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Found 8 results

  1. Dean Pomerleau

    Inspiring Oldsters

    [Admin Note: Several of these first posts are from other threads. I've collected them here on a thread devoted to "Inspiring Oldsters". --Dean] Sthira, I appreciate your advocacy for the image of centenarians, and I mean them no offense, but I think supercentenarians generally look like crap in photos because they look like crap in real life. They are suffering the ravages of the aging process, and by our hard-wired standards of physical attractiveness, these folks ain't it. Honestly, I expect the photographers are doing their best to make them look ok. But while there may not be many (any?) attractive supercentenarians, there are centenarians who still look quite good. This Pinterest channel has lots of pictures of them. But Pinterest is a PITA, blocking anyone without an account from view its pictures. So I've screen captured several of the most striking (reportedly) centenarians and linked to them below. Pretty impressive, both the individuals and the photography. --Dean
  2. All, I'm usually reluctant to post studies that try to associate single nucleotide polymorphisms (SNPs) with health or longevity outcomes. There are several reasons to be skeptical of such gene studies, including: They often fail to replicate across different populations The effects of individual SNP variations are often quite small - since there are usually many genes and polymorphisms that contribute to any important health/longevity outcome Often it's not even clear from the study what the specific allele variation(s) the authors are evaluating You often can't even find out what variant of an allele you have - since only some of us have our own genetic data and even that is only partial coverage through 23andMe. There is nothing you can do about it anyway - your genes are your genes. These polymorphisms and their effects often have nothing to do with CR. But this new meta-analysis [1] posted by Al Pater (thanks Al!) seems to suffer from none of these shortcomings. It focuses on a SNP in the FoxO3 gene (rs2802292) which has been previously associated with longevity - is it overrepresented in centenarians [2], as discussed here, and summarized as: [T]he odds ratio for reaching 100 years of age for rs2802292(G;G) vs (T;T) carriers was 2.75 (p = 0.00009; adjusted p = 0.00135). One's odds of living to 100 with one copy of 'G' for rs2802292 (i.e. G:T), appears to be about 1.5-2 times greater than people with T:T. Those results were encouraging, but didn't address causality, and was limited to a homogeneous population of men. Plus it only seemed relevant for people without other 'gotchas' (genetic or otherwise) that might kill them off long before reaching 100. What about the rest of us mortals, who may not be destined to live that long? Does having copies of the 'G' allele for rs2802292 do the rest of us any good on the way to extreme longevity? Apparently - Yes! Study [1] followed three pretty large groups of Americans with Japanese (N ≈ 3600), Caucasian (N ≈ 1600), or African (N ≈ 1000) ancestory for 17 years to assess the association between SNP rs2802292 status and mortality. Interestingly, the frequency of being a lucky 'G' Allele Carrier (GAC) for this SNP varied between the three populations - 47% of Japanese, 58% of Caucasian and 92% of African ancestry folks were GACs. Across all three populations, being a GAC was associated with a 10% reduction in all-cause mortality over the 17 year follow-up, with virtually all of the benefit resulting from a 26% reduction in heart disease mortality. Here is the most important figure from the free full text: As you can see the effect was quite consistent across the three populations. The difference in the confidence interval for the three groups was a result of the different population sizes. The cool thing is that those of us with 23andMe data can find out our status for SNP rs2802292. Simply log in to 23andMe and follow this link. I'm fortunate to be in the ~60% of caucasian people who is a 'G' carrier for this allele (I've got one copy). But for anyone who isn't lucky enough to be a GAC for this allele, there is still hope. Why? Because FoxO3 gene activity is something we know quite a bit about, including ways of boosting its activity, like the G allele for rs2802292 apparently does. Curiously, cider vinegar appears to upregulate DAF-16, the C. Elegans equivalent of FoxO3, which in turn resulted in the worms living 25% longer, as discussed here. So maybe cider vinegar is worth including in one's diet. I do. But even more relevant, we know that both CR and cold exposure increase FoxO3 gene expression largely by upregulating SIRT1, as discussed recently here. So everybody wins! --Dean ------------------ [1] The FoxO3 gene and cause-specific mortality. Willcox BJ, Tranah GJ, Chen R, Morris BJ, Masaki KH, He Q, Willcox DC, Allsopp RC, Moisyadi S, Poon LW, Rodriguez B, Newman AB, Harris TB, Cummings SR, Liu Y, Parimi N, Evans DS, Davy P, Gerschenson M, Donlon TA. Aging Cell. 2016 Apr 13. doi: 10.1111/acel.12452. [Epub ahead of print] Free Article