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  1. The longevity Live Chat is growing really fast and more and more people are connecting. Lots of detailed discussions on what is new in anti aging. Conversations about SENS, Aubrey De Grey, and many other initiatives that are getting us closer to the end goal of keeping aging under medical control. The live chat can be found here: https://discord.gg/ftSbffu It's great for us to be connected and work together. I'll keep making youtube videos on Longevity / aging, as well as help introduce people from different lines of work to each other with the end goal of hopefully speeding up the research and development of anti aging therapies. Cheers!
  2. Aubrey remains pretty skeptical of the benefits of CR in humans. http://www.planettechnews.com/interviews/ptn-interviews-dr-aubrey-de-grey-researcher-and-a-thought-leader-in-anti-aging-regenerative-medicine Here is the relevant section from this Q&A article : Q: You comment in your talks that tinkering with metabolism is not a viable approach, because it is too complicated and impossible to modify without causing "more harm than good". However, it seems a number of anti aging companies, focused on drugs and genetic engineering, seem to be pursuing this route. Can you explain this disagreement? Aubrey: Great question. The short answer is that there is one exception to my comment, but it’s an exception that doesn’t seem likely to have much practical significance for humans. The exception is calorie restriction. The drugs and other simple interventions (including genetic ones) that companies are looking at are almost all focused on making the body behave as if it is in a famine. The motivation, of course, is that famine (and these drugs) can greatly postpone aging in short-lived laboratory organisms like mice, rats and (even more so) worms. But it turns out - and for very obvious evolutionary reasons - that this doesn’t work nearly so well in long-lived species as in short-lived ones. The most that I think humans can possibly benefit by that kind of approach is a couple of years.
  3. Here is something technical I've been wondering about for a while now. I'm hoping one of the resident experts on science of aging (Michael, James, Brian?) can help to clarify it for me. Back in the old days, about a decade ago, it seems from my recollection that there was a distinction between the concept of "Intrinsic Aging" (IA) and the diseases of aging. IA was an inexorable process that wasn't well understood, other than that it proceeded in the background, accelerated over time (maybe leveling off at some extreme age), and eventually and almost inevitably leads to one or more of the diseases of aging, which are almost always what kills a person. People almost never die of "old age" per se, but some specific cause resulting from the body's inability to indefinitely keep itself in good repair. Furthermore, under this model, certain interventions, like exercise or a healthy diet, were able to "square the mortality curve" and extend mean lifespan by preventing some of the damage associated with the diseases of aging, but they couldn't slow down the underlying IA process itself, and so couldn't extend "maximum lifespan" - which I understood to be something like the age an organism could reach if it wasn't killed off prematurely by a disease of aging. But there was one intervention that was known to be different - calorie restriction. CR, it was said, could slow the rate of IA, sometimes quantified as "mortality doubling time" and hence it was able to extend maximum lifespan, not just mean lifespan. Nothing else anyone had discovered was able to do this. Fast forward 10 years and it seems like the idea of IA isn't as popular or prevalent, at least as far as I can see. Instead, aging is described by experts like Aubrey as the accumulation of damage, which Aubrey and company have compartmentalized into the famous seven categories. As an example, one such category is the accumulation of intracellular junk, like when macrophages swallow toxic byproducts of cholesterol which they can't effectively break down, leading to their accumulation in the walls of arteries and eventually atherosclerosis, the plaques in our arteries that are responsible for heart disease. But the thing is, interventions like a healthy diet and exercise can impact the rate of accumulation of damage caused by at least some of these seven categories, including the accumulation of intracellular junk in the form of toxic cholesterol byproducts. So while exercise and a healthy diet were previously seen as completely ineffective at slowing intrinsic aging, now it seems they can positively influence at least one of (actually several of) the underlying causes of aging - the accumulation of damage from the seven categories. And so it would seem they are capable of slowing what amounts to the aging process. From this perspective, it would seem to me that exercise and a healthy diet would now have to be considered bona fide anti-aging interventions (albeit relatively narrow and therefore ultimately ineffectual ones), whereas they didn't used to be considered anti-aging interventions at all, at least by the formal definition used in the gerontology community. So am I understanding this correctly and there has been a shift in what scientists believe aging amounts to, or am I missing something? More specifically, is intrinsic aging now an outdated concept? And as a corollary, is calorie restriction just a better (although only modestly better if you ask Aubrey) anti-aging intervention than a good diet or exercise because it is more comprehensive i.e. it obviates a wider range of damage categories, a wider range of damage types within a category and the degree of damage of a given type it prevents? --Dean
