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  1. The secret to a longer lifespan? Gene regulation holds a clue May 26, 2022 What accounts for longer lifespan? According to new research from biologists at the University of Rochester, a key piece of the puzzle lies in the mechanisms that regulate gene expression. (Getty Images photo) AddThis Sharing Buttons Share to Facebook Share to TwitterShare to LinkedInShare to More Rochester biologists who study the genetics of lifespan suggest novel targets to combat aging and age-related diseases. Natural selection has produced mammals that age at dramatically different rates. Take, for example, naked mole rats and mice; the former can live up to 41 years, nearly ten times as long as similar-size rodents such as mice. What accounts for longer lifespan? According to new research from biologists at the University of Rochester, a key piece of the puzzle lies in the mechanisms that regulate gene expression. In a paper published in Cell Metabolism, the researchers, including Vera Gorbunova, the Doris Johns Cherry professor of biology and medicine; Andrei Seluanov, professor of biology and medicine; and Jinlong Lu, a postdoctoral research associate in Gorbunova’s lab and the first author of the paper, investigated genes connected to lifespan. Their research uncovered specific characteristics of these genes and revealed that two regulatory systems controlling gene expression—circadian and pluripotency networks—are critical to longevity. The findings have implications both in understanding how longevity evolves and in providing new targets to combat aging and age-related diseases. Comparing longevity genes The researchers compared the gene expression patterns of 26 mammalian species with diverse maximum lifespans, from two years (shrews) to 41 years (naked mole rats). They identified thousands of genes related to a species’ maximum lifespan that were either positively or negatively correlated with longevity. They found that long-lived species tend to have low expression of genes involved in energy metabolism and inflammation; and high expression of genes involved in DNA repair, RNA transport, and organization of cellular skeleton (or microtubules). Previous research by Gorbunova and Seluanov has shown that features such as more efficient DNA repair and a weaker inflammatory response are characteristic of mammals with long lifespans. The opposite was true for short-lived species, which tended to have high expression of genes involved in energy metabolism and inflammation and low expression of genes involved in DNA repair, RNA transport, and microtubule organization. Two pillars of longevity When the researchers analyzed the mechanisms that regulate expression of these genes, they found two major systems at play. The negative lifespan genes—those involved in energy metabolism and inflammation—are controlled by circadian networks. That is, their expression is limited to a particular time of day, which may help limit the overall expression of the genes in long-lived species. In comparing the gene expression patterns of 26 species with diverse lifespans, Rochester biologists Vera Gorbunova and Andrei Seluanov found that the characteristics of the different genes were controlled by circadian or pluripotency networks. (University of Rochester illustration / Julia Joshpe) This means we can exercise at least some control over the negative lifespan genes. “To live longer, we have to maintain healthy sleep schedules and avoid exposure to light at night as it may increase the expression of the negative lifespan genes,” Gorbunova says. On the other hand, positive lifespan genes—those involved in DNA repair, RNA transport, and microtubules—are controlled by what is called the pluripotency network. The pluripotency network is involved in reprogramming somatic cells—any cells that are not reproductive cells—into embryonic cells, which can more readily rejuvenate and regenerate, by repackaging DNA that becomes disorganized as we age. “We discovered that evolution has activated the pluripotency network to achieve longer lifespan,” Gorbunova says. The pluripotency network and its relationship to positive lifespan genes is therefore “an important finding for understanding how longevity evolves,” Seluanov says. “Furthermore, it can pave the way for new antiaging interventions that activate the key positive lifespan genes. We would expect that successful antiaging interventions would include increasing the expression of the positive lifespan genes and decreasing the expression of negative lifespan genes.”
  2. Many of us here are fairly robotic, and eat the same thing day in and day out. Some of us enjoy more diversity and enjoy exploring culinary aspects of foods. Yet for many people browsing this forum, they aren't exactly sure what our meals looks like. Let us share our wonderful food creations with one another! I just enjoyed a delicious lunch. It consisted of the following: Purple sweet potato, chick peas, broccoli, cauliflower, carrots, mushrooms, 1 tsp of olive oil, 1 tbsp of 20-spice mix, garlic, oregano, parsley, cilantro, chili peppers, and 2 oranges for dessert. Ingredients were organic when possible. I also get centenarian status for eating Okinawan sweet potato, right? Calorie total was about 700-800, but I don't watch that closely. I just eat more or less depending on what the scale says each day. Did I mention the food was incredibly delicious? Bon appetit!
  3. Here is a really interesting article on the short tenure enjoyed by most holders of the title of world's oldest person. Here is a cool graphic from article, showing how old all the recent record holders have been, and how long they've reigned: As you can see, since 2000 the oldest living person (invariably a woman) has been between the age of 114 and 117, and they've held the title for a short time relative to the 9 years that Jeanne Calment was at the top. Despite dramatic increases in recent average lifespan, the age of the oldest person alive has remained pretty stable lately: The average age of the oldest-ever people has increased over the past 40 years from around 112 to around 114. --Dean
  4. https://www.sciencenews.org/article/lizard-like-tuatara-mitochondrial-genomes-cold-tolerance?utm_source=Editors_Picks&utm_medium=email&utm_campaign=editorspicks013121
  5. Dear ALL, I've just received the letter below, from Dr. Luigi Fontana. It describes his latest book, and includes an attached video. Enjoy, -- Saul Dear Saul, how are you? Hope you are doing well in these difficult times. I am writing to bring to your kind attention a new book, entitled the ‘Path to Longevity’, that summarizes more than 20 years of research, clinical practice and my accumulated knowledge on healthy longevity. Here, a video interview with Sunrise TV that encapsulates some of the key topics: https://youtu.be/bho1IfJqCBw My ultimate dream is that by reading this book people might start to examine their current level of physical and psychological health, and their subconscious expectations for the future. I hope that by becoming more aware of their full potential they will unlock a profoundly felt need for transformation and possibly help the world become a better place. Warmest regards, Luigi PROFESSOR LUIGI FONTANA, MD, PhD, FRACP Professor of Medicine and Nutrition Leonard P Ullmann Chair in Translational Metabolic Health Director, Healthy Longevity Research and Clinical Program Charles Perkins Centre | Sydney Medical School (Central Clinical School) Faculty of Medicine and Health The University of Sydney
  6. 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
  7. Arg.... Forum ate my post. Take 2. ---------- Dean, I have the same results as you, also on the 5th SNP, rs3751812! By the way, there's a much easier way to check status on any SNP than logging into 23andMe. Use SNPTips with FireFox. Yes, we learn a lot about the thin phenotype, but I think the real question is the effect on the possibility of benefitting from CR. CR might be easier for you and me, one might guess. I'd say almost the opposite: being thin is easier, but that's not the goal. Someone with the opposite genetic tendency might go from a BMI of 30 to a BMI of 22 or 21 on CR, benefit tremendously, not look scrawny -- maybe not have really low testosterone, etc. -- whereas we, on CR, go from a BMI of 22 or 23 to 18 or less, and maybe don't get as many CR benefits, and get a lot of the downsides. Maybe. Leanness per se confers some health benefits, according to some studies. But being in "survival mode", as you rightly have called it, might be the real goal. And we might not be able to be in extreme survival mode without being dangerously fat-less. Here's where a citizen science project might be very useful! Zeta
  8. I follow Dr. Greger's NutritionFacts.org and today he released a video on higher heart rate risk factors for morbidity. I'm curious to know if any one here practices any lifestyle changes to lower heart rate (exercise/meditation/etc) to improve one's chances of living longer. If so, how low is your resting heart rate? I try to practice daily meditation and I know it helps me lower my heart rate and blood pressure, but I'm still quite average in terms of heart rate, probably around 70bpm. I wonder if lowering my resting heart rate to 50bpm or lower would be a good idea or not. I'd prefer not to do excessive endurance exercise (for time and physical stress reasons) to lower it. I'd love to hear what other people think of the topic!
