Longevity Meme Newsletter, January 01 2007

LONGEVITY MEME NEWSLETTER
January 01 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.

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CONTENTS

- A Year-End Message From the Methuselah Foundation
- Backing Success to Generate More Success
- Discussion
- Latest Healthy Life Extension Headlines

A YEAR-END MESSAGE FROM THE METHUSELAH FOUNDATION

A review of the year past and prospects for the year ahead in healthy life extension and advocacy can be found at the Methuselah Foundation:

http://blog.methuselahfoundation.org/2006/12/a_yearend_message_from_the_met.html

"The most significant development in the MF's activities during 2006 is that we are now a fully-fledged grant-making body. Until a year ago, we were focused predominantly on just one of our two strategies for promoting life-extension research, namely the Mprize, which had grown by the end of 2005 to well over $1m in cash and about $2m in pledges. But this year we have begun to place equal emphasis on the other arm of our operations, the direct funding of specific research projects.

"A major effort of the MF during 2006 will become public only in the fall: a popular science book describing SENS in depth for a general audience. It will be published by St. Martin's Press, a major New York publishing house. The text was written partly by Aubrey but mostly by his full-time research assistant, Michael Rae.

"The book will be launched contemporaneously with the next Cambridge SENS conference, which will take place on September 6-10. We'll be opening the conference website for registrations very soon. At the previous conference there was a great clamour for more frequent SENS conferences, especially somewhere in North America, so we're delighted that one of our long-standing and most active volunteers, Kevin Perrott, has managed to put together exactly that in Edmonton on March 30-31 and we encourage you to come along!

"We'll continue to expand our SENS research program, with more manpower at our main LysoSENS site (Arizona State University), additional LysoSENS work at Rice University, a probable doubling of effort on the MitoSENS project in Cambridge, and with several other projects lined up to begin as we obtain the needed funds. Our public outreach activities will be much enhanced in 2007, not least by a professional redesign of our websites. And we will be aiming to allocate substantial resources to building an organisation of the size needed to defeat aging, including hiring a professional fundraiser and making more frequent visits to meet key potential supporters."

BACKING SUCCESS TO GENERATE MORE SUCCESS

From my - admittedly biased - point of view, it seems clear that the Methuselah Foundation is a focal point for success in advancing healthy life extension science over the years ahead. The all-volunteer organization has secured more than $8 million in cash and pledges to date, all aimed squarely at the defeat of degenerative aging and age-related frailty, and shows no sign of slowing down. This includes a $3 million matching pledge from Peter Thiel - every donation to SENS research is matched at 50%. If you have an interest in seeing real progress in the medicine of longevity and rejuvenation within your lifetime, then consider helping to reinforce this success in 2007.

http://www.longevitymeme.org/projects/join_the_three_hundred.cfm
https://www.fightaging.org/archives/000979.php

DISCUSSION

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!

Reason

Founder, Longevity Meme

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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/

On Longevity Insurance (December 31 2006)
http://www.pantagraph.com/articles/2006/12/31/money/doc45970259ec07b165223006.txt
Pantagraph.com discusses longevity insurance in a piece that provides more of the nuts and bolts details than my recent post on the subject at Fight Aging! "In its simplest form, the premise of longevity products is that by making a one-time payment, you will start receiving guaranteed lifetime income at a designated point in the future. Your projected income stream is calculated at the time that you invest. ... The insurance companies rely on the fact that people aren't going to live that long to provide the payouts to the select few that will ... financial planners were critical because the investments, while similar to annuities, carried high commissions and lacked some of the flexibility traditional annuities offer, such as inflation protection and return-of-premium benefits ... Insurers have since added some of these options. But such features add considerably to the cost, which leads critics to still question whether such products are worth the investment." And of course, whether these insurers are going to be ambushed by rapidly rising longevity in the old, thanks to modern biotechnology, and thus rendered unable or unwilling to meet their obligations.

