Nothing gets me bristling quite like questions about healthy life extension that involve words such as "allowed," "permitted" and so forth. Whatever happened to the presumption of freedom? A commenter on a post about the SENS Challenge proffers an interesting exchange for consideration:

Both Nuland and the Editor of Technology Review, Jason Pontin, made clear that they believe extending the human lifespan is a terrible thing which could adversely and irrevocably effect our species by transforming our nature in dangerous ways.

...

I therefore thought it would be timely for me to publish an exchange of letters I had with Jason Pontin. (There did not appear to be anything in Jason Pontin's letter which suggested he would want it kept private or which would be embarrassing to him.)

It certainly seems that Pontin comes to view healthy life extension in a manner similar to Leon Kass when it comes down to it. There is the presumption of central authority making decisions for us - controlling our future access to healthy life extension technologies - and the sense that "something could be done" to prevent people from extending their healthy life spans. As I've pointed out in past posts, that something is called murder, no matter how you might go about organizing or whitewashing it. See this comment from Pontin, for example:

That said, you raise the issue of personal freedom. Does personal freedom--including the freedom to life--trump all other interests? Societies traditionally limit personal freedom, even the freedom to live, for any number of reasons. I am not saying this is a good thing--but I don't think the argument of "choice" can decide whether or not Immortality is a Good Thing.

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Some thoughts on whether and how chronic pain and the process of degenerative aging tie together from Randall Parker at FuturePundit:

Do the various pains have a common cause? Does chronic pain indicate a generally faster rate of aging?

I'd like to see a follow-up of this study with people over the age of 50 where stem cells get extracted from knees and other regions of pain and also from the blood. The goal would be to measure telomere lengths and compare them between people with and without pain to see if people with more pain are biologically older than age equivalent people who suffer less pain. Telomeres are caps on the ends of chromosomes and their lengths provide an indication of how many times a cell has divided. The more times a cell divides the shorter the telomeres get. I bet that the people with more chronic pains have shorter telomere lengths. Also, I bet that people with shorter telomere lengths will have lower life expectancies on average.

A study that looks for correlations between stem cell age and extent of aches and pains would provide evidence for whether development of stem cell treatments should gain priority in treatment of arthritis and other diseases that cause pain with age. Advocates for Strategies for Engineered Negligible Senescence (SENS) such as Aubrey de Grey argue that it would be more productive to develop rejuvenation therapies than to try to develop treatments for every disease of old age. If aches and pains are the result of cellular aging and of a lack of young stem cells to supply replacements for repair then more rapid development of rejuvenating stem cell therapies would provide better solutions for the pains of old age than surgery, anti-inflammatory drugs, anti-pain medication, and other current approaches.

From an engineering, reliability theory point of view, it seems like a sensible proposition and certainly worthy of further investigation. Do older people who are suffering chronic pain have, on average, bodies that are more worn - more damaged - by the processes of aging?

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A spirited discussion has been taking place on the Gerontology Research Group list with respect to the $20,000 SENS Challenge issued by the MIT Technology Review yesterday. Some folks in favor of the whole venture, some against, but here are biomedical gerontologist Aubrey de Grey's thoughts in response to other comments and an anecdote from biochemist Steven Spindler regarding the perniciousness of journalists:

Steve Spindler has summed it up best -- and I can add to his story by telling you that he did so good a job of refusing to ridicule me that the broadcaster (NBC) never aired the segment. The challenge has been brought into existence as a joint enterprise by Technology Review and the Methuselah Foundation. The reason from TR's point of view is that they have done themselves a lot of harm by doing a hatchet job on me without being able to back it up with authoritative names and they're keen to remedy that. (Jason Pontin is actually very ambivalent on the desirability issue -- one should not interpret Sherwin Nuland's views as representing Jason.) The reason from my (and [the Methuselah Foundation]'s) point of view is much more charitable: I know that most of my colleagues are inclined to be less conscientious than Steve when asked to opine on me, and I also know why, namely (a) that my conclusion in terms of potential life expectancy is very extreme and thus politically unpredictable, and (b) that the particular approach I advocate, the piecemeal engineering approach, is antithetical to mainstream thinking and thus tends to threaten funding for work that is currently in favour. The fact that I have no experimental training is an easy hook upon which to hang a curt dismissal of anything uncomfortable that I might have to say. I am therefore doing my colleagues a big favour with this: I am letting their silence help me rather than hurt me, They mostly know that I'm not an idiot and that they are unequipped to critique my proposals in detail, but they don't like to say so. Now, they don't need to say so -- I'll gain credibility, and more with every day that passes, just from their silence.

Just so.

