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  1. All, There is a new paper out [1] (popular account) that seems to me to do a pretty good job summarizing what we know about the different causes of aging. They have the same perspective as Aubrey, Michael & SENS - namely that at its root aging is a result of metabolic damage accumulation. But they appear to have a slightly different taxonomy than Aubrey's "7 deadly causes", although I'll leave it to Michael to map between the two. Here is there graphic showing the "Hallmarks of Aging": One thing that jumped out at me (and that I've highlighted above in yellow) was the role peroxisome proliferator-activated receptor-gamma coactivator 1alpha (PGC1α) appears to play in the various hallmarks of aging. In fact, a drop in PGC1α signalling is implicated in four of the nine hallmarks of aging. This interests me, because PGC1α promotes mitochondria biogenesis, and is upregulated by cold exposure [2], as we've seen many times on the cold exposure thread. Sadly, the authors don't mention cold exposure as a potential means to ameliorate the aging process. Instead they focus on CR, amino-acid restriction, CR-mimetics, time-restricted feeding, and exercise as the most promising longevity interventions. Oh well, someday the benefits of cold exposure will be more widely recognized. Overall it's an fascinating paper covering both the mechanisms of aging and (some of) the best ideas we have for what can be done about it today. --Dean ---------- [1] Cell 166, August 11, 2016 Metabolic Control of Longevity Carlos Lo´ pez-Otı´n,1,* Lorenzo Galluzzi,2,3,4,5,6,7 Jose´ M.P. Freije,1 Frank Madeo,8,9 and Guido Kroemer Free full text: http://www.cell.com/cell/pdf/S0092-8674(16)30981-3.pdf Several metabolic alterations accumulate over time along with a reduction in biological fitness, suggesting the existence of a ‘‘metabolic clock’’ that controls aging. Multiple inborn defects in metabolic circuitries accelerate aging, whereas genetic loci linked to exceptional longevity influence metabolism. Each of the nine hallmarks of aging is connected to undesirable metabolic alterations. The main features of the ‘‘westernized’’ lifestyle, including hypercaloric nutrition and sedentariness, can accelerate aging as they have detrimental metabolic consequences. Conversely, lifespan-extending maneuvers including caloric restriction impose beneficial pleiotropic effects on metabolism. The introduction of strategies that promote metabolic fitness may extend healthspan in humans. PMID: Not available DOI: http://dx.doi.org/10.1016/j.cell.2016.07.031 ------------ [2] Adv Physiol Educ. 2006 Dec;30(4):145-51. PGC-1alpha: a key regulator of energy metabolism. Liang H(1), Ward WF. Author information: (1)Department of Cellular and Structural Biology, Audie Murphy Veterans Administration Medical Center and University of Texas Health Science Center, San Antonio, Texas 78229-3900, USA. Peroxisome proliferator-activated receptor-gamma coactivator (PGC)-1alpha is a member of a family of transcription coactivators that plays a central role in the regulation of cellular energy metabolism. It is strongly induced by cold exposure, linking this environmental stimulus to adaptive thermogenesis. PGC-1alpha stimulates mitochondrial biogenesis and promotes the remodeling of muscle tissue to a fiber-type composition that is metabolically more oxidative and less glycolytic in nature, and it participates in the regulation of both carbohydrate and lipid metabolism. It is highly likely that PGC-1alpha is intimately involved in disorders such as obesity, diabetes, and cardiomyopathy. In particular, its regulatory function in lipid metabolism makes it an inviting target for pharmacological intervention in the treatment of obesity and Type 2 diabetes. DOI: 10.1152/advan.00052.2006 PMID: 17108241
  2. Since this is a forum about general health and longevity, I thought these two infographics were quite relevant, interesting, and informative. The first shows the leading causes of death in the UK, with each circle proportional to the number of people who die from each cause. The US data is similar: The next I found even more interesting. It represents the risk factors leading death, again in order of frequency. What surprised me most was how low down the list I had to look to find any that CR folks engage in or experience: We've all must die of something (at least for now), but from this list it is hard to say what is going to kill off a CR practitioner! --Dean
