Some interesting research on flies sheds more light on the way in which double strand breaks in DNA are repaired:

"DNA double strand breaks are regarded as one of the primary causes of cancer," says Kusch. "While there are natural mechanisms within an organism to detect and repair these breaks, factors involved in DNA damage repair must first bypass histones. Histones are proteins that condense DNA and protect it from mechanical and other stresses, but also make DNA rather inaccessible."

...

"These findings answer fundamental questions about DNA double-strand break repair," says Robb Krumlauf, Ph.D., Scientific Director of the Stowers Institute. "They may ultimately help to formulate new strategies of cancer therapy."

For more context on what we know and surmise about double strand breaks as related to aging and cancer, you may want to read a fascinating discussion between Robert Bradbury, Aubrey de Grey and Joao Magalhaes here at Fight Aging: Part One, Part Two.

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Three items over at Betterhumans caught my eye today.

Another potential source of multipotent stem cells:

Testicles from newborn mice have yielded stem cells that could rival those from embryos in their treatment potential.

Japanese researchers led by Takashi Shinohara from Kyoto University report that they have established a line of potent cells from neonatal mouse testes using a special cell culturing method.

Treatment for wet age-related macular degeneration:

Two new trials have shown that a drug injected into the eye can effectively treat a potentially blinding form of age-related macular degeneration (AMD).

...

The wet form of AMD represents about 10% of the disease's overall prevalence but is responsible for 90% of severe vision loss. In wet AMD, abnormal blood vessels grow under the central retina and cause a progressive loss of central vision. This interferes with everyday tasks such as driving.

Debating the ethics of human enhancement:

American bioethicists Arthur Caplan and Carl Elliott recently debated the issues in the open-access journal PLoS Medicine. Caplan is chair of the Department of Medical Ethics at the University of Pennsylvania School of Medicine in Philadelphia. Elliott is associate professor at the Center for Bioethics at the University of Minnesota in Minneapolis, as well as the author of Better than Well: American Medicine Meets the American Dream.

...

Ultimately, [opposition to enhancement] posits a static vision of human nature to which the [opposition activists] mandate we reconcile ourselves. If anything is clear about human nature, it is that this is not an accurate view of who we have been or what we are now, or a view that should determine what we become.

Quite aside from concepts of freedom and the merits of letting anyone control or restrict medical research and access to healthy life extension technologies (any such thing is hugely immoral in the libertarian worldview), Caplan has it right in his comment above. It is in our nature to change ourselves, to reach for what we can envisage. We can envisage longer, healthier lives and the technologies required to get there - those who stand in the way are guilty of prolonging death and suffering on an enormous scale.

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Bruce Klein of the Immortality Institute has posted the latest in a series of previews for Exploring Life Extension, the film currently in production. This time it's an interview with Michael Rose, an evolutionary biologist known for his work on increasing the life span of fruit flies, amongst other things.

My major scientific focus over the last fifteen years has been experimental tests of evolutionary theories for the evolution of aging, fitness, life-histories, etc., on Drosophila melanogaster , although I collaborate with other investigators using different species. We have experimentally tested the general theory that aging evolves because of a decline in the force of selection with adult age.

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CNet is running an interview with Ray Kurzweil on the topic of his approach to healthy life extension.

His regimen for longevity is not everyone's cup of tea (preferably green tea, Kurzweil advises, which contains extra antioxidants to reduce the risk of heart disease and cancer). And most people would scoff at his notion that emerging trends in medicine, biotechnology and nanotechnology open a realistic path to immortality--the central claim of a new book by Kurzweil and Dr. Terry Grossman, a physician and founder of a longevity clinic in Denver. "I am serious about it," said Kurzweil, a wiry man with few lines on his face for a 56-year-old. "I think death is a tragedy. I think aging is a tragedy. And going beyond our limitations is what our species is all about."

The scoffing is something that we advocates must continue to work on - the science behind the path to much, much longer lives (if not immortality in the traditional meaning of the word) is very sound. Still, having serious people talk seriously about immortality is, I think, very good for the wider healthy life extension movement. It provides a much better outrageous extreme, a topic I explored a while back:

The middle of the road, "reasonable" position in public or political debate tends to gravitate to midway between what are perceived to be the two opposite outrageous extremes, regardless of the actual merits of any of these positions.

With this in mind, it is occurring to me that part of the ongoing problem in the modern political debate over healthy life extension is that our "outrageous extreme" has always been a tentative, reasonable proposal that medical research carry on and that near-term technology would seem to allow us all to live a little longer…say, to 150. When the outrageous extreme from the other side - from the Bush administration, Leon Kass of the President's Council on Bioethics, and others - is that no-one should be permitted to research ways of extending healthy life span, we can see that the average between these two positions is not very favorable to our future health and life span. We wind up where we are right now: anti-research factions in governments worldwide are restricting and legislating against all of the most promising fields of medicine, while attempting to force through complete bans on stem cell research, theraputic cloning and other promising technologies.

We need a better outrageous extreme.

When immortality is on the table for respectable discussion, proposals to significantly fund research into rejuvenation therapies and a cure for aging will be more successful.

You can read an illustrative excerpt from Ray Kurzweil and Terry Grossman's "Fantastic Voyage" over at the Longevity Meme.

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This is promising:

Biologists at the University of California, San Diego have found a fundamental mechanism used by embryonic stem cells to assure that genetically damaged stem cells do not divide and pass along the damage to daughter stem cells.

Their discovery, detailed in an advance online publication of the journal Nature Cell Biology, solves the longstanding mystery of how embryonic stem cells, which have the potential to divide an unlimited number of times and differentiate to make all of the cell types in the body, are able to avoid duplicating cells that have sustained genetic damage.

...

The scientists, who included Tongxiang Lin, a UCSD postdoctoral fellow and the first author of the study, and Connie Chao, a graduate student in Xu's laboratory, discovered that p53 activated by DNA damage in mouse embryonic stem cells directly suppresses the expression of a gene called Nanog, which is necessary for the self renewal, or unlimited duplication, of these stem cells. The suppression of Nanog promotes embryonic stem cells to differentiate into other cell types.

"The end result of all of these actions by p53 is to deprive embryonic stem cells with DNA damage the ability to self renew themselves and pass the DNA damage onto their daughter cells," says Xu. "p53 also contributes to the eventual elimination of DNA damage in the embryonic stem cells that have already differentiated into specific cell types, thus preventing the development of cancerous cells."

I'm sure that we can all think of a number of ways to make use of this information, assuming that the same mechanism is used in human embryonic stem cells. (This research used mouse cells, so it's fairly likely to be the same). You can find out more about the Nanog gene, uncovered in 2003, here:

The research group at the Institute for Stem Cell Research, University of Edinburgh, have shown that the Nanog gene, which is only expressed in pluripotent cells, plays an essential function in maintaining stem cells. Dr Ian Chambers who isolated the Nanog gene said: "Nanog seems to be a master gene that makes embryonic stem cells grow in the laboratory. In effect this makes stem cells immortal. Being Scottish, I therefore chose the name after the Tir nan Og legend."

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This seems to be an appropriate time of year to remind folks about calorie restriction, a lifestyle and diet option that has been demonstrated to bring dramatic health benefits.