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The frustration of Jason Pontin, editor of the MIT Technology Review, over the inexplicable reluctance of A-list bioscientists to deliver a good scientific critique of Aubrey de Grey's Strategies for Engineered Negligible Senescence (SENS) has born fruit. From Pontin's latest post, we have the announcement of the SENS Challenge:

The most widely read story in Technology Review in 2005 was "Do You Want to Live Forever?," a profile of Dr. Aubrey de Grey, a British theoretical biologist and computer scientist at the University of Cambridge's Department of Genetics.

De Grey believes that aging, like a disease, can in principle be treated and defeated. He proposes approaching aging as a problem in engineering through something he calls "Strategies for Engineered Negligible Senescence." SENS claims to identify the 7 causes of human aging and describes how each cause might be circumvented. De Grey is also the guiding genius behind The Methuselah Foundation, an organization which offers monetary awards to biologists who make significant advances towards reversing aging in mice.

...

In my reply to our readers, whilst conceding nothing, I promised to find a working biogerontologist who would take on de Grey's ideas. But while a number of biologists have criticized SENS to me privately, none have been willing to do so in public.

This silence is puzzling (de Grey, less charitably, calls it "catatonia"). If de Grey is so wrong, why won't any biogerontologists say why he is wrong? If he is totally nuts, it shouldn't be so hard to explain the faults in his science, surely?

One possible explanation for the silence of biogerontologists is that criticizing SENS would require time and effort - and that working scientists are too busy to waste time on something so silly. Another explanation (one obviously preferred by de Grey) is that biogerontologists reject SENS out of hand without examining its details.

Technology Review thinks it would be useful to determine which of the two explanations is correct. If SENS has some validity, then we should take it seriously. Because if we can significantly extend healthy life, we will have to ask - should we?

Regardless of which explanation is correct, biogerontologists apparently need an incentive to consider SENS. To that end, Technology Review is announcing a prize for any molecular biologist working in the field of aging who is willing to take up the challenge: submit an intellectually serious argument that SENS is so wrong that it is unworthy of learned debate, and you will be paid $20,000 if it convinces independent referees. In the case that even $20,000 is insufficient to motivate the relevant experts, we also invite contributions to the fund; anyone wishing to pledge should contact me.

Pontin is not pro-life-extension, needless to say - and, sadly, still appears to be willing to describe Aubrey de Grey as "nuts." I don't agree with a number of his opinions on the workings and nature of science, even if he clearly understands where he should be going with respect to the circulation of his magazine. However, if the Technology Review staff pull this off, or even generate significant additional publicity for serious attempts to greatly extend the healthy human life span, I might just be willing to forgive some of their past transgressions.

Go and read the full post for the terms of the SENS Challenge. You might also find Aubrey de Grey's "The Curious Case of the Catatonic Biogerontologists" to be well worth reading in the present context.

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A nice set of comments on current aging research are lined up at ScienceWeek for your reading pleasure. Richard Miller's points are interesting:

Is it safe to conclude that oxygen molecules are the true culprits in causing aging? Can we now turn our attention to the secondary questions of how they cause physiological decline in the superannuated? There are still some grounds for skepticism. The search for antioxidant drugs that slow aging and extend life span in mammals has produced much frustration and an absence of authentic anti-aging pills.

...

Mice can live reasonably long and healthy lives despite unusually high levels of oxidative damage ... Mutations that extend worm longevity also typically lead to, and perhaps act through, increased resistance to multiple forms of stress. Thus, it seems plausible that many age-retarding mutations may work by inducing cellular signaling pathways, still poorly defined, that augment defenses against a multitude of insults, including the oxidative ones.

While it's true that scientists would seem to have nailed down all the major root causes of age-related damage, there is a way to go yet in understanding how genetic and biochemical changes influence aging. Yet our lack of knowledge regarding specific mechanisms doesn't have to hold us back from developing medical technologies capable of repairing the age-related damage we understand. You don't have to be a meterologist to fix the guttering after a rainstorm - or to build a better gutter that will withstand the next storm. So less conservatism and more research into real anti-aging therapies!

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For the past couple of years, various modes of first generation adult stem cell therapy for heart disease have been trialed - mostly outside the US prior to 2004, thanks to the heavy, unaccountable, keep-my-own-job-safe hand of the FDA. These are comparatively simple therapies; forms of transplant using either donor stem cells, usually from bone marrow, or cultured stem cells from the patient to avoid immune rejection. An update on one of the latest trials:

Two patients have already been enrolled at Hopkins in a Phase I clinical trial, which is designed to test the safety of injecting adult stem cells at varying doses in patients who have recently suffered a heart attack. In total, 48 patients will participate in this study, which is happening at several sites across the country. Results are not expected until mid-2006.

...

The researchers are using a special kind of stem cell in an early stage of development, called adult mesenchymal stem cells, to avoid potential problems with immunosuppression, in which every human's immune system might attack stem cells from sources other than itself.