  3. All, I'm sometimes asked by friends and family who aren't quite as obsessive as I am about health & longevity for a few tips they might be able to adopt that might help them stay healthier longer but without "going overboard" like I do. Today I stumbled across an article that I think fits the bill really well, and that I'll point such people to in the future. It is titled 13 Habits Linked to a Long Life (Backed by Science) and it is from the website AuthorityNutrition.com, which I've never considered much of an authority on nutrition, but this article is quite good so I may have to reconsider... Here is the list: Avoid Overeating Eat Some Nuts Use The Spice Turmeric Eat Plenty of Healthy Plant Foods Exercise and Be Physically Active Don’t Smoke Keep Your Alcohol Intake Moderate Prioritize Your Happiness Avoid Chronic Stress and Anxiety Nurture Your Social Circle Increase Your Conscientiousness Drink Coffee or Tea Develop a Good Sleeping Pattern Each of the 13 is explained in clear, easy to understand language. The article describes the science to back up the recommendations, and has references for people who want to learn more. Finally, it's really brief for those with a short attention span. There are three additional items I can think of that I would add to the list: 14. Don't Sit Too Much (ref) 15. Practice Good Oral Hygiene (discussion, discussion) 16. Ask Your Doctor - Get regular medical checkups and recommended tests after age 50, or earlier if you've got risk factors (discussion) Anyone else have health and longevity "best practices" you would or do suggest to friends/family that aren't included on the list? --Dean
  4. Al posted a new study [1], that appears to me to support the theory I've been promulgating for a while that what's important for health and longevity is the quality of one's diet and lifestyle, rather than the quantity of calories one eats. The study followed over 90,000 postmenopausal women for about 13 years to see how the baseline quality of their diet (as quantified by 4 popular dietary quality metrics) impacted subsequent mortality. The dietary quality metrics were designed to gauge how well the women adhered to commonly-accepted 'good' dietary patterns, like following a Mediterranean Diet, or a DASH-like diet. All four shared much in common (emphasize fruits & vegetables, whole grains, avoid red & processed meat, etc.), and fortunately all four resulted in similar outcomes in this study, so I'll collapse all four in my brief discussion of the results below into a single notion of a "good diet". What they found was the women who had the best diet (i.e. were in the highest quintile of 'good diet' score relative to lowest quintile) had about a 20-25% lower risk of dying during the 13 year follow-up period. They also had a lower BMI (25-26 vs. 28-29) although weren't especially slim, and the exercised more than the women who ate the crappiest diet, although the researchers attempted to factor out BMI, exercise, and calories (see next point) from their statistical analysis to focus on the link between diet quality and mortality. On average the women who were eating the best diet and hence were healthier & longer-lived didn't report eating any fewer calories than the women eating the crappiest diet (although as we know food frequency questionnaires are fraught with difficulties...), they were just eating healthy foods rather than unhealthy ones. In short, this is yet one more study showing that dramatic improvements in health/longevity, on par with what we hope to achieve via CR, seem to be attainable by following a healthy obesity-avoiding diet & lifestyle, but without calorie restriction. --Dean -------- [1] Comparing indices of diet quality with chronic disease mortality risk in postmenopausal women in the Women's Health Initiative Observational Study: evidence to inform national dietary guidance. George SM, Ballard-Barbash R, Manson JE, Reedy J, Shikany JM, Subar AF, Tinker LF, Vitolins M, Neuhouser ML. Am J Epidemiol. 