  4. Here is a new 20min video interview of Aubrey de Grey on Youtube in which he covers some interesting topics, including: The self-experimentation Liz Parrish from Bioviva has done to modify expression of genes telomerase & for preventing sarcopenia. Aubrey says there some evidence these modifications could be beneficial. But both have their potential downsides as well (e.g. cancer for telomerase). He admires Parrish for her boldness, and for bringing the possibility of genetic manipulation in humans for health / longevity to the public debate. But he worries that it will be very difficult to identify any measureable benefits that might result from these interventions, since Parrish is young and healthy The newly FDA-approved study of metaformin as a potential anti-aging drug. He is skeptical of CR mimetics like metaformin, due to his skepticism that CR will have much longevity benefit in long-lived species. He applauds the effort to study aging as a disease that can be treated, as this study attempts. CRISPR-cas9 gene editing technology He sees lots of potential for this technology to facilitate the kind of health / longevity interventions his SENS Foundation is investigating He doesn't see a lot of benefits/advantages (yet) for using the other recently publicized DNA technology, DNA_Origami, for drug delivery relative to other drug delivery methods. --Dean
  5. Nickola from Singularity Webblog has a new interview with Dr. Michael Fossel, an expert on telomeres and telomerase. Quite an interesting interview. He has a new book, called the Telomerase Revolution and new company, called Telocyte, focused on extending telomerase to lengthen telomeres, and he claims, slow & reverse aging. Pretty big claims, and honestly he came across in the interview as a bit of a salesman... Unfortunately I can't seem to embed the video to start up at specific times, so I'm going to list the times of a couple interesting sections in the video, so you can jump ahead manually in the video embedded below: At 16:25 Nickola reads a single sentence summary of Fossel's "Telomere Theory of Aging" from his book. - He's basically saying that aging is a programmed result of changes in gene expression as the organism gets older, orchestrated by telomeres. When the relative length (not absolute length, he's clear to point out), of telomeres shortens, it changes which genes and especially how quickly genes get expressed, i.e. get read and translated into proteins. Without the right protein mix, bad things happen in cells, or more specifically, bad things continue to be generated, but they are no longer broken down at a fast enough rate. So they accumulate, and that is the major cause of cellular aging. So things like beta amyloid, or advanced glycation end products (AGEs), which can be broken down effectively in young animals, accumulate when telomeres get short and proteins aren't created to break them down. At 24:20 Fossel talks about why (teleologically) he thinks we age. That is, if its possible to keep the protein mix in cells "young" (via telomerase or some other method), why doesn't the body do this all the time? I was thinking he was going to say it's a tradeoff with cancer. But no, he doesn't. He says (to paraphrase) we age because the quicker a population turns over, the quicker it can adapt to a changing environment. For example, viruses that reproduce quickly can adapt very quickly via mutation. So organisms are designed to die off so that their mutated progeny can inherit the earth (or at least their parent's niche). I'm pretty dubious of this model... It doesn't seem to jibe with the "selfish gene" theory which seems pretty well established. But what do I know... At 33:40 and again at 40:30 he talks about the effectiveness (or lackthereof) of existing telomerase activator compounds, particularly astragalus. He says there is some evidence it works, but the supplements are either really expensive (like $200/mo) from reputable companies, or likely contain little astragalus if they are a lot cheaper. Josh Mitteldorf talks about telomerase and astragalus in several posts, like this one about a guy who has been taking high doses of astragalus since 2007. At 36:00 Fossel talks about the data in animals that suggests resetting telomere length can reverse aging as measured by quite a number of biomarkers. At 42:40 he talks about the potential side effects of lengthening telomeres, and specifically cancer. He makes an argument that cancer is unlikely to be significantly increased, but acknowledges there is the possibility that it would. His argument that it won't cause cancer is that extra telomerase upregulates expression of genes that repair