Longevity Meme Newsletter, July 24 2006

July 24 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.



- A Welcome to the New Folk
- Aubrey de Grey on the SENS Challenge
- Discussion
- Latest Healthy Life Extension Headlines


Rather a lot of new folk joined the list this week: a warm welcome to you all! To get into the Longevity Meme mindset, I strongly recommend you read the following pages, if you haven't already done so:

An Introduction to Healthy Life Extension

No Silver Bullet For Degenerative Aging ... Yet

In short, a wonderful future of longer, healthier lives awaits us - but we all have to put in the work to help make new medical technologies a reality. One group of volunteers and activists in particular makes it possible for you to help advance scientific progress towards healthy life extension medicine without all the fuss and mess: the Methuselah Foundation. If you are interested in living a longer, healthier life, please do take a look at their approach:


Meanwhile, time and aging march on for all of us. Fortunately, a small number of well-known and scientifically proven strategies for reducing the risk of age-related disease and extending your healthy longevity do exist now. More correctly, I should say strategies for avoiding some of the damage that comes with a modern lifestyle; you would not be extending your healthy life span so much as not reducing it to the same degree as everyone else. At the top of this list is calorie restriction:


Everything worthwhile takes some effort - one of the goals of the Longevity Meme is to make the first steps of your research and connection with the healthy life extension community a great deal easier. So make the most of it! The next few decades will be a wondrous time of transformation and progress; why not do the best you can to ensure it will be a time of health and vigor?


SENS, the Strategies for Engineered Negligible Senescence, is an ethical rallying call; a proposed research and development plan aimed at producing effective first generation medical technologies capable of reversing aging - and producing these results fast enough to make a difference to you and I. If you are unfamiliar with SENS and the SENS Challenge hosted by the MIT Technology Review, please do leaf through the background at the following links:


Biomedical gerontologist Aubrey de Grey was kind enough to pen a few words for the newsletter - in his own inimitable style - on the recent SENS Challenge results and the future:

"MIT Technology Review's 'SENS Challenge' is an invitation to mainstream gerontologists, with a $20,000 incentive, to compose a denunciation of SENS powerful enough to convince an independent expert panel that discussing SENS in detail - let alone funding it - is unwarranted.

"The Technology Review received three submissions that were all rejected by the panel. Given the eminence of the panel in both biology and technology - and of the submitters in biogerontology - a popular conclusion is that it was singularly unwise of some of my colleagues in gerontology to be quite so outspoken in their opinions of SENS given how poorly they had in fact studied it. A second conclusion is that there was merit on both sides, since the panel were certainly not convinced that SENS would succeed.

"I concur with the first conclusion, but sharply disagree with the second. My view is the exact opposite: that the detail of SENS is what makes it feasible. Hence a panel who came in with essentially no knowledge of SENS and studied it only quite briefly would be almost certain to doubt its feasibility. That they accept its admissibility as a credible topic of discussion *despite* harbouring such doubts makes their refutation of the position of my more intemperate critics even stronger.

"However, it is not my purpose to be in any way triumphalist. I feel that no time should be spent flagellating my colleagues with the SENS Challenge's demonstration that their judgement in signing up to a denunciation of SENS was unduly hasty and short-sighted. Everyone makes mistakes; and the best course, here as always, is to learn from them but not to dwell on them. There are, to be sure, a rump of genuine SENS opponents (as opposed to skeptics) who have nailed their colours so firmly to that mast that they may have no choice but to bluster on to oblivion. The field in general is not so narrow-minded as to ignore the view of minds so eminent as the SENS Challenge panel, however. There is much work to be done to implement SENS, and the time to focus on that work is now.



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/

Looking at the Aging Immune System (July 23 2006)
Researchers have made progress in recent years in identifying and understanding the mechanisms of decay and inefficiency in the aging immune system. Here, 50connect.co.uk looks at other threads in this work: "the most abundant form of white blood cells, whose job it is to defend against invading microbes, are only half as effective in people aged over 65 as they are in younger people ... What is particularly exciting about this finding is that in laboratory experiments we can improve the efficiency of white blood cells by adding DHEAS. We are now going to explore whether treating patients with this hormone can help them fight infections." Another study finds that "cells from older people had fewer receptors to direct the T lymphocytes to where they are needed, than younger people. This deficit resulted in less T lymphocytes reaching the infection site. ... older people have a specific immune response deficit in their skin, not necessarily a generalised lack of immunity."

Towards Progeria Therapies (July 23 2006)
As noted briefly by Medical News Today, scientists are making progress towards the first therapies for the accelerated aging condition progeria (HGPS): "HGPS is caused by a mutation in the Lamin A gene (LMNA) that results in the synthesis of a mutant prelamin A (also called progerin). Progerin undergoes farnesylation but cannot be further processed to mature lamin A, a key structural component of the cell nucleus. In HGPS cells, progerin accumulates at the rim of the nucleus, causing misshapen nuclei. ... [researchers] suspected that protein farnesylation might be crucial for the aberrant targeting of progerin to the inner nuclear membrane and were able to show that blocking farnesylation with an inhibitor would prove therapeutic." Given that the same cellular problems are seen to a lesser but still significant degree in "normal" aging, it seems likely that any successful progeria therapy would also prove beneficial for the rest of us.

