Longevity Meme Newsletter, January 30 2006

January 30 2006

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.



- Questions to Ponder
- Changing the Aging Research Paradigm
- Discussion
- Latest Healthy Life Extension Headlines


I thought I'd present a pair of open questions from Fight Aging! for you to ponder; they depart somewhat from the "first things first" ethos of healthy life extension that I like to maintain, but feel free to jump in and add your comments by following the links below.

Firstly, in relation to the practice of cryonic suspension, how do you make your resources, modest or otherwise, work for you when you're not there to defend your decisions? We'd all like to think that we'll live long enough to see the era of real, working anti-aging medicine, but clearly some of us will not. Cryonics is the best of the available alternatives to the grave, and as in all forms of insurance, financial or otherwise, it pays to take a little time to think things through:


This matter of resources is something of a fundamental question for all cryonicists, since at least some portion will be used to support their suspended state. Are the greatest challenges to cryonics - and the chances of those undergoing cryonic suspension - those of human nature rather than the development of advanced technology for revival?

On to the second question: what will be the principle age-related causes of death 30 years from now? We can make some educated guesses based on looking at the pace and direction of medical science today:


Pick a major cause of age-related death today - I think you'll find that in each case there's a large, well-funded research community that is plausibly within 10-20 years of a cure. Bearing that in mind, what will health and longevity prospects in 2036 look like for those of us reading this today?


The lesson to take away from this examination of future mortality rates and causes is that the present dominant paradigm of medical research - identify the symptoms, patch up the problem, move on to the next issue - may extend our healthy life spans, but it is too slow and too costly. There are simply too many potential problems, too many leaks in the dam. Each time a new problem is found, everyone in the first decade or two of the queue is dead of it before the research infrastructure can react. Patching in response to emergencies is no way to keep complex machinery running, as any mechanic or programmer will tell you - and it's certainly not the best way to help us live longer, healthier lives.

A much more efficient methodology is needed, one that looks to the root causes of all these problems. Twenty year olds aren't falling apart at the seams - so instead of the endless, expensive, ultimately unsuccessful paradigm of searching for ways to patch up fatal symptoms of aging in 80-year olds, more time and money should go to finding out how to repair and reverse the underlying changes that make that 80-year old frail:



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



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/

Mitochondrial Transfer as Healing? (January 29 2006)
A most interesting New Scientist article looks at hints of an existing mechanism by which age-damaged mitochondria could be repaired. Given the central role played by mitochondrial degeneration in aging, this would be a very big deal if it could be exploited: "Healthy cells seem to have shown an amazing ability to breathe new life into damaged ones by rejuvenating their defunct mitochondria. It is an extraordinary and controversial claim. But if confirmed it could offer a way to prevent a range of harrowing metabolic diseases that affect millions of people. Experts in mitochondrial research have yet to be convinced. They say the work purporting to show the effect has yet to be comprehensively peer-reviewed, and is so potentially ground-breaking that more evidence is needed."

Exploring Life Extension (January 29 2006)
The Immortality Institute film Exploring Life Extension can now be found at Google Video thanks to Institute volunteers. You can also order a free DVD beta cut, or search for one of the several bittorrents. The film is a much condensed summary taken from hundreds of hours of interviews with members of the healthy life extension community, and a good first effort from the film crew. There's much more to be mined in the source material, however. A version two, with the benefit of greater editing experience and some fresh eyes on the interviews would be a worthy project. There's a lot to be said for this sort of community anthropology as a way of effectively delivering a message to a wider audience: radical life extension is a noble, plausible, possible goal.

More Klotho Research (January 28 2006)
Kevin Perrott notes new research on the Klotho gene: "Released just yesterday are two papers which describe more detail of the story behind Klotho, unravelling some nuances which in days gone by would have taken further years or even decades to uncover. The first paper describes how Klotho exerts its anti-aging effects by binding to and increasing the influence of a factor on cell growth while the second paper shows Vitamin D to play a direct role in this factors activity, showing a potential link between Klotho and Vitamin D." I'm still skeptical of the earlier Klotho experiments, but it seems there's something of interest in the biochemistry. Still, all this metabolic tinkering is no path towards radical life extension - that will require more ambitious, directed strategies.