  9. Hi. I'm new to this forum. I’ve always wanted to live longer, ever since I was a kid. I'm still pretty young but I recently decided to go on a calorie restricted diet. The thing is that I’m not sure how to do that and I could really use some help. I’ve been relatively skinny most of my life. My BMI is around 19 and has been around that since I was a 15-16. I suffer from Hashimoto’s (autoimmune hypothyroidism) and have recently had to eat relatively little to maintain my weight and look and feel like my normal self. I work out 6-8 hours per week of relatively intense exercise and eat around 1600-1800 calories a day. I try to eat nutritious food. I’m sensitive to fiber so I have to restrict my vegetable intake. Eating more than 20 g of fiber per day makes me very gassy and prevents nutrients from getting absorbed. I try to eat nutritious foods that are low in fiber. The way I understand this diet is that people cut calories to the point where their metabolism slows down and their bodies barely get enough calories to survive. But their diet is rich enough to provide all the necessary nutrients by eating lots of vegetables and fiber. What do I need to do if my metabolism is already crawling. I’m on medication so I’m not currently hypo but my metabolism is very slow compared to the way it was before I had thyroid issues. My thyroid hormones are currently in the normal range but they're very close to hypo (my FT3 is at the low end of the healthy range and my FT4 is not that far above it). Do I need to slow down my metabolism more? Do I need to eat less if my BMI is already relatively low? How can I do this diet if I can’t eat fiber.
  10. I want to create food with 0 calories for me to eat my whole life!
  11. Valter Longo's work has been discussed around here quite frequently as of late, particularly his work on the fasting mimicking diet. In typical Rich Roll fashion, he goes long form and tries to gain deep insight into Longo's understanding of nutrition, longevity, and health. Rich says that he considers it one of his most important conversations to date.
  12. From this new article from the BBC: "Across mammals alone, expected lifespan can vary 100-fold, from shrews that live for no longer than 1.5 years to the bowhead whales that can live for more than 200. It is as if, for various reasons, natural selection has somehow pushed certain creatures to evolve their own elixir of life." The writer goes on to talk to scientists studying genes and gene expression in whales, bats and naked mole rats, in hopes of discovering how they live so long, and in particular avoid cancer. The article talks about the possibility of using gene therapy to replicate some of the longevity-promoting genetic changes observed in these long-lived animals in people someday. One of the researchers talks about a study I'd sign up for - comparing bowhead whale gene expression to the gene expression of people practicing CR! It reminds me of the study [1] Luigi Fontana did on our muscle tissue - namely comparing our gene expression to that of CRed rats. Note: This is yet another example of a post that would be fit better on a "Science of Health & Longevity" forum, rather than here on the "CR Science & Theory" forum. How about it Brian/Tim? --Dean ---------------------------- [1] Mercken, E. M., Crosby, S. D., Lamming, D. W., JeBailey, L., Krzysik-Walker, S., Villareal, D. T., Capri, M., Franceschi, C., Zhang, Y., Becker, K., Sabatini, D. M., de Cabo, R. and Fontana, L. (2013), Calorie restriction in humans inhibits the PI3K/AKT pathway and induces a younger transcription profile. Aging Cell, 12: 645–651. doi: 10.1111/acel.12088. Full Text: http://onlinelibrary.wiley.com/doi/10.1111/acel.12088/full
  13. Been thinking about this ever since I read Kurzweil’s book ‘Transcend’. Many people might already be familiar with his ideas and his theory of exponential growth and how that will affect our health and longevity. Here’s the latest interview with him where he succintly summarizes his predictions about the future of health, aging and biotechnology: [media]https://www.youtube.com/watch?v=lpzXWGrngTw[/media] Thoughts? What do you think are the holes/blind spots in his arguments?
  14. Hi all, I'm creating a monthly newsletter that describes the latest advances in longevity sciences. The newsletter is intended for a non-technical audience without a formal background in chemistry and biology. Content Includes: Summaries of the latest research Basic overview of the science behind longevity Tests for personalized diagnostics of age-related diseases Database of the latest FDA drug and device submissions If you're interested, click on this landing page link http://www.mylanderpages.com/filez/LongevityDigest it enter your email. I will email you the newsletter once it's ready.
  15. All, I know there are a couple Dr.. Greger detractors on the forum, but he's got a new video talking about the diets and lifestyles of the long-lived Okinawans and vegetarian Adventists that I think people will find interesting.. He mentions that both groups eat a mostly plant-based diet.. He cites [1], which found that the vegetarian Adventists who also practiced a healthy lifestyle had average lifespans of 87 (men) and 90 (women).. That's 10-14 years longer than the general population, and even longer than the traditional Okinawans (77.6 for men and 86.0 for women). For those who don't like to watch videos, I've included the transcript at the bottom, along with all his references. My one criticism of this video is his claim that: The plant-based nature of the diet may trump the caloric restriction, though, since the one population that lives even longer than the Okinawa Japanese don’t just eat a 98% meat-free diet, they eat 100% meat-free. The Adventist vegetarians in California, with perhaps the highest life expectancy of any formally described population. His claim may be true, but its a big stretch to try to argue it from a comparison between the Okinawans and the vegetarian Adventists, to say nothing of attributing the (small) difference to the 98% vs..100% meat-free diet. There are plenty of other differences between the two groups that could explain they longevity difference besides the (perhaps) tiny bit more meat eaten by the Okinawans relative to the vegetarian Adventists - things like access to healthcare. Here is the gist of the Adventist paper he's referencing [1]: High physical activity [> 15min 3x / week vigorous exercise], frequent consumption of nuts [>5 times/wk], vegetarian status [eating meat less than once per month], and medium body mass index [not specified, but presumably 22.5 - 25.0] each result in an approximate 1.5- to 2.5-years gain in life expectancy compared with the corresponding high-risk values [high risk for BMI wasn't specified, but was presumably > 25.0]. The sum of these independent effects (9.7 years in men and 10.4 years in women) is similar to those predicted in subjects who have contrasting values for all variables simultaneously. So from this we can conclude the following two interesting things: Being vegetarian ("low risk" as defined by the authors as eating meat less than once per month, although mostly not vegan - the authors say "few Adventists in this study were vegans") vs. eating meat once a week or more ("high risk" as defined by the authors), provided a 1.5-2.5 year gain in life expectancy, and Having a medium BMI (vs. low or high) provides a longevity advantage. First BMI. The fact that having a medium BMI was better than a low BMI in this Adventist study, while having low BMI was better than medium BMI in this other Adventist Study [2] discussed a couple days ago in this post can best be explained by the fact that this study followed subjects for only 12 years, and excluded only the first 4 years of mortality data in an attempt to eliminate the confounding effects of pre-existing conditions. As we saw from [2], the lingering effects of pre-existing conditions (esp. respiratory problems and a prior history of smoking) have an impact on both BMI and mortality for much longer than 4 years. So I think it's safe to say that this study's conclusion that a medium BMI is better than a low BMI should be taken with a big grain of salt in light of the better evidence of the opposite on another group of Adventists in [2]. Regarding the extra 1.5-2.5 years gain from being vegetarian vs. eating meat more often than once per week. Consider what the following graph from [1] shows