http://onlinelibrary.wiley.com/doi/10.1111/acel.12452/full http://onlinelibrary.wiley.com/doi/10.1111/acel.12452/pdf Abstract The G allele of the FOXO3 single nucleotide polymorphism (SNP) rs2802292 exhibits a consistently replicated genetic association with longevity in multiple populations worldwide. The aims of this study were to quantify the mortality risk for the longevity-associated genotype and to discover the particular cause(s) of death associated with this allele in older Americans of diverse ancestry. It involved a 17-year prospective cohort study of 3584 older American men of Japanese ancestry from the Honolulu Heart Program cohort, followed by a 17-year prospective replication study of 1595 white and 1056 black elderly individuals from the Health Aging and Body Composition cohort. The relation between FOXO3 genotype and cause-specific mortality was ascertained for major causes of death including coronary heart disease (CHD), cancer, and stroke. Age-adjusted and multivariable Cox proportional hazards models were used to compute hazard ratios (HRs) for all-cause and cause-specific mortality. We found G allele carriers had a combined (Japanese, white, and black populations) risk reduction of 10% for total (all-cause) mortality (HR = 0.90; 95% CI, 0.84-0.95; P = 0.001). This effect size was consistent across populations and mostly contributed by 26% lower risk for CHD death (HR = 0.74; 95% CI, 0.64-0.86; P = 0.00004). No other causes of death made a significant contribution to the survival advantage for G allele carriers. In conclusion, at older age, there is a large risk reduction in mortality for G allele carriers, mostly due to lower CHD mortality. The findings support further research on FOXO3 and FoxO3 protein as potential targets for therapeutic intervention in aging-related diseases, particularly cardiovascular disease. KEYWORDS: FOXO3; heart disease; longevity; mortality PMID: 27071935 -------------- [2] Proc Natl Acad Sci U S A. 2008 Sep 16;105(37):13987-92. doi: 10.1073/pnas.0801030105. Epub 2008 Sep 2. FOXO3A genotype is strongly associated with human longevity. Willcox BJ(1), Donlon TA, He Q, Chen R, Grove JS, Yano K, Masaki KH, Willcox DC, Rodriguez B, Curb JD. Author information: (1)Pacific Health Research Institute, 846 South Hotel Street, Honolulu, HI 96813, USA. bjwillcox@phrihawaii.org Human longevity is a complex phenotype with a significant familial component, yet little is known about its genetic antecedents. Increasing evidence from animal models suggests that the insulin/IGF-1 signaling (IIS) pathway is an important, evolutionarily conserved biological pathway that influences aging and longevity. However, to date human data have been scarce. Studies have been hampered by small sample sizes, lack of precise phenotyping, and population stratification, among other challenges. Therefore, to more precisely assess potential genetic contributions to human longevity from genes linked to IIS signaling, we chose a large, homogeneous, long-lived population of men well-characterized for aging phenotypes, and we performed a nested-case control study of 5 candidate longevity genes. Genetic variation within the FOXO3A gene was strongly associated with human longevity. The OR for homozygous minor vs. homozygous major alleles between the cases and controls was 2.75 (P = 0.00009; adjusted P = 0.00135). Long-lived men also presented several additional phenotypes linked to healthy aging, including lower prevalence of cancer and cardiovascular disease, better self-reported health, and high physical and cognitive function, despite significantly older ages than controls. Several of these aging phenotypes were associated with FOXO3A genotype. Long-lived men also exhibited several biological markers indicative of greater insulin sensitivity and this was associated with homozygosity for the FOXO3A GG genotype. Further exploration of the FOXO3A gene, human longevity and other aging phenotypes is warranted in other populations. PMCID: PMC2544566 PMID: 18765803
  3. Dean Pomerleau

    Optimal Late-Life BMI for Longevity

    Mike Lustgarten has penned an interesting blog post in which he looks at data from several sources, including these two meta-analyses [1][2]. Study [1] found the optimal BMI for adults in general (median age 58), was pretty flat and optimal between BMI of 19-25. Here is the graph: But [2] found in older adults (65+) the optimal BMI was much higher: As we've discussed here, this late-life "obesity paradox" might be a result of latent disease making people thin and more likely to die. Or it could simply be that heavier people have more metabolic reserves, which is important to enable the elderly to weather the "slings and arrows" of aging / decrepitude (e.g. falls & fractures, hospitalization, sarcopenia, loss of appetite, etc.) But the most interesting graphic from Mike's post is this one, in which Mike looked through a bunch of references (see his blog post for the list of references) and apparently did his own meta-analysis of the average BMI of centenarians (thanks Mike!): As you can see, most centenarians have a BMI between 19 and 24. He concludes: Centenarians have a BMI between 19.3-24.4 