Longevity Meme Newsletter, March 24 2008

March 24 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.



- Incentive Prizes For Our Folding@Home Team
- Views From the Cage
- Discussion
- Latest Healthy Life Extension Headlines


I'm pleased to report that the Immortality Institute incentive prize program is underway for members of the Longevity Meme Folding@Home team:


"The Longevity Meme has teamed up with the Immortality Institute to offer a quarterly prize to people who contribute to the Stanford Folding@home distributing computing project - aimed at curing disease through understanding the basics of protein folding.

"Winners will be determined by how many points are accumulated over the course of three months as reported at the Stanford Folding@home statistics site. The first quarter of competition begins at 12:00 a.m. Eastern daylight time (U.S.) April 2nd and ends at 12:00 midnight, Eastern daylight time, on June 30th. "

New members are welcomed with open arms - please do jump on in and help the team climb the ranks.



We are far more constrained by what we choose to believe than by any other form of limit. The cage of the human condition, collectively and personally, is shaped by the goals we are willing to see as possible.


"It is utterly false to present a choice of working to prevent dementia or working to prevent cancer and heart disease. All can be done - there's no shortage of resources in the world. But this fellow is well with the cage of his preconceived limits: in his world, we must all suffer and die from some age-related disease. Not doing so isn't even a possibility. How odd to hear a researcher argue this point; one might almost think about pushing him back a century to argue about whether consumption or yellow fever is best to be adopted as the death of choice, and therefore no cures should be sought.

"We live in an age on the verge of repairing the damage of aging, preventing all age-related disease, and extending the healthy human lifespan through other means besides. How can any medical researcher debate which age-related degeneration should be left alone as the accepted mode of suffering and death? The strongest bars are found in the cages of the mind that we build for ourselves by accepting the world in its present form."


"So why is it that most people care so much more about the shiny, distracting trinkets of the now, a few years more or a few years less than someone else, in comparison to the far more important issue of the desired future and how to get there?

"We are all doomed unless we dig ourselves out of the hole of aging via the future of medical technology. What does it matter that some of us are a handful of percentage points more or less doomed than others, largely through our own actions in exercise, diet and other controllable factors? It's still doom, and we'll all be just as rescued by technologies capable of repairing the damage that is aging."


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/

An X Prize For Longevity Science? (March 21 2008)
History teaches us that research prizes are a great way to drive progress in science and its application. Competition is fundamental to human endeavor and achievement. In our neck of the woods, we can see that the Mprize for longevity science has gone a long way towards turning the aging research community away from its conservatism and reluctance to discuss extending healthy human longevity. More is always better, however. Via Cosmic Log I see that the X Prize Foundation is considering a prize for longevity research: "Even as the X Prize Foundation kicks off its $10 million competition for super-efficient automobiles, it's working on plenty more prizes to come. X Prize co-founder Peter Diamandis says he’s aiming for two new prizes every year, focusing on five fields. ... Diamandis is already deep into the strategic planning for the next X Prizes. ... We've refined our strategy, and we are planning X Prizes in five vertical fields that we've defined. ... We are looking at life science-related X Prizes, where the Archon X Prize for Genomics is the first. We're looking at areas such as cancer and human longevity."

Sun, Inflammation and Aging Skin (March 21 2008)
Inflammation caused by long-term exposure to sunlight hastens the damage of aging in skin, much as it does in many other tissues and systems in the body. From Science News: "Older skin cells turned up production of enzymes called proteases that break down collagen and elastin, proteins that give skin its spring and structure ... As collagen breaks down, skin collapses into wrinkles. ... It's the equivalent of taking the air out of a balloon. The tension goes out of it, and it begins to sag and fold in on itself. ... Inflammation also sets off other skin-damaging processes, such as inhibiting skin's regenerative abilities and changing fatty acid and cholesterol metabolism, which lead to erosion of the protective barrier that holds in moisture. ... sun exposure hastens "this chronic march down the calendar." ... Exposure to ultraviolet radiation from the sun increases inflammation, speeding the aging process."

Deciphering Telomerase (March 20 2008)
Telomerase, the enzyme responsible for lengthening telomeres, is important in many areas of aging and cancer research. However, as ScienceDaily reports, scientists are still working on understanding it and lowering the cost of researching it: researchers have now "identified two new proteins that make up the telomerase complex and have a lead on several more. This is the first significant step toward understanding the makeup of telomerase since 1999. ... describe two protein components of telomerase. They also show that disabling one of the proteins brings telomerase to a grinding halt. Although the work was done in cells in a lab dish, the findings suggest that a drug blocking that protein may be a useful tool against cancer. ... one problem with studying telomerase is that it's available in such small quantities. Growing huge vats of cancer cells in the lab still only results in miniscule amounts of protein. Until recently, no technology was sensitive enough to analyze proteins at such minute levels." This is the path that leads to cheaply produced telomerase for research, as well as better approaches to manipulate its actions in cells.

Something New For Insulin (March 20 2008)
EurekAlert! notes a newly discovered role for insulin in metabolism: researchers report "that insulin inhibits a master gene regulator protein known as SKN-1, and that increased SKN-1 activity increases lifespan. SKN-1 controls what is called the Phase 2 detoxification pathway, a network of genes that defends cells and tissue against oxidative stress - damage caused by elevated levels of free radicals (byproducts of metabolism) - and various environmental toxins. The new finding was demonstrated in experiments on the digestive system of C. elegans, a microscopic worm often used as a model organism. ... You can manipulate the expression of SKN-1 and the worms live longer ... The idea down the line is that fine-tuning the activity of SKN-1 may lead to increased resistance to chronic diseases and influence longevity, he said. The work could be important as it relates to diabetes and the many problems associated with the disease, particularly vascular and renal complications. But, today's finding may be most important for what it teaches about aging in general." It may go some way towards explaining some of the unknowns related to IGF-1 signaling and lifespan.