FuturePundit On CETP VV (December 31 2006)
http://www.futurepundit.com/archives/003990.html
Randall Parker of FuturePundit comments on the latest results from studies of the long-lived and centenarians: "CETP is on one of the 3 pathways that transfer cholesterol from HDL particles in the blood into the liver. So CETP is involved in regulating the amount of cholesterol in the blood. ... Work is underway to develop a drug that emulates the effect of this life-extending version of the CETP gene. But I'd much rather get a gene therapy that'd enhance my liver cells to express the genetic variant for CETP that slows aging. I've long thought the liver a key target for slowing whole body aging because it regulates blood lipid, lipoprotein, and cholesterol levels. This CETP gene variant (called CETP VV) is likely just one of many genetic variations waiting to be found that are expressed in the liver and can raise life expectancy." As I've said before, this sort of complex work to tweak metabolism to slow the rate of age-related damage does not seem to be the best use of scientific resources, at least when compared to the path of periodically repairing damage.

Funding and Progress in Alzheimer's Research (December 30 2006)
http://www.businessweek.com/print/magazine/content/07_02/b4016060.htm
Interesting views on the structure and progress of the Alzheimer's research community - and its funding - can be found in a recent BusinessWeek article: "A few years behind Alzhemed and Flurizan are promising treatments [that] provoke an immune response against the disease. Nearly 60 other drugs designed to modify the disease are also in clinical trials, including one from AC Immune of Switzerland that caught the attention of biotech giant Genentech Inc. best known for its cancer treatments. Genentech just announced plans to invest $300 million for the rights to AC Immune's drug. ... It's a whole new era. At least some of these medications are likely to work, and once we have disease-modifying drugs, we have opened the door to prevention. ... Certainly any disease could benefit from more funding, but with Alzheimer's the need for effective treatments is especially urgent. It is the only major cause of death in the U.S. where the numbers are getting worse, not better. That's because Alzheimer's is a disease of success. As people live longer and benefit from new treatments for common killers such as heart disease and cancer, the odds they will succumb to Alzheimer's increase."

More of the Right Attitude (December 30 2006)
http://www.americanchronicle.com/articles/viewArticle.asp?articleID=18446
I am always pleasantly surprised to see a very positive, mindful article on healthy life extension in the media, especially coming from reaches of the community I was unaware existed. It's a sign of growth, that the concepts of progress in longevity science and support for research are spreading. From the American Chronicle: "History unequivocally demonstrates that money is essential for invention. It shows that the larger the share of the economy that goes into research and development, the larger the amount of discoveries. It is a very straightforward correlation. Therefore, the larger the amount of cash that goes into biomedical gerontology, the sooner will humanity possess a technology that will allow people to live to two hundred years. ... What could possibly be more important than that? What could be more relevant than that? There is obviously nothing worthier than life. Most people believe there is such a thing as the right time to die. There is no such thing. ... if what we have today is good, then living to two hundred will also be good."

Reducing Stroke Damage (December 29 2006)
http://www.eurekalert.org/pub_releases/2006-12/uoc--ntp122806.php
EurekAlert! notes a demonstration of a comparatively straightforward method of mitigating stroke damage: "In one study, rats' brains were subjected to ischemia - severely reduced blood flow - for two hours in a model of stroke. Researchers then administered nicotinamide adenine dinucleotide, or NAD+, immediately after "reperfusion," or resumption of blood flow. Reperfusion is the time when stroke damage actually occurs because brain cells are suddenly exposed to highly reactive and unstable oxygen molecules, which are toxic. The researchers found that NAD+ reduced brain cell death from reperfusion by 70 to 86 percent compared with rats not given the treatment ... NAD+ plays a number of essential roles in cell metabolism. One role is supporting the activity of the DNA repair enzyme PARP-1, which normally repairs cell damage from brain infection. In response to reperfusion following ischemia or brain trauma, PARP-1 is overactivated. As a result, it quickly depletes all available NAD+, in a sense its 'fuel,' and is unable to repair cell damage, leading to brain cell death."

