LONGEVITY MEME NEWSLETTER
October 05 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.
- A Special Mprize Award
- The Respectable Nature of Longevity Science
- Singularity Summit 2009
- The Correlation of Fat, Death, and Disability
- An Interview With Aubrey de Grey
- Latest Healthy Life Extension Headlines
A SPECIAL MPRIZE AWARD
The Mprize for longevity science is the Methuselah Foundation's best foot forward: putting money on the table to encourage greater effort and competition in improving longevity-enhancing biotechnology. You might take a look at the competitor listings, which includes numerous videos of the researchers discussing their work:
Later this week, the Foundation folk will be presenting a special Mprize award:
"Methuselah Foundation will award Z. David Sharp, Ph.D. the Special Mprize Lifespan Achievement Award for the first pharmaceutical intervention to successfully extend the life of laboratory mice. The study, published this summer in the journal Nature, showed that when aging mice were given the drug rapamycin, they lived longer than other mice."
You'll find more on that study, published a few months ago, back in the Fight Aging! archives:
"This is actually good enough to be worth running in the Rejuvenation Prize component of the MPrize for longevity science - it's about the same as the record for late onset calorie restriction started at that age. It has to be said that I'm surprised to see a presently available drug capture a similar level of additional longevity given the past few years of less stellar results from sirtuin-manipulating drugs."
THE RESPECTABLE NATURE OF LONGEVITY SCIENCE
It is sometimes (and, for some, conveniently) hard to remember that researchers who proposed intervening in the aging process had a very difficult time with their colleagues only a decade ago - those at the top or in positions of influence wanted nothing more than all such talk to go away. Researchers who talked openly about extending life were seen as rocking the boat or threatening existing funding strategies, so almost all such talk took place in private and went nowhere. The change in attitudes in the aging research community since then has been nothing short of sweeping, however:
"Thankfully minds change as evidence accrues. It's very hard to ignore the sound science that shows the potential to repair the damage of aging, and even harder to ignore the many demonstrations of extended longevity in mammals, achieved through genetic and metabolic engineering. That is not to mention the siren song of possible personal gain, amplified by the acquisition of Sirtris Pharmaceuticals last year - a huge market awaits anyone who can develop working longevity medicine."
SINGULARITY SUMMIT 2009
The Singularity Summit took place this last weekend. The concept of the technological singularity is enjoying its time in the sun these days; accelerating change is in the air:
Of all the ideas emerging from the transhumanist community over the past few decades, the technological singularity is perhaps the most successful in terms of its present spread and engagement. While the singularity is ostensibly about the development of self-improving artificial intelligence rather than the general acceleration of advances in technology (such as in biotechnology), there is a great overlap between the community of AI advocates and the community of longevity science advocates. They attend the same conferences, talk to the same funding sources, and their organizations share both members and movers and shakers.
A fair few bloggers covered the Summit as it happened. You might take a look at the h+ Magazine editor's blog, for example:
You'll also find videos from the event at the Summit media page:
THE CORRELATION OF FAT, DEATH, AND DISABILITY
The weight of evidence from long-term studies of large numbers of people shows that being overweight strongly correlates with greater disability in later life and earlier death. Being fat also correlates with being poor and having a lower IQ measure - but for those items you won't find a direct biochemical link to cause the damage of aging:
"I think that the evidence is very strong for extra body fat - visceral fat, to be specific - as a major contributory cause of accelerated age-related degeneration. By this I mean a direct and biochemical cause, not merely a correlation; people aren't degenerating more rapidly as a direct result of a lack of dollars or IQ points, but changes to the operation of human biochemistry brought about by the presence of larger visceral fat deposits are very damaging over the long term. Aging is absolutely a matter of how much damage your biochemistry has sustained, and the present consensus is that fat-induced inflammation has a lot to do with accumulated damage."