2014 Sep 15;180(6):616-25. doi: 10.1093/aje/kwu173. Epub 2014 Jul 17. PMID: 25035143 Free PMC Article http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4157698/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4157698/pdf/kwu173.pdf Abstract Poor diet quality is thought to be a leading risk factor for years of life lost. We examined how scores on 4 commonly used diet quality indices-the Healthy Eating Index 2010 (HEI), the Alternative Healthy Eating Index 2010 (AHEI), the Alternate Mediterranean Diet (aMED), and the Dietary Approaches to Stop Hypertension (DASH)-are related to the risks of death from all causes, cardiovascular disease (CVD), and cancer among postmenopausal women. Our prospective cohort study included 63,805 participants in the Women's Health Initiative Observational Study (from 1993-2010) who completed a food frequency questionnaire at enrollment. Cox proportional hazards models were fit using person-years as the underlying time metric. We estimated multivariate hazard ratios and 95% confidence intervals for death associated with increasing quintiles of diet quality index scores. During 12.9 years of follow-up, 5,692 deaths occurred, including 1,483 from CVD and 2,384 from cancer. Across indices and after adjustment for multiple covariates, having better diet quality (as assessed by HEI, AHEI, aMED, and DASH scores) was associated with statistically significant 18%-26% lower all-cause and CVD mortality risk. Higher HEI, aMED, and DASH (but not AHEI) scores were associated with a statistically significant 20%-23% lower risk of cancer death. These results suggest that postmenopausal women consuming a diet in line with a priori diet quality indices have a lower risk of death from chronic disease. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health 2014. This work is written by (a) US Government employee(s) and is in the public domain in the US. KEYWORDS: diet; diet quality indices; mortality risk; postmenopausal women; prospective cohort study
  5. There has been a lot of media attention over the last few days about whether cancer is caused mainly by "intrinsic factors" (i.e. "bad luck" - i.e. mutations that just happen when stem cells replicate which lead to cancer) or "extrinsic factors" (colloquially, "bad behaviors" - i.e. our lifestyle choices, like smoking, diet, exercise, etc.). The controversy stems from two recent papers, [1] and [2], both of which seem to come to conflicting conclusions. In [1], the authors looked at different organs and compared the cancer rates in those organs with the number of stem cell divisions that occur in those organs. They found a high correlation - i.e. the more stem cells have to divide to maintain an organ over a person's or animal's lifetime, the more likely it is that cancer will occur in that organ. The authors of [1] (and especially the media covering the study when it first came out earlier this year) appear to interpret this to mean that most incidents of cancer can be chalked up to 'bad luck', rather than bad lifestyle choices or other environmental factors. To quote from the abstract of [1]: These results suggest that only a third of the variation in cancer risk among tissues is attributable to environmental factors or inherited predispositions. The majority is due to "bad luck," that is, random mutations arising during DNA replication in normal, noncancerous stem cells. In what appears to be a direct response to [1], the authors of [2] did a somewhat different analysis, using epidemiological data to show that the relatively simple model to predict various cancer rates from the number of stem cell divisions doesn''t fit the data well at all. They conclude instead that 70-90% of cancer rates are a result of extrinsic factors, like exposure to carcinogens from smoking, foods, environment etc. It isn't from this paper, but here is a very interesting table from this popular press article (originally from the American Cancer Society) estimating the percentage of risk coming from extrinsic factors, and what those specific extrinsic factors are, for various types of cancer: So how to reconcile the seemingly conflicting studies? One of the authors of [2] had what I thought was a good analogy in this interview to explain the apparent discrepancy. He likened cancer to playing Russian roulette. Some organs have a high rate of stem cell division, correspond to spinning the chamber and pulling the trigger many times, while other organs require you to "take a chance" with stem cell division much less often. This represents the intrinsic difference between various organs. In this analogy, extrinsic factors (e.g. smoking, diet, lifestyle, etc.) determine the number of bullets in the gun's chamber. With more bullets in the chamber, there is a greater chance that on any one round (i.e. stem cell division), you'll get unlucky and the division will go badly, resulting in cancer. Take home message - since we can't really change the number of stem cell divisions our organs require to function and maintain themselves, it is important for cancer prevention to minimize our exposure to extrinsic factors that increase the risk of bad stem cell divisions that result in cancer, by following a healthy diet and lifestyle. --Dean ------------- [1] Science. 