Another Alzheimer's Mechanism (January 28 2006)
The biochemistry of Alzheimer's is complex indeed, as illustrated by the fact that after 10 years of massive funding, researchers are still uncovering and debating the significance of possible mechanisms and causes. "The emerging lesson is that cognitive problems in [Alzheimer's] are related to defects in the machinery controlling neuronal connections, not the lesions observed by pathologists ... This new study implicates the PAK enzyme-signaling pathway, which is known to play a role in synapse formation and developmental cognitive deficits, or mental retardation. The PAK enzymes form a family that includes two members known to localize to synapses (PAK1 and PAK3). Both are known to play critical roles in learning and memory. Humans with genetic loss of PAK3 have severe mental retardation. Both PAK1 and PAK3 are abnormally distributed and reduced in Alzheimer patients to an extent sufficient to contribute to cognitive decline."

SIRT6 and Accelerated Aging (January 27 2006)
Scientists are discovering all sorts of interesting things now that mainstream calorie restriction research is focused on sirtuins: "The research on SIRT6 is part of a broad effort in the Alt laboratory to study the role of a family of seven known mammalian sirtuin genes. These studies were prompted by findings some two decades ago that a yeast counterpart called Sir2 maintains genomic stability and regulates aging in yeast cells. Researchers had also found that enhancing the activity of Sir2's counterparts in the roundworm and fruit fly extended their life span. ... we've found that the SIRT6 knockout produces the most dramatic effects ... The researchers do not know whether the accelerated aging-like effects of losing [SIRT6] relate to its role in DNA repair. Nor do they know whether the degenerative effects are relevant to the natural aging process. However, they said, the discovery offers an intriguing new model for studying DNA repair, as well as its possible role in aging-related degeneration."

Designing Advanced Nanomedicine (January 27 2006)
As an estimate, scientists are probably 10 years from building proof of concept nanomachines of the sort proposed by Robert Freitas, or shown in this Nanotechnology News Network article. It'll be at least another decade after that to proceed to mass production - but the benefits will be astounding. (Poorly) translated from the Russian: "How we can see, proposed worm design can collect and digest more microorganisms than microbivore. It can move in blood, so it will multiply number of collected bacteria. Nanorobot in bloodstream can collect bacteria and fungus. Worm can also crawl on the tissue surface, so I can imagine worms, crawling on vein's surface to clean out atherosclerosis conglomeration. Worm will be constructed from diamondoid with high precision molecular assembling technology. Worm tracks technology allows fully reprogrammable binding sites, which can make Worm multipurpose device - it can collect not only bacteria or viruses, but toxic enzyme too."

Bona Fide Dopamine Neurons (January 26 2006)
Via EurekAlert news of a good step forward for the future of regenerative medicine: researchers have "discovered a 'master determinant' that turns embryonic stem cells into bona fide dopamine neurons, brain cells that degenerate in those with Parkinson's disease. The findings hold promise for the future of cell replacement therapy for the debilitating and incurable disease ... The results also underscore the general importance of a thorough understanding of development for producing authentic cells of a desired type from stem cells. ... We spent a lot of effort and are now confident that these are authentic dopamine neurons. If we want to treat Parkinson's patients with stem cells, it will only work if we are able to generate authentic dopamine cells. In the use of stem cells for therapy, it is of utmost importance to make the correct cell type. In the brain, there are at least 1000 different types of neurons, only one of which is clinically relevant to Parkinson's disease."

Other Regenerative Strategies (January 26 2006)
Wired takes a brief look at regenerative methodologies outside the mainstream of stem cell based therapies: "Hydra Biosciences is working a regeneration drug that stimulates heart muscle-cell regrowth, and could lead to better recoveries for heart attack sufferers. The protein-based drug induces mature cells to become a little bit like stem cells. It causes heart cells to 'dedifferentiate' partially, reverting them to an earlier stage of development and activating their ability to generate more muscle cells. ... The dogma has always been that heart muscle cannot regenerate. But it's possible in animals, and now we have drug candidates that may do the same thing in humans. ... He estimates human trials of the protein compounds will begin within the next few years."