Evolutionary Skepticism on CR (July 22 2006)
As research into the mechanisms of healthy life extension through calorie restriction (CR) continues, the skeptics are finding their feet: "Calorie restriction is known to increase lifespan in many but not all species and may perhaps not do so in humans. ... Given the variety of physiological responses to variation in food supply that are possible, evolutionary life history theory indicates that an increased investment in maintenance in response to resource shortage will not always be the strategy that maximises Darwinian fitness. Additionally, for the well-studied species in which life extension is observed, there is considerable variation in the response. This suggests that it is not an ancient ancestral response, which has been conserved across the species range." For all that, the positive benefits on human health and resistance to common age-related diseases have been quite amply demonstrated.

Who Is This "We?" (July 22 2006)
A typically mixed article on healthy life extension from the Times Online: "But while headlines trumpet about modern-day Methusalahs, philosophers, sociologists, anthropologists and the public are beginning to ask a vital question that the scientists may have forgotten: are we getting so carried away with the possibility of extended life that we're forgetting to ask whether we want it?" Who is this "we?" Be very wary of people who use this sort of language; they are almost certainly trying to stop you from exercising your freedoms - such as the vital freedom of research. "The leading medical charity the Wellcome Trust takes the bull by the horns next week with a debate on whether science has looked at all the angles when it comes to living a full, long life. Speakers will examine the implications on lifespan of, for example, stem-cell technology for rebuilding damaged organs and our growing understanding of the molecular and cellular processes that lead to age-related disease."

On Elder Life Expectancy (July 21 2006)
(From the Harvard University Gazette). Life expectancy statistics can provide a number of apparently counterintuitive points; for all it appears a straightforward enough concept, it is not: "Life expectancy in this country has been rising steeply since 1990, and the National Center for Heath Statistics concludes that the older you are today, the greater the age you are likely to reach. Men and women who make it to age 75 in 2006 can expect to still be around in 2016 and 2017, respectively. At age 85, the odds are good that you'll reach 91. ... people who study aging trends believe that life expectancies for the old will continue to grow longer. The main reason is that the three biggest killers of older people - heart disease, cancer, and stroke - are being treated more successfully." These are the results of the first impact of modern biotechnology on therapeutics. It can get much, much better - if the funding is there for directed research into repairing the cellular damage that causes age-related degeneration.

On Public Support For Aging Research (July 21 2006)
Kevin Perrott pointed out a presentation prepared for the White House Council on
Aging 2006 - an event I hope I was sufficiently dismissive of - at the behest of the Alliance for Aging Research and AFAR: "Scientists say the field is on the threshold of a new way of thinking, shifting focus from specific illnesses to searching to understand aging itself as a biological process. The report suggests that many of the scientists' concerns about the public's understanding of these issues emanate from political arguments or media coverage rather than actual public opinion at large. For example, researchers are generally pessimistic about public support for funding, but the research suggests the public seems to be far more supportive of basic aging research than the official political voices might lead scientists to believe."

Cryonics Documentary From Zig Zag (July 20 2006)
The Guardian notes that Zig Zag's documentary on cryonics will be aired in the UK. "The first ever footage of a person being cryonically frozen is to be broadcast in a Channel Five documentary that will follow a woman who is terminally ill with cancer before and after her death. ... We're really very proud of what we have achieved with this programme - the human and emotional journey we captured with one contributor in particular, filming prior to her death and the subsequent process of her preservation, in conjunction with the amazing scientific and ethical questions raised by this subject, makes for one of our most challenging and fascinating productions to date." Filming was earlier this year, according the Alcor newsletter; I'm hoping this turns out to have more of a respectful positioning than the Guardian article suggests. Cryonics is an essential insurance policy; the best and only option available to all too many people who will die before the onset of meaningful healthy life extension technologies.

Biomarkers and Programmed Aging (July 20 2006)
Via EurekAlert!, recent research in which biomarkers of cellular aging - genetic activity in this case - and programmed aging are discussed in the same breath. In fact these are quite separate topics; programmed aging is not necessary to explain common forms of change in gene expression with tissue age, nor longevity differences between species. "Why animals and even people age at different rates prompted Kim to look deeper into the processes that control aging. His new study suggests that the cell has a molecular homeowner that keeps up repairs until a predetermined time, when the owner picks up the welcome mat and moves out. Once that process kicks off, the decay happens as a matter of course. The homeowners in tortoise cells stick around for hundreds of years delaying the decay, while those in fly cells move out within weeks ... [the] work doesn't identify what triggers that process, it does provide a way of detecting the point a cell has reached in its life span." Remember that cellular longevity doesn't necessarily have to have anything to do with your longevity.

