LONGEVITY MEME NEWSLETTER
July 16 2007
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.
- Stephen Spindler Seeks Research Suggestions
- Ending Aging Another Month Closer
- Latest Healthy Life Extension Headlines
STEPHEN SPINDLER SEEKS RESEARCH SUGGESTIONS
Noted aging researcher Stephen Spindler is taking suggestions from the healthy life extension community for his ongoing mouse longevity studies:
"Does anyone have suggestions of single or groups of supplements, food additives or drugs to test in mouse lifespan studies? I have funding for such studies. If you do, please forward your suggestions to me. Please include some information about the rationale for the suggestions."
Spindler goes on to list a large range of compounds under consideration; I'm sure some of the readers here will be able to suggest plausible additions.
That said, I'm not sure that I see this sort of work as the wave of the future. Consider that a few decades from now, simulated mice on silicon will be cheap, and millions of compounds will be testable every year. Just how great a benefit can the study of a few thousand compounds between now and then gain versus, say, research aimed at advancing biomolecular repair technologies aimed directly at the known and suspected causes of aging?
ENDING AGING ANOTHER MONTH CLOSER
The release of biomedical gerontologist Aubrey de Grey's "Ending Aging: The Rejuvenation Breakthroughs That Could Reverse Human Aging in Our Lifetime" is another month closer:
The book stands as a bridge between presently available layman's summaries of Strategies for Engineered Negligible Senescence (SENS) science and the wealth of published scientific papers on SENS and related lines of research, walking a non-scientific reader through the details in a careful, step-by-step fashion.
The TED Conference European Director recently interviewed de Grey on the topics of Ending Aging and progress in ongoing SENS research:
"The Methuselah Foundation has gone from strength to strength. ... We are currently sponsoring research by three teams (in Phoenix, Houston and Cambridge UK) on two of the most important SENS strands - LysoSENS, the identification and exploitation of microbial enzymes to break down molecules that we cannot naturally degrade, and MitoSENS, the incorporation of modified copies of the mitochondrial DNA into the chromosomal DNA so that mitochondrial mutations will have no effect. Both these projects are going really well, results coming out of the LysoSENS project have already been presented at two meetings and a paper has been submitted for publication in a prominent journal."
You can read more about SENS at the SENS website, naturally, including some of those papers mentioned earlier:
For a good feel of the breadth of medical research relevant to SENS, you might also browse the rather long list of submitted abstracts for this year's SENS3 conference:
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!
Founder, Longevity Meme
LATEST HEALTHY LIFE EXTENSION HEADLINES
To view commentary on the latest news headlines complete with links and references, please visit the daily news section of the Longevity Meme: http://www.longevitymeme.org/news/
Radical Life Extension and the Singularity (July 13 2007)
I agree with this point made by Michael Anissimov. The technological Singularity - in its older, more useful definition relating to information and intelligence - has little to do with greatly extended longevity. "Radical life extension (people living to 100, 200, 300, and beyond) seems very plausible to me, and I believe that we are going to be experiencing this ourselves in our lifetimes, unless an existential disaster occurs. A Berkeley demographer found that maximum lifespan of human beings is increasing at an accelerating rate. However, life extension has very little, if anything, to do with the Singularity, other than that the Singularity is sometimes associated with technological progress and that technological progress may result in radically extended lifespans. This is somewhat like how house mice are somewhat associated with raccoons because both live in areas dense with human populations." This is a useful reminder that a future of greater healthy life extension is not a given: the future doesn't arrive on a conveyor belt, delivered deus ex machina. Desired futures are only achieved when we band together and help to make them real.
Another Telomere Length and Longevity Study (July 13 2007)
There is definitely a relationship between telomere length and human longevity; it remains to definitively and fully describe the mechanisms involved. Is this sufficiently close to the biochemical roots of aging - is it an independent form of accumulated damage - that the many research groups working to lengthen telomeres are onto something? This paper demonstrates the relationship once more: "Many studies have demonstrated the association between telomere length in mitotic cells and carcinogenesis and mortality, but little attention has been focused on post-mitotic cells and human life expectancy. We assessed the relationship between telomere length in cerebral gray and white matter and longevity in 72 autopsied Japanese patients aged 0-100 years ... the 90-100-year age group possessed significantly longer telomeres than the 70s ... Autopsy protocols showed a decrease in the rate of cancer death in individuals in their [80s and 90s] versus those in their 60s, and in their 80s the mean telomere length in the gray matter from cancer death patients was significantly shorter than that of patients who died of other diseases ... These data suggest that innate telomere lengths are maintained very well in the cerebrum, and are associated with longevity."