More Use It Or Lose It For the Brain (January 25 2006)
More studies linking metal exercise with improved resistance to degeneration are rolling in: "complex mental activity across people's lives significantly reduces the risk of dementia. The researchers found that such activity almost halves the incidence of dementia. ... It is a case of 'use it or lose it'. If you increase your brain reserve over your lifetime, you seem to lessen the risk of Alzheimer's and other neurodegenerative diseases. ... individuals with high brain reserve have a 46 percent decreased risk of dementia, compared to those with low brain reserve. All the studies assessed agreed that mentally stimulating leisure activities, even in late life, are associated with a protective effect. ... brain reserve is not a static property, nor that it is determined by early life experiences such as level of education, socio-economic deprivation or poor nutrition. It is never too late to build brain reserve."

Regenerating Stroke Damage (January 25 2006)
ScienCentral reports on a potential method of regenerating damage caused by a stroke: "In the developing systems of young people and other animals, the central nervous system (CNS), which consists of around ten billion nerve cells, have the ability to spontaneously grow new nerve cell connections. ... We know that adults have the same capacity to re-grow, it's just that they're being stopped from re-growing ... Nogo-A is one of the major inhibitors to new growth, there are others but, Nogo appears to be one of the major ones ... In tests on stroke-damaged rats Kartje and her research team used a very specific antibody, an immune-system protein, to stop Nogo-A from binding to receptors on nerve cells. Without the inhibitory affect of Nogo-A, the injured nerve cells were able to re-grow, restoring lost movement to the front paws of the rats."

East Bay Calorie Restriction (January 24 2006)
A feature article in the East Bay Express takes a look at calorie restriction: "Years of studies have shown that severe dietary restriction indeed prolongs life, in lab creatures at least. Yeast on a [calorie restricted, optimal nutrition] diet can live up to three times longer than normal, fruit flies double their average lifespan, and mice that normally live two years can live three or more. Studies on monkeys are ongoing, since primates are naturally long-lived, but so far the calorie-restricted monkeys appear to get fewer lethal chronic diseases and may indeed outlive their well-fed peers. These animals not only live longer, but seem to retain their youthfulness. They are smaller than their counterparts, but more active. They look younger and healthier, are mentally more agile, and have bolstered immune-system activity. The results suggest that eating far less might prevent or slow the onset of a host of human age-related conditions ... The observed changes occur quickly and bring longevity benefits at any age."

It's All in the Delivery Method (January 24 2006)
The art of destroying bad cells could halt today, and we'd still have very impressive medicine ten years from now due to dramatic improvements in selective delivery technologies. Destroying cells is easy - destroying just the right cells is very hard. Via Newswise: "The disease-finding capability of these scaffolds is due to the specially engineered virus that displays a peptide that matches a protein receptor "zip code" on the tissue of interest. ... previous work revealed that the human vascular system contains unique molecular addresses, depending on the site of an organ or tissue, and that blood vessels also acquire abnormal signatures on diseased organs. ... these nanoplatforms could potentially locate damaged areas on arteries that have been caused by heart disease, and then deliver stem cells to the site."

A View of Proposition 71 (January 23 2006)
Via the Scripps Howard News Service, a look at the state of Proposition 71 and the California Institute for Regenerative Medicine. The opposition of those determined to prevent the development of embryonic stem cell science and resulting cures for age-related disease has put a strong brake on progress - resources poured into battling for control rather than into advancing beneficial medical research. "Instead of financing an accelerating research agenda this year, officials are reduced to begging for handouts to avert closing down by June, when existing funds run out. They also implemented a freeze on most staff hiring. ... It will take about $2.5 million in additional donations, Hall said, for the institute to 'remain active, remain visible and build the infrastructure on which we will launch this big program in the spring of '07.'"

Yet Another Heart Stem Cell Trial (January 23 2006)
A great deal of work is presently taking place on first generation regenerative therapies for heart damage. Here is another example: "The first-of-its-kind study in heart attack patients will seek to demonstrate the safety, and roughly measure efficacy, of three intravenous doses of adult human stem cells versus placebo in lessening damage to heart muscle within ten days of first heart attack. The treatment recently passed an early safety test and has been approved for study in more patients at higher doses. That process will get underway shortly ... The potential to re-build damaged heart muscle by implanting stem cells that then become new muscle cells is one of the most exciting in cardiology."



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