A calorie restriction diet aims at reducing your intake of calories to 20-40% less than is typical, while still obtaining all the necessary nutrients and vitamins.

...

The Proceedings of the National Academy of Sciences has published an impressive set of statistics on the effects of calorie restriction (CR) in humans, based on ongoing US research. It makes for compelling reading: "It's very clear from these findings that calorie restriction has a powerful protective effect against diseases associated with ageing. [Practitioners will] certainly have a much longer life expectancy than average because they're most likely not going to die from a heart attack, stroke or diabetes."

Calorie restriction has been proven to extend healthy life span in most animals - including mice and primates - and the weight of evidence suggests that it does the same in humans.

A human study by John O. Holloszy, a professor of medicine at Washington University in St. Louis, published earlier this year noted that 18 people who had been practicing CR for three to 15 years showed dramatically reduced risk of developing diabetes or clogged arteries. ... It's very clear that calorie restriction has a powerful, protective effect against diseases associated with aging ... We don't know how long each individual actually will end up living, but they certainly have a much longer life expectancy than average because they're most likely not going to die from a heart attack, stroke or diabetes.

Calorie restriction has even been demonstrated to slow the progression of specific age-related conditions, such as Alzheimers:

Restricting the diets of mice reduces the build-up of plaques in the brain that are linked to Alzheimer's disease, according to a new study that offers further evidence of the benefits of calorie restriction. Obese people are already considered to be at a higher risk for developing Alzheimer's but the findings offer some insight into a possible explanation for this trend.

If you haven't already investigated calorie restriction as a means to a longer, healthier life, you certainly shouldn't wait any longer.

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The relationship between telomeres and aging is likely to be anything but simple. A recent thread at sci.life-extension offers a short selection of interesting complications and links:

Interesting that telomeres appear to play no role in either human skin aging, or bone marrow aging.

...

Aged skin was associated with thinning of the epidermis, decreased proliferation, and increased apoptosis below the granular layer. This was associated with increased epidermal expression of Fas and FasL. Telomerase activity was similar in aged and young epidermis. CONCLUSIONS: Fas/FasL-mediated apoptosis, along with decreased proliferation, may have a role in changes of human epidermis during ageing. Telomerase activity did not appear to be limiting in young vs. old human epidermis.

...

It is quite surprising that some major manifestations of aging such as skin and muscle atrophy can be reversed in old animals (or induced in young animals) by transplantion and/or joining of blood streams (parabiosis). It would be interesting to know how many signs of aging are due to immunological and systemic factors rather than tissue specific factors like telomeres.

We know that telomeres generally become shorter with age. We also know that errors in telomere mechanisms - much more common for shortened telomeres - are a root cause of many cancers. We know that telomere malfunctions are implicated in Werner's syndrome, an accelerated aging condition. Beyond this, the story seems to get much more complex - stay tuned.

You might want to read up on recent insights into the way in which the immune system deteriorates with age - scientists are closing in on the precise mechanisms by which this happens. This is a very promising sign for the prospects of future rejuvenative therapies for the immune system.

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I received an interesting e-mail yesterday from a visitor to the Longevity Meme:

I am interested in your work on longevity and would normally support it. However, I have a real problem with your portrayal of the stem cell debate. Contrary to what is on your site, I believe most advances to date have stemmed [pun intended] from adult stem cells. You state the most promising advances are linked to embryonic stem cells and I believe that is untrue at this time.

I am very concerned about the push to use and create embryos for research and your position on this matter (both the factual claims you made which I believe are misleading) and the lack of concern over moral issues related to use of embryonic stem cells makes it difficult for me to wholeheartedly support or contribute to this longevity project. No doubt you would consider this a form of 'cutting the nose off to spite the face' but longevity is not everything. Any thoughts either on the relative contributions from adult vs embryonic? Any thoughts on how important it is to address the moral issues involved in embryonic stem cell research?

To which I made the following response:

I agree that my more commonly accessed static pages on stem cell research need to be updated on the topic of embryonic stem cell research - those pages tend to lag a little behind my evolving opinions, new science and the political debate. Comments like yours help to bump these items up the priority list.

You'll find a short synopsis of the important part of my position on embryonic research here:

http://www.fightaging.org/archives/000203.php

In short, a collection of living cells has to be capable of feeling pain, be capable of thought, or be essential to the use of a meaningful amount of complex data amassed as the result of thought in order for it to have moral worth for me. Heritage and potential aside from these points count for nothing.

I am morally opposed to causing suffering in animals in the course of medical research, for example, but I don't see a meaningful alternative at the present time in order to avoid even greater human suffering - a suffering-free world is something we need to work towards in the long term, but you just can't do it all at once. The embryos used in stem cell research (small collections of cells without any meaningful differentiation) cannot suffer or feel, and are no different in this respect from any other non-essential cells taken from a human. You can probably extrapolate my opinions on other related topics such as abortion from these views.

Regarding embryonic stem cell research from a results-oriented point of view, it all comes down to a matter of time and consequences. I have no doubt that, even if hobbled and blocked at every turn, scientists will eventually understand how to turn any type of cell into any other type of cell - or create cells from scratch if need be. They will eventually understand how all of the most serious diseases do their damage at the genetic and molecular level. The relevant questions are how long it will take and how much very real, otherwise avoidable human suffering and death will be caused by delays - the death toll alone increases by 150,000 people each and every day.

The fastest way to understand cellular processes in order to cure many serious diseases is through embryonic stem cell research. Scientists use embryonic stem cell lines in order to understand the biochemical and genetic progression of many of these conditions - as well as to understand basic cellular processes that still remain a mystery. Adult stem cell therapies of the type being trialed now seem very suited to repairing certain types of tissue damage - but we know that because this research has not been blocked or suppressed to anywhere near the same extent as embryonic stem cell research. It is no surprise that adult stem cell research is far ahead, even in these comparatively crude first generation treatments.

(Although there is a good therapy in the works for spinal cord damage that uses embryonic stem cells:

http://www.longevitymeme.org/news/view_news_item.cfm?news_id=1384

This research group is aiming for human trials in 2006).

Embryonic stem cell research is very necessary; it is indeed essential for the most promising medical research of the next few decades. My comments above should serve to explain why I see this to be the case.

Insofar as we were talking about your support for increased human longevity, I would suggest that it is perfectly possible to support longevity research and serious anti-aging science while being opposed to specific activities within the broader research community. I certainly don't approve of everything that goes in the name of longevity research around the world, and nor am I representing a unified community voice in any way, shape or form. Finding a place in the community that you are happy with is a matter of finding the right groups to support and expressing your own opinions clearly and loudly.

What do you folks think? What needs to be updated or made more clear on my main pages on stem cell research?

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The transcript for the SAGE Crossroads interview with James Vaupel is now online. You may recall recent press on Vaupel's demographic research and suggestions that life expectancy in countries like the US could actually decline in years ahead. This interview serves to clarify his views and place those remarks in a wider context - Vaupel sounds like he agrees with the Reliability Theory of aging. Some excepts:

It used to be thought that there was nothing that could be done about aging, and that there was nothing that could be done to extend the length of life for humans.