More Arguments For and Against Engineered Longevity (March 19 2008)
It's always pleasant to see the signs of greater awareness of healthy life extension and longevity science out there in the world. Here's one: a student-produced video of arguments for and against engineered longevity. It manages to catch most of the major points aired by both sides. "Here's our final video. It looks into the pros and cons of extending our human lives beyond their normal capacity. To enhance the feeling of a debate we decided to animate our parts of the script separately then link them together so that there would be a clear distinction between the arguments for (white text) and against (black text) life extension. We also agreed to leave the debate open so that the viewer is left to decide where they stand on the issue." From where I stand, the point that trumps all others is the ongoing tide of age-related death and pain. More than 100,000 people age to death each and every day, and uncounted millions more suffer terribly. There is no practical level of effort we could devote to the repair aging that would be appropriate to the loss suffered with the passing of every single day.

Exercise, Twins, Telomeres and Aging (March 19 2008)
Via the LEF News, a reminder that taking care of the health basics makes a big difference to the state of your biochemistry over the years: "Inactive people may be 10 years older biologically than their active counterparts, say researchers who measured the length of telomeres in the white blood cells of more than 2,400 twins (mostly women). Telomeres are sequences of DNA that cap chromosomes, protecting them from degrading. ... Each time a cell divides, its telomeres erode, so shorter telomeres are a sign of aging. Twins who were most active during their leisure time (they averaged half an hour of activity a day) had significantly longer telomeres than their twins who were least active (they averaged just two minutes a day). Scientists don't know how exercise protects telomeres from erosion, but other studies suggest that activity may help by curbing inflammation and oxidative stress. Both can shorten telomere length. What to do: Start moving. Any exercise is better than none."

Calorie Restriction and the Hippocampus (March 18 2008)
Adding to the growing list of calorie restriction (CR) benefits: "CR can increase lifespan reliably in a wide range of species and appears to counteract some aspects of the aging process throughout the body. The effects on the brain are less clear, but moderate CR seems to attenuate age-related cognitive decline. Thus, we determined the effects of age and CR on key synaptic proteins in the CA3 region of the hippocampus and whether these changes were correlated with differences in behavior on a hippocampal-dependent learning and memory task. ... We also found that both CR and ad libitum (AL) fed animals exhibited age-related cognitive decline on the Morris water maze task. However, AL animals declined between young and middle age, and between middle age and old, whereas CR rats only declined between young and middle age. Thus, the decrease in key synaptic proteins in CA3 and cognitive decline occurring across lifespan are stabilized by CR. This age-related decrease and CR-induced stabilization are likely to affect CA3 synaptic plasticity and, as a result, hippocampal function."

Manipulating Retinal Regeneration (March 18 2008)
ScienceDaily notes continued progress towards manipulating human regenerative processes: scientist "have discovered what chemical in the eye triggers the dormant capacity of certain non-neuronal cells to transform into progenitor cells, a stem-like cell that can generate new retinal cells. ... with aminoadipate, the newly minted retinal cells migrated to where they might be needed in the retina and turned into desirable cell types. Specifically, [the researchers] showed that by injecting the chemical below the retina, the cells give rise to new photoreceptors -- the type of cells that are lost in retinitis pigmentosa or macular degeneration, as a result, leading to blindness. ... This study is very significant. It means it might be possible to turn on the eye's own resources to regenerate damaged retinas, without the need for transplanting outside retinal tissue or stem cells. If our next steps work in animal disease models, we believe that clinical testing could happen fairly quickly."

Simulation As the Future of Biomedical Research (March 17 2008)
MSNBC looks at where exponentially growing computational power leads us - why run ten experiments in the real world if you could run a thousand in simulation for the same cost in time and money? Medicine will move to look much more like other branches of engineering today in that respect: "I would predict that this century is going to be dominated by our ability to handle biomedical problems in a computational domain ... The increasing ability of computers and biochips to mimic brain chemistry, internal organs, and the interactions between drugs and viruses such as HIV could help reduce the reliance on animal testing to understand the potency and side effects of pharmaceuticals. A more informed leap between experiments on dish-grown cells and lab animals, in turn, could lead to a better drug development process. And eventually, the technology could usher in a new era of personalized medicine in which rapid tests tell doctors which treatments have the best chances of success for individual patients. ... Devices that look at what happens within the body as a whole could eventually take over many roles played by the lab rat [and] the range of simulations being worked on now will increasingly approach reality."

MicroRNAs and Regeneration (March 17 2008)
An update on research into the enhanced regenerative mechanisms of lower animals: "Tiny wonders of the aquarium world, zebrafish can regenerate organs and tissues, including hearts, eye parts and fins. When a fin is lost, the fish regenerates a perfect copy in two weeks by orchestrating the growth of many tissue types, including bone, nerves, blood vessels, connective tissue and skin. ... In zebrafish, one or more microRNAs appear to be important to keep regeneration on hold until the fish needs new tissue ... In response to an injury, the fish then damp down levels of these microRNAs to aid regrowth. The team discovered that the ability of zebrafish to replace amputated fins is particularly sensitive to levels of a particular microRNA called miR-133. ... They probably need to have mechanisms to reduce the potential for unwelcome growth. The implication is that in order to make human tissue regenerate more effectively, we might want to look at some of these microRNAs as potential targets."



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