Longevity Meme Newsletter, February 13 2006

February 13 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.



- Simultaneously Inevitable and Horrible
- How Rapidly Could We Beat Aging?
- Discussion
- Latest Healthy Life Extension Headlines


Degenerative aging has been simultaneously inevitable, horrible and common knowledge for all human existence, but humans are pretty poor at dealing with constant stress. Stress literally makes us sick, causing detrimental biochemical changes if it continues unabated, so it makes sense that the most successful human genes and cultures would be those that provide a way to deal with the problem of a universal horrible truth.

We all know the end of this story, of course, which is that humans are very good at taking inevitable, horrible things and painting them as wonderful - or putting them out of sight and out of mind. Or both. It's an evolved and selected defense mechanism, and it works pretty well. The trouble is that this defense mechanism is now the biggest obstacle to actually getting out of the hole we're trying so hard to ignore.

For the first time in human history, we have entered an era - the era of biotechnology - in which there is a chance of turning aging into a treatable medical condition, alleviated by the application of advanced medical technology. There is a chance that no one would have to involuntarily suffer from age-related cellular damage and disease, that we could life far longer, healthier lives. There is a chance that this could come about in our lifetimes. Reaching for that chance will take widespread support and large-scale funding - the crafting of a culture and infrastructure to rival that of cancer research today.

We won't get there if everyone keeps their eyes tightly shut - instead, we'll all suffer exactly the horrible fate that people want to put out of sight and out of mind:


Looking at your own future health and prospects with eyes wide open is the first step to supporting healthy life extension research. Take it with measured strides.


How rapidly could we beat aging? Therein lies the question - certainly faster for every additional individual who stands up to support, advocate or advance medical research. I take a look at biomedical gerontologist Aubrey de Grey's published timescales in this Fight Aging! post:


Is a span of a few decades plausible or not? Is it possible it could take that long just to ramp up the funding machinery and win over a public determined to put aging out of their minds? What of spectacular gains in biotechnology and nanomedicine predicted for the next 20 years - how does that fit in to the picture?


See what you think and speak your mind if the fancy takes you.


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/

A Profile of the Buck Institute (February 12 2006)
The Sacramento Bee profiles the Buck Institute for Age Research: "Today, 61 percent of the Buck's $25.6 million budget is supplied by grants, mostly from the government. The Buck Trust makes up 23 percent, donations 14 percent and licensing income, interest and miscellaneous the remaining 2 percent. That supports the work of 15 laboratories studying aging and age-related disease at the level of cells and genes. Lithgow, who left a tenured faculty position at the University of Manchester in England to join the Buck, said the allure of the institute is that everyone there agrees that the mechanism of aging - in and of itself - is worth trying to understand. Some do it through studying Parkinson's disease, others through human embryonic stem cells, or through cancer or nutrition or DNA damage."

Anything But Change (February 12 2006)
Far too many people would rather suffer pain and death than admit radical change into their lives and the world at large; here is an Observer column from one such person. Fear of change makes for a poor futurist - if you don't like to think about the future in any meaningful way at all, you'll extrapolate very poorly. Hence this piece is a good example of many of the errors of thinking about healthy life extension that seem very hard to get rid of. In particular, the Tithonus error - that longer life will mean more infirmity rather than many more healthy, active years - and the idea that the present concept of retirement will continue as-is are featured prominently. I am reminded that people who don't like life are not likely to be enthused by more of it - but please let the rest of us get on with building a better, longer-lived future.

Removing Senescent Cells (February 11 2006)
Dealing with the accumulation of senescent cells is one of the seven Strategies for Engineered Negligible Senesence (SENS). This profile of researcher Judy Campisi at The Scientist gives some insight into where the mainstream of aging research is on this topic: "senescent cells not only exist in vivo but also accumulate in aging tissue. ... in culture, these nonreplicating cells are far from inert. They produce a plethora of unpleasant proteins that can, among other things, destroy the structural integrity of the tissue that surrounds them. ... The critical test would be to create an organism in which you prevent senescent cells from accumulating ... She and her colleagues are working on devising a system to do that test. They are developing a mouse in which an inducible promoter allows them to activate a gene that will selectively eliminate senescent cells."