But now we know that there is a lot that can be done about aging, and that people can live much longer than they used to live. So that's the plasticity of longevity.

...

That life expectancy is a measure of current conditions. It is not a prediction about how long somebody will live. But it's a measure of how long a person, a baby would live if that baby was confined to this year, could not get out of this year, was stuck with the conditions of this year.

So a more meaningful projection for most people would be, how long do we think that a newborn would live given mortality improvements?

The result is quite astounding. The result is that a newborn baby, in the developed world today—Europe, Japan, the United States—of those newborn babies, half will probably celebrate their hundredth birthday.

...

So the progress [in life expectancy prior to 1950] was largely due to saving lives below age sixty-five, especially children.

But after 1950 the improvements to life expectancy have largely been due to saving lives after age sixty-five, to this extension of life, to this giving—adding years to the life of older people.

So it's been a remarkable shift, and the shift has been due to the fact that since 1950 we've had various kinds of interventions that could help save people from heart disease, that could intervene with various infectious diseases that were killing very old people, so the antibiotics and so on helped older people a lot.

When Vaupel makes predictions, I think it's important to note that these are extrapolations; they do not and cannot take into account fundamental paradigm shifts in medical science. This is illustrated by any number of other competent, well-informed folks - such as Ray Kurzweil - making very different sorts of analytical predictions about the future of medical technology and human life span. The following pretty much says it all regarding extrapolation:

So when I'm criticized for saying that newborn babies will live to a hundred, I think the most powerful criticism is that I can't describe how they are going to live to a hundred. What's going to happen that will let them live to a hundred?

Then what I say is that I think heart disease death rates are going to come down. I don't know exactly how. I think we are going to find a cure or a way of preventing Alzheimer's, but I don't know exactly how. I think we are going to find ways of preventing or treating cancer, but I don't know exactly how.

So there are a lot of uncertainties about how this is going to be done. Basically, what I'm saying is that if life expectancy has gone up by two and a half years per decade for 160 years, it is likely to continue to go up. We are learning a lot about biomedical interventions, by health interventions. But I can't describe the details.

I have to say that I fall into the school of making it happen rather than the school of making projections. The capacity to influence the aging process is clearly not too far away under the right circumstances - getting there is a matter of finding the funding and will, and sooner is better.

Vaupel has a fairly sensible (if state-centric) view of the role of retirement in a longer life:

Well, there's a notion that's been developed mainly over the last hundred years, to separate life into three boxes. The first box you get educated, so you finish high school, you finish college, you finish graduate school and you are educated.

Then the second box is you work.

The third box you spend decades in forced leisure.

It doesn't make any sense to me to divide life up that way. But life has been divided up that way, and the number of people in most developed countries—once again, especially—this is especially Europe—the number of people who are working after age sixty has fallen dramatically, especially over the last twenty years.

So people have sort of—people have developed an assumption that they have a right to decades of leisure at age sixty or age sixty-five.

I don't see where this right comes from. People have a responsibility to contribute to society. We have to maintain the economy. If there are very large numbers of people who are not working at older ages, then that's going to be a burden on younger people.

I would have said "responsibility to support themselves," but we all know my leanings in that area.

One quote that jumped out:

Suppose you wanted to live to a hundred or I wanted to live to a hundred. How could we do it? What can you do? There is actually very little that an individual can do to extend an individual's life span by twenty years.

If the current human calorie restriction research continues to produce the same sorts of results as it has to date, then this lifestyle choice would seem to be a good shot at getting a fair chunk of those extra healthy years. Vaupel is right, however, in that what we have access to right now is pretty poor longevity medicine in the broader context of what is possible.

In summary, James Vaupel comes across as bullish on the prospects for increasing healthy life span through improved medicine - but he's in much the same ballpark as folks like S. Jay Olshansky or Richard Miller when it comes to the expected timeframe for these improvements. There are a fair number of other interesting items in there to find, so go and read the whole transcript.

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The most interesting pieces of research have a way of turning up on sci.life-extension - the regulars there keep a good ear to the ground. In this case, the research in question is an examination of advanced regenerative capacities in a strain of mice:

The reaction of cardiac tissue to acute injury involves interacting cascades of cellular and molecular responses that encompass inflammation, hormonal signaling, extracellular matrix remodeling, and compensatory adaptation of myocytes. Myocardial regeneration is observed in amphibians, whereas scar formation characterizes cardiac ventricular wound healing in a variety of mammalian injury models. We have previously shown that the MRL mouse strain has an extraordinary capacity to heal surgical wounds, a complex trait that maps to at least seven genetic loci. Here, we extend these studies to cardiac wounds and demonstrate that a severe transmural, cryogenically induced infarction of the right ventricle heals extensively within 60 days, with the restoration of normal myocardium and function. ... The myocardial response to injury observed in these mice resembles the regenerative process seen in amphibians.

Understanding the process by which lower forms of animal life regenerate serious wounds has been a desirable goal for some time now:

Studies of expression profiles, functional assays, and cloning of mammalian orthologues of genes that promote regeneration are aimed at designing a molecular cocktail of genes and/or proteins that will reverse tissue damage and lead to regeneration from the body's own cells. The limb provides information that will lead to the regeneration of muscle, bone, skin, and nerves. The work on eye will help us regenerate lens, retina and optic nerve, and the studies of spinal cord to reverse paralysis.

It is interesting and potentially very promising that a similar regenerative process has been found in a mammal - indicating a much shorter, although still resource-intensive, jump to therapies that will work for human injuries.

Our laboratory has determined that the MRL mouse strain is unique in its capacity for regenerative wound healing, as shown by the closure of ear punches with normal tissue architecture and cartilage replacement reminiscent of amphibian regeneration as opposed to scarring. Furthermore, we have mapped the genes involved, identified a minimum of six different loci on five chromosomes, and shown that this is a complex multigenic trait.

Using this mouse strain in the present study, we show that the MRL heart, when injured with a cryoprobe, is capable of growing and replacing wounded tissue without fibrosis. We show that cardiomyocytes are capable of dividing near and filling the wound site with a mitotic index equivalent to that of amphibians. We also show that granulation tissue resolves quickly with restoration of normal myocardial architecture and a markedly reduced extent of scarring. Finally, myocardial function seems to recover from the injury.

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There is an opportunity for us all to help the M Prize for serious anti-aging research receive another large end of year donation. See the following from Methuselah Foundation fundraiser April Smith:

Michael Cooper would like to drive us above the $100,000 cash mark before the end of the year and is committed to donate $23,700 of NYSE stock to the Longevity Prize. He will do this IF we get what it takes to top the $50,000 mark in the Longevity Prize - which will trigger Bob Gelfond's $5,000 challenge funds. Reason is willing to put a $2,000 donation towards the Longevity Prize, all of which puts us in shouting distance.

The short of it is that we need only another $2000, but we need it fast. Between our own resources and those of our immediate friends in the life-extension world, I believe we can. Can you help?

Bob Gelfond's challenge was issued quite early in the history of the prize, and I'll admit that I wasn't expecting the chance to trigger it quite so soon. But onwards and upwards!

