Resveratrol Reduces the Effects of Aging

Reduce the Effects of Aging

Funding Aging Research

Resveratrol™s Real Importance

posted on September 29, 2009

For the past year and a half, the press has bombarded us with news of resveratrol and its life-extending potential. Resveratrol is found in the skin of red grapes and is a constituent of red wine, but not in sufficient amounts to explain why the French suffer a relatively low incidence of coronary heart disease, despite having a diet relatively rich in saturated fats. When a description of this paradox was aired on 60 Minutes in 1991 with the proposal that red wine decreases the incidence of cardiac diseases, the consumption of red wine increased 44% and some wineries began lobbying for the right to label their products "health food".

Last year, a study found that high doses of resveratrol mimicked some of the benefits of caloric restriction (including reduced effects of aging) in mice. Now, millions clamor after low-dose supplements in hopes of extending their lives.

It™s probably very good for you, and I take it every day. In fact, GlaxoSmithKline thought enough about it to buy the rights for $720 million. They are developing a high concentration resveratrol diabetes drug.

Dr. David Sinclair of Sirtris, the company that sold the rights to Glaxo isn™t bashful about expressing his opinion about how resveratrol has the potential to extend lives and that it might eventually be a potent anti-aging drug, even though it cannot be prescribed for life extension purposes. He also has positive opinions about life extension in general.

In an article by Reason from the archives, we see such an opinion:

"¦In truth, we're fighting aging and extending lifespan every time a doctor prescribes a statin drug or recommends a healthier diet to a patient. And the fact remains that science has not yet discovered an indisputable biological 'expiration date' for a human life, nor is there good evidence that one exists.

"In time, the idea of an inevitable, debilitating decline starting at age 50 will seem as horrifying and primitive as it does for us, in the age of potent antibiotic cocktails, to imagine a young person in the 19th century dying from an infection caused by a splinter. As a society, we should not accept a terrible period of suffering, dependence, sickness, and frailty if we don't have to. There's nothing more natural than marshalling the body's own defenses to treat and heal itself, and that is precisely what longevity genes like SIRT1 do."

SIRT1 is the gene that resveratrol activates.

Last week, I wrote how the Hollywood crowd is not yet well versed on extreme life extension possibilities, but they do embrace it once they hear a little about it. I found they are a more receptive than most and lots more receptive than many.

However, even the least receptive, including those who object to extreme life extension, clamor for the latest anti-aging rage such as resveratrol.

This is very encouraging to me. Many think we will have lots of resistance, and even organized resistance to supporting longevity research. We see it now. But the positive reaction to a potentially mild life extending supplement such as resveratrol has those same people rushing to the health food stores. Imagine what will happen when we develop and announce a dramatic life extender. Imagine how many will finally line up to invest in technologies that will help ensure your longevity.

So I think the biggest contribution resveratrol makes to the life extension movement is not its potential life-extending properties. I think it is the attention it has drawn to anti-aging and the demonstration we see that even people resistant to longevity will reverse their opinions once they see hope for themselves.

The survival mechanism has a way of overriding all sorts of philosophical viewpoints. Let™s work to introduce an opinion reversing œkiller app soon.


You'll find an Aubrey de Grey reprint in the latest issue of Discover: "Many people, when thinking about the idea of adding years to life, commit the 'Tithonus error' - the presumption that, when we talk about combating aging, we're only talking about stretching out the grim years of debilitation and disease with which most people's lives currently end. In fact, the opposite is true. The defeat of aging will entail the elimination of that period, by postponing it to indefinitely greater ages so that people never reach it. There will, quite simply, cease to be a portion of the population that is frail and infirm as a result of age. It™s not just extending lives that I'm advocating; it's the elimination of the almost incalculable amount of suffering - experienced not only by the elderly themselves, of course, but by their loved ones and caregivers - that aging currently visits upon us. Oh, and there's the minor detail of the financial savings that the elimination of aging would deliver to society: It's well established that the average person in the industrialized world consumes more health care resources in his or her last year of life than in an entire life up to that point, irrespective of age at death, so we're talking about trillions of dollars per year."

Researchers still have much to learn about telomere biochemistry and how it interacts with degenerative aging: "The decline in the neuromuscular function affects the physical performance and is a threat for independent living in later life. The age-related decrease in muscle satellite cells observed by the age of 70 can be specific to type II fibers in some muscles. Several studies have shown that different forms of exercise induce the expansion of satellite cell pool in human skeletal muscle of young and elderly. Exercise is a powerful non-pharmacological tool inducing the renewal of the satellite cell pool in skeletal muscles. Skeletal muscle is not a stable tissue as satellite cells are constantly recruited during normal daily activities. Satellite cells and the length of telomeres are important in the context of muscle regeneration. It is likely that the regulation of telomeres in vitro cannot fully mimic the behavior of telomeres in human tissues. New insights suggest that telomeres in skeletal muscle are dynamic structures under the influence of their environment. When satellite cells are heavily recruited for regenerative events as in the skeletal muscle of athletes, telomere length has been found to be either dramatically shortened or maintained and even longer than in non-trained individuals. This suggests the existence of mechanisms allowing the control of telomere length in vivo."