On the subject of chronic inflammation, such as that produced by visceral fat, you might read this past post:
AN INTERVIEW WITH AUBREY DE GREY
This interview with biomedical gerontologist and longevity advocate Aubrey de Grey is worth a look, as some fresh topics are discussed with the Singularity Summit in mind:
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
EXPLORING THE MECHANISMS OF PROTEIN RESTRICTION (October 02 2009)
Lowered dietary protein leads to a longer life, acting in much the same way as calorie restriction. Here researchers delve more deeply into the underlying mechanisms: "Mitochondria act as the 'powerhouse' of the cells. It is well known that mitochondrial function worsens with age in many species ... Our study shows that dietary restriction can enhance mitochondrial function hence offsetting the age-related decline in its performance ... The researchers report the unexpected finding that while there is a reduction in protein synthesis globally with the low protein diet, the activity of specific genes involved in generating energy in the mitochondria are increased ... That activity, which takes place at the level of conversion of RNA to protein, is important for the protective effects of dietary restriction ... There have been correlative studies that show mitochondria change with dietary restriction, this research provides a causal relationship between diet and mitochondrial function ... mitochondrial genes are converted from RNA to protein by a particular protein (d4EBP). Flies fed a low protein diet showed an uptick in activity of d4EBP, which is involved in a signaling pathway that mediates cell growth in response to nutrient availability called TOR (target of rapamycin). ... d4EBP is necessary for lifespan extension upon dietary restriction. When the activity of the protein was genetically 'knocked out' the flies did not live longer, even when fed the low protein diet. When the activity of d4EBP was enhanced, lifespan was extended, even when the flies ate a rich diet."
ON REVERSIBLE CRYOPRESERVATION (October 02 2009)
From Depressed Metabolism: "I think in the next 20 years more small animal organs, and perhaps some human organs, may be reversibly cryopreserved. The best scenario for cryonics would be improved, and possibly demonstrably reversible, cryopreservation of animal brains. It has been long observed that if reversible solid-state brain preservation could be demonstrated, then cryonics revival becomes a purely technical problem (albeit very complex one) of tissue regeneration. There would be no remaining doubt about whether the preservation itself was viably preserving human beings ... Reversible solid-state cryopreservation of whole mammals is a very difficult problem with existing technology. This is why when asked about it people will often defer to nanotechnology. References to nanotechnology as a solution to a medical problem basically say, 'We have no idea how to solve this problem with existing tools, but future abilities to completely analyze and repair tissue at the molecular level will be implicitly sufficient.' It's a valid argument, but saying that a medical problem will be solved when someday technology exists to solve every medical problem is not very illuminating about time lines or nature of the problem."
SENS RESEARCH WINS THE 3BANANA CONTEST (October 01 2009)
I see that, thanks to the vigorous response of the pro-longevity community, the SENS Foundation has won $5,000 for longevity research: "The challenge, launched this September, was sponsored by 3banana as a philanthropic crowdsourcing contest helping health, environment and education-focused non-profit organizations raise money and exposure for their respective causes while testing the sharing features of the company's online and mobile note-taking software. ... 'We are very honored to accept this prize. This contest has really opened our eyes to the possibilities of furthering our cause using social networks,' said Dr. Aubrey de Grey, Chief Science Officer for the SENS Foundation. 'Thousands of our supporters shared their words of encouragement for our mission, and this effort has created more dialog between our organization and our supporters.'" As the cost of biotech research falls, I think we're going to see much more grassroots fundraising of this nature - see, for example, the laser ablation of lipofuscin research that was funded earlier this year via online efforts.