You might also want to take a look at this Immortality Institute thread on the donation challenge:

The short of it is that we need only another $2000, but we need it fast. Between our own resources and those of our immediate friends in the life-extension world, I believe we can. Can you help us relieve Michael Cooper of his precious stock before the end of the year runs out?

As I've said before.. I'm no millionaire but I believe strongly that it will take putting my money where my mouth is to encourage others to do the same, and it is only by action that we will see change, so I'm putting a $100 bucks in over and above my regular MPrize commitment. Anyone else?

So what are you waiting for? Pitch in a few dollars and help us net a large donation of stock for the prize fund.

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It is good to see that the UC Riverside newsroom is covering the inaugural award of the Methuselah Mouse Rejuvenation Prize to biochemist Steven Spindler. From the article in question:

University of California, Riverside Professor of Biochemistry Stephen Spindler has received the inaugural Methuselah Mouse Rejuvenation Prize for his research in calorie restriction and its role in reversing aging in middle-aged laboratory mice, while extending their overall lifespan.

...

The aim of the prize is to speed the development of anti-aging interventions and promote public awareness of the prospects for them. According to a foundation statement, the research was "astounding because it worked on mice later in life."

According to Spindler's research, the fewer calories an animal consumes - provided malnutrition is avoided - the slower an animal ages and the lower the death rate from cancer, heart disease and diabetes. Spindler has served on several advisory groups and committees for the National Institute on Aging and National Institutes of Health.

He has been probing the life-extending effects of calorie restriction using advance gene chip technology, which is used to monitor and measure changes in gene expression. The major conclusions from his study are that many of the life-extension effects of calorie restriction happen rapidly and that these effects can be shown not only in young animals but also in older animals not previously on calorie restriction.

Spindler's intervention extended the average and maximum lifespan of the mice by about 15 percent and reduced the number of deaths from cancer.

You can find out more about Steven Spindler's research into the mechanisms of calorie restriction and longevity at his faculty webpage.

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The Immortality Institute film project - a wide-ranging series of interviews with members of the healthy life extension community - is progressing well. I'm sorry to say that I missed my interview opportunity with Bruce Klein for the silliest of organizational errors on my part, but we will hopefully get that done the next time he is in the neighborhood.

The latest sample of work to date is a video interview with Joe Waynick, the CEO of Alcor, the well-known cryonics provider. Waynick has been instrumental in steering Alcor towards a much more professional, growth-oriented culture - I've said before that I believe this sort of change is essential for the cryonics industry. The industry serves a very necessary purpose:

Death is not a topic that people like to think about, and that is just as true of healthy life extension advocates as anyone else. We have to recognise, however, that the future of healthy life extension (regenerative medicine, stem cell therapies, understanding the biochemical processes of aging, and nanomedicine, to name a few fields) will not arrive soon enough to benefit everyone. Many people are too old, or suffer from other conditions that will kill them before cures can be developed. This is an unpleasant reality that we must face.

Do we just write these people off and forge ahead regardless? Of course not. Instead, we turn to the science and business of cryonics, a serious effort to solve this problem that has been underway since the early 1970s.

Cryonics is the only option for life extension open to many older and seriously ill people: those who cannot wait for the promised therapies of the next few decades. It is the science of placing humans and animals into a low-temperature, biologically unchanging state immediately after clinical death, with the expectation that advances in medical technology may eventually enable full restoration to life and health. A small industry of cryonics providers exists to freeze your body on death, in the hopes that future scientists (most likely using nanotechnology and nanomedicine) will be able to revive and repair you.

In order to serve this purpose for everyone who might want to take advantage of it in the future, however, cryonics must become much more progressional, grow, legitimize and publicize itself. This is not to demean the sterling efforts of many volunteers over the years, but for real growth, cryonics must move beyond volunteerism and amateurs - no matter how dedicated and skilled they might be. We can hope that this process is underway.

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The Milken Institute is funding an effort called FasterCures, aiming to:

Evaluate the current systems of identifying and delivering cures

Identify barriers to progress that currently exist in these systems

Engage individuals and organizations in our mission to accelerate solutions

Create action plans to clear the path to faster cures

Clearing out the undergrowth of political, regulatory and protectionist parasitism that holds back scientific progress and its commercial application is a good thing for everyone, especially those of use who advocate healthy life extension and aging research. In our case, time is very much of the essence. Even the fastest plausible paths for future development of medical technology mean that meaningful rejuvenation therapies will come too late for many.

Still, it is a promising sign that an organization like FasterCures exists - it shows that recognition of the magnitude of regulatory and organizational problems in medicine has led to well-backed efforts to do something about it. I wish the FasterCures team the best of luck in achieving their goals.

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I'm very pleased to see the following press release. One of the many benefits of volunteering with the Methuselah Foundation is that I have early access to good news like this (before it makes it to the M Prize website, even).

Ammunition for the War on Aging - $100,000 sponsorship accelerator

British Visionary supports mission of Methuselah Foundation with large gift

WASHINGTON, DC For Immediate Release

On November 23, 2004, British entrepreneur David Fisher, learned that the first Rejuvenation M Prize - the prize for Rejuvenation and reversal of aging in middle-aged mice – was awarded to Dr. Stephen Spindler. Impressed by the power of Prizes to accelerate investment in scientific research to reverse aging, Fisher decided to donate well over $100,000 in cash to the Methuselah Foundation which the foundation will use to accelerate its efforts to grow the M Prize fund.

"The biggest causes of suffering in the developed world are degenerative diseases, and by attacking the aging process itself, we can intervene in all of these simultaneously," said Fisher. "The Prize is obviously a model that works. Rather than funding only one group of researchers, it inspires scientists from all over the world to compete for the reward and recognition of a large, public prize. The success of the Ansari X Prize is an excellent example of this. I believe that the fundraising efforts that my donation will make possible will greatly increase the M Prize fund and most certainly bring about similar success."

Fisher has also joined the Three Hundred, a group of devoted individuals who have committed to donating $1000 a year for the next twenty-five years to the M Prize fund. Membership in The Three Hundred has climbed dramatically since the announcement of Spindler's success.

Fisher went on to say “People from all over the world have joined The Three Hundred. Their commitment shows that ordinary people are willing to make extraordinary sacrifices in their everyday lives and budgets in order to bring about the reversal of aging. I’m following their example and hope I will be an example to others to join so the prize can grow in size and power as quickly as possible."

Fisher's sponsorship is the first major donation to be given via the Methuselah Foundation's newly established affiliate in the United Kingdom. The Foundation’s UK affiliate was established to provide tax deductibility for donations by citizens of the United Kingdom and to generally extend the Methuselah Foundation's efforts to advance Rejuvenation research and results into the international sphere.

The Methuselah Foundation will be adding more affiliate countries next year as it works to bring the strength of the international community to the cause – and to increasingly incite the competitive spirit of nations to substantially increase support and research into ending the diseases and suffering caused by aging.

For more information about The Methuselah Foundation, its M Prize competition and how to support the Foundation’s mission, see www.MPrize.org or contact us via e-mail at media@mprize.org.

CONTACT:

David Gobel : 202 306 0989 : media@mprize.org : http://www.mprize.org

Onwards and upwards, it seems!

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You may recall I mentioned research into the genetics of aging using kidney tissue a little while ago.