us. The interesting thing about this graph is its left-to-right structure. Here is the text describing the figure: The first bar shows life expectancy when all variables take medium-risk values. Then passing from left to right through the figures, additional variables are also set at either high- or low-risk values, those variables to the right of a particular bar being still at medium-risk values. In the final contrast, when all variables are at either low- or high-risk values, the differences in the expected ages at death are 10.8 years (men) and 9.8 years (women). So for men who are in the "medium risk" category for all these health factors, their average lifespan was 85.1 years (first, white bar on left). Now consider the first 3 bars in the graph above. Keeping all the other factors at their "medium risk" category, eating meat less than once per month (i.e. vegetarian) resulted in a mean lifespan of 85.3. Eating meat more than once per month but less than once per week (semi-vegetarians) resulted in a lifespan of 85.1. And eating meat once per week or more resulted in a lifespan of 83.8. Given the confidence intervals, there really wasn't any difference between almost never eating meat and eating it occasionally (but less than once per week). This is virtually exactly what the Okinawans do, since according to the video, they get about 1% of their calories from fish and < 1% from meat. Here is a cool pie chart of the traditional Okinawan diet: The limited benefit from being a very strict vegetarian Adventist vs. an Adventist who occasionally eats meat is further supported by [2], which found that the subpopulation of Adventist "vegetarians" [sic] with the lowest mortality rate were the pesco-vegetarians, followed by the vegans, lacto-ovo-vegetarians and semi-vegetarians, in that order: The adjusted hazard ratio (HR) for all-cause mortality in all vegetarians combined vs nonvegetarians was 0.88 (95% CI, 0.80-0.97).. The adjusted HR for all-cause mortality in vegans was 0.85 (95% CI, 0.73-1.01); in lacto-ovo-vegetarians, 0.91 (95% CI, 0.82-1.00); in pesco-vegetarians, 0.81 (95% CI, 0.69-0.94); and in semi-vegetarians, 0.92 (95% CI, 0.75-1.13) compared with nonvegetarians. So as much as it pains me to say it , and contra what Dr. Greger suggests, being a strict vegetarian, as opposed to eating meat (esp. fish) occasionally like the Okinawans, doesn't appear likely to be responsible for much of the lifespan advantage enjoyed by the Adventists relative to the Okinawans, which is substantial for men (average of Adventists man with best diet/lifestyle = 87.0 years, average Okinawan man = 77.6 years). --Dean Transcript: The Okinawa Diet: Living to 100 The dietary guidelines recommend that we try to choose meals or snacks that are high in nutrients but lower in calories to reduce the risk of chronic disease.. By this measure, the healthiest foods on the planet, the most nutrient dense, are vegetables, containing the most nutrient bang for our caloric buck.. So, what would happen if a population centered their diet around vegetables? They might end up having among the longest lives. Of course, any time you hear about long-living populations, you have to make sure it’s validated, as it may be hard to find birth certificates from the 1890’s.. But validation studies suggest that, indeed, they really do live that long. The traditional diet in Okinawa is based on vegetables, beans, and other plants.. I’m used to seeing the Okinawan diet represented like this, the base being vegetables, beans, and grains, but a substantial contribution from fish and other meat, but a more accurate representation would be this - if you look at their actual dietary intake.. We know what they were eating from the U.S.. National Archives, because the U.S.. military ran Okinawa until it was given back to Japan in 1972, and if you look at the traditional diets of more than 2000 Okinawans, this is how it breaks down. Less than 1% of their diet was fish; less than 1% of their diet was meat, and same with dairy and eggs, so it was more than 96% plant-based, and more than 90% whole food plant based—very few processed foods either.. And, not just whole food plant-based, but most of their diet was vegetables, and one vegetable in particular, sweet potatoes.. The Okinawan diet was centered around sweet potatoes—how delicious is that? Could have been bitter gourd, or soursop—but no, sweet potatoes, yum. So, 90 plus percent whole food plant-based makes it a highly anti-inflammatory diet, makes it a highly antioxidant diet.. If you measure the level of oxidized fat within their system, there is compelling evidence of less free radical damage.. Maybe they just genetically have better antioxidant enzymes or something? No, their antioxidant enzyme activity is the same; it’s all the extra antioxidants that they’re getting from their diet that may be making the difference—most of their diet is vegetables! So, 6 to 12 times fewer heart disease deaths than the U.S.—you can see they ran out of room for the graph for our death rate, two to three times fewer colon cancer deaths, seven times fewer prostate cancer deaths, and five and a half times lower risk of dying from breast cancer. Some of this protection may be because they were only eating about 1800 calories a day, but they were actually eating a greater mass of food, but the whole plant foods are just calorically dilute.. There’s also a cultural norm not to stuff oneself. The plant-based nature of the diet may trump the caloric restriction, though, since the one population that lives even longer than the Okinawa Japanese don’t just eat a 98% meat-free diet, they eat 100% meat-free.. The Adventist vegetarians in California, with perhaps the highest life expectancy of any formally described population. Adventist vegetarian men and women live to be about 83 and 86, comparable to Okinawan women, but better than Okinawan men.. The best of the best were Adventist vegetarians who had healthy lifestyles too, like being exercising nonsmokers, 87 and nearly 90, on average.. That’s like 10 to 14 years longer than the general population.. Ten to 14 extra years on this Earth from simple lifestyle choices.. And, this is happening now, in modern times, whereas Okinawan longevity is now a thing of the past.. Okinawa now hosts more than a dozen KFCs . Their saturated fat tripled.. They went from eating essentially no cholesterol to a few Big Macs' worth, tripled their sodium, and are now just as potassium deficient as Americans, getting less than half of the recommended minimum daily intake of 4700 mg a day.. In two generations, Okinawans have gone from the leanest Japanese to the fattest.. As a consequence, there has been a resurgence of interest from public health professionals in getting Okinawans to eat the Okinawan diet, too. References: D C Willcox, G Scapagnini, B J Willcox.. Healthy aging diets other than the Mediterranean: a focus on the Okinawan diet.. Mech Ageing Dev.. 2014 Mar-Apr;136-137:148-62. A Drewnowski, J Hill, B Wansink, R Murray, C Diekman.. Achieve Better Health With Nutrient-Rich Foods.. Nutrition Today: January/February 2012 - Volume 47 - Issue 1 - p 23–29. D C Willcox, B J Willcox, H Todoriki, M Suzuki.. The Okinawan diet: health implications of a low-calorie, nutrient-dense, antioxidant-rich dietary pattern low in glycemic load.. J Am Coll Nutr.. 2009 Aug;28. S Davinelli, D C Willcox, G Scapagnini.. Extending healthy ageing: nutrient sensitive pathway and centenarian population.. Immun Ageing.. 2012 Apr 23;9:9. B J Willcox, D C Willcox.. Caloric restriction, caloric restriction mimetics, and healthy aging in Okinawa: controversies and clinical implications.. Curr Opin Clin Nutr Metab Care.. 2014 Jan;17(1):51-8. M Poulain.. Exceptional Longevity in Okinawa:: A Plea for In-depth Validation..Demographic Research;Jul-Dec2011, Vol.. 25, p245. N S Gavrilova, L A Gavrilov.. Comments on Dietary Restriction, Okinawa Diet and Longevity.. Gerontology.. 2012 Apr; 58(3): 221–223. B J Willcox, D C Willcox, H Todoriki, A Fujiyoshi, K Yano, Q He, J D Curb, M Suzuki..Caloric restriction, the traditional Okinawan diet, and healthy aging: the diet of the world's longest-lived people and its potential impact on morbidity and life span.. Ann N Y Acad Sci.. 2007 Oct;1114:434-55. D C Willcox, B J Willcox, H Todoriki, J D Curb, M Suzuki.. Caloric restriction and human longevity: what can we learn from the Okinawans? Biogerontology.. 