TOWARDS THE RESTORATION OF AGED MUSCLES (October 01 2009)
Via ScienceDaily: "adult muscle stem cells have a receptor called Notch, which triggers growth when activated. Those stem cells also have a receptor for the protein TGF-beta that, when excessively activated, sets off a chain reaction that ultimately inhibits a cell's ability to divide. The researchers said that aging in mice is associated in part with the progressive decline of Notch and increased levels of TGF-beta, ultimately blocking the stem cells' capacity to effectively rebuild the body. This study revealed that the same pathways are at play in human muscle, but also showed for the first time that mitogen-activated protein (MAP) kinase was an important positive regulator of Notch activity essential for human muscle repair, and that it was rendered inactive in old tissue. ... For old human muscle, MAPK levels are low, so the Notch pathway is not activated and the stem cells no longer perform their muscle regeneration jobs properly ... When levels of MAPK were experimentally inhibited, young human muscle was no longer able to regenerate. The reverse was true when the researchers cultured old human muscle in a solution where activation of MAPK had been forced. In that case, the regenerative ability of the old muscle was significantly enhanced. ... In practical terms, we now know that to enhance regeneration of old human muscle and restore tissue health, we can either target the MAPK or the Notch pathways. The ultimate goal, of course, is to move this research toward clinical trials."
UTILITY AND ENGINEERED LONGEVITY (September 30 2009)
Here's a long post on the utility of contributing to engineered longevity versus the other forseeable technology most likely to dramatically reshape the world - self-improving artificial intelligence (AI). The author puts that goal in advance of contributing now to advancing longevity science, but I think that a point is missed along the way. Even if your contributions made now don't lead to technologies arriving in time to extend your life, they will bring forward the dates at which the medicine of engineered longevity does emerge in each region of the world. Every day gained in this fashion saves approximately 100,000 lives at present population levels. From the post: "The crux of my conflict is whether there is greater utility in putting money toward longevity or strong AI. ... . And for now, let's pretend that longevity escape velocity (LEV) occurs 25 years from now without any of my investment. Now lets say I buy 5 years of 'progress' in longevity, so it happens only 20 years from now. I think it's likely that within the first few decades of LEV, most of the change in life expectancy will come from wealthy old people in prosperous nations. I just saved and improved many lives, but not a whole bunch ... probably under half a billion. Infectious and lifestyle diseases, accidents and wars still exist, and those who can't afford treatment still die when they get old, even when AI shows up."
AN ANIMATION OF PAST AND FUTURE LONGEVITY TRENDS (September 30 2009)
Via Calculated Risk, an animated chart that aptly illustrates the gains in life expectancy over the past 60 years and a set of very conservative projections out to 2050. "The population data and estimates are from the Census Bureau. Watch for the original baby bust preceding the baby boom. Those are the people currently in retirement. With the original baby bust now at the age of peak health care expenses, these are the best of times (from a demographics perspective) for health care. Animation updates every 2 seconds." You might compare this with Anders Sandberg's recent models - at some point over the next decade or so we should expect to see the "official" projections adjusted upward or shown to be overly conservative. The uncertainty introducted by advancing biotechnology is a very important topic in actuarial circles these days; a great deal of money rests on being right about the future of longevity, and being right is now harder than ever.
MODERN GENETICS: DISABLE THE GENE AND SEE WHAT HAPPENS (September 29 2009)
Here is a good example of the way in which modern genetic studies tend to proceed: genes of interest are disabled one by one to confirm exactly what it is they do. This is how researchers are exploring the complex feedback loops and interlinked mechanisms surrounding calorie restriction induced longevity, for example: "Dietary restriction is the most widely used intervention to promote longevity; however, the mechanisms underlying the effect of dietary restriction remain elusive. In a previous study, we identified two novel genes, nlp-7 and cup-4, required for normal longevity in Caenorhabditis elegans. nlp-7 is one of a set of neuropeptide-like protein genes; cup-4 encodes an ion-channel involved in endocytosis by coelomocytes. Here, we assess whether nlp-7 and cup-4 mediate longevity increases by dietary restriction. [RNA interference] of nlp-7 or cup-4 significantly reduces the life span of the eat-2 mutant, a genetic model of dietary restriction, but has no effect on the life span of long-lived mutants resulting from reduced insulin/IGF-1 signaling or dysfunction of the mitochondrial electron transport chain. The life-span extension observed in wild-type N2 worms by dietary restriction [is] prevented significantly in nlp-7 and cup-4 mutants. ... We conclude that two novel pathways, NLP-7 signaling and endocytosis by coelomocytes, are required for life extension under dietary restriction in C. elegans."