2015 Jan 2;347(6217):78-81. doi: 10.1126/science.1260825. Cancer etiology. Variation in cancer risk among tissues can be explained by the number of stem cell divisions. Tomasetti C(1), Vogelstein B(2). Full text via sci-hub.io: http://www.sciencemag.org.sci-hub.io/content/347/6217/78.full Some tissue types give rise to human cancers millions of times more often than other tissue types. Although this has been recognized for more than a century, it has never been explained. Here, we show that the lifetime risk of cancers of many different types is strongly correlated (0.81) with the total number of divisions of the normal self-renewing cells maintaining that tissue's homeostasis. These results suggest that only a third of the variation in cancer risk among tissues is attributable to environmental factors or inherited predispositions. The majority is due to "bad luck," that is, random mutations arising during DNA replication in normal, noncancerous stem cells. This is important not only for understanding the disease but also for designing strategies to limit the mortality it causes. PMID: 25554788 -------- [2] Nature. 2015 Dec 16. doi: 10.1038/nature16166. [Epub ahead of print] Substantial contribution of extrinsic risk factors to cancer development. Wu S(1,)(2), Powers S(1,)(2,)(3), Zhu W(1,)(2), Hannun YA(2,)(3,)(4,)(5). Free Full text: http://www.nature.com/articles/nature16166.epdf Recent research has highlighted a strong correlation between tissue-specific cancer risk and the lifetime number of tissue-specific stem-cell divisions. Whether such correlation implies a high unavoidable intrinsic cancer risk has become a key public health debate with the dissemination of the 'bad luck' hypothesis. Here we provide evidence that intrinsic risk factors contribute only modestly (less than ~10-30% of lifetime risk) to cancer development. First, we demonstrate that the correlation between stem-cell division and cancer risk does not distinguish between the effects of intrinsic and extrinsic factors. We then show that intrinsic risk is better estimated by the lower bound risk controlling for total stem-cell divisions. Finally, we show that the rates of endogenous mutation accumulation by intrinsic processes are not sufficient to account for the observed cancer risks. Collectively, we conclude that cancer risk is heavily influenced by extrinsic factors. These results are important for strategizing cancer prevention, research and public health. PMID: 26675728
  6. Dean Pomerleau

    Telomeres, Diet & Longevity

    It's not clear whether telomere shortening is a cause or a side-effect of aging, and Aubrey de Grey is concerned that direct manipulation of telomeres to make them longer (i.e. via increased expression of the telomerase enzyme) is likely to be a bad idea due to concern about allowing cancer cells to replicate more readily. But longer leukocyte telomeres do seem to be associated with longevity: study [2] found that centenarians have leukocyte telomeres as long as people who are much younger than themselves (and therefore unlikely from a statistical perspective to make it to 100), and the offspring of centenarians have longer telomeres than age and gender matched offspring of parents who died at a "normal" age. So having longer telomeres might be a sign of healthy aging (I can hear Michael Rae revving up his engines now :)). With this in mind this new study [1] (provided to me by Al Pater - thanks Al !), found that components of a person's diet was predictive of their telomere length 10 years later. From the abstract: The first factor labeled 'prudent dietary pattern' was characterized by high intake of whole grains, seafood, legumes, vegetables and seaweed, whereas the second factor labeled 'Western dietary pattern' was characterized by high intake of refined grain, red meat or processed meat and sweetened carbonated beverages. In a multiple linear regression model adjusted for age, sex, body mass index and other potential confounding variables [including from the full text - income status, smoking status, alcohol consumption status, physical activity and calorie intake, and presence of hypertension, diabetes mellitus or hypercholesterolemia], the prudent dietary pattern was positively associated with [leukocyte telomere length - LTL]. In the analysis of particular food items, higher consumption of legumes, nuts, seaweed, fruits