2006 Jun;7(3):173-7. G E Fraser, D J Shavlik.. Ten years of life: Is it a matter of choice? Arch Intern Med..2001 Jul 9;161(13):1645-52. D C Willcox, B J Willcox, Q He, N C Wang, M Suzuki.. They really are that old: a validation study of centenarian prevalence in Okinawa.. J Gerontol A Biol Sci Med Sci.. 2008 Apr;63(4):338-49. M Suzuki, B J Wilcox, C D Wilcox.. Implications from and for food cultures for cardiovascular disease: longevity.. Asia Pac J Clin Nutr.. 2001;10(2):165-71. M Suzuki, D C Wilcox, M W Rosenbaum, B J Willcox.. Oxidative stress and longevity in okinawa: an investigation of blood lipid peroxidation and tocopherol in okinawan centenarians.. Curr Gerontol Geriatr Res.. 2010;2010:380460. ----------- [1] Arch Intern Med. 2001 Jul 9;161(13):1645-52. Ten years of life: Is it a matter of choice? Fraser GE(1), Shavlik DJ. BACKGROUND: Relative risk estimates suggest that effective implementation of behaviors commonly advocated in preventive medicine should increase life expectancy, although there is little direct evidence. OBJECTIVE: To test the hypothesis that choices regarding diet, exercise, and smoking influence life expectancy. METHODS: A total of 34 192 California Seventh-Day Adventists (75% of those eligible) were enrolled in a cohort and followed up from 1976 to 1988. A mailed questionnaire provided dietary and other exposure information at study baseline. Mortality for all subjects was ascertained by matching to state death tapes and the National Death Index. RESULTS: California Adventists have higher life expectancies at the age of 30 years than other white Californians by 7.28 years (95% confidence interval, 6.59-7.97 years) in men and by 4.42 years (95% confidence interval, 3.96-4.88 years) in women, giving them perhaps the highest life expectancy of any formally described population. Commonly observed combinations of diet, exercise, body mass index, past smoking habits, and hormone replacement therapy (in women) can account for differences of up to 10 years of life expectancy among Adventists. A comparison of life expectancy when these factors take high-risk compared with low-risk values shows independent effects that vary between 1.06 and 2.74 years for different variables. The effect of each variable is assessed with all others at either medium- or high-risk levels. CONCLUSIONS: Choices regarding diet, exercise, cigarette smoking, body weight, and hormone replacement therapy, in combination, appear to change life expectancy by many years. The longevity experience of Adventists probably demonstrates the beneficial effects of more optimal behaviors. PMID: 11434797 ----------- [2] JAMA Intern Med.. 2013 Jul 8;173(13):1230-8.. doi: 10.1001/jamainternmed.2013.6473. Vegetarian dietary patterns and mortality in Adventist Health Study 2. Orlich MJ(1), Singh PN, Sabaté J, Jaceldo-Siegl K, Fan J, Knutsen S, Beeson WL, Fraser GE. Author information: (1)School of Public Health, Loma Linda University, Loma Linda, CA 92350, USA. morlich@llu.edu Comment in JAMA Intern Med.. 2014 Jan;174(1):168-9. JAMA Intern Med.. 2014 Jan;174(1):169. JAMA Intern Med.. 2013 Jul 8;173(13):1238-9. Dtsch Med Wochenschr.. 2013 Sep;138(39):1930. IMPORTANCE: Some evidence suggests vegetarian dietary patterns may be associated with reduced mortality, but the relationship is not well established. OBJECTIVE: To evaluate the association between vegetarian dietary patterns and mortality. DESIGN: Prospective cohort study; mortality analysis by Cox proportional hazards regression, controlling for important demographic and lifestyle confounders. SETTING: Adventist Health Study 2 (AHS-2), a large North American cohort. PARTICIPANTS: A total of 96,469 Seventh-day Adventist men and women recruited between 2002 and 2007, from which an analytic sample of 73,308 participants remained after exclusions. EXPOSURES: Diet was assessed at baseline by a quantitative food frequency questionnaire and categorized into 5 dietary patterns: nonvegetarian, semi-vegetarian, pesco-vegetarian, lacto-ovo-vegetarian, and vegan. MAIN OUTCOME AND MEASURE: The relationship between vegetarian dietary patterns and all-cause and cause-specific mortality; deaths through 2009 were identified from the National Death Index. RESULTS: There were 2570 deaths among 73,308 participants during a mean follow-up time of 5.79 years.. The mortality rate was 6.05 (95% CI, 5.82-6.29) deaths per 1000 person-years.. The adjusted hazard ratio (HR) for all-cause mortality in all vegetarians combined vs nonvegetarians was 0.88 (95% CI, 0.80-0.97).. The adjusted HR for all-cause mortality in vegans was 0.85 (95% CI, 0.73-1.01); in lacto-ovo-vegetarians, 0.91 (95% CI, 0.82-1.00); in pesco-vegetarians, 0.81 (95% CI, 0.69-0.94); and in semi-vegetarians, 0.92 (95% CI, 0.75-1.13) compared with nonvegetarians.. Significant associations with vegetarian diets were detected for cardiovascular mortality, noncardiovascular noncancer mortality, renal mortality, and endocrine mortality.. Associations in men were larger and more often significant than were those in women. CONCLUSIONS AND RELEVANCE: Vegetarian diets are associated with lower all-cause mortality and with some reductions in cause-specific mortality.. Results appeared to be more robust in males.. These favorable associations should be considered carefully by those offering dietary guidance. PMCID: PMC4191896 PMID: 23836264 ------------- [2] Int J Obes Relat Metab Disord.. 1998 Jun;22(6):544-8. Body mass and 26 y risk of mortality among men who never smoked: a re-analysis among men from the Adventist Mortality Study. Lindsted KD(1), Singh PN. Author information: (1)Center for Health Research, Loma Linda University, CA 92350, USA. OBJECTIVE: To re-analyse the previously reported linear relation between Quetelet's body mass index (BMI) and mortality, among men from the Adventist Mortality Study after accounting for effects due to age at measurement of BMI, smoking history and race. DESIGN: Prospective cohort study.. To specifically account for effects due to age at measurement of BMI, smoking history and race, our methodology includes: 1, computing hazard ratios for BMI quintiles from a proportional hazard regression, with 'time on study' as the time variable, and age at baseline as a covariate; 2, conducting separate analyses of middle-aged (age 30-54y) and older (age 55-74y) men; and 3, restriction of the analyses to never-smoking, non-Hispanic white males. SUBJECTS: 5062 men (age: 30-74 y, BMI: 14-44 kg/m2) from the Adventist Mortality Study. MEASUREMENTS: Subjects reported data on anthropometric, demographic, medical, dietary and lifestyle characteristics at baseline and were enrolled in mortality surveillance during a 26y study period (1960-1985). RESULTS: During the early years of follow-up (years 1-8, 9-14), we found some evidence of excess risk among the leanest men that was probably due to the effects of antecedent illness.. During the later years of follow-up (years 15-26), effects due to antecedent illness were not apparent and a significant positive, linear relation between BMI and all-cause mortality was consistently found among middle-aged (30-54 y) and older (55-74 y) men.. Disease-specific analyses of the later follow-up (years 15-26) revealed that the positive linear trends with all-cause mortality, were primarily due to excess risk of cardiovascular disease and cancer among the heavier men.. Among older men, a significant inverse relation between BMI and respiratory disease mortality risk was identified during later follow-up (years 15-26), but this effect attenuated after restriction of the analyses to men with no baseline history of respiratory disease. CONCLUSIONS: The re-analysis confirms the findings of a positive, linear relation between BMI and all-cause mortality, reported in the original study. PMID: 9665675
  16. 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
  17. 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