DNA Repair, Mitochondrial Dysfunction (February 11 2006)
Kevin Perrott comments on recent research into DNA repair and the effects of damage: "a DNA repair protein called NEIL1 coded in the nucleus had also been found in liver mitochondria implicating it, and possibly its relatives role, in the repair of mitochondrial DNA mutations. ... The researchers mutated both copies of NIEL1 in mice expecting an increased incidence of cancer but what they got were massively obese rodents with diabetes accompanied by liver and kidney disease and elevated of triglycerides in the blood, all hallmarks of metabolic syndrome. Hypothesizing that impaired mitochondrial function due to lack of NEIL1 function might be the cause, the confirmed that the mitochondrial DNA of the mutant mice indeed suffer from a great deal of breaks and damage." It is encouraging that work is underway to develop repair technologies for mitochondrial DNA.

On Inkjet Bioprinting (February 10 2006)
ABC News catches up with research and development of inkjet technology for tissue engineering: "The promise of tissue engineering and the promise of 'organ printing' is very clear: We want to print living, three-dimensional human organs. That's our goal, and that's our mission. ... The concept behind organ printing is one that's been used in the manufacturing world for years, 'rapid prototyping.' ... Rapid prototyping is nothing more than layer-by-layer deposition of any materials. What is new is that instead of ceramic, instead of polymer, instead of some other nonorganic stuff, we use living tissue and living cells." The technology is in its very earliest stages - a long way to go yet, but it's most promising.

Review of the Genetics of Aging (February 10 2006)
A review paper on genes, aging and drug discovery in the American Journal of Clinical Nutrition is interesting for having come from Elixir Pharmaceuticals staff: "Aging is not a passive activity, but an actively regulated metabolic process. Specific genes have been identified that regulate aging, although aging, and consequently longevity, is only partially under genetic influence. ... type 2 diabetes, a disease of glucose homeostasis, can be conceptualized as a form of accelerated aging. ... Because aging and diabetes are intimately related at a molecular level, diabetes may be able to provide the link between disease treatment (eg, diabetes) and the prevention of age-related diseases. If specific molecular pathways controlling the rate of aging can be modulated genetically, then perhaps they can be modulated pharmacologically."

Genetic Influence on Life Span (February 09 2006)
Scientists are starting pin down the bounds of the influence of genes on aging and life span, as demonstrated in this PubMed entry: "We study the genetic influence on human lifespan and how it varies with age using the almost extinct cohorts of Danish, Finnish and Swedish twins born between 1870 and 1910 comprising 20,502 individuals followed until 2003-2004. We first estimate mean lifespan of twins by lifespan of co-twin and then turn to the relative recurrence risk of surviving to a given age. ... While the estimated overall strength of genetic influence is compatible with previous studies, we find that genetic influences on lifespan are minimal prior to age 60 but increase thereafter. These findings provide a support for the search for genes affecting longevity in humans, especially at advanced ages." This goes nicely with the Reliability Theory of aging.

The Art of Overthinking (February 09 2006)
More coverage of Demos and Better Humans can be found at Spiked, veering from sensible in places to knee-jerk overthinking in others: "It's because this area is really a debate about values that it is interesting. Do we want to live longer - if not, why not? How do we use technologies to extend ourselves rather than avoid ourselves?" I still find it amazing that some people are willing to expend so much effort to avoid concluding that curing disease, preventing pain and suffering, and offering people the choice of living longer, healthier lives are very good things. It's equally amazing that folk can even debate the possibility of blocking the development and use of healthy life extension technologies if they don't like your reasons for doing so.