DNA, so that will reduce cancer rate, balancing out with the extra ability for cells to divide. At 46:00 he says that's one reason they are targeting Alzheimer's Disease in their first clinical trial, because AD is a death sentence and these people are old anyway, so cancer won't have that long to proliferate and spread even if it is slightly increased by telomerase therapy. At 48:15 he talks about Liz Parrish and her "N=1" experiment with gene therapy, including telomerase activation. He understands her frustration with the slow progress of anti-aging research, but he is pretty skeptical that we'll be able to learn anything from her, because she is so young and healthy. He says she'll basically have zero credibility because of the way she's gone about it, without oversight, FDA approval, etc. He says they are going to go through the right FDA clinical trial process with their own efforts, at Telocyte. At 58:00 he talks about Aubrey and "longevity escape velocity". He says people 100 years from now will look back and identify the coming decade as the time frame when we cured aging. He says at 1:01:15 that there will be an "inflection point" that dramatically slows aging, whether you want to take the therapy or not, and whether there may be side effects or not, and that breakthrough will occur in the "next few years". He also disses Aubrey as not quite understanding the genetics involved in aging, and therefore being too conservative"by mistake", both in the timeframe for curing aging, and in the value of telomere therapy... At 1:02:00 he talks about the biotech company he started last year, Telocyte. They are planning a clinical trial to show they can "prevent and cure" Alzheimer's disease. If things go really well, he hoping to start a phase 1 clinical trial with a handful of AD patients around the end of 2016, have results 6 months later, and hopefully phase 2 trials shortly after that, if the phase 1 goes well. At 1:06:30 he talks about the clinical trial timeline in detail. At 1:10:20 he fields a question about how telomerase therapy can (or can't) deal with the other types of damage that accumulate with age. Like lipofuscin. He says "no problem", longer telomeres should do the trick. Not an entirely satisfying answer... At 1:15:40 he disses Aubrey again, as misunderstanding the relationship between senescent cells and aging. Dubious... At 1:17:40 if you look carefully he does the "finger twirl around the ear" gesture in reference to Aubrey, a gesture that is typically associated with someone being crazy, although with his words he says "Aubrey isn't thinking about the pathology [of senescent cells] well." At 1:19:50, he makes an interesting statement. He says that most people (hint - Aubrey) say that damage causes aging. He says that's backwards. Instead, aging permits damage to occur, or "aging causes damage". As we grow older, our telomeres shorten, causing changes in gene expression that results in poorer cellular repair and increased damage. Overall, as I said at the top, he comes across more as a salesman, rather than a researcher. He's very optimistic, and it would be great if he's right, and gets a chance to prove it, or be disproven, pretty soon... It seems like targeting AD might be a pretty good strategy to start with. --Dean
  6. In this Quora Q&A, Aubrey share's his perspective on calorie restriction in humans with a 20 year-old thinking about starting CR. Its really quite a sensible answer, and he mentions the CR Society! Question: If I am in my early twenties, should I bother with caloric restriction or should I sort of rely on medicine to advance enough by the time I would be old enough for it to make a difference? (Personally, I maintain an active lifestyle including regular strength training so I actually eat *a lot*.) Aubrey de Grey Answer: There is a wide spectrum of opinion within the academic biogerontology community concerning the likely benefit of CR in humans. I personally am rather pessimistic, for reasons that I set out several years ago here: http://www.ncbi.nlm.nih.gov/pubmed?term=15711074 But to answer your question directly: interventions that bring aging under genuine medical control, actually rejuvenating people rather than just slowing aging down, are still too far off for us to have any idea of exactly how far. So, no matter how young or old you are today, anything you can do to stay alive and healthy for as long as possible increases your chances of being around when those therapies do arrive. If you find it not too stressful to do CR, and you do it knowledgeably (according to the recommendations of the CR Society, for example), it probably won't hasten your aging - and if I'm wrong in my pessimism above, it might be worth doing. --Dean