  18. Low testosterone (hypogonadism), besides potentially reducing quality of life (a commonly held notion the validity of which many of us male CR folks would contend...), has been thought to be potentially associated with increased mortality, particularly from cardiovascular disease, at least among the general (non-CR) population. Here again is a situation where we hope that our low testosterone (as frequently but not universally experienced by CR men) has different health/longevity implications than hypogonadism in the general population, where it is frequently associated with obesity and other indicators of ill-health. Well, this study posted by Al Pater (thanks Al!) from the Framingham Heart Study may help ease those doubts and concerns. It found that even in a general population of 254 elderly men (avg age 75), neither low testosterone nor absolute level or change in other sex hormones were associated with increased mortality at either 5 or 10 year follow-up, once other confounding factors were statistically factored out. The confounders they corrected for were age, body mass index, smoking, total cholesterol, high-density lipoprotein cholesterol, type 2 diabetes, systolic blood pressure, and antihypertensive medication - all of which seem reasonable to factor out. To quote from the discussion of the free full text: Leveraging the unique data set and design of the community-based FHS, the present study is the first to investigate longitudinal trajectory patterns of serial sex steroid and gonadotropins measurements and their associations with 5-year and 10-year risk of incident clinical CVD and all-cause mortality. We observed no consistent association of sex steroids, gonadotropins, and their trajectories with incident clinical CVD or all-cause mortality risk in 254 elderly men in the community. In other words, it appears that if you are a healthy elderly man (i.e. without the confounders listed above, which hopefully most CR folks do/will avoid), having low testosterone is not associated with an increased risk of cardiovascular disease or overall mortality. So we've got that goin' for us... --Dean ----------- [1] Association of sex steroids, gonadotrophins, and their trajectories with clinical cardiovascular disease and all-cause mortality in elderly men from the Framingham Heart Study. Haring R, Teng Z, Xanthakis V, Coviello A, Sullivan L, Bhasin S, Murabito JM, Wallaschofski H, Vasan RS. Clin Endocrinol (Oxf). 2013 Apr;78(4):629-34. doi: 10.1111/cen.12013. PMID: 22901104 Free PMC Article http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4161203/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4161203/pdf/nihms622794.pdf Abstract BACKGROUND: Emerging data from longitudinal studies suggest that low sex steroid concentrations in men are associated with increased cardiovascular risk and mortality. The impact of longitudinal trajectory patterns from serial sex steroid and gonadotrophin measurements on the observed associations is unknown to date. METHODS: We prospectively evaluated 254 elderly men (mean age, 75·5 years) of the Framingham Heart Study with up to four serial measurements of serum total testosterone (TT), dehydroepiandrosterone sulphate (DHEAS), follicle-stimulating hormone (FSH), luteinizing hormone (LH) and total estradiol (EST); and constructed age- and multivariable-adjusted Cox proportional hazard regression models relating baseline hormone concentrations and their mean, slope and variation over time (modelled as continuous and categorized into quartiles) to the incidence of clinical cardiovascular disease (CVD) and all-cause mortality at 5- and 10-year follow-up. RESULTS: We observed no association between baseline concentrations of sex steroids, gonadotrophins and their trajectories with incident clinical CVD over 5- and 10-year follow-up. Although higher baseline TT concentrations were associated with lower mortality risk at 5 years (hazard ratio per quartile increment, 0·74; 95% confidence interval, 0·56-0·98), correction for multiple statistical testing (P < 0·005) rendered this association statistically nonsignificant. Repeat analyses at the 10-year follow-up time point also demonstrated no significant association between sex steroids, gonadotrophins or their trajectories and mortality. CONCLUSION: Investigating longitudinal trajectory patterns of serial sex steroid and gonadotrophin measurements, the present study found no consistent associations with incident clinical CVD and all-cause mortality risk in elderly men from the community.
  19. Hello, I have a medical background and created an app to help you understand which of 10 habits could reduce your mortality risk (based on scientific research) and develop them using gamification. I'm looking for testers, so let me know if this could be useful to you. Thanks.
  20. AlPater

    Future Predictions for 2017-2045

    And, CBC had an article on the likelihood of a human marrying a robot by 20XX. Future Predictions for 2017-2045 Posted on Jan. 6, 2017, 1:18 p.m. in Industry News Artificial Intelligence Biotechnology Longevity Medical Technology http://www.worldhealth.net/news/future-predictions-2017-2045/ Dr Robert Goldman, Co-Founder & Chairman-World Academy of Anti-Aging Medicine, weighs in with his latest set of predictions for health and technology. Future Predictions for 2017-2045 It is estimated that the doubling time of medical knowledge in 1950 was 50 years; in 1980, 7 years; and in 2010, 3.5 years. In 2020 it is projected to be 0.2 years—just 73 days. Computer power is doubling every 18 months, so massive increases in scope and scale. Once nanotechnology and nano circuitry, stem cells, and genetic engineering, come on board, the world as we know it will be unrecognizable. Get ready for the first complete synthetic human brain, moon mining, chips implanted in our brains, self-driving cars, trucks and planes, robotic moon bases and maybe even high-speed rail linking London to Beijing. The most popular movie super heroes demonstrate cellular regeneration like 'Wolverine' allowing mutations to enable rapid cellular repair & healing achieving Immortality, or Captain America in 1942 using Hormone Therapy/Steroid Augmentation to become an athletic Super Hero and with Cryonics/suspended animation freezing him into the 21st century. This Brave New World is coming into being faster than we imagined. To have the great jobs and careers of the future, you must embrace and see it before it arrives. Radical Life Extension Billions of dollars have recently flowed into Anti-Aging Medical research, from the likes of Silicon Valley & Biotech Startups chasing after the 'Fountain of Youth', such as Calico (Google), Johnson & Johnson, Human Longevity Inc, Elysium Health, Synthetic Genomics, GlaxoSmithKline / Sinclair, Startup Health, Mayo Clinic, Scripps Research, Roche , Novartis (Rapamycin), AstraZeneca, AbbVie, Pfizer, Sanofi, Medtronic/Covidien, IBM Watson Healthcare, Quest, Apple, Microsoft, Qualcomm, Facebook, Amazon, Novo Nordisk and other giants. They finally realize that Anti-Aging & Regenerative Medicine is the next generation of healthcare -the age of PRACTICAL IMMORTALITY, where lifespans of 120 to 150 in superior health may become commonplace and may be seen as early as 2029. Others such as Oracle co-founder Larry Ellison, for example, has given more than $430 million toward anti-aging research because he finds the quiet acquiescence of mortality “incomprehensible.” XPRIZE entrepreneur Peter H. Diamandis co-founded Human Longevity, which, in conjunction with StartUp Health, launched the Longevity Moonshot, whose mission is “to extend and enhance healthy life by 50+ years and change the face of aging.” Google co-founder Larry Page launched a biotech company called Calico, which aims to extend the human life span by a century. Calling it “a longer-term bet,” Page said he was confident they “can make good progress within reasonable timescales with the right goals and the right people.” PayPal co-founder Peter Thiel created Breakout Labs to fund scientists and start-ups that include some working on achieving immortality, and he invested millions in funding research to treat aging as an engineering problem to be solved at the cellular level by reprogramming cells to stop aging. The anti-aging literature is loaded with technologies to prolong lifespan by 20-40%, at least in lab animals. Interventions such as caloric restriction, rapamycin, stem cells, genetic engineering, nanotechnology and metformin, etc have been studied for decades for their anti-aging capacity. In the past several years, multiple scientific teams demonstrated the rejuvenating powers of young blood. A study published in the esteemed journal Nature found that eliminating senescent cells in aged mice boosted their lifespan by a hefty 30%. Hundreds of anti-aging drugs are now in the pipeline and billions of dollars are being expended to find real answers. The FDA finally recognized 'Aging' as a disorder that the medical community could target and potentially treat, something the