Longevity Meme Newsletter, July 14 2008

July 14 2008

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.



- Folding@Home Prize Update
- Longevity Advocacy at the Idea City Conference
- Mitochondrial DNA Deletions in Your Brain
- Discussion
- Latest Healthy Life Extension Headlines


The Immortality Institute's Folding@Home prize contest continues:


"Many thanks to all of the visionaries and contributors who made the inaugural quarter of the F@H Prize a resounding success! The Longevity Meme folding team rose from rank 199 to 172 (as of June 24th) while increasing its point per day output by 150 percent! The 2nd quarter of competition is beginning on July 1st (all competitor's scores will be reset to zero) and even more cash is up for grabs thanks to a generous donation by Maciek K. So get ready to rev up your PS3s, overclock your CPUs and, max out your GPUs."

It's not too late to jump on in to help the team - and win some money as well. Head on over to the Immortality Institute to find out how to sign up:


To find out more about the science of the folding project, look here:


"We feel strongly that a Distributed Computing project must not just run calculations on millions of PCs, but DC projects must produce results, especially in the form of peer reviewed publications, public lectures, and other ways to disseminate the results from FAH to the greater scientific community. ... More recently (2006-present), we have been putting a great deal of effort into studying proteins relevant for diseases, such as Alzheimer's and Huntington's disease."


A number of well-known faces from the healthy life extension community were at the Idea City conference in June:


"[Longevity science was] a major focus of a recent conference in Toronto organized by Moses Znaimer, the 66-year-old media mogul who built his career on youth-driven television channels such as CityTV and MuchMusic and is now bent on rebranding 50-plus as the new watershed age for hip and active lifestyles. 'If you are having a good time and you are not in discomfort or disarray, we all want to live forever. Who wouldn't want to extend a happy and productive life?' he said."


Damage to mitochondrial DNA (mtDNA), the blueprint for your cell's power plants, is an important component of aging. When one or more of a few important genes in a mitochondrion are damaged or deleted, that mitochondrion begins to malfunction. This leads to a growing chain of molecular and cellular damage, expanding to disease and degeneration of health. Now researchers are peering into individual cells to catalogue the damage they see:


"By employing quantitative single cell techniques, we were recently able to show significantly high levels of mtDNA deletions in dopaminergic substantia nigra (SN) neurons from [Parkinson's disease] patients and age-matched controls. In the present study we used the same approach to quantify the levels of mtDNA deletions in single cells from three different brain regions (putamen, frontal cortex, [substantia nigra]) of patients with [Alzheimer's disease] as compared to age-matched controls."

The short of it: we all have a lot of deletions when we get old, as expected in the mitochondrial free radical theory of aging. Some regions of the brain get hit worse than others, such as the population of neurons whose loss causes Parkinson's disease, but it's a universal problem - and not just in the brain.

As I point out in the post linked above, there are a good half-dozen methods presently in early conceptual or laboratory demonstration stages for replacing entire mitochondria, replacing damaged mitochondrial DNA, or restoring function without repairing damage. These are important technologies for the future of our health, as we all suffer from the results of degraded mitochondrial DNA. This research should be receiving much more attention and funding than it is at present - and that is something we can all help with. Start by showing your support for the MitoSENS project of the Methuselah Foundation:



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!




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/

Naked Mole-Rats and Stress Resistance (July 11 2008)
Long-lived naked mole-rats are little goldmines of information on how metabolism and membrane composition relates to species longevity. From Ouroboros, a new twist: "Stress resistance at the cellular level is correlated with longevity at the organismal level, to such an extent that one can screen for longevity mutants by first identifying stress-resistant animals. ... It would therefore come as a surprise if a long-lived organism turned out to be unusually sensitive to stress - and in particular, sensitive to particular stresses. In one fell swoop, this would falsify both the general, well-accepted correlative pattern (stress resistance = longevity) and the somewhat more fanciful model of a central [stress resistance mechanism related to longevity]. ... Short version: naked mole rats are more resistant than mice and rats some stressors, but not all of them. Heat and starvation, two of the classic and longest-known types of stress known to correlate with longevity, work in the expected direction, with the mole rat more resistant. Beyond that, curiously, it’s hard to find patterns." If you have to bet on biology, always bet that it's going to turn out to be more complex than presently thought.