OBESITY AND AGING (September 29 2009)
In Search of Enlightenment ponders obesity and aging: "When it comes to a disease like progeria, which is an extreme form of accelerated aging, I assume we would all agree that we should seek ways of preventing the disadvantage that comes with the disease. No child deserves to be robbed of the opportunity to have a healthy childhood and develop into a healthy adult. Progeria is very rare, affecting about 1 in 8 million births. When it comes to obesity, which also accelerates aging (though is less severe than progeria, but much, much more prevalent) we also think we should strive to prevent this. No one deserves diabetes or heart disease in their 50's or 60's. But what about the 'regular' rate of aging, which is less severe but much, much more prevalent than obesity, what should our attitude be? The inborn aging process limits average life expectancy of humans to around 85. Shouldn't we aspire to retard that rate of molecular and cellular damage if it would help prevent disease and death? Does anyone actually believe people (our to make the point more vivid, their parents, children or spouse) deserve heart disease, stroke, AD, cancer, etc. in late life? [Yet] aging research is grossly underfunded and that young scientists who want to make the world a better place gravitate towards goals like trying to control the global climate or finding a cure for just one disease of aging (e.g. cancer) rather than investigating the aging process itself."
REVISITING OVARIES AND LONGEVITY IN MAMMALS (September 28 2009)
It has been known for some years that manipulation or transplant of ovaries can influence longevity in mammals, a fact that might be compared with the mechanisms linking germ cells to nematode longevity. Here is a recent demonstration: "Previously we reported that prepubertally ovariectomized mice that received young transplanted ovaries at a postreproductive age showed a 40% increase in life expectancy. To study this phenomenon in greater detail, 11-month-old ovariectomized and ovary-intact CBA/J mice underwent ovarian transplantation with 60-day-old ovaries or a sham surgery. Results from observations on transplant recipients in the current study extended our previous results. Whereas intact control mice lived an average of 726 days, transplant recipients lived an average of 770 days (i.e., 780 days for intact recipients and 757 days for ovariectomized recipients). If intact recipients had ceased reproductive cycling by the time of transplant, we observed a further increase in mean life span to 811 days. These results demonstrate that young ovaries enhanced longevity when transplanted to old mice and that ovarian status, examined by means of ovariectomy and ovarian transplantation, clearly influenced the potential of young transplanted ovaries to positively impact longevity." We still await an understanding of the biochemical mechanisms involved in this method of life extension.
THE THIEL FOUNDATION (September 28 2009)
The Thiel Foundation is the public face of investor Peter Thiel, noteworthy for his funding of SENS Foundation research. "Freedom is always under siege. Around the world, authoritarian regimes deprive millions of people of basic economic and social rights. Even elected governments can burden their citizens with labyrinthine bureaucracies and complex, unnecessary laws. And while some regimes are obviously worse than others, they all have apologists who obscure these conditions by twisting the relationship between freedom and human fulfillment. The Thiel Foundation defends and promotes freedom in all its dimensions: political, personal, and economic. How do we do this?
(a) By supporting innovative scientific research and new technologies that empower people to improve their lives. (b) By championing organizations and individuals who expose human rights abuses and authoritarianism in all its guises. (c) By encouraging the exploration of new ideas and new spaces where people can be less reliant on government and where freedom can flourish." The goal of freedom taken to its logical ends means not just freedom from human-engineered oppression, but also freedom from the limitations, suffering, and cruelties inherent in the human condition and human biology - such as degenerative aging.