kg/m2. Shouldn’t that be the BMI reference range for those interested in living past 100? On the CR Society Facebook Group discussion of Mike's blog post, I question his rationale for this statement, saying: To play devil's advocate, it seems like the only way to answer [the question of the optimal BMI for living past 100] is to see if [the centenarians] have maintained that BMI from a much younger age, or have only gotten that thin as a results of sarcopenia and other unintended weight loss. Or maybe they've gained weight relative to their younger selves. There just isn't enough information to know what is optimal based on late-life BMI in the extremely old. I further suggest something we've discussed before (in the thread mentioned above): The optimal strategy may be to remain thin until one's elderly years to gain the benefits of CR, then put on weight to serve as a metabolic reserves when adverse events are likely to require them in old age. --Dean ------- [1] Berrington de Gonzalez A, Hartge P, Cerhan JR, Flint AJ, Hannan L, MacInnis RJ, Moore SC, Tobias GS, Anton-Culver H, Freeman LB, Beeson WL, Clipp SL, English DR, Folsom AR, Freedman DM, Giles G, Hakansson N, Henderson KD, Hoffman-Bolton J, Hoppin JA, Koenig KL, Lee IM, Linet MS, Park Y, Pocobelli G, Schatzkin A, Sesso HD, Weiderpass E, Willcox BJ, Wolk A, Zeleniuch-Jacquotte A, Willett WC, Thun MJ. Body-mass index and mortality among 1.46 million white adults. N Engl J Med. 2010 Dec 2;363(23):2211-9. doi: 10.1056/NEJMoa1000367. Erratum in: N Engl J Med. 2011 Sep 1;365(9):869. ---- [2] Winter JE, MacInnis RJ, Wattanapenpaiboon N, Nowson CA. BMI and all-cause mortality in older adults: a meta-analysis. Am J Clin Nutr. 2014 Apr;99(4):875-90.
  4. Here is a cogent argument that aging researchers should focus more attention on the oldest of the old, both because it is a growing demographic and because the causing of aging (and eventual death) of the really old are different from the "young old", those in their 60s and 70s who are dying from the usual lineup of chronic diseases (heart disease, cancer, diabetes, etc), and so studying the really old could teach us a lot about the true causes of aging (or causes of true aging?): http://www.longevityreporter.org/blog/2015/9/8/anti-aging-old While the writer does mentioned gunk (amyloid) building up as part of the mechanism of aging in the very old (one of Aubrey's seven deadly sources of damage), overall his argument seems to be in somewhat interesting contrast to Aubrey De Grey's perspective (at least as I've seen him express recently). Aubrey seems to be focusing the efforts of the SENS research projects on reversing the damage that accumulates on the path to our common killers (e.g. genes from bacteria that can break down oxidized cholesterol which leads to heart disease), calling this accumulation of damage the true hallmark and cause of aging (my paraphrasing). Perhaps the author and Aubrey are not that far apart, but I've found Aubrey's blurring the line between aging "proper" and the "diseases of aging" very interesting. Intuitively Aubrey's perspective makes a lot of sense to me: accumulation of damage is just what it means to age, and when enough of it accumulates, it manifests itself as one of the diseases of aging and you die. But at the same time it seems like something other than the diseases of aging are very consistently limiting practical human lifespan to about 115-116 years (with Jean Calmet as an extreme outlier), as if there is something else going on in the background that will eventually get you even if the diseases of aging don't. --Dean
  5. All, I was quite surprised to see in this study [1] posted by Al (thanks Al!) that among a population of nearly 1500 elderly people (age 75-96), two thirds said they didn't want to live to see 100. And these folks were apparently not institutionalized, but instead were "community dwelling" and recruited randomly by mail from the Helsinki's population registry. So they should have been a pretty good sample of older folks, if anything skewed towards being healthier than average rather than decrepit since they were able to respond to the survey. The two factors that correlated most strongly with desiring to make centenarian status were being male and being in good subjectively-reported health - so most of us have that goin' for us. For those who said no to the question of living to 100, their reasons were a litany of complaints about life and old age - pretty depressing actually: Among those not wishing to live to be 100, by far the largest proportion gave anticipatory explanations, seeming to believe that disease or poor functioning would be inevitable in a long life (n = 226): ‘Too many diseases!’ ‘Probably I would be too frail’ (Table 3). Emerging attitudes were mainly pessimistic. Many of the participants seemed to experience that life is meaningless (n = 111), ‘Not worth living’, or they conveyed indifference (n = 82) or even bitterness (n = 72): ‘Pointless suffering’; ‘Society is so cruel’. In addition, these old people were concerned about being a burden to others (n = 96): ‘It is a strain on yourself and your loved ones’. Some people expressed more positive attitudes, such as integrity (n = 16) or belief (n = 10): ‘I have led a rich life’; ‘I’m grateful every day’. In addition to rational reasons or attitudes, fear of the future was the third theme. Fear of loss of autonomy was striking (n = 98): ‘I’m afraid of frailty and helplessness’. Also loneliness (n = 23) and pain (n = 17) fed fear of the future. It shows how important it is to maintain one's health and especially a positive attitude. Obviously it's not so easy for the vast majority of people, at least in Finland - which is ironic, because Finland is perennially recognized as one of the happiest countries on Earth (#5 of 157), and it appears Finland has a darn good safety net for the elderly. I'm frightened to know what a survey of oldsters from the US (ranked #13) would reveal... --Dean --------- [1] Do you want to live to be 100? Answers from older people. Karppinen H, Laakkonen ML, Strandberg TE, Huohvanainen EA, Pitkala KH. Age Ageing. 2016 Apr 13. pii: afw059. [Epub ahead of print] PMID: 27076523 http://sci-hub.io/10.1093/ageing/afw059 Abstract BACKGROUND: little is known about the oldest-olds' views on ageing. OBJECTIVE: to investigate older people's desire and the reasons they give for wanting to live to 100. DESIGN: a postal questionnaire, analysed both quantitatively and qualitatively. SETTING: population based in Helsinki, Finland. SUBJECTS: a random sample (response rate 64%;N= 1,405) of community-dwelling older people (aged 75-96). METHODS: a structured self-completed questionnaire with an open-ended question on the reasons why/why not participants wished/did not wish to live to 100. RESULTS: one-third (32.9%) of home-dwelling older people wanted to live to be 100. Those who did were older, more often male and self-rated their health better than those who did not. Often the desire for long life was conditional: 'Yes, if I stay healthy'. Among the reasons is that many were curious to see what would happen. Many stated that they loved life, they had twinkle in their eye or significant life roles. Those who did not want to live extremely long lives gave various rationales: they would become disabled, life would be meaningless, they were reluctant to become a burden to others or they feared loss of autonomy or suffering pain or loneliness. Some people also shared the view that they should not intervene in destiny or they felt that they had accomplished what they wanted in life. CONCLUSIONS: one-third of the oldest-old participants wanted to live to 100. Identifying what motivated them to desire long life could be a resource in their care plans. KEYWORDS: centenarian; older people; oldest-old; qualitative; will-to-live
  6. Al Pater posted this review article [1] from way back in 2002 on the question of whether or not worldwide life expectancy is really beginning to level off, or is marching higher at the same 1/4 of a year per year rate that it has for the last 150 years. Here are two graphs from the paper, the first showing how striking and consistent the trend towards a higher lifespan has been, and how virtually everyone predicts it is going to level off (dashed red lines at the top): The authors postulate that the impression people have that lifespan is constantly on the verge of plateauing is an illusion with a few different causes. One interesting one is political. Politicians tend to low-ball when it comes to estimating future gains in life expectancy to make the cost of social programs, particularly those directly at the elderly like social security, medicare, look less costly and burdensome on the future. More interestingly, and with more evidence it would seem, they suggest the apparent leveling off in life expectancy gains is a result of the fact that the leading nation in life expectancy improvements keeps changing, with some countries (like the US) falling off the cutting edge, while other countries, like Japan, pick up the torch and push life expectancy higher at the same old rate of 1/4 of a year per year. So for the citizen in most countries, they fact is that lie expectancy improvements have levelled off. They give as evidence for this effect this graph: As you can see, Japan comes up after WWII to overtake the rest of the world in life expectancy, and keep us on the linear curve of life expectancy increases. Here are the authors' three rather bold assertions in the concluding paragraph of the paper: This mortality research has exposed the empirical misconceptions and specious theories that underlie the pernicious belief that the expectation of life cannot rise much further. Nonetheless, faith in proximate longevity limits endures, sustained by ex cathedra pronouncement and mutual citation (1, 8, 9). In this article we add three further lines of cogent evidence. First, experts have repeatedly asserted that life expectancy is approaching a ceiling: these experts have repeatedly been proven wrong. Second, the apparent leveling off of life expectancy in various countries is an artifact of laggards catching up and leaders falling behind. Third, if life expectancy were close to a maximum, then the increase in the record expectation of life should be