American Academy of Ant-Aging Medicine (A4M) (www.Worldhealth.net, www.A4M.com) has been stating for decades. Notes A4M President Dr Ronald Klatz, "'Aging is Not Inevitable' and we are seeing the largest paradigm shift in the history of medicine." We know that lifespan has essentially been going up roughly 1 year in every 4, but healthspan is not going up at anywhere near the same rate. The United States spends 19% GDP on healthcare, most of which is used in the last 6 months of a person’s life. If u want an exciting career, the anti-aging & regenerative medicine marketplace is one to look at seriously. We can no longer practice the 'disease based' medicine of the past...preventative anti-aging & regenerative medicine is the only viable solution to prevent bankrupting of the national budgets due to massive chronic healthcare costs. The Robots are Coming Robotics is a rapidly emerging technology which will penetrate every aspect of business and our daily lives. This will replace massive numbers of manufacturing jobs and manual labor. Japan is expecting one in three of its population to be over the age of 65 by 2030, and one in five to be over 75, creating a major requirement for the care of the elderly. Japan is now using robots to service the elderly. A hotel opened in Japan in 2015 with lifelike robots, called 'Actroids', serving as the check-in staff. Aid assistance in nursing facilities is on the horizon, meaning many of the entry-level jobs in those areas will become obsolete just like bank tellers. Look at the field of Robotics, AI (Artificial Intelligence) and VR (Virtual Reality) technologies for massive growth industries. Coastal Changes Climate change will have a strong economic impact in the future. It is anticipated that by 2050, more than 40% of the world’s population will live under severe water stress, resulting in floods or drought that, combined, can put the economic value of assets at risk to record highs. Becoming efficient with resources is socially responsible and cost beneficial. Organizations need to adapt to increasing regulations controlling energy efficiency, waste, water leakage, urban congestion, transportation efficiency, land degradation, freight impact, and other factors. Allowing employees to work virtually also reduces the need for facilities and helps organizations minimize their carbon footprints. New Energy Sources Where we get our energy from will change dramatically. The U.S. military has pledged to get half its energy from renewable resources by 2020, and the Navy whole-heartedly believes it can turn to 50 percent biofuels by then. It makes political sense not to rely on volatile regions for energy, and this push could mean both cleaner vehicle fleets and a major bump in the competitiveness of biofuels in the market. The strangle hold that Middle Eastern oil holds will soon be an ancient memory. Biofuels and renewable clean energy are growth industries of the future..Oil and coal are on their way out. 3D Print Your Organs and Meat 3D Printable Organs are already in process via 3D “bioprint” organ tissues, a process that involves depositing a “bio-ink” made of cells precisely in layers, resulting in a functional living human tissue for use in the lab. These tissues should be better predictors of drug function than animal models in many cases. In the long-term, this has the potential to pave the way to “printing” human organs, such as kidneys, livers and hearts. By 2020, the goal is to have the technology be broadly used by pharmaceutical companies, resulting in the identification of safer and better drug candidates and fewer failures in clinical trials. ...This same 3D Printed technology via stem cells, is also being applied to meat production for human consumption. (Keith Murphy, CEO of Organovo -World Economic Forum) World Will Get Very Small There is major globalization shift in where business is conducted and is occurring now. McKinsey estimates that half of the world’s largest companies will be headquartered in what are now emerging markets, such as Brazil, India, and eastern European countries. Pressure from global competition and other factors resulted in over 40% of the companies that were in the Fortune 500 in 2000 falling off the list in the next several years. These were replaced largely by new global entrants and technology companies. This will continue to shift to farther parts of the planet. The Job Skills/Info Gap The Job Skills Gap and information Gap is the problem and not that workers are unskilled; it’s that workers don’t know what skills employers need. Technology is already disrupting existing jobs, and creating new jobs that never existed before. In fact, the top 10 in-demand jobs in 2010 did not even exist in 2004. Change is happening so rapidly that 65 percent of today’s grade school kids in the U.S. will end up at jobs that haven’t even been invented yet. If u wish to be competitive you must enhance your tech skill levels for future industries not yet mainstream. (Alexis Ringwald, Cofounder and CEO, LearnUp, -World Economic Forum) Water as a Major Asset Water is an asset not a liability. Driven by global population growth and rising water scarcity, the UN reports that 75 percent of the world’s available freshwater is already polluted. Under-investment in water management is exacerbating the problem, causing serious impacts on human health and the environment. A key challenge is the high capital cost, and high energy requirements, of current wastewater treatment and management systems. Desalination plants will spring up worldwide to create massive needed fresh water from sea ocean water. The ability to use biotechnology to extract resources, such as energy, from waste, and the dropping cost of industrial automation, will begin to change our approach to managing water globally. Rather than a liability, wastewater will be viewed as an environmental resource, providing energy and clean water to communities and industry, and ushering in a truly sustainable and economical approach to managing our water resources. (Matthew Silver, CEO of Cambrian Innovation-World Economic Forum) Super Computers Replacing Your Doctor? Supercomputers with artificial intelligence taking better care of you than your Doctor? IBM Watson has partnered with Celgene to better track negative drug side effects and IBM is applying its cognitive computing AI technology to recommend cancer treatment in rural areas in the U.S., India, and China. For example, IBM Watson could read a patient's electronic medical records, analyze imagery of the cancer, and even look at gene sequencing of the tumor to figure out the optimal treatment plan for a particular person. The IBM Watson programs are able to instantly scan the world's medical literature data for making a diagnosis and treatment plan, so in the future a nurse or tech may be able do a more detailed evaluation than even team of doctors. And coupled with advanced MRI, CT and PET scans, view the inner body in mind boggling ways and even treating cancers and other issues at the microscopic level. This will turn the medical profession on its ear. (Fortune Magazine) The Nanobots are Coming Nanobots (miniaturized robots as small as an atom or electron) could become commonplace and in the future, may even integrate with our brain matter allowing us to merge with computers and the 'Cloud' for a 'Singularity' or merging of our minds with machines & computers. Nanotechnology ("nanotech") is manipulation of matter on an atomic, molecular, and supramolecular scale. The earliest, widespread description of nanotechnology referred to the particular technological goal of precisely manipulating atoms and molecules for fabrication of macroscale products, also now referred to as molecular nanotechnology which is the manipulation of matter with at least one dimension sized from 1 to 100 nanometers and such technologies deal with the special properties of matter which occur below the given size threshold potential applications (including industrial and military). Governments have invested billions of dollars in nanotechnology research and can be as diverse as surface science, organic chemistry, molecular biology, semiconductor physics, microfabrication, molecular engineering, etc. The associated research and applications are equally diverse, ranging from extensions of conventional device physics to completely new approaches based upon molecular self-assembly, from developing new materials with dimensions