On Advancing Technology (July 12 2007)
Michael Anissimov talks about the nature of technology: "We realize that the longer you look forward, the more uncertain the predictions get, but one thing is quite certain: if a [technology] is physically possible and obviously useful, human (or transhuman!) ingenuity will see to it that it gets built eventually. As we gain ever greater control over the atomic structure of matter, our technological goals become increasingly ambitious, and their payoffs more and more generous. ... Gene therapy replaces bad genes with good genes, and RNA interference can selectively knock out gene expression. Together, they give us an unprecedented ability to manipulate our own genetic code. By knocking out genes that code for certain metabolic proteins, scientists have been able to make mice that stay slim no matter how much junk food they eat. Lou Gehrig's disease has been cured in mice, and it could only be a few years before we develop a therapy that can cure it for humans too. Aubrey de Grey’s SENS (Strategies for Engineered Negligible Senescence) research program contains various prescriptions for the use of gene therapy. Within a couple decades or so, progress in anti-aging therapies will improve to the point where we are gaining more than an extra year of lifespan per year, reaching so-called 'longevity escape velocity' eventually culminating in indefinite lifespans. Like many transhumanist technologies, gene therapy is really exciting because it's just beginning."
Return on Investment for Medical Research (July 12 2007)
The Scientist looks at return on investment for research - especially medical and biotechnology research - and misses the point. We're not in a gentle race to an ephemeral crown with other demographic groups overseas. Rather, we're in a nail-biting contest to defeat disease, degeneration and aging, amidst an ongoing tsunami of death that dwarfs any other cause of misery in the world. The sheer scale of economic devastation suffered daily, monthly and yearly due to aging is hard to visualize; as Robert Freitas notes, "the worldwide natural death toll of 52 million people in the Year 2001 represents an economic loss of about $100 trillion dollars. Every year. How big of an economic calamity is this? Taking Federal Reserve figures for the total tangible wealth of the United States, including all financial assets, all real estate, and all consumer durables, net of debt, and applying the ratio of U.S. to world GDP gives us an estimate of total global tangible net worth of $91 trillion dollars. So this means that every year, natural death robs us of human capital equivalent in value to the entire tangible wealth of the world." Nations have mobilized to oppose economic damage a fraction of this value. No practically attained level of resources directed towards the fight to defeat aging could ever be said to be sufficient.
Antagonizing Antagonistic Pleiotropy (July 11 2007)
Chris Patil examines a contrarian viewpoint on antagonistic pleiotropy and the evolution of aging: "the idea is that genes which benefit an organism early in life but hurt fitness later on can nonetheless be selected, since extrinsic causes of mortality and the inexorable logic of exponential population growth cause the strength of selection to decrease with time ... The theory is an attractive one that has gained popularity among biogerontologists, as more and more findings are announced that appear consistent with its predictions. ... But every theory has detractors as well as adherents ... In a recent opinion in Biogerontology, Parsons launches a spirited attack on the generality of antagonistic pleiotropy ... The author’s main argument is that the requisite conditions for antagonistic pleiotropy are extremely rare in naturally occurring populations, and that environmental stress should be a major driving force in the evolution of longevity. Negative consequences of selectable traits should be less important at the levels of energy intake that actually occur in the wild, he argues; furthermore, he proposes that some of the data in favor of antagonistic pleiotropy are artifacts of the artificially benign environments we create in the lab."
The Biology of Human Longevity (July 11 2007)
Gerontologist Caleb Finch has a new book out this month, entitled "The Biology of Human Longevity: Inflammation, Nutrition, and Aging in the Evolution of Lifespans." Here, US News takes a gander: "In the last 200 years, one year of extra lifespan has been added for about every four years of historical time. Life expectancy has doubled since the industrial revolution, from about 40 years to near 80 years. ... Aging processes in humans are directly related to the nutritional and inflammatory aspects of the environment. One example is Alzheimer's disease: Research from our lab has shown that the senile plaques that build up in that disease are related to inflammatory processes in the brain. And we now know that inflammation intensifies atherosclerosis, the hardening of the arteries that can contribute to stroke and heart attack. Longer life spans have been a worldwide phenomenon associated with improvements in hygiene and medical care and reductions in infectious disease. Some have explained this through the reduction of infant mortality. But we're also living longer because we're staying healthier - kids have fewer infectious diseases to fight with. This reduction of inflammation and infection, along with the improvement of nutrition, has contributed to longevity by slowing many of the diseases of aging."