slowing. It is not. For 160 years, best-performance life expectancy has steadily increased by a quarter of a year per year, an extraordinary constancy of human achievement. As I said - bold words. So that was in 2002. It's been almost a decade and a half since the paper was written. Have gains in life expectancy continued their "steadily increased by a quarter of a year per year" that the authors observe happening for the last 160 years? Nope - Not quite at least. Japan remains #1, and here is a graph of Japanese life expectancy that includes the period between 2002 through 2014: The paper reports in 2002 the life expectancy of a Japanese female was "almost 85 years", and in 2014 it was almost 87 years. So that is a life expectancy increase of 2 years in 12 years, or one sixth of a year per year, rather than the quarter of a year per year trend the authors point to. That equates to an average yearly shortfall in lifespan gains of 33% relative to the authors' prediction. Of course, this may be just a short-term deviation away from the long-term trend. Perhaps new advances in treatments or therapies for the diseases of aging (e.g. stem cell therapy, CRISPR-based gene therapy) will come along and keep us on the curve. It reminds me of the supposedly inexorable Moore's Law that futurist and immortality-optimist Ray Kurzweil likes to point to, namely that computer power (actually transistor count) doubles every two years, like clockwork, and has been for at least the last 40-50 years, and much longer than that if you ask Kurzweil. Unfortunately, I looks like we're falling off that curve too, according to this recent article in Nature (Feb '16): Next month, the worldwide semiconductor industry will formally acknowledge what has become increasingly obvious to everyone involved: Moore's law, the principle that has powered the information-technology revolution since the 1960s, is nearing its end. Similarly, at this point we seem to be slowing down rather than speeding up increases in life expectancy which would move us toward longevity escape velocity, where life expectancy increases by (at least) one year per year. --Dean ---------- [1] Science. 2002 May 10;296(5570):1029-31. No abstract available. Demography. Broken limits to life expectancy. Oeppen J, Vaupel JW. Free Full text: http://www.econ.ku.dk/okocg/VV/VV-Economic%20Growth/articles/artikler-2006/Broken-limits-to-life-expectancy.pdf Summary Is human life expectancy approaching its limit? Many--including individuals planning their retirement and officials responsible for health and social policy--believe it is, but the evidence presented in the Policy Forum suggests otherwise. For 160 years, best-performance life expectancy has steadily increased by a quarter of a year per year, an extraordinary constancy of human achievement. Mortality experts have repeatedly asserted that life expectancy is close to an ultimate ceiling; these experts have repeatedly been proven wrong. The apparent leveling off of life expectancy in various countries is an artifact of laggards catching up and leaders falling behind. PMID: 12004104
  7. 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
  8. Michael R

    At the Edges of "Natural" Lifespan

    All: I BELIEVE she is the first person other than Calment to hit that age; I am checking on this and will update. This is yet more significant than it seems; despite Calment's example, it has seemed as if there is some kind of maximum lifespan brick wall around 114 years. Aubrey de Grey's latest editorial pushes back on that, but also refers to recent research that disproves the notion of a "tail" in the Gompertz lifespan curve (exists in fruit flies and some other invertebrates, but is an illusion in mammals), which Michael Rose (mis)interpreted as a "period of immortality" (sic: agelessness) reached after the unleashed disruptive forces of residual antagonistic pleiotropy are exhausted, which could in principle (he argued, in a way I think is rather less than syllogistic even on its premises) be pushed back by tuning gene expression into a more adaptive mode, so that we would stop aging while still in youthful good health. For some stabs at this argument: DOES AGING STOP? BOOK REVIEW BY R. MICHAEL PERRY Cryonics / February 2013 Interview with Dr. Michael R. Rose Cryonics / September 2013 SEPTEMBER 2013 • VOLUME 34:9 http://www.impactaging.com/papers/v1/n5/full/100053.html http://www.kurzweilai.net/how-to-achieve-biological-immortality-naturally http://www.genescient.com/ais-superflies-and-the-path-to-immortality/ Even if you think you can make that argument for flies, however, recent evidence from better data at the extremes of the natural lifespan shows even the premises underlying the argument don't hold in humans or laboratory rodents. http://biomedgerontology.oxfordjournals.org/content/70/1/1 http://paa2015.princeton.edu/uploads/152897 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4318539/ http://longevity-science.org/pdf/Demografie-English-2011.pdf Dr. de Grey has dug even more deeply into these data, and thinks he has identified a novel finding therein, with some quite interesting implications — stay tuned.