  7. Whenever I've heard Aubrey de Grey speak about defeating aging, he usually seems to downplay the potential impact on society and the planet that success in his project might have, and (to his credit) points out that it shouldn't be up to us to decide whether or not future generations should live a lot longer, and risk harming the planet by doing so - it should be up to them, and it is our moral responsibility to develop the tools to give them that choice. So it was with interest that I read this new study [1], sponsored by Aubrey's SENS research foundation, and the accompanying editorial by Aubrey [2], on statistical models of just what impact defeating aging in the coming century might have on human demographics and planetary sustainability. In [2], Aubrey says policymakers need to take into account the societal impact of defeating aging as projected in [1], but seems to downplay the magnitude of the impact, saying: [The projections from [1] show that] the actual, plausible trajectory of population growth following the arrival of effective rejuvenation biotechnologies only rather modestly exceeds the ‘‘base case’’ in which such technologies are never developed... Is "modestly exceeds" the base case scenario (no curing of aging) a fair way to characterize the projected impact of effective rejuvenation technologies described in [1]? I'm not so sure, and it doesn't seem like the authors of [1] are so sure either, at least by my reading. First, here are the two scenarios the authors of [1] using in their projects, based on differing mortality rates, one is the "base case" (people continue dying at a similar rate as today for the remainder of the century) and the other is the "Negligible Senescence" scenario (NegSens) in which scientists figure out how to stop aging in the next few years and it gets deployed over the next couple decades, at which point very few people will be dying: Based on this very low rate of people dying after the year 2040, the authors predict population growth based on three different fertility rates compared with the baseline scenario. In the baseline scenario, worldwide fertility rate drops from its current level of around 2.5 children per woman averaged over the entire world to 1.9 children per woman. In the (seemingly unrealistic) high fertility scenario, women start having more children than today once aging is defeated, with the fertility rate rising to 3.0, perhaps because they are living longer and are fecund for longer as well. In the mid-fertility scenario, the fertility rate is the same as the baseline scenario, i.e. 1.9 children per woman. This seems fairly reasonable it would seem, since childbearing / childrearing is an important part of many people's lives, giving them pleasure and their life meaning. In the low fertility scenario, fertility drops to 1.0 children per woman, "due to some combination of a reduced sense of self 'replacement' and 'old-age care' needs and of societal needs to limit fertility substantially to slow the rapid population growth of the underlying scenario." This last, low-fertility scenario may happen, but I'm skeptical societal attitudes about having kids will change that quickly, to the point that couples around the world on average only have a single child. But given these four scenarios (baseline and three NegSens fertility rates), here is the graph of population growth over time: The baseline agrees with most population projects demographers are currently making - namely that the global population will asymptote at around 10 billion around mid-century and then starts gradually declining. If women seriously curtail the number of kids they have, the low fertility NegSens scenario shows population growing only gradually to around 12 billion by the turn of the century - not too dramatic. But if women continue to have nearly two kids each, population will continue growing, to around 15 billion by the turn of the century. The high fertility NegSens scenario has population growing to a whopping 20 billion by the end of the century. In the remainder of the paper the authors pretty much ignore this high fertility scenario, as unrealistic and/or too depressing... One of the most interesting projections is the impact of the various scenarios on greenhouse gases. The authors point out that it is obviously quite sensitive to the mix of energy production methods (i.e. fossil fuels vs. renewables), but the authors project that neither the low nor medium fertility rates will substantially change carbon dioxide equivalents level in the atmosphere relative to the baseline scenario, with all three resulting in a pretty substantial increase in greenhouse gases over today's level of around 400 ppm to around 600 ppm by the turn of the century, or 800 ppm if we continue to use a lot of coal and other fossil fuels in our energy production mix. Those numbers are pretty depressing, given the temperature rise and climate effects the scientists are predicting unless we reverse the trend and keep greenhouse gases well below the current level of 400 ppm... In terms of worldwide hunger, the authors predict that with better food production / distribution methods, and a stable population, the baseline scenario will result in a dramatic reduction in hunger and starvation around the world by the turn of the century. But with a growing population as a result of defeating aging, we could see a world where hunger and starvation remain a problem of similar magnitude as today, as illustrated in the graphs below: Here is the most important paragraph from the author's conclusion: Finally, our results point to perhaps the greatest challenge facing a world of negligible senescence, those relating to the sustainability of our natural resources and