on the nanoscale, to direct control of matter on the atomic scale. Nanotechnology may be able to create many new materials and devices with a vast range of applications, such as in nanomedicine, nanoelectronics, biomaterialsenergy production, and consumer products. On the other hand, nanotechnology raises many of the same issues as any new technology, including concerns about the toxicity and environmental impact of nanomaterials, and their potential effects on global economics, as well as speculation about various doomsday scenarios. These concerns have led to a debate among advocacy groups and governments on whether special regulation of nanotechnology is warranted.. So with nano circuitry, we may be able to live, basically, in a virtual world — Matrix style....and perhaps even Reincarnate deceased ones virtually and be able to "bring back" those lost through artificial intelligence states some scientists. By the 2030s perhaps we send nanobots into people's brains to extract memories of loved ones. Augment that with a DNA sampling of the deceased, and it may be possible to create a convincing virtual version of somebody who's passed on. This progress is so profound, that within 30 years, computational power of artificial intelligence will be a billion times that of human intelligence, allowing us to upload our minds and maybe even our very souls to a computer, leading to a form of connective 'Singularity', a term created by Google scientist Ray Kurzweil. Even Stephen Hawking thinks it's possible; "I think the brain is like a program in the mind, which is like a computer, so it's theoretically possible to copy the brain on to a computer and so provide a form of life after death," the physicist said. This may in fact lead to virtual bodies like the wild video games and Virtual Reality (VR) and Artificial Intelligence (AI) devices we seeing exploding on the scene: (PopSci.com) Self-Driving Trucks and Cars The push for self-driving cars is not just because motorists would rather let the machine do the work. It’s because taking humans out of equation could mean safer travel and smarter traffic flow. To look forward to how we will drive in 2020 you just have to look back to 1957. The US electricity industry ran a newspaper ad promising a life of leisure in the future with a now iconic image showing a near empty highway and a family in a self-driving car with a glass bubble roof. Instead of worrying about the road ahead, the family are doing what all families do in their downtime apparently — they play dominoes and clearly don’t have a care for skin cancer. When it comes to self-driving cars, the year 2020 doesn’t just mark a vision of the future but a deadline. Nissan and Mercedes-Benz have set 2020 down as when they plan to introduce cars that can navigate city streets without the need for a driver. Volvo, which will soon begin trialling self-driving cars in Australia, has taken that one step further. Back in 2008, Volvo’s lead safety expert Anders Eugensson predicted that “by 2020, nobody shall be seriously injured or killed in a new Volvo”. Since then, Volvo has added some fine print to that bold prediction. Volvo safety expert Trevor Rourke admitted earlier this year that “not even the Pope is infallible” but said the trend was towards zero fatalities by 2020. No matter how attentive a human driver can be, a self-automated car with lasers, radar, sonar and video sensors gives the car the edge in keeping an eye on the road. In many ways Google is leading the charge towards self-driving cars with its autonomous vehicles now having driving nearly 3 million self-autonomous kilometres with only a handful of minor accidents and most of them caused by drivers running into the self-driving car because they are distracted by the Google logo and sensors on the top. But other new players working on autonomous cars include Uber, Tesla and, if the rumours are true, Apple. As Telstra Chief Technology Officer Vish Nandlall says, we’re already down. Driverless Trucks Driverless trucks will be safer and cheaper than their human-controlled counterparts, but that doesn’t mean America’s 3.5 million professional truck drivers are giving up to the machines without a fight. Across the US, truckers collectively haul more than 10 Billion tons of freight each year, but it’s a tough job – the hours are long and lonely, the pay is low and the lifestyle is sedentary. In many ways it’s a job ripe for disruption; robots v truckers. “Picture the taxi drivers around the world acting in response to Uber,” says Andy Stern, the former former president of the Service Employees International Union, referring to protests and violence that erupted in many cities as the $62.5 Billion Silicon Valley on-demand ride-hailing firm challenged conventional, regulated taxis. “Truck drivers will follow a similar pattern,” says Stern. “There will be disruption in different places. You can imagine people ringing state capitals with their trucks.” Much has been written about the advent of the driverless car, with rival versions being developed by Google, Uber and Tesla, yet driverless trucks are likely to roll out at scale much sooner. “Individuals can make their own choices about whether they want to get into a driverless car or taxi, but labour-saving technology will be deployed by businesses much quicker,” explains Stern, whose book Raising the Floor explores the need for a universal basic income as technology replaces jobs. Mining giant Rio Tinto already uses 45 240-ton driverless trucks to move iron ore in two Australian mines, saying it is cheaper and safer than using human drivers. Now the race is on to put driverless trucks on public roads. In May 2015, the first self-driving truck hit the American road in the state of Nevada, and there have been several tests around the world since then including a convoy that drove across Europe to the port of Rotterdam. That convoy used a new automated driving technology called platooning, which connects trucks using Wi-Fi, sensors, GPS and cameras. The leading vehicle dictates speed and direction, while the rest automatically steer, speed up and slow down in close convoy. In San Francisco, former Googlers have launched a startup called Otto, which promises to retrofit vehicles with driverless capabilities for just $30,000. The average trucker’s wage is around $40,000 per year. The potential saving to the freight transportation industry is estimated to be $168 Billion annually. The savings are expected to come from labor ($70 Billion), fuel efficiency ($35 Billion), productivity ($27 Billion) and accidents ($36 Billion), before including any estimates from non-truck freight modes like air and rail. It’s regulation, and not technology that stands in the way of eliminating people from behind the wheel. Although trucking companies are likely to lobby hard for the legal reform so they can save on labor, which represents an estimated 34% of operational costs per mile, Morgan Stanley conservatively estimates that the freight industry could save as $168 Billion annually by harnessing autonomous technology – $70 Billion of which would come from reducing staff. In addition to cost savings, fleets of automatedtrucks could save lives. Crashes involving large trucks killed 3,903 people in the US in 2014, according to the National Highway Traffic Safety Administration, and a further 110,000 people were injured. More than 90% of the accidents were caused at least in part by driver error. What next for drivers? Where does this leave the 3.5 million truckers whose livelihoods depend on the need for a human behind the wheel? Truck Driver is not a profession for the future. Internet of Things It’s the simplest of terms that is obsessing the tech industry and confusing the public: The 'Internet of Things'. There are currently 13.4 billion things connected in the world — smartphones, smart TVs, computers, tablets and the odd fridge and robotic vacuum. Juniper Research predicts that figure will reach 38.5 billion by 2020. Technology analysts Telsyte predict the number of connected devices in the average Australian home will jump from the current figure of nine to at least 24 and the internet-enabled white good will become the norm, just as smart TVs are now standard. This is another career growth area in the tech fields. So we either prepare for these future high tech/Info tidal waves and embrace them, or be swept away by them.
  21. 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!