From In Search of Enlightenment, more to go along with a recent Fight Aging! post on misplaced priorities: "Of all the incredible things that humans have accomplished, our ability to think rationally and consistently about an uncertain and unpredictable long-term future is not one of our strongest attributes. For the vast majority of human history we had a short life expectancy (under 30 years) and thus the cognitive capacities we have inherited from our Darwinian past reflect the reality that, historically, it was much more important to think clearly about short-term goals (like finding food and a mate) than the complex long-term goals facing societies in the 21st century. When I reflect upon the issues of what constitutes a harm for humans (as both individuals and collectively as a society), and what it may be possible to do this century if we invest in certain areas of knowledge and innovation, one particular issue stands out far above the rest - global aging. These harms are a 100% certainty if we do not modify the aging process. We don't need computer models to accurately predict that middle aged people today will age and become frail." Yet comparatively little attention is given to the rapidly evolving science of aging and enhanced longevity - so there is comparatively little done.

Anders Sandberg has built simple models to aid in a discussion of possible futures of enhanced human longevity: "Dirk Bruere on the Extrobritannia mailing list asked a provocative question: 'Any serious H+ predictions of longevity trends between now and (say) 2050 for various age groups? I would expect our predictions to start to deviate from the 'official' ones at some point soon.' This led me to develop a simple model of life extension demographics. I'm not a professional demographer and it depends on various assumptions, so take this with a suitable amount of salt. Summary of my results: I do not see any unexpected demographic changes before life extension breakthroughs, and age at death will not rise until a while after - despite potentially extreme rises of cohort life expectancy. (Flickr photostream [of charts]). I also think we 30+ transhumanists should be seriously concerned about speeding basic and transitional research, and look at alternative possibilities (cryonics, possibly [whole brain emulation]). What about our chances? It all depends on when we think the basic solutions are going to be discovered. My personal intuition is that we are not far from early research breakthroughs (they might have occurred already). I end up with the general life extension social breakthrough somewhere 2040-2060. Great news for current kids, a bit more worrying for us at 30+."

HELP RAISE $5,000 FOR SENS RESEARCH (September 23 2009)
Via Ouroboros, a chance to help raise funds for longevity science: "The SENS Foundation (which organizes the Strategies for Engineered Negligible Senescence conferences) is in the running for the $5000 grand prize in 3banana's Share to Win event. The contest seeks to raise money 'for causes serving unmet needs in health, education and environment.' And you can help. It™s pretty simple: All you have to do is leave a comment on this page. (The award goes to the cause with the most comments.) You can sign on using a Google account if you already have one of those, or register for a free one-off account. It's painless and takes about thirty seconds. Your comment/vote makes a difference! Right now, SENS is neck-and-neck with the competition - as of this post, they're 17 votes behind first place. (Well, sixteen, since I just commented.) So don't just sit there - this is your opportunity to help send real money to a very important cause, at no cost to yourself. Post your comment now. There are only four days left in the contest, so time is of the essence."

MECHANISMS OF HEALING (September 22 2009)
Greater understanding of the mechanisms of healing brings more opportunities to enhance the body's natural powers of regeneration. Here, researchers "provide conclusive proof that, when a muscle is injured, white blood cells called macrophages play a crucial role in its regeneration. The scientists also uncovered the genetic switch that controls this process, a finding that opens the door for new therapeutic approaches not only to sports injuries but also to diseases such as Duchenne muscular dystrophy. After clearing [an injured region], macrophages stop [releasing] pro-inflammatory factors, and start making anti-inflammatory factors that promote repair in the damaged area. This shift from clearing debris to promoting building is known as macrophage polarization ...  Normally, inflammatory factors trigger an increase in C/EBP-beta production, which in turn activates genes that cause the macrophage to polarize. From a medical point of view, it would seem that the trick to improve muscle repair is finding a way to increase C/EBP-beta production and keep it high. If we can now figure out exactly which key genes C/EBP-beta controls, that will give us even more potential targets [to enhance healing].

Yet another single gene manipulation to extend life in mice is reported here, with some implications for potential longevity drugs in humans: "Angiotensin II (Ang II) [has] a role in the etiology of hypertension and in pathophysiology of cardiac and renal diseases in humans. Other functions of Ang II include effects on immune response, inflammation, cell growth and proliferation, which are largely mediated by Ang II type 1 receptor (AT(1)). Several experimental studies have demonstrated that Ang II acts through AT(1) as a mediator of normal aging processes by increasing oxidant damage to mitochondria and in consequences by affecting mitochondrial function. Recently, our group has demonstrated that the inhibition of Ang II activity by targeted disruption of the Agtr1a gene encoding Ang II type 1A receptor (AT(1A)) in mice translates into marked prolongation of life span. The absence of AT(1A) protected multiple organs from oxidative damage and the alleviation of aging-like phenotype was associated with increased number of mitochondria and upregulation of the prosurvival gene sirtuin 3. AT(1) receptor antagonists have been proven safe and well-tolerated for chronic use and are used as a key component of the modern therapy for hypertension and cardiac failure, therefore Ang II/AT(1) pathway represents a feasible therapeutic strategy to prolong life span in humans."

LOOKING FORWARD (September 21 2009)

From The National: "The 20th century saw a string of world-changing technological breakthroughs  - mass-produced automobiles, television, space travel, computers and the internet - that would have been met with incredulity just a few decades before. But the astonishing speed at which 21st-century medicine is advancing looks set to outstrip even those giant leaps for mankind. It is possible that over the course of our lifetime, vaccines will help prevent or cure many of our most lethal cancers; we will be able to grow an unlimited supply of hearts, kidneys and other organs in the lab for transplantation (rendering irrelevant the current drastic shortage of donors); stem-cell technology will cure some forms of blindness and help paralysed, spine-damaged patients regain mobility; and nanotechnology will allow us to develop drug-dispensing devices no bigger than a molecule. It may sound like science fiction, but these technologies - and many others, too numerous to list here - are either available now, or at least will be in the next decade or two."

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