The Coming $1000 Genome (July 19 2006)
A great deal more than DNA sequencing is going on in the bioinformatics field, but the cost of sequencing seems to have become the chip speed of that industry - a commonly used measure for present capabilities and speed of progress. "The goal now being pursued by the N.I.H. and by several manufacturers [is] to drive the costs of decoding a human genome down to as little as $1,000. At that price, it could be worth decoding people's genomes in certain medical situations and, one day, even routinely at birth. ... As we drop the price and increase the capability, there are applications that couldn't be done before, [like] a researcher being able to screen a thousand patients for cancer mutations." We're heading for a real influx of information; vast, ever-growing databases to accelerate medical research and spur development of new technologies to engineer longer healthy life spans.

Progranulin and Frontotemporal Dementia (July 19 2006)
Medical News Today provides surprisingly good news about a common age-related condition: Frontotemporal Dementia (FTD), "the second most common form of dementia after Alzheimer's disease, is a group of brain disorders that affect the frontal and temporal lobes of the brain ... What we've found is a little bit different than what we've found in other common neurodegenerative diseases. What we're looking at here is simply the loss of progranulin that is causing the disease ... One copy of the progranulin gene has been knocked out by the mutation, and therefore we have less progranulin produced, which is enough on its own to cause the disease." We don't expect neurodegenerative conditions to be easily prevented or cured - but every so often something goes our way. "Replacing progranulin is the obvious therapeutic approach ... That might be possible through gene therapy."

A Longevity Regulator Gene? (July 19 2006)
It's good to see that the Paul F. Glenn Laboratories for the Biological Mechanisms of Aging is already appearing on published research. Via PubMed: "Eukaryotes have evolved elaborate mechanisms to survive periods of adversity. By manipulating genes that control these mechanisms, researchers have found they can generate more stress resistant, longer-lived organisms. One of these is the PNC1 gene of [budding yeast], a master 'longevity regulatory gene' that translates a variety of environmental stresses into lifespan extension by activating the sirtuin family of longevity deacetylases. ... We propose that there is a functional equivalent of PNC1 in mammals called Nampt (a.k.a. PBEF/Visfatin), a stress-responsive gene that would coordinately regulate metabolism, cell defenses, and resistance to diseases of aging." There are those who see this sort of metabolic research as a dead-end: interesting and useful within its range, but not likely to produce ongoing significant healthy life extension.

The Alzheimer's-Diabetes Link (July 18 2006)
Researchers continue to quantify the level of risk linking diabetes and Alzheimer's: "failure of diabetic patients to maintain control of their blood-sugar levels increased their risk of developing dementia 10 years down the road by as much as 78 percent ... Glycosated hemoglobin - known as HbA1c - kept under 10 percent in the blood appeared to be the point where the likelihood of developing dementia begins ... [another study] described how patients with borderline diabetes were 67 percent more likely to develop dementia nine years after diagnosis and were 77 percent more likely to develop Alzheimer's disease after nine years." Diabetes appears to be a condition most people could avoid; if you let your metabolism and lifestyle slide into causing more cellular damage, it shouldn't be a surprise that you suffer more rapid and greater age-related degeneration.

Inflammaging (July 18 2006)
Via the Financial Times, another reminder of the importance of reducing chronic inflammation and the damage it causes: "in old age, a failing immune system frequently triggers inflammation in many parts of the body. This in turn causes chronic disease. ... There is a strong inflammatory element in all the major diseases of ageing. The body tries to adapt by producing anti-inflammatory compounds [but] human biology eventually fails. ... Our immune system has evolved to get rid very efficiently of acute infections in young bodies but it has not been selected to get rid of subclinical viral infections in old age. ... The constant attempt to suppress slow-acting viruses such as cytomegalovirus (CMV) could eventually throw the immune system out of balance ... CMV is a passive infection in many old people - and more and more of the immune system is devoted to fighting it."

Metabolic Supermice (July 17 2006)
Forbes reports on interesting research into metabolism and inflammation: "Called aP2, the protein has no useful function in the body. It only appears during the course of disease, and seems to cause adverse effects on blood sugar levels and fatty acid metabolism. It previously has been found in fat cells and macrophages (a type of immune cell) in people with obesity, diabetes and heart disease. ... [researchers have] found aP2 in the lining of the human lung, where it appears to regulate the inflammation associated with asthma. ... To study the effects of aP2, the researchers created genetically engineered mice that could not produce the protein. ... They're metabolic supermice. We cannot make them obese, diabetic or atherosclerotic. They don't develop fatty liver disease, and they don't develop asthma ... pharmaceutical companies have developed aP2-blocking drugs. ... They work very well in animal models and produce the same effects we've seen in genetically engineered mice. But all the work is pre-clinical."

Leukemia Stem Cells (July 17 2006)
Since cancer stem cells - and the implications for future cancer therapies - seem to be the topic of the moment, I should point out this news of progress from EurekAlert!: researchers "have isolated rare cancer stem cells that cause leukemia in a mouse model of the human disease. The leukemia stem cells isolated proved to be surprisingly different from normal blood stem cells - a finding that may be good news for developing a drug that selectively targets them. ... scientists showed that they could create leukemia stem cells, which also are self-renewing, from partially committed, non-self-renewing progenitor cells. The latter are short-lived cells that can turn into several types of blood cells ... in the future we should be able to specifically target leukemia stem cells without killing normal stem cells."



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