Sonia Arrison on Aging 2008 (July 11 2008)
From TechNewsWorld: "More than 200 scientists and longevity activists gathered at UCLA recently to discuss advancements in repairing humans. New technology is making it possible to imagine a world with ever greater life spans, but old world issues pervaded the discussions. ... 'We should mount a war on aging where it is not a disease, it is THE disease,' said Gregory Stock, Ph.D., director of the UCLA Program on Medicine, Technology and Society. To do this, Stock proposed an 'aggressive publicly funded program.' While no one challenged this idea on the panel, during the two days of the conference, it was clear that some questioned the efficacy of such a plan. Indeed, in a less formal setting, [Bruce] Ames lamented the fact that under the mostly government-run system of science grants, the 'true visionaries are not getting funding.' This is not surprising, given that government agencies are by nature political, making decisions with an eye toward public opinion, not necessarily the best and brightest ideas. Agencies like the U.S. National Institutes of Health and particularly the Food and Drug Administration typically become risk averse over time, as it's easier to deny approval for an idea or product that no one ever finds out about than it is to take a chance on a revolutionary idea and have it flop."

On Long-Term Brain Maintenance (July 10 2008)
Anne C. ponders long-term maintenance of the brain: "One of the most fascinating things about the brain is how it must simultaneously change constantly over time (in response to new information and other inputs) and maintain the aspects of its structure that permit it to keep functioning as a person wants it to as he or she ages. This is true for the body as a whole, of course, but particularly interesting to consider in the case of the brain, as (unlike other organs and parts, which can be transplanted or replaced by prostheses) the brain is unique to each individual in such a way that you wouldn't ever be able to replace it with another and expect to get 'the same person' as a result. ... It is this uniqueness and irreplaceability of brains that makes them of special concern in thinking about healthcare across the lifespan. ... I [think] it more than reasonable to surmise that the conditions presently grouped together as 'the dementias' will likely someday: (a) subsume the phenomenon of milder memory loss and progressive cognitive difficulty currently considered 'normal aging', and (b) become amenable to preventative, maintenance, and rejuvenation treatments."

AGEs and DNA Damage? (July 10 2008)
A research group is proposing that buildup of advanced glycation end-products (AGEs) causes DNA damage in addition to known other issues: "The scientists studied semen samples from men with diabetes who were receiving insulin therapy. ... when we looked for DNA damage, we saw a very different picture. Sperm RNA was significantly altered, and many of the changes we observed are in RNA transcripts involved in DNA repair. ... Diabetics have a significant decrease in their ability to repair sperm DNA, and once this is damaged it cannot be restored ... We found a class of compounds known as advanced glycation end products (AGEs) in the male reproductive tract. These [accumulate] during normal ageing. They are dependent on life style - diet, smoking etc - and in many diabetic complications are centrally implicated in DNA damage. ... The scientists intend to follow up their work by trying to determine how AGEs cause and contribute to DNA damage. They believe that they may have uncovered a new role for AGEs, and that their influence goes far beyond diabetes and its complications." I think that this is proposed on a fairly weak correlation, but we'll see where it goes.

The Longevity Dividend Message (July 09 2008)
Via EurekAlert!, advocacy from those who believe that engineering metabolism to slow the accumulation of age-related damage is the only way ahead: "The traditional medical approach of attacking individual diseases -- cancer, diabetes, heart disease, Alzheimer's disease and Parkinson's disease -- will soon become less effective if we do not determine how all of these diseases either interact or share common mechanisms with aging ... all living things, including humans, possess biochemical mechanisms that influence how quickly we age and, through dietary intervention or genetic alteration, it is possible to extend lifespan to postpone aging-related processes and diseases. ... We believe that the potential benefits of slowing aging processes have been underrecognized by most of the scientific community. We call on the health-research decision-makers to allocate substantial resources to support and develop practical interventions that slow aging in people." Meanwhile, initiatives to raise funding to develop the means to repair - rather than just slow - the damage of aging continue. I believe those initiatives to be the superior path forward, as they seem likely to be less complex, less costly, and more effective.

