dermatol Venereol24p977-8(2010 Aug)
-)
-Angiotensin-II behaves as an endogenous pro-inflammatory molecule.
-Das UN
-J Assoc Physicians India53p472-6(2005 May)
 {{tag>diseases}}
+<nodisp>
 ===== Notes and comments =====
+//Lee// " I am 70 now (not 65) when we started this conversation ...lolDr's were amazed that I was in such good shape and all fractures were closed and healed well. I would like to say I may not bicycle ride now ..but it's a family thing and I probably will "
+  (({{pmid>long:000}}))
 <DiseaseHierarchy>
-  * [[http://www.marshallprotocol.com/forum37/10103.html]] s259
+  * [[https://www.marshallprotocol.com/forum37/10103.html]] s259
-  * [[http://www.marshallprotocol.com/view_topic.php?id=9759&forum_id=37&jump_to=126260#p126260]] s263
+  * [[https://www.marshallprotocol.com/view_topic.php?id=9759&forum_id=37&jump_to=126260#p126260]] s263
@@ Line 409: / Line 190: @@
 <blockquote> As far as I can see, Th1 pathogens start to dictate the 'health' of just about everyone as they age. If you draw a graph of 25-D levels vs age, they drop steadily after age 40. Something is happening, even during 'healthy aging', that we really ought to understand a little more :)
-There is a branch of medicine which is starting to look at Immunity and Aging. Here is a short letter I recently wrote to the editor of one of the journals: [[http://www.immunityageing.com/content/3/1/12/comments]]
+There is a branch of medicine which is starting to look at Immunity and Aging. Here is a short letter I recently wrote to the editor of one of the journals: [[https://www.immunityageing.com/content/3/1/12/comments]]
 //**Trevor Marshall, PhD**// </blockquote>
@@ Line 418: / Line 199: @@
 {{ :home:pathogenesis:cawthon3.gif|Association of telomere length with mortality}}
-Cawthorn et al examined the [[http://en.wikipedia.org/wiki/Telomere|telomeres]] of 143 people over the age of 60.(({{pubmed>long:12573379}})) Telomeres are DNA sequences on the ends of chromosomes that are gradually lost as cells replicate. The team found that those with shorter telomeres in blood DNA had significantly poorer survival, attributable in part to a 3.18-fold higher mortality rate from heart disease and, tellingly, a 8.54-fold higher mortality rate from infectious disease.
+Cawthorn et al examined the [[https://en.wikipedia.org/wiki/Telomere|telomeres]] of 143 people over the age of 60.(({{pmid>long:12573379}})) Telomeres are DNA sequences on the ends of chromosomes that are gradually lost as cells replicate. The team found that those with shorter telomeres in blood DNA had significantly poorer survival, attributable in part to a 3.18-fold higher mortality rate from heart disease and, tellingly, a 8.54-fold higher mortality rate from infectious disease.
 A number of the sickest patients on the Marshall Protocol, who are killing intracellular bacteria at the fastest rate possible, take over three years to completely recover their health. This hints at the large amount of pathogen-altered DNA that many people, even those who are not yet displaying the hallmarks of Th1 disease, are carrying.
-Study shows that most older adults have signs of brain damage [[http://bacteriality.com/2008/01/04/brain/]]
+Study shows that most older adults have signs of brain damage [[https://bacteriality.com/2008/01/04/brain/]]
@@ Line 431: / Line 212: @@
 People who haven’t completed the MP consider it inevitable that as they age, they will need to stock up on any number of medications including thyroid medications, cardiac meds, statins, NSAIDS, B/P meds, etc. But people who have reached the later stages of the MP see no reason why they cannot take their level of healing to a maximum – to a point where they will never need these medications and may experience great health during their elder years.
-//**Amy Proal**, [[http://bacteriality.com/2008/02/23/misconceptions/#13|Top 14 misconceptions about the MP: addressed and explained]]//</blockquote>
+//**Amy Proal**, [[https://bacteriality.com/2008/02/23/misconceptions/#13|Top 14 misconceptions about the MP: addressed and explained]]//</blockquote>
@@ Line 457: / Line 238: @@
-<blockquote>Hypothesis: The Aging Paradox and Autoimmune Disease(({{pubmed>long:1822969}}))
+<blockquote>Hypothesis: The Aging Paradox and Autoimmune Disease(({{pmid>long:1822969}}))
 Authors: Eyal Talora; Noel R. Rosea
@@ Line 491: / Line 272: @@
 the cells is good, bad or indifferent.
-http://www.nytimes.com/2011/11/03/science/senescent-cells-hasten-aging-but-can-be-purged-mouse-study-suggests.html
+https://www.nytimes.com/2011/11/03/science/senescent-cells-hasten-aging-but-can-be-purged-mouse-study-suggests.html
 </blockquote>
-===== References =====
+===== References =====</nodisp>

home/diseases/aging.txt · Last modified: 09.14.2022 by 127.0.0.1