Anti-Inflammatory News (February 08 2006)
Inflammation is a major cause of some types of accumulated cellular and biomolecular damage, which is why sources of inflammation are linked to age-related conditions - acquire damage faster and your systems wear out faster. From EurekAlert: "We have done what many others have been trying to do for years. We have made a therapeutic antibody against one of the most potent inflammatory agents in the body and used it to cure arthritis in mice. The next step is to translate the highly effective outcome we see in mice to human patients. If we can do this, we will have a revolutionary new treatment for a number of important human diseases ... We anticipate that our antibody will be a significant improvement over current therapies because it acts at a different and earlier point in the inflammatory process compared with current anti-inflammatory therapies."

Seizing the Chance To Live To 150 (February 08 2006)
More coverage of biomedical gerontologist Aubrey de Grey, the path to radical life extension and transhumanism - as seen by the Demos think tank - can be found at the Financial Times: "As medicine becomes more powerful, we will inevitably be able to address ageing just as effectively as we address many diseases today ... equally significant are the ripples of interest that Mr de Grey is generating outside the scientific community. He has rapidly emerged as the British figurehead of a new political movement, which has steadily been gaining ground on both sides of the Atlantic. This movement is known as transhumanism, and its central belief is that advances in science and technology will liberate us from the constraints of illness and ageing and enable us to live longer, healthier lives."

Review of "The Long Tomorrow" (February 07 2006)
A positive review of evolutionary biologist Michael Rose's "The Long Tomorrow" can be found at the American Scientist: "The [premise] is that the ultimate cause of senescence is natural selection and that evolutionary biology holds the key that will unlock the secret of longer, healthier lives for humans. ... Rose and his colleagues have succeeded in bringing about this paradigm shift by weight of evidence and prolific publication of articles, mostly in top-tier peer-reviewed journals. Most scientists studying senescence now accept the rather remarkable idea that natural selection accounts for such a seemingly maladaptive trait, although there is still debate over the specifics of some mathematical models and the interpretation of some data. Rose was not alone in his efforts to move evolutionary biology to the forefront of aging research, but as outlined in this book, he was the first to publish compelling data."

Genes and Alzheimer's (February 07 2006)
Forbes reports on the genetic component of Alzheimer's: "Genes may play a much bigger role in Alzheimer's disease than previously thought, a new study involving twins suggests. In fact, Alzheimer's disease may have a genetic cause in up to 80 percent of cases ... The study, which involves data on nearly 12,000 elderly participants in the Swedish Twin Registry, is 10 times larger than any previously done." From what researchers presently know, Alzheimer's is the end result of biochemical processes that take place in everyone. Your genes likely determine the rate at which harmful side-effects accumulate, and the degree to which you resist that harm. Live long enough and you'll suffer neurodegeneration - which is why curing Alzheimer's and other age-related neurodegenerative conditions is so important for the future of healthy life extension.

Stem Cells Versus Type 2 Diabetes (February 06 2006)
(From Medical News Today). A modest study on type 2 (age-related) diabetes using the patient's own stem cells shows good results: "84% of the patients that had received the autologuous bone marrow cells could also abandon the drugs that stimulate insulin production or the insulin that they had been receiving previously. There were no complications at all, demonstrating the safety of the technique ... The most likely reason of this improvement is that the implanted autologuous stem cells regenerate the destroyed beta cells in the Islets of Langherhans in the pancreas of diabetes patients. It is also possible that they originate new beta cells which produce the new insulin."

Resveratrol News (February 06 2006)
I'll admit to being skeptical on resveratrol, despite some interesting science lurking in there somewhere - the compound appears to pull some of the same biochemical triggers as calorie restriction. This EurekAlert report looks at research in short-lived fish: "Recently, a small fish species with a captive lifespan of only three months was described by Cellerino and colleagues. In the new work, the researchers used this short-lived fish to test the effects of resveratrol on aging-related physiological decay. The researchers added resveratrol to daily fish food and found that this treatment increased longevity and also retarded the onset of aging-related decays in memory and muscular performance." Of course, there's always the possibility that they failed to control for actual calorie restriction - that happens a lot.



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