and dairy products and lower consumption of red meat or processed meat and sweetened carbonated beverages were associated with longer LTL. So for what is may be worth (he says, expecting to be corrected and chastised by Michael :) for oversimplifying and ignoring important evidence...), eating what is considered by most to be a healthy diet may help to preserve your telomeres, and improve your chances of healthy aging. --Dean ----------- [1] Eur J Clin Nutr. 2015 Sep;69(9):1048-52. doi: 10.1038/ejcn.2015.58. Epub 2015 Apr 15. Association between dietary patterns in the remote past and telomere length. Lee JY(1), Jun NR(1), Yoon D(2), Shin C(2,)(3), Baik I(1). BACKGROUND/OBJECTIVES: There are limited data on the association between dietary information and leukocyte telomere length (LTL), which is considered an indicator of biological aging. In this study, we aimed at determining the association between dietary patterns or consumption of specific foods and LTL in Korean adults. SUBJECT/METHODS: A total of 1958 middle-aged and older Korean adults from a population-based cohort were included in the study. Dietary data were collected from a semi-quantitative food frequency questionnaire at baseline (June 2001 to January 2003). LTL was assessed using real-time PCR during the 10-year follow-up period (February 2011 to November 2012). RESULTS: We identified two major factors and generated factor scores using factor analysis. The first factor labeled 'prudent dietary pattern' was characterized by high intake of whole grains, seafood, legumes, vegetables and seaweed, whereas the second factor labeled 'Western dietary pattern' was characterized by high intake of refined grain, red meat or processed meat and sweetened carbonated beverages. In a multiple linear regression model adjusted for age, sex, body mass index and other potential confounding variables, the prudent dietary pattern was positively associated with LTL. In the analysis of particular food items, higher consumption of legumes, nuts, seaweed, fruits and dairy products and lower consumption of red meat or processed meat and sweetened carbonated beverages were associated with longer LTL. CONCLUSIONS: Our findings suggest that diet in the remote past, that is, 10 years earlier, may affect the degree of biological aging in middle-aged and older adults. PMID: 25872911 -------------------------- [2] Exp Gerontol. 2014 Oct;58:90-5. doi: 10.1016/j.exger.2014.06.018. Epub 2014 Jun 27. Leukocyte telomere length and prevalence of age-related diseases in semisupercentenarians, centenarians and centenarians' offspring. Tedone E(1), Arosio B(2), Gussago C(3), Casati M(4), Ferri E(3), Ogliari G(3), Ronchetti F(3), Porta A(3), Massariello F(3), Nicolini P(4), Mari D(2). Centenarians and their offspring are increasingly considered a useful model to study and characterize the mechanisms underlying healthy aging and longevity. The aim of this project is to compare the prevalence of age-related diseases and telomere length (TL), a marker of biological age and mortality, across five groups of subjects: semisupercentenarians (SSCENT) (105-109years old), centenarians (CENT) (100-104years old), centenarians' offspring (CO), age- and gender-matched offspring of parents who both died at an age in line with life expectancy (CT) and age- and gender-matched offspring of both non-long-lived parents (NLO). Information was collected on lifestyle, past and current diseases, medical history and medication use. SSCENT displayed a lower prevalence of acute myocardial infarction (p=0.027), angina (p=0.016) and depression (p=0.021) relative to CENT. CO appeared to be healthier compared to CT who, in turn, displayed a lower prevalence of both arrhythmia (p=0.034) and hypertension (p=0.046) than NLO, characterized by the lowest parental longevity. Interestingly, CO and SSCENT exhibited the longest (p<0.001) and the shortest (p<0.001) telomeres respectively while CENT showed no difference in TL compared to the younger CT and NLO. Our results strengthen the hypothesis that the longevity of parents may influence the health status of their offspring. Moreover, our data also suggest that both CENT and their offspring may be characterized by a better TL maintenance which, in turn, may contribute to their longevity and healthy aging. The observation that SSCENT showed considerable shorter telomeres compared to CENT may suggest a progressive impairment of TL maintenance mechanisms over the transition from centenarian to semisupercentenarian age. PMID: 24975295