Thou Shalt Not Overhype (December 29 2006)
http://genesandaging.blogspot.com/2006/12/ageing-genes-back-in-news.html
From Genes&Aging, a justifiable note of complaint about the way the press has presented recent research: "researchers in the US have identified a gene which is reponsible both for longevity and for the retention of mental sharpness. 'Wow!', thinks I, 'my work has been done for me, we can all go home.' ... It's a nice paper, and the results are interesting and may direct research into useful areas. But: (1) It's a small study (158 people); (2) The results are only just statistically significant; (3) Other factors (other genes, environment, nutrition, exercise...) appear to be more important in influencing the phenotype than the gene itself; (4) "Cognitive function" was measured with a single test. ... Neither the general public, nor the researchers, nor science itself is done any good by hyping results such as these into news of supergenes which are going to turn us all into centenarian geniuses. It's never that simple." You have to read the popular science press with a critical eye.

Cryonics in Teen Fiction (December 28 2006)
http://rationallongevity.blogspot.com/2006/12/transhumanism-meets-teen-lit.html
Via Existence is Wonderful, a look at spreading awareness of cryonics in unexpected places: "I grew up reading science fiction, so I am no stranger to the subject of suspended animation -- however, it is odd and strangely compelling to see this subject pop up in something so far removed from sci-fi as the bubblegum world of novels written for an audience of eighth-grade girls. Could it be that the cryonics meme is, in fact, propagating through mainstream culture? ... The book's overall tone is one that assumes that being alive is inherently good, and that freezing -- er, vitrifying -- people is a compassionate and proper thing to do in the event of fatal illness. ... It is more than refreshing to read a book, albeit one aimed at teen girls, that not only presents life extension technology in a positive light, but that is completely devoid of annoying, moralizing messages about how death is somehow 'natural' and that cryonics is some kind of abomination."

A Look Inside Geron (December 28 2006)
http://biotech.seekingalpha.com/article/23090
If you like to see how the sausage is made, Seeking Alpha takes a look inside Geron, a company representative of the messy business of developing the latest regenerative medicine and cancer therapies: "Geron has two telomerase-based cancer drugs in human trials, though both are early stage. For metastatic prostate cancer, the company is injecting telomerase into patients, hoping to provoke a more aggressive immune response - a therapeutic vaccine. ... On the stem cell front, Geron is testing GRNOPC1 to treat spinal cord injuries. The drug was given to rats with injuries that prevented them from using their legs, and GRNOPC1 helped them regain control of their legs. ... A second drug, GRNIC1, uses embryonic stem cell-derived islet clusters treatment to treat diabetes. ... Geron plans to begin its initial human testing of the drug in 2007 ... GRNCM1, the third stem cell based drug candidate, is a potential treatment for myocardial infarction."

Apoptosis Drugs Versus Cancer (December 27 2006)
http://www.sciencedaily.com/releases/2006/11/061116100836.htm
To live longer, healthier lives, we must find safe, effective ways to defeat cancer - but for the most part, drugs to kill cancer cells also kill healthy cells. This is why better targeting via nanomedicine is a productive way forward. An alternative approach is to blanket the body with drugs that hurt cancer cells far more than healthy cells; progress in one such long-running attempt is outlined at ScienceDaily: "ABT-737 is a drug with a different strategy for attacking cancer. Rather than attempting to poison the rogue cells, the new drug attempts to reactivate the healthy and normal cell death program that failed to kill the unwanted cells on cue. ... Normally, the cell death machinery is switched on when damaged cells need to be removed. The failure of the machinery to be turned on when it should can lead to cancer. ABT-737 is a 'switch flicker' that kicks the cell death machinery into action. Much more remains to be done to assess the drug's safety and effectiveness in patients, but early results from the laboratory are promising. Our hope is that the new drug will prove to be more effective while having fewer side effects."

More On Wnt and Zebrafish Regeneration (December 27 2006)
http://www.eurekalert.org/pub_releases/2006-12/uow-hda122606.php
Via EurekAlert, more details on the role of Wnt signaling in the regeneration of complex organs in zebrafish: regeneration "involves creating cells that can take any number of new roles. This can be done by re-programming cells that already have a given function or by activating resident stem cells ... a particular kind of cell-to-cell communication, called Wnt/Beta-catenin signaling, regulates the fate of these as-yet undeveloped cells as an embryo forms. ... These streams of signals also tell stem cells in adult organisms what functions to undertake. Once tissue formation starts, something has to tell it to stop before growth gets out of hand. ... We show that Wnt/Beta-catenin signaling is activated in the regenerating zebrafish tail and is required for the formation and subsequent proliferation of the progenitor cells of the blastema ... It is most likely the inability of humans to form a blastema in the first place that renders us unable to re-grow arms and legs ... the same genes for turning on and turning off growth and development are found in humans, and drugs exist that can regulate this pathway."