The findings, from different tissue groups within the kidney, suggest that the same changes in gene activity with age occur in all tissue types. This would certainly be hopeful news if verified - dealing with one type of process will require far less time and research funding than if there were a different process for every tissue type in the body. This "study doesn't suggest what factors drive the aging process, only that once it starts it follows the same path even in different organs ... whatever happens once aging begins, the mechanism that kicks off the process is probably genetically determined."

Randall Parker has followed up with his own more in-depth commentary:

The next obvious experiment would be to repeat this study with tissues from other organs and see if the same genes have changing levels of activity as tissue ages. Do some organs age at more rapid rates? Does this happen for everyone? One might expect some variability between humans due to genetic variants that accelerate aging in particular organs and also due to dietary habits and other habits that impose larger harm on certain organs (e.g. smoking on lungs or drinking on livers or fried meats on intestines).

Note that gene microarrays have gotten so powerful that these researchers were able to check the expression levels of all the known genes in a human cell. Chronological age is not always the same as age as measured by molecular genetic expression profile.

...

I'd love to see a longitudinal study where tissues are taken from a number of elderly people and assayed for gene expression to see if onset of diseases and mortality can be predicted from how far along the cells in a person seem to have aged according to gene expression levels.

As pointed out in that post, you can read the full paper online. Open scientific publishing is a very good thing; one has to hope that this new publishing model wins out over the established journal system.

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The Washington Post has been running a series of online discussions in question and answer format for a while now. The latest features Chris Mooney and is entitled "Is Politics Stifling One of the Most Promising Avenues of Aging-Related Research?" It focuses, as you might expect, on the California research initiative and stem cell research politics elsewhere in the US. Some quotes:

As bioethicists David Magnus and Arthur Caplan wrote recently in the San Jose Mercury News, "While it is hard to tell from the media coverage in the wake of the presidential election, the citizens of California brought the stem-cell debate to a screeching halt. There will now be ample public funding for that research."

...

In my view, thanks to what has happened in California, the debate in Washington hardly even matters any more. Unless, of course, Senator Sam Brownback's bill to ban all forms of cloning--including "therapeutic cloning" or cloned embryo research--somehow passes the Senate. Then we would have a federalism showdown pitting the feds versus the Golden State, which has green-lighted this work. And at that point there are all sorts of interesting legal possibilities in terms of who would win...but barring that, I think Washington has been largely superseded in this debate.

...

The attempt to use the United Nations as a backdoor means of banning "therapeutic" cloning, or cloning for research, has failed for two years in a row now. Each time, defenders of the research have rallied and prevented such a misguided action by the UN. I think the people who have been fighting this fight are extremely relieved, and they don't expect to have to go another round any time soon.

Rather than a global treaty calling for a ban on all forms of cloning, the UN will instead be adopting a "declaration" on this subject. It will be the product of negotiation and, therefore, will likely contain language that pleases everybody. So, in short, this is a huge victory for supporters of research.

I don't expect more significant action at the U.N. anytime soon, then. In Congress the big possibility, as I've said before, is that Senator Sam Brownback's bill to ban all forms of cloning--including for research--starts to move.

As Chris Mooney points out, the danger of a Federal ban on therapeutic cloning still exists. This technology is vital to the most promising research into regenerative medicine - attempts to ban it are just as damaging as attempts to ban or restrict embryonic stem cell research. If you would like to make a difference to the future of medicine, health and longevity, you should contact your elected representatives and make your opinions heard.

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While California officials are working on building the California Institute for Regenerative Medicine authorized by the passage of Proposition 71, politicians in other states are considering, reconsidering and pushing for their own public funding. Here is a small sample of current activity around the US:

Connecticut:

State funding for embryonic stem cell research could reach $10 million to $20 million, if Gov. M. Jodi Rell has her way. Rell wants to use state money to create a fund to help spur research institutions to finance studies in Connecticut. The governor wants to target biomedical research companies, universities and pharmaceutical firms. The fund would be "seed money" to match these interested parties.

Illinois:

State Comptroller Dan Hynes proposes a $1 billion bond issue over 10 years to fund the Illinois Regenerative Medicine Institute, which would distribute loans and grants to universities and medical research facilities in Illinois. The funds would pay for research involving embryonic, adult and cord blood stem cells. The effort is modeled on one in California, where $3 billion in public funding for stem-cell research will be set aside.

To pay for the bonds, Hynes has proposed a tax on elective cosmetic surgery, such as "tummy tucks," face-lifts and botox injections. A 6 percent tax would generate $15 million the first year if voters approve the plan in a statewide referendum in November 2006.

Minnesota:

Under a plan proposed by state Rep. Phyllis Kahn, DFL-Minneapolis, Minnesotans’ tax dollars could soon be used to pay for stem cell research at the University. Kahn said she plans to introduce a bill in the upcoming legislative session that would allow state money to pay for the University’s stem cell research, including work on embryonic stem cells. The bill, co-authored by Kahn and several other Democratic representatives, is largely similar to the one she introduced last year.

Texas:

Senator Kay Bailey Hutchison says Texas needs to pursue stem-cell research, and state leaders should work with Governor Rick Perry and the Legislature to develop a policy on stem-cell research. Hutchinson says it's necessary to keep the state from being -- quote -- "left in the dust by California.", referring to a landmark three billion dollar initiative to fund stem-cell research passed by California voters in November.

Leaving aside my opinions regarding the ultimately destructive nature of public funding (and the taxes and wasteful processes it requires), I would just like to point out that competition is a marvelous thing. Competition is the alchemy though which the basest of human motives are converted into shining towers of accomplishment.

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A new study in rhesus monkeys demonstrates one possible way in which calorie restriction protects against neurodegenerative conditions - Parkinson's in this case:

Researchers say the study suggests that calorie restriction may lessen the natural loss of dopamine that occurs with age and may reduce the risk of developing Parkinson's disease. Dopamine is a chemical used by the brain to control movement.

Although dopamine levels in the brain decline naturally with age, this decline becomes accelerated in people with Parkinson's disease and causes problems with movement and uncontrollable muscle tremors.

Researchers say previous studies have shown that people who eat a low-calorie, low-fat diet and those who exercise appear to have a lower risk of developing Parkinson's disease.

...

The study showed that the calorie-restricted monkeys had higher levels of movement compared with monkeys fed an unrestricted diet. Levels of dopamine in the brain were higher in the monkeys fed the calorie-restricted diet. Those monkeys also had higher levels of a substance known as GDNF that helps dopamine cells survive longer.

Researchers say these preliminary results suggest that long-term calorie restriction may reduce the risk of Parkinson's disease by increasing the production of GDNF and preventing the destruction of dopamine cells.

The weight of science backing calorie restriction suggests that it is the best and easiest currently available method of improving your health and increasing your healthy life span. On the grand scale of what is possible, however, calorie restriction is just a small step in the right direction. This is why those of us who want to live well for far longer must do more than just take care of our own health - we must devote time and energy to ensuring that the healthy life extension medicine of the future arrives in time.