  22. Hang in, there aging calorie restricters. Help may be on the way (eventually, alas): http://tinyurl.com/zy5hnj8 ("DNA-editing breakthrough could fix 'broken genes' in the brain, delay ageing and cure incurable diseases" -- Independent [uK])
  23. OK - everyone has got to watch this tongue-in-cheek music video called Forever Young, produced by Humanity Death Watch (itself a very funny website). It is about immortality, the Singularity, Ray Kurzweil, and has cameos by the "big three" Anti-AI spokespeople (Hawking, Gates & Musk). Sthira, you are going to love this. It is without question the most hilarious thing I've seen in a long time. If we can't laugh at ourselves, what's the point? Note - I've pasted the lyrics below the video for curmudgeons who don't have time to watch a 4min video. Enjoy! --Dean Produced by Humanity Death Watch Directed by Dorian & Weston Lyrics: Mr. Kurzweil please stay for a while. Singularity’s near, we’re only watching the clock. Hoping for the best but expecting robots Are they gonna kill us all or not? Don’t let me die young I want to live forever My body is fragile so replace it with metal. Living as a cyborg, I’ll be on a God-trip It’s all about transcendence. Our bodies and computers will be as one Superintelligence will be such fun! Thanks to our leader we’ll always be new with brains wired to self improve. Forever young I want to be forever young. With Ray I want to live forever Forever, and ever. Forever young I want to be forever young Yes I really want to live forever Forever young. Some are just downers, some refuse to see Some won’t transcend their biology. Sooner or later they all will be gone While my guy stays young. It’s so hard to get old, I’d rather not I’ll never perish with my nanobots Me and Ray we’re enlightened ones And we’ll evolve together. Uploading our consciousness before death Saved in the cloud to be born again. So many dreams comin’ out of the blue They all will come true! Forever young I want to be forever young. With Ray I’m gonna live forever Forever, and ever. Forever young I want to be forever young. Yes I really want to live forever Forever, and ever. Forever young I want to be forever young! I’m gonna sing this song forever! Written by Paul Babb Directed by Dorian & Weston Cinematography by Neil Lokken Animation & Models by Weston Getto Allen Art Assistants: Rebecca Cook, & Berenice Delfuego Suchilt Original Song Performed by Alphaville Parody Lyrics by Paul Babb & Dorian Electra Starring: Dorian Electra Featuring: Christopher Crawford & Montana Ridge
  24. The Observer

    Motivation for Practicing CR?

    [Admin Note: Observer (the OP) and others - I apologize for moving this post around. After (nearly) completing a long response, I realize just how interesting Observer's questions are, and how they deserve their own thread in the CR Practice Forum. Thanks Observer! I'll be posting a detailed response shortly. - Dean] Great, now you guys somewhat discouraged me in throughout this thread. Just when I was getting a little bit more serious about starting a proper CR regime, after ~10 years of hesitation. But now you convinced me CR probably doesn't do much for us humans, compared to just eating/exercising healthy and staying slim. I am currently on some mild-CR plan with one 24-hour fast every week and my BMI is 21.5. Was planning on lowering it down do 19-20, but now I don't see a reason for doing it anymore. :( Before I believed I would gain at least 5-8 additional years, especially because of my own anecdotal evidence. I am somewhat a unique human specieman in that I was basically on CR for most of my life, unknowingly.. I simply rejected food, never liked sweets and was always semi-anorexic. As a result (I guess) I was developing slower as a child and always looked much younger than my peers. Even now in my late 30's people think I look 25-30 and I do agree my biological age must be closer to 30. Then again, what do I know? Now reading your posts Dean, you seem like a reasonable individual and you convinced me that we probably cannot gain more than ~2 years through CR and possibly even shorten our lifespan.. So the obvious question is, why do you - and others - even continue practicing it? Why not simply live healthy lives? I'm thinking perhaps I should only concentrate on fasting and autophagy that comes with it? What are your thoughts on that Dean, if you don't mind answering?
  25. All, It's been argued by respected aging researchers like Luigi Fontana that CR is likely to extend human lifespan through its effects on the somatotropic axis [2] - the signalling pathway involving growth hormone, insulin and IGF-1. In fact, Luigi argues that the monkeys in the NIA CR longevity trial may not have benefited because they may not have been restricted enough to show the biomarkers of CR-induced extended longevity, which especially includes low IGF-1, as has been observed in CRed rodents, and like he has observed in long-term human CR practitioners from the CR Society. This new review article [1] begs to differ. It uses two lines of reasoning to argue that modulation of the IGF-1 pathway via CR, genetic manipulation or drugs, won't extend human lifespan. The first argument is an evolutionary one that has been made before (e.g. by Aubrey) - that humans use different strategies unavailable to rodents and other lower organisms for dealing with food shortage - i.e. migration, and so humans wouldn't have had the evolutionary pressure to maintain the genetic machinery to hunker down and boost longevity when faced with famine. The second line of argument looks at data from a variety of non-rodent animal and human studies of the association between the IGF-1 pathway and longevity. He suggests the fact that CR didn't work in the NIA monkeys suggests it won't work in humans, although as mentioned above it's unclear how restricted the NIA CR monkeys were, or whether the CR monkeys' IGF-1 pathway was downregulated (somewhere on these forums Michael points to evidence that it was...). The author also points to data from dwarf humans with congenitally low IGF-1 who he says don't live longer. He looks at studies of gene polymorphisms involving expression of IGF-1 and says people with genetically-low IGF-1 levels don't live longer. He says studies of IGF-1 levels of centenarians and their offspring have been equivocal at best. He criticizes data showing shorter people live longer, and even questions the longevity of traditional Okinawans. He's a real skeptic, concluding: The main conclusion of this article is that modulation of the somatotropic axis does not explain longevity variations of ad libitum-fed animals but is a tool to face food shortage, leading to increased longevity in some species only. One can hope that a better knowledge of this axis could help to fight various pathologies, such as obesity not linked to an excessive food intake. However, one should give up the idea that it could help to modulate the ageing process and increase longevity of people not suffering from metabolic disorders. This post by Brett Black argues that low IGF-1 is likely to be detrimental, while the two that follow it in that thread (by me and Michael), suggest the opposite - that lower IGF-1 is indeed associated with improved longevity in humans, contra what the current paper [1] suggests. It seems hard to say who's right on this, given the evidence available to us about the effect of IGF-1 on human longevity, and (unfortunately) the evidence likely to be available to us during our lifetimes... --Dean ---------- [1] Biogerontology. 2016 Apr;17(2):421-9. doi: 10.1007/s10522-015-9632-6. Epub 2015 Dec 28. The somatotropic axis may not modulate ageing and longevity in humans. Le Bourg É(1). Full text: http://sci-hub.io/10.1007/s10522-015-9632-6 Studies in nematodes and mice have shown that the somatotropic axis can modulate their longevity and it has been argued that it could also modulate human longevity. Thus, like nematodes and mice, human beings should live longer when facing starvation and genetic variation of the somatotropic axis should be linked to longevity. This article argues that, because the life-history strategies of humans are very different from those of mice, these hypotheses are not warranted. PMID: 26712318 -------- [2] Aging (Albany NY). 2013 Jul;5(7):507-14. Will calorie restriction work in humans? Cava E(1), Fontana L. Author information: (1)Division of Geriatrics and Nutritional Science and Center for Human Nutrition, Washington University School of Medicine, St. Louis, MO 63130, USA. Calorie Restriction (CR) without malnutrition slows aging and increases average and maximal lifespan in simple model organisms and rodents. In rhesus monkeys long-term CR reduces the incidence of type 2 diabetes, cardiovascular disease and cancer, and protects against age-associated sarcopenia and neurodegeneration. However, so far CR significantly increased average lifespan only in the Wisconsin, but not in the NIA monkey study. Differences in diet composition and study design between the 2 on-going trials may explain the discrepancies in survival and disease. Nevertheless, many of the metabolic and hormonal adaptations that are typical of the long-lived CR rodents did not occur in either the NIA or WNPRC CR monkeys. Whether or not CR will extend lifespan in humans is not yet known, but accumulating data indicate that moderate CR with adequate nutrition has a powerful protective effect against obesity, type 2 diabetes, inflammation, hypertension, cardiovascular disease and reduces metabolic risk factors associated with cancer. Moreover, CR in human beings improves markers of cardiovascular aging, and rejuvenates the skeletal muscle transcriptional profile. More studies are needed to understand the interactions between CR, diet composition, exercise, and other environmental and psychological factors on metabolic and molecular pathways that regulate health and longevity. PMCID: PMC3765579 PMID: 23924667