MSNBC On Calorie Restriction (July 09 2008)
How far we've come in the past five years, from the days in which the mainstream media poured scorn on the practice of calorie restriction. If there is a lesson here, it is to observe the way in which the Calorie Restriction Society engaged and encouraged the research community: progress in science is a necessary accompanyment to progress in advocacy for a cause. From MSNBC: "While the quest for the proverbial Fountain of Youth is endless and typically fruitless, one method known to extend the human lifespan by up to five years has quietly become accepted among leading researchers. The formula is simple: Eat less. It could add years to your life, several experts now say. And done in moderation, it could at least help you live a more healthy life. The only question is: Will the average person do it? ... Here's a rough rule of thumb that many experts generally agree on now: Eat 15 percent less starting at age 25 and you might add 4.5 years to your life ... Eating fewer calories also reduces age-related chronic diseases such as cancers, heart disease, and stroke in rodents. That's important because it suggests ways to not just make us live longer, but to allow us to age more gracefully, healthwise."

p53 and Insulin-Like Signaling (July 08 2008)
An interesting paper: "In higher organisms dependent on the regenerative ability of tissue stem cells to maintain tissue integrity throughout adulthood, the failure of stem cells to replace worn out, dead, or damaged cells is seen as one mechanism that limits lifespan. In these organisms, tumor suppressors such as p53 are central participants in the control of longevity because they regulate stem cell proliferation. Several recent reports have identified p53 as a longevity gene in organisms such as Caenorhabditis elegans and Drosophila melanogaster, which lack proliferative stem cells in all but the germline and have relatively short lifespans. This has forced us to reevaluate the role of p53 in the control of lifespan. We discuss how p53 might regulate longevity in both long- and short-lived species by controlling the activity of insulin-like molecules that operate in proliferating and non-proliferating compartments of adult somatic tissues. We also discuss the hierarchical structure of lifespan regulation where loss of p53 has lifespan extending effects. Finally, we suggest a molecular mechanism by which p53 might facilitate the response to severe nutrient deprivation that allows metabolically active cells to survive periods of starvation. Paradoxically, loss of p53 function in these cells would compromise lifespan."

The First Hourglass Aging Science Carnival (July 08 2008)
The inaugural Hourglass carnival of aging and longevity science is hosted at Ouroboros: "Welcome to the first installation of Hourglass, a blog carnival devoted to the biology of aging. This first issue corresponds with the second blogiversary of Ouroboros, but mostly I consider it a celebration of the excellent (and growing) community of bloggers who are writing about biogerontology, lifespan extension technologies, and aging in general ... BrainHealthHacks writes about recent evidence that smarter people live longer. This is true whether your metric of intelligence is education (which could be problematic, as education levels are often correlated with lifelong affluence and access to medical care) or whether you're looking at individual genetic variations correlated with both longevity and intelligence. It's a giant post that quotes several articles from the primary literature as well as studies by international organizations." You'll find an interesting view of ongoing calorie restriction studies too.

FuturePundit on Resveratrol Results (July 07 2008)
FuturePundit comments on the latest resveratrol research: "Surprisingly, resveratrol extends life of those on the calorie restriction diet. I say 'surprisingly' because calorie restriction is already causing most of the changes that resveratrol causes. But note that mice on the middle range calorie diet did not live longer as a result of resveratrol treatment. ... Maybe on the [every other day feeding] mice the resveratrol worked by mimicking the effects of calorie restriction on the feeding days? ... My reaction to this study is mild disappointment. Resveratrol did not work nearly as well as calorie restriction in extending life. You still need to starve yourself to assure a longer life." It's convenient verbal shorthand, but the practice of calorie restriction is not "starving yourself." It's important to be correct in these matters - calorie restriction is elimination of calories above those needed to be healthy, while still obtaining an optimal level of micronutrients. Many slim, healthy people are already practicing a form of mild calorie restriction when measured against commonly recommended dietary intake. Still, my fervent hope is that calorie restriction will become irrelevant and outstripped by the first medical interventions to extend healthy life, hopefully within the next 20 years. My money is on technologies of mitochondrial replacement and repair.

Methuselah Foundation Undergrad Research Initiative (July 07 2008)
From the Methuselah Foundation: "Are you an undergraduate interested in the Strategies for Engineered Negligible Senescence and other avenues of longevity science? Have you considered volunteering with the Methuselah Foundation to help advances towards the repair of aging? Then you should visit the MFURI website to learn more about the Methuselah Foundation Undergraduate Research Initiative. ... the initiative provides students with the knowledge and logistical support to develop their own projects to further the agendas of the Methuselah Foundation, a non-profit organization which supports research and advocacy for radically extending healthy human life. As a means for promoting student interest, thousands of dollars in scholarship funds, grants, and man hours are provided annually. These support mechanisms, coupled with the logistical support of numerous dedicated, professional volunteer coordinators, provide unprecedented opportunity for student development and success in most any academic discipline. In addition to becoming eligible for scholarships and general support, MFURI students are also given the choice to perform projects and initiatives for university credit virtually anywhere within the United States."



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