biosphere. Given widespread concern that our economic way of life is already unsustainable, the potential addition of billions of people would concern many, especially given that this population (in the absence of negative feedbacks from environmental constraints) would see a GDP per capita 30% above the already substantial economic growth built into our Base Case. Energy demand levels, even with quite optimistic assumptions about efficiency gains and renewable contributions, would drive atmospheric CO2 levels above 600 ppm and, if coal were more heavily drawn upon without carbon sequestration, to 800 ppm or above. In the absence of food production technologies that are currently not on the forecast horizon, it might become nearly impossible to reduce the portion of the world's population that is undernourished. So in a sense Aubrey is right - global resources would be strained by defeating aging, but given a reasonably projection of fertility changes (dropping to 1.9 kids per woman worldwide), things won't go completely off the rails, at least by the turn of the century. Of course history won't end at 2100 (hopefully!), and in this 1.9 fertility rate scenario, population will continue to climb steadily, while the planet and its resources won't be getting any bigger... Perhaps by that time Elon Musk will have succeeded and we'll be colonizing Mars, so will have a lot more room and resources for humanity to expand. But I'm not holding my breath on that one, given the challenges of making Mars habitable and getting people there en mass. We live in interesting & challenging times, and it seem like things are only going to get more interesting & challenging. My primary reason for pursuing health / life extension is so that I can be around to see how things turn out - it promises to be quite a show! --Dean ------ [1] Technological Forecasting and Social Change, Volume 99, October 2015, Pages 77–91 doi:10.1016/j.techfore.2015.06.031 Opportunities and challenges of a world with negligible senescence Barry B. Hughesa, Randall Kuhnb, Eli S. Margolese-Malina, Dale S. Rothmana, José R. Solórzanoa Free full text: http://www.sciencedirect.com/science/article/pii/S0040162515001985 Abstract The development of anti-aging technologies could have dramatic implications for a world already challenged by population aging. We explore how the world might evolve given the development and deployment of technologies capable of nearly eliminating mortality and morbidity from most causes. We consider both the great benefits and some of the complex sociopolitical rebalancing resulting from such advances. We use the International Futures (IFs) long-term, multi-issue, global forecasting system in our analysis of the interactions among demographic changes, the related changes in health costs and government finances, shifts in labor force participation, resultant economic transformations, and the environmental sustainability of the dramatically-altered human demands that emerge. We find that the widespread deployment of anti-senescence technologies would cause populations to surge—making fertility rates an issue of tremendous social import—while a much larger, healthier, labor force would spur economic growth. But this is not a given; the cost of treating entire adult populations could prove unbearable to non-high-income economies without significant transfers within and across societies. In the absence of new transformative production technologies, life-pattern financing would require the virtual elimination of retirement and a major restructuring of government finances. Pressures on the environment would also greatly intensify. --------- [2] Rejuvenation Research. October 2015, Vol. 18, No. 5: 387-388 What Will a Post-Aging World Really Be Like? Finally, A Tool to Help Us Predict de Grey Aubrey D.N.J. Full text via sci-hub.io: http://online.liebertpub.com.sci-hub.io/doi/full/10.1089/rej.2015.1786 Excerpt: ... I am gratified to say that the findings reported in this article accord very strongly with my historical intuition. The conclusions are presented in a suitably cautious manner, incorporating stern warnings of the consequences if humanity fails to anticipate the impact that the arrival of these medicines will have on demands for food, sustainable energy, and, of course, the medicines themselves. However, that is indeed the purpose for which we sponsored this work—for two reasons. First, by setting out properly evidence-based projections through to the year 2100 of a few sample scenarios of how the various regions of the world will fare and what they will experience in a post-aging world, the paper lays to rest the far more pessimistic knee-jerk assumptions so vocally expressed by so many when the topic is discussed. The actual, plausible trajectory of population growth following the arrival of effective rejuvenation biotechnologies only rather modestly exceeds the ‘‘base case’’ in which such technologies are never developed, and it is vital that opinionformers and policy-makers should understand that fact if they are to make wise decisions concerning near-term investment in the long-term future.
  8. 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
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