Glenn and Millard Foundations Support SENS3 (July 10 2007)
When looking at the most impressive list of presentations set out for this year's Strategies for Engineered Negligible Senescence conference (SENS3), we should take a moment to acknowledge the generous donors who help to make it possible: "$25,000 from the Millard Foundation; $10,000 from the Glenn Foundation; $1,000 from HMX, Inc.; $1,000 from the Supercentenarian Research Foundation; $1,000 from Legendary Pharmaceuticals. Thank you all! Regular readers will recognize the Glenn Foundation as a major supporter of the Methuselah Foundation, as well as the force behind the Paul F. Glenn Laboratories for the Biological Mechanisms of Aging, and some of the other groups as long-time donors and associates. Gary Hudson of HMX, Inc. is well on his way through the six figure range - a true champion for healthy life extension science. For those of you with a mind for the history of computing - many, I know - you'll be interested to know that the Millard Foundation is the philanthropic face of William Millard, visionary pioneer of the PC industry and founder of Computerland. Pleased to have you on board!"
More On Stem Cells Versus Parkinson's (July 10 2007)
Researchers continue to move towards the use of stem cells to treat neurodegenerative conditions like Parkinson's. Via PhysOrg.com: "[The] study showed that only a small number of stem cells turned into dopamine-producing cells - not enough to improve the primates' function by replacing missing neurons. Instead, some stem cells turned into astrocytes, a supportive brain cell that produces neuron-nourishing chemicals. ... [we] have been arguing, for some time now, that stem cells are important for brain repair because they provide growth factors and because they send signals to the brain to help it repair itself. This study in primates showed the same effects that the stem cells are there to act as facilators of repair versus the original hypothesis that stem cells are transplanted to merely replace an injured cell ... We hear about new sources of stem cells monthly, but how we take those cells and treat disease is going to be a significant amount of translational work. This is one of the first studies that starts that process - looking at primates before going into people with Parkinson's disease ... Pending further preclinical studies, the results so far from the current study are supportive for developing a safe and effective stem cell treatment for Parkinson's disease."
The Problem, Illustrated (July 09 2007)
Why, despite the great range of potential applicable biotechnology, do we not see hundreds of millions of dollars invested in startups attempting to address the aging process? The answer is buried in this New York Times article on Sirtris: "Dr. Westphal and Mr. Sinclair stress that they are not working to 'cure' aging, a condition that, so far at least, is common to all humanity and that most physicians do not consider a disease. 'Curing aging is not an endpoint the federal drug agency would recognize,' Dr. Westphal says dryly. Instead, both men say, they are working to ameliorate the diseases of aging." For so long as unelected government employees can declare, with no accountability and full force of law, what medicine is permitted and what is not, there will be no direct venture funded efforts to cure aging - or even to take the first steps by aiming to repair specific, identified age-related damage in order to intervene in the aging process. There is no lack of companies, research groups and billions of dollars ready to be directed to that end, as any brief survey of the biotechnology marketplace will show you - but the ignorant few who write policy continue to bury all that potential. The work that could have gone to advance the cause of healthy longevity is instead confined towards the backwaters of patching specific age-related conditions.
Cancer Gene Therapies Improving (July 09 2007)
Effective gene therapies for cancer are becoming more plausible for the near future, as illustrated by this report from EurekAlert!: "A molecularly engineered therapy selectively embeds a gene in pancreatic cancer that shrinks or eradicates tumors, inhibits metastasis, and prolongs survival with virtually no toxicity ... The researchers call the system a versatile expression vector - nicknamed VISA. It includes a targeting agent, also called a promoter, two components that boost gene expression in the target tissue, and a payload - in this case a gene known to kill cancer cells. It's all packaged in a fatty ball called a liposome and delivered intravenously. ... In a test of the therapy against two aggressive lines of pancreatic cancer in two different types of mice, researchers loaded the VISA system with a mutant version of a gene named Bik, which expresses a protein that naturally forces cancer cells to kill themselves. The team created the more lethal mutant and named it BikDD. Untreated control mice in both experiments all died within 40 days. Mice treated with the mutant gene delivered via a less-targeted viral promoter driven expression system employing cytomegalovirus (CMV) all died within 90 days, most much earlier. In both trials, the VISA-BikDD mice lived longer, with at least half surviving for 14 months with no detectable sign of cancer recurrence."