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Since I mentioned research into Werner's syndrome (a rare condition causing accelerated aging, or at least the appearance and consequences of accelerated aging) a couple of days ago, some interesting further work was drawn to my attention. It seems that gene expression changes due to Werner's syndrome closely resemble those accompanying normal aging:

Werner syndrome (WS) is a premature aging disorder, displaying defects in DNA replication, recombination, repair, and transcription. It has been hypothesized that several WS phenotypes are secondary consequences of aberrant gene expression and that a transcription defect may be crucial to the development of the syndrome.

...

Transcription alterations in WS were strikingly similar to those in normal aging: 91% of annotated genes displayed similar expression changes in WS and in normal aging, 3% were unique to WS, and 6% were unique to normal aging. We propose that a defect in the transcription of the genes as identified in this study could produce many of the complex clinical features of WS. The remarkable similarity between WS and normal aging suggests that WS causes the acceleration of a normal aging mechanism. This finding supports the use of WS as an aging model and implies that the transcription alterations common to WS and normal aging represent general events in the aging process.

Progeria, another accelerated aging condition, has already been confirmed to actually produce accelerated aging. If Werner's syndrome is also really accelerated aging, then understanding its mechanisms and finding a cure should help in the fight to defeat the normal aging process.

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It sounds like Alcor - the cryonics provider - has wrapped up the legal unpleasantness with the family of Ted Williams. From their latest newsletter:

The court has finally issued a final judgment in the TW matter as it pertains to the rights of the nephews to examine the document of gift.

...

While we consider this judgment a significant victory, Alcor reserves the right to exhaust our legal remedies in this case and we will review the order with legal counsel to determine if further legal action is required prior to the December 30th deadline.

This judgment puts the TW affair to rest for now. However, that does not mean to say that John Heer will not try to come back with another attack.

As wrapped up as it gets in these matters, in any case. There is a real lesson here with regard to ensuring that your relatives are not going to try and destroy your cryopreserved body after death. If you're new to this story, you can use Google to find a wide range of articles and commentaries (biased in all directions) from various points in the drama.

Also worthy of note is the announcement of a new cryonics documentary in the works:

Alcor has given the green light for creating a high-quality documentary about cryonics. The documentary is being filmed in HDTV by a professional film crew and it is being produced by Debra Johnson, a professional producer with many years of experience in the television industry. This film will take a scientific approach to the subject of cryonics and it will contain many interviews with leading scientists throughout the industry. It will also contain member interviews and footage of the Alcor facility. The finished product will be made available to members to use as a recruiting tool. It will also be used on selected broadcast media stations to publicize Alcor and the field of cryonics.

This is a part of Alcor's new publicity and awareness program - a very good and necessary thing in my view.

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Werner's syndrome is one variety of apparently accelerated aging. It is less aggressive than Progeria, the other most common varient of this class of rare conditions, but still horrible enough. Scientists have already shown that Progeria is accelerated aging (rather than just appearing to be accelerated aging), a fact that makes this condition even more compelling for aging researchers. Curing Progeria should pave the way for advances in our understanding of the aging process in healthy adults.

But back to Werner's Syndrome. An article from the ever-reliable Betterhumans brings us up to date on the latest:

A new discovery about a protein's role in a premature aging disease has given researchers a better understanding of the illness and provided insight into normal aging.

The disease, Werner's syndrome, causes young people who would be otherwise healthy to suffer from such aging-related conditions as osteoporosis, heart disease, cataracts, wrinkled skin and grey hair.

Sufferers are known to lack a protein called RecQ helicase WRN. However, until now scientists were unsure why the absence of this protein affected so many different cells.

...

Telomeres are like ticking clocks, normally shortening when cells divide and initiating cell death when they get too short. But without RecQ helicase WRN, Karlseder and colleagues found, telomeres can often be lost instead of just shortening.

The researchers believe that the lost telomeres can lead to chromosomal instability which can result in cancer. This could explain why many Werner's sufferers die of cancer by middle age.

"The finding that the loss of individual chromosome ends (telomeres) can induce cellular aging is significant for aging in general, since it contradicts the hypothesis that all telomeres in a cell gradually erode, and at a certain critical length induce an aging program," says Karlseder.

...

"The biggest implication of our studies lies in the understanding of age-related cancer development," says Karlseder. "One could hypothesize that avoiding individual telomere loss (by that I mean loss of a telomere from a single chromosome) would avoid genome instability and therefore cancer."

So it comes back to telomeres, just like many other threads of modern research into aging and cancer. Developing therapies for Werner's may bolster our understanding of telomere science, and thus aid the fight to cure aging and cancer.

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Aubrey de Grey (and others, like Chris Lawson) have suggested that radical life extension using technologies that could be attained in a matter of decades would lead to life spans of 5,000 years or so. Where does this figure come from?

Once our medical technology has passed the stage of what Aubrey de Grey calls acturial escape velocity - the point at which the effects of aging are being defeated faster than we age - our life spans will be limited only by accident and violence. The odds of death under these circumstances are very well researched for our current Western societies:

The odds of dying from an injury in 2001 were 1 in 1,781.

If you take the statistics for a healthy person in the prime of life and keep calculating the odds of death based on present day statistics, you wind up with a projected life span of thousands of years. As Chris Lawson says, it is perhaps more appropriate to consider ageless individuals to have half-lives in the same fashion as radioactive elements:

[An ageless man] who has lived 500 years has a 50% chance of living another 500 years. And should [he] survive that to reach 1000 years of age, he still has a 50% chance of living another 500 years. This is always true: no matter what [his age], he has a 50% chance of surviving another half-life.

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I'll give the Aubrey de Grey profile at PopSci a mention at the Longevity Meme tomorrow (wider human audience, fewer machine aggregators), but in the meanwhile here are some good quotes for you:

Aubrey de Grey’s ideas are often met with skepticism, but, he says, "I haven’t been thrown out of any rooms yet."

...

Aubrey de Grey has no victory pronouncements to make as of yet, but he is vigorously pursuing an even more challenging project. Using the legacy that Watson and Crick bequeathed us, he proposes to tinker with the essential biochemical pathways that drive the aging process. De Grey contends that we know enough to intelligently map out a program of anti-aging intervention research such that sometime in the next 100 years, and quite possibly much sooner, the average human life span may be 5,000 years, a figure brought short of outright immortality by the small number of people who will die from non-age-related diseases and everybody else who, given the boggling amount of time available to them on the planet, will eventually do something unlucky or stupid like walk in front of a moving rocket car. In de Grey time, the 400-year span between Shakespeare's England and today would be but the blink of an eye.

...

The key to this rosy scenario is a sort of biological Ponzi scheme that de Grey has dubbed "escape velocity." The idea is simple. If scientists can find ways to intervene in the cellular processes that cause our bodies to age—managing to keep middle-aged people alive an additional 40 years, say—that extra 40 years will buy enough time for biogerontological engineers to solve other damage problems before they emerge. Think of the body as a leaky boat. You don’t have to keep it bone-dry to stay afloat; you just have to bail out the water at the same rate it’s coming in. Or, as de Grey says, "You don’t have to fix everything you’re ever going to get. You only have to fix things in time."

...

Whatever else you can say about de Grey, he gives a good PowerPoint presentation. My favorite image from his bag of lectures is a chart that compares aging with fox hunting. Both are traditional, both are effective ways to keep a population down, and both are "fundamentally barbaric."

