LONGEVITY MEME NEWSLETTER
September 28 2009
The Longevity Meme Newsletter is a weekly e-mail containing news, opinions, and happenings for people interested in healthy life extension: making use of diet, lifestyle choices, technology, and proven medical advances to live healthy, longer lives.
- An Aubrey de Grey Interview
- A Look at the Maximum Life Foundation
- Illustrating the Aging Immune System
- Latest Healthy Life Extension Headlines
AN INTERVIEW WITH AUBREY DE GREY
A short video interview with Aubrey de Grey is currently running at MSNBC - links in this Fight Aging! post:
In addition, you'll note that we're coming to the close of an online contest to win $5,000 for de Grey's SENS research. A startup is rather cannily running a contest based on comments in their system (no doubt both a good test and good publicity) - the nonprofit cause that encourages the most people to leave a comment wins. SENS research is currently very close to winning, and every dollar does help. So take a few moments to add a comment if you haven't done so already. Instructions and links can be found in this Longevity Meme news item:
A LOOK AT THE MAXIMUM LIFE FOUNDATION
The Maximum Life Foundation is the initiative and online presence of entrepreneur David Kekich:
"The Maximum Life Foundation was founded in 1999, and thus predates most of the latest generation of serious ventures in advocacy and fundraising for longevity science, such as the Methuselah Foundation, SENS Foundation, or Immortality Institute. This is reflected in the messaging of the Maximum Life Foundation and its founder, which comes across as a hybrid of two eras: on the one hand the past era of supplements and hopes epitomized by the Life Extension Foundation; on the other hand, the present era of biotechnology and a real chance at medicine that can slow or reverse aging. All, of course, heavily filtered through Kekich's view on markets, health, self-actualization, and progress."
Kekich has recently published a book on the march towards engineered longevity, in which he takes the ideas developed in the community over the past decade and presents them in the style of gonzo self-help or "for dummies" books. You can download it from the Maximum Life Foundation website, or order it from Amazon. To the best of my knowledge, no-one in the pro-longevity advocacy community has given that a serious try yet - so we'll see how it goes. It is my belief that growth in advocacy and fundraising in the future depends upon expanding the community of people who "get" the basic message: that we stand at the edge of a fantastic opportunity to use biotechnology to extend healthy life, but it won't happen in time to benefit us unless we all get behind the wheel and push.
ILLUSTRATING THE AGING IMMUNE SYSTEM
The way in which the immune system fails with age is one of the most structured forms of degenerative aging. Your immune system is, by its very nature, set up to fail over time, and researchers today understand why that is the case. There are two issues at work: (a) that the supply of new immune cells dries up as your thymus, where those cells are nurtured, is programmed to cease its function early on in life, and (b) you can only support at fixed maximum number of immune cells, which is important because of viruses like cytomegalovirus (CMV). Whilst CMV is fairly harmless, the body cannot effectively remove it. But the immune system keeps trying, with the result that increasing numbers of immune cells become CMV-specialized memory cells rather than the killer cells that can destroy new threats. In effect your immune system becomes ever more focused upon CMV at the expense of its ability to perform all its other vital jobs:
"The next step in immune research should be to do something about these problems. On the one hand, we would want to understand how to safely keep the thymus active, and on the other hand establish methodologies to regularly eliminate CMV-specific immune cells and thus free up capacity. Fortunately, both of these goals look to be very plausible for the next decade of development. Researchers in the cancer science community have been demonstrating methods of safely killing specific cell populations identified by their surface markers for some years now, using either nanoparticles or engineered viruses. Killing specific immune cells should be well within the capabilities of this emerging field. As to the thymus, we can look to regenerative medicine and tissue engineering, a vast and well funded field devoted to restoring and recreating fully functional organs using a patient's own cells. If you can build a heart from scratch, a thymus can't be many years behind."
The highlights and headlines from the past week follow below.
Remember - if you like this newsletter, the chances are that your friends will find it useful too. Forward it on, or post a copy to your favorite online communities. Encourage the people you know to pitch in and make a difference to the future of health and longevity!
LATEST HEALTHY LIFE EXTENSION HEADLINES
A MODEST PROPOSAL: HOW TO STOP AGING ENTIRELY (September 25 2009)
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."
TELOMERE LENGTH IN MUSCLES (September 25 2009)
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."
MORE THOUGHTS ON PRIORITIES (September 24 2009)
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.
MODELING THE FUTURE OF ENGINEERED LONGEVITY (September 24 2009)
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+."
THE FUTURE OF ALCOR (September 23 2009)
Depressed Metabolism here critiques cryonics provider Alcor: "Alcor's recent news item about its 2009 Annual Board Meeting and Strategic Meeting contains a number of encouraging statements. On the front of institutional reform, however, there is not much news to report. The passage about the need to balance recruiting new Board members and preserving institutional memory reads as a rather uninspired defense of the Board's recent decisions. In light of the growing recognition that most of Alcor's problems over the years can be tracked back to the composition and functioning of the Board of Directors, one would have expected more innovation on this front. ... One of the most positive items in Alcor's report is the recognition that Alcor would benefit from substantial cost savings in its operations. Throughout most of Alcor's history the organization has been dependent on (unpredictable) donations from wealthy members to sustain normal operations. Obviously, this way of funding the operations of a cryonics organization (as opposed to long term patient care) constitutes an irresponsible gamble. Donors should be commended for being reluctant to contribute to Alcor (any further) until Alcor has shown evidence of getting its financial house in order. A number of sensible proposals were discussed to generate more structural income for the organization such as increasing membership dues, raising cryopreservation minimums, introducing a recommended funding level (as opposed to just a minimum funding level), and creating income-generating endowments."
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."
RESEARCHING THE MECHANISMS OF OSTEOPOROSIS (September 22 2009)
This ScienceDaily release provides insight into present mainstream research into the mechanisms of osteoporosis and rheumatoid arthritis: a matter of scientists investigating and debating mechanisms to find the next and better target for viable drug development. "Bone is continually recycled to maintain its strength through the competing action of osteoclasts, cells that break down aging bone, and osteoblasts, which build new bone. Osteoclasts also play a central role in common diseases that erode bone, where two signaling molecules, TNF-alpha and RANKL, cause too much bone breakdown. ... the current study argues that TNF-alpha and RANKL have different effects on levels of a key inhibitory protein [called] NF-kappaB p100 ... We believe NF-kappaB p100 limits not only osteoclast maturation, but also the number of inflammatory cells attracted to the joints in response to TNFalpha. If confirmed, it would mean that p100 has more than one role in more than one major bone disease, and thus would create new opportunities to reverse disease by manipulating p100 levels."
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].
ANGIOTENSIN II AND THE AGTR1A LONGEVITY GENE (September 21 2009)
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."