A Year-End Message From the Methuselah Foundation (December 26 2006)
http://blog.methuselahfoundation.org/2006/12/a_yearend_message_from_the_met.html
A look back at 2006 and some of what is to come in 2007 from the Methuselah Foundation (MF) founders: "A major effort of the MF during 2006 will become public only in the fall: a popular science book describing [the Strategies for Engineered Negligible Senescence (SENS)] in depth for a general audience. It will be published by St. Martin's Press, a major New York publishing house. ... The book will be launched contemporaneously with the next Cambridge SENS conference, which will take place on September 6-10. ... We'll continue to expand our SENS research program, with more manpower at our main LysoSENS site (Arizona State University), additional LysoSENS work at Rice University, a probable doubling of effort on the MitoSENS project in Cambridge, and with several other projects lined up to begin as we obtain the needed funds. Our public outreach activities will be much enhanced in 2007 ... will be aiming to allocate substantial resources to building an organisation of the size needed to defeat aging, including hiring a professional fundraiser and making more frequent visits to meet key potential supporters."

Longevity Gene, Cholesterol (December 26 2006)
http://www.eurekalert.org/pub_releases/2006-12/aeco-gtt121906.php
Cholesterol metabolism remains a focus in the work of Nir Barzilai on the genetics of the long-lived. "A gene variant linked to living a very long life - to 90 and beyond - also serves to help very old people think clearly and retain their memories ... Known as CETP VV, [this] protein affects the size of 'good' HDL and 'bad' LDL cholesterol, which are packaged into lipoprotein particles. Centenarians were three times likelier to possess CETP VV compared with a control group representative of the general population and also had significantly larger HDL and LDL lipoproteins than people in the control group. Researchers believe that larger cholesterol particles are less likely to lodge themselves in blood vessels. So people with the CETP VV gene (and the larger cholesterol particles they produce) run a lower risk of heart attacks and strokes, which may explain their unusual longevity. ... CETP VV also protects the cognitive integrity of the brain - either through the same vascular 'anti-clogging' benefit that prevents heart attacks and strokes or through an independent protective mechanism that remains to be found."

Who's Who in Gerontology (December 25 2006)
http://whoswho.senescence.info
Researcher Joao Pedro de Magalhaes maintains a number of interesting databases at his senescence.info website. One I haven't pointed out is a Who's Who of gerontology, with listings for better-known people and companies hard at work on the biology of aging. "I hope senescence.info can also make people aware of the problem that is aging. Aging will likely be the major cause of suffering and death of those you love. It is the main reason why great artists, scientists, sportsmen, and thinkers die. ... Even so, few resources are aimed at tinkering with the biological causes of aging and most people are not even aware of that research is done on the biology of aging. Rivers of money, both in the industry and academia, flow to fight specific age-related diseases, but not to fight the aging process. Less than 20% of the National Institute of Aging's budget goes to research the basic causes of aging, which pales in comparison with the resources available to other medical problems like neurodegenerative diseases or cancer. Hopefully, senescence.info can contribute to make the public aware of the work done by gerontologists."

LA Times on Longevity Science (December 25 2006)
http://www.latimes.com/features/health/la-he-lifespan25dec25,1,77391,full.story
The LA Times takes a high-level look at longevity science that has attracted media attention this year: calorie restriction, resveratrol, centenarian studies and other metabolic manipulations intended to slow the accumulation of age-related damage. This is but one weak side of the coin; when thinking in these terms "Phelan says he doesn't think there will ever be a way to significantly extend human life span. 'Millions of years and billions of people living a variety of lifestyles that result in life spans that never exceed 122 demonstrate that it is unlikely that some new method will dramatically extend this.' Which might be true if you restrict yourself to manipulating metabolism - it's like tuning up a car; there are definite limits to performance within the present architecture and state of repair. But this leaves out the concept of using modern biotechnology to identify and repair the damage that causes aging. That is the real path forward - fix the failing engine, don't tune it.

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