...

And sitting opposite de Grey and me at the Eagle is John Archer, a bona fide Cambridge professor and a leading authority on bioremediation, the use of microbes to clean up toxins in the environment. De Grey has sold Archer on the feasibility of identifying tenacious strains of bacteria in soil ("You can find bacteria that digest rubber," de Grey says), genetically modifying them for compatibility with humans, then delivering the bacterial genes to human cells to aid with the never-ending job of breaking down the metabolic waste that leads to macular degeneration (the leading cause of blindness in the elderly), heart disease and Alzheimer’s. "It's sort of human engineering," Archer says. "It crosses boundaries, and that’s exciting."

...

De Grey has carved a middle way between geriatric medicine and gerontology; he aims to reach what he calls "engineered negligible senescence." His is a pragmatic approach, he tells me emphatically over another pint, because by the time the gerontologists have cracked the mysteries of cellular metabolism, we'll all be worm’s food. We’re at an unprecedented time in the history of science, he says, having learned enough about the genetic and biochemical processes that lead to metabolic damage that we can begin to sketch out a plan to repair it.

The Methuselah Foundation gets a good mention too, as well it should. It's one of the most important initiatives in aging research advocacy currently underway. The full article is long - I could fill another few screens with good quotes, so get thee hence and read it all.

Two other related items are also up at PopSci:

Seven Deadly Sins:

We must intervene to halt these aging processes, says Aubrey De Grey. the rub is, no one has figured out how.

How Would Transhumanists Modify the Body?:

While most of us science-literate folks are watching the biotech revolution with tentative optimism, hoping for innovations like medicines that have no side effects because they’re tuned to a patient's genes, or livers and kidneys grown to order for people with organ failure, some intrepid souls are taking much larger leaps.

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While I'm following up on items mentioned at the Longevity Meme, here is another one you (with thanks to Chris Mooney for pointing it out). This post goes into more detail on the science - what little we know of it at least - behind the latest Bioethics Council mutterings.

The first proposal might not yield any stem cells at all. If it did produce stem cells, they would probably be seriously defective.

The second proposal would probably yield only defective cells. Moreover, it looks like a solution to the problem only given a hokey and implausible view of what counts as an embryo.

So, alas, neither looks like a real solution.

Go and read the whole thing - there's a lot more leading up to that conclusion. I think my initial take in the Longevity Meme post was accurate; it's a fuss over abitrary definitions and bioethicists doing what they do best - trying to find ways to slow down the advance of medicine. The only problem here is that research in this field is neither free enough nor fast enough for those who are suffering and dying from conditions that could soon be treated.

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As a followup to a couple of items I pointed out at the Longevity Meme recently, here are some interesting posts from Randall Parker at FuturePundit.

Harmful Reduction In Immune System Cell Diversity With Age:

In a way the TCE cells pose a problem similar to cancer. They divide too much and squeeze out cells that do necessary jobs. In another way the TCE cells are similar to the T cells that cause auto-immune diseases. They propagate too much to create antibodies that are not needed (in the case of TCEs) or even harmful (in the case of T cells causing auto-immune disorders). It would be interesting to know whether some auto-immune disorders are caused by TCE cells and whether people who suffer from auto-immune disorders have less diverse T cell populations.

In a way this report is good news for people suffering frmo auto-immune disorders because it focuses attention on the need to be able to very selectively eliminate large subsets of immune system cells. A therapy developed to eliminate TCE cells might also be adaptable to use against T cells that are causing auto-immune disorders.

Effectively the pool of people who need to have their immune systems selectively pruned back has just gotten a lot larger. This increases the odds of more resources being deployed to develop such therapies.

Muscle Myoblast Stem Cells Cure Incontinence:

This treatment is a far greater economic value because it is of similar cost to existing treatments but works better because it actually fixes the cause of the problem.

...

Think about the economic value of stem cell treatments. Our problem in the United States isn't that we spend $1.6 trillion (as of 2002 - surely higher now) per year on medical care. Our problem is that so much of that care does not really fix the underlying causes of various medical conditions. Imagine medical treatments were capable of fixing everything that breaks just as auto mechanics can fix cars. Imagine you could therefore live in perfect health. Then I for one would not complain if that takes 15+% of the GDP.

...

What I find great about this report is that it shows that stem cell therapies that really fix what is wrong are moving into regular clinical practice. Stem cell therapies are not some distant prospect. They are happening now and every year that goes by from here on out we will have more stem cell therapies that successfully treat more diseases and disorders.

The economic argument is a good one (and I haven't been saying enough on that topic of late). The way to a healthier life is to greatly reduce the cost of curing and preventing disease. One way to achieve this end is to move beyond treating the symptoms of chronic conditions and repair the underlying problem. Medical research is expensive, but nowhere near as expensive as no medical research.

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If you scroll down to the bottom of the seminar download page at the Long Now Foundation, you will find an audio download for a talk by Michael West entitled "The Prospects of Human Life Extension."

The latest seminar (Ken Dychtwald on "The Consequences of Human Life Extension") isn't up for download yet - and not having read much of him or his materials yet, I can't tell you whether he's on the side of light or darkness (or even really involved for that matter) in the anti-aging marketplace. Any of you folks who know more than I are welcome to educate me in this matter.

The Dychtwald seminar was blogged and it sounds fairly sensible from this report. Another fellow had the following to say:

Last night, I went to the Long Now seminar with densaer. Ken Dychtwald on the consequences of human life extensions, and the like. Relatively short-term stuff, and relatively standard content, but he's a good speaker.

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People are fascinated by folks who make an effort to follow their own rules on appearance and mannerisms - so half of this Guardian piece is taken up with a discussion of Howard Trevor Jacobs' taste in clothing rather than the minor details of his research and acceptance of the Descartes prize. This fellow is one of the scientists organizing and contributing to recent important insights into the role of mitochondrial DNA damage in aging.

His multinational project, which involves scientists from Britain, Italy, Finland and France, promises not only to help in the creation of treatments for a host of illnesses, including deafness and diabetes, but to achieve the Holy Grail of medical science: a way to extend healthy human life.

...

Mitochondria are the power packs of the cell, with their own DNA, separate from the genes that direct the growth of rest of our bodies. As Jacobs puts it: 'Mitochondrial genomes are the cinderellas of genetics - you inherit them through the maternal line, and no one in science pays them much attention.'

Or that was the case. Thanks to work by Jacobs and other groups, it has been found that errors in mitochondrial genes can lead to the development of various inherited conditions, and that understanding their role offers an opportunity to correct these flaws.

Moreover, experiments using mice bred to accumulate high numbers of errors in their mitochondrial DNA produced startling results. The mice, aged less than a year, acquired a hunchback appearance. They also suffered from hair loss, osteoporosis, loss of fertility, heart disease and brain changes such as those seen in humans with Parkinson's disease.

In short, they got senile although only a few months old. 'This will lead to a much fuller understanding of ageing, and to rather straightforward ways of prolonging a healthy lifespan,' said Jacobs.

You'll find some more discussion of this linkage between mitochrondrial damage and aging - as well as some interesting related work aimed at manipulating mitochondrial DNA - here at Fight Aging!

There are still some notes of caution to sound with respect to this work - just because you can produce what looks like accelerated aging in mice doesn't mean you have the keys to an extended healthy life span. The next step (already underway) is to build the tools needed to repair and regenerate mitochondrial DNA in mice. Then we can see if this a truly a path to greatly extended healthy life spans. Personally, I am cautiously optimistic - there is a fair weight of science behind the theories backing this sort of work.

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Biogerontologist Aubrey de Grey is getting a fair amount of press again the moment - all for the good. The more people exposed to the debate over serious anti-aging research the better.

Before getting to the latest mainstream articles, I should point out this excellent post from April. Highlights from a discussion of the Methuselah Mouse Prize at the recent Calorie Restriction (CR) Society conference:

We need a large amount of money, directed only at the actual prevention/reversal of aging. The problem with this is that nobody wants to fund it with venture capital because guess what... it takes a long time to see if people will die! As soon as a CR mimetic drug looks promising, for example if it looks like it can also be a cancer drug or some such thing, then all the capital goes into that, since a profit can be made right now, and the studies are shorter term.

...

So now we come to one of my favorites of de Grey's points: people are so convinced that stopping aging is impossible, that they don't even want to try. They're willing to put massive resources into searching for the cure for diseases, but when you start to talk about curing aging itself, people look at you like you just stepped out of a science fiction movie.

...

Questioner 1: "We all agree that we need to fund the research. I think we might be able to fund the real anti-aging research by generating interest in a normal, mainstream sounding foundation that will help people be healthy. We obviously need large, huge amounts of money. How can this be raised without appealing to a broader audience than life-extensionists like ourselves?"

Michael: "What we need to do is convince more people to believe that curing aging is possible, then get them to do something about it."

Questioner 2: "But Michael, what if you can't get normal people to believe that?"

Michael: "That's the whole point of getting people involved who know how to change other people's minds. It's going to take more than just scientists to cure aging... we have to mobilize the political will to fund the project. I believe we can do it... and April, people like you can play an important role. You have great skills at organizing, persuading, and supporting people in the formation of mass movements, even in the face of peoples' aquired defeatism and false consciousness. Not to make you personally responsible for changing the world or anything..."

There's lots more good stuff there for those of us who are advocacy-minded. Go read it all.

But on to the mainstream media. The BBC is collecting articles on aging science at a fair rate. Aubrey de Grey makes his case in the latest piece, facing off against the opinions of S. Jay Olshansky. Both have commented here on Fight Aging! before - in essence, their principle differences lie in the timescale of serious anti-aging research and the way in which science can and should interact with the media, new and old. This public discussion (and the less public discussion that goes on within the scientific community) has a great deal of influence on funding decisions.

Glenn Reynolds sums up a common, sensible response:

I don't know who's right, but I know who I hope is right.

What do we have to lose in a serious, go-for-broke medical Manhattan Project - private, public, or philanthropic - to understand and cure aging? Aside from money, that is ... and you know what they say about taking that with you.

The BBC feature was also mentioned in a Slashdot posting. Examining the comments made there and to a previous post featuring Aubrey de Grey is certainly an educational exercise for those of us who want to extend public support and understanding of healthy life extension. Aging and life span really are a strange sort of sacred cow in our societies - but we can't let that hold back or divert the possibility of creating technology to enable greatly extended healthy life spans in our lifetimes.

Lastly for the moment, here is a report at Samizdata of a talk given by Aubrey de Grey at a recent meeting of a UK transhumanist society. It focuses on the Methuselah Mouse Prize, perhaps the most interesting of Aubrey de Grey's current projects - at least from the perspective of those of us outside the scientific community. The Prize gives each and every one of us a way to contribute directly to the process of invigorating and expanding serious anti-aging research - that's a big deal, because that opportunity was not previously available to average folks like you and I.

You may recall that the Methuselah Foundation recently inaugurated its Rejuvenation Prize - this is a worthy effort that is continuing to grow.

UPDATE: The Winter 2004 Advances contains a great article on Aubrey de Grey that I have mentioned at the Longevity Meme.

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Fight Aging! suffered an aggressive comment spam attack last week that forced the hosting ISP to take the server down for a while. The problem with the version of MovableType that we were using (2.661) was that it will rebuild several static pages after each comment - so a few hundred comments over a short period of time will bury the server. The very useful MT-Blacklist was installed, but that particular version is no protection against unrecognized, new spam URLs.

There are numerous ways of dealing with this, but I decided to upgrade to the latest version of MovableType and MT-Blacklist. The anti-spam functionality is improved and I've configured the new software to deal with the rebuild problem. All comments issued to older posts are now held for moderation rather than being posted immediately. In addition - something I should have done a while back - I have shifted the location of the comment submission script to a new, non-standard location.

We'll see if all that helps. In the meanwhile, you folks shouldn't see any differences on the site - but do let me know if you run into anything that looks like an upgrade bug.

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The passage of Proposition 71 and the prospects of $300 million in public embryonic stem cell research funding each year for the next decade is having a widespread effect on the research community. It has spurred on similar efforts in New Jersey and Massachusetts, while prompting discussions in other states with large research establishments. The threat of companies and talent moving to California is taken seriously these days:

Prior to the passage of a $3 billion stem cell research initiative in California last month, the institutions of Houston's Texas Medical Center seemed guaranteed a pre-eminent position in the research field some feel will revolutionize medicine. Now the lure of all that Golden State seed money might draw research talent away from the Texas Gulf Coast.

...

"We're very concerned about losing research scientists who are interested in stem cell biology and medicine to California," comments Dr. James Willerson, a cardiologist and stem cell researcher. He's also the president-elect of the Texas Heart Institute and president of the University of Texas Health Science Center in Houston.

So, for better or worse, I think we'll be seeing much more public funding for embryonic stem cell research and related fields at the state level in the next few years.

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I mentioned the recent linking of psychological stress and shortened telomeres, but Randall Parker has a lot more information at FuturePundit. In particular, other ways in which short telomeres have been linked to aging and health risks:

For those of you asking "What are telomeres and why are they important?" here is the short version: Telomeres are caps on the ends of chromosomes. They are made up of a very simple repeating sequence of DNA. Every time a cell divides its telomere gets shortened. Eventually the telomere gets so short that somehow as a result the cell can no longer divide or can divide only slowly and with increasing genetic damage.

...

My guess on the study reported above is that the mechanism of telomere shortening the researchers are observing is that stress causes certain classes of cells to divide more rapidly. Keep in mind that not all cells divide. For example, most nerve and heart cells are what are called post-mitotic. They no longer go through mitotic cell division. But skin cells and the various types of adult stem cells divide. One major cause of aging is that adult stem cell reservoirs throughout the body go through so many divisions that their telomeres get too short and they can't divide very well to provide cells to do repair.

Evidence has previously been found linking telomere length to mortality risk. The length of telomeres in endothelial progenitor cells (a type of adult stem cell) is linked to increased risk of cardiovascular disease. So those cells would be logical candidates to check for telomere length in women who have been under sustained stress.

Also, see an earlier thread here for good commentary on telomeres and the prospects for making them longer in a safe, reliable fashion.

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