This trial uses cells from sources other than the patient, and performed very well in animal studies. If regulatory matters and commercialization proceed at the normal pace for the US medical system, some form of effective stem cell therapy for heart disease should be a widely available option by 2010.

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It seems evident that much of the gain in healthy life span over the past hundred years is the result of a large reduction in chronic disease - less disease means less acculumated damage to the complex machinery of your body, which leads to a better chance at a longer life, at least according to the Reliability Theory of aging. It is also established that at least a few age-related conditions are caused by or aggravated by forms of chronic infection. The latest article from SAGE Crossroads takes a look at this topic:

Since the discovery of Alzheimer's disease (AD) a century ago, researchers have probed many possible causes for the brain-ravaging illness, from nutrient deficiencies to the aluminum in cooking pans. But if an unorthodox hypothesis proves correct, the cause of AD was right under our noses all the time - or even inside them. According to a growing band of scientists, many of old age's scourges - including atherosclerosis, AD, and some cancers - stem from infections by bacteria and viruses. The evidence so far is inconclusive, but if research confirms the contention, doctors might be able to use the arsenal of antimicrobial weapons to prevent or even treat some of the most dreaded illnesses of old age.

Calls for greater government intervention aside (no surprise considering the source), it's clear that much more work needs to be done to conclusively link common age-related conditions to infectious agents. It is an attractive idea, as identifying a problem species of bacteria or virus would open the door to new and effective prevention strategies. The attraction doesn't mean these theories are necessarily right in the cases we'd like them to be, however. More research would seem to be justified, but bear in mind my earlier comments:

I point this out as a matter of interest - it is of course still that case that far more progress in healthy life extension can and should be made by directed research into extending the healthy human life span. We do need cures for chronic age-related conditions (infectious agents or not), but a great deal of funding is already invested in that research. Not so for the fight to cure aging, alas.

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If you want to take the long term view, articles like this one from the BBC are at least modestly promising. People are slowly opening their eyes and talking about aging in a more positive way, as something that can be changed and improved upon. Recognizing that there is an issue - that degenerative aging is extremely unpleasant for everyone who suffers and eventually dies from it - and that sufficient investment in science can make a difference is the first step.

Rising life expectancy could mean older people having to endure more years of ill health at the end of their lives, say peers. A House of Lords Science and Technology Committee report says more must be done to make older people healthier and to improve their quality of life. It calls on the government to apply scientific resources to improve health in old age.

We advocates must continue in our work to promote serious, scientific anti-aging research to those who have finally come to the conclusion that aging is not immutable, and that scientific research to ameliorate age-related suffering and ill-health is a good idea.

(I'll pragmatically refrain from commenting on the knee-jerk British reaction to address matters, especially matters medical, through horribly inefficient and unaccountable government programs).

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The healthy life extension community has certainly grown and become more mainstream over the past five years. This is all to the good, especially when the concepts of radical life extension and the prospects for research to achieve it are becoming more widely understood, both inside and beyond the scientific community. As Gandhi famously said, "First they ignore you, then they laugh at you, then they fight you, then you win." On this scale, we're doing pretty well - scientifically literate folks aren't laughing any more, and the laughter fades from other segments of the population as media coverage spreads. Instead, we see a battle of ideas between those opposed to the very idea of healthy life extension, scientists arguing over timescales, funding and possibilities, and advocates for longer, healthier lives telling them to get on with it.

One common form of advocacy movement can be thought of as a pyramid; a large number of supporters and hard workers support a few people who are deliberately placed to catch and focus media and public attention. We humans have brains designed for village life - we like to relate to individuals rather than organizations or causes, and organizations providing individuals for that purpose tend to outperform. The apex of one of the pyramids I am involved in is biomedical gerontologist Aubrey de Grey, author of the Strategies for Engineered Negligible Senescence (which I'm sure comes as no surprise to regular readers). By acting as a focal point for a portion of the healthy life extension community, Aubrey finds doors are opened that would otherwise be shut. Media coverage, organizational support and a network of supportive contacts are required in order to generate more of the same - in much the same way that the easiest way to make money is to start with a pile of money. It's a positive feedback look - growth and success inspires more growth and success. Every avalanche starts with a pebble, but it's a great deal of hard work to get the first few hundred pebbles to see it your way. After that, the options become more interesting.

Aubrey de Grey, and by extension the rest of us, are seeing new opportunities on the horizon. Invitations to self-important global conferences beyond the scientific community (such as TED) are a currency that can be grown and eventually bartered into relationships with wealthy philanthropists ... and thus funding. Give it a couple of years at the present rate of growth (of the Mprize for anti-aging research, of media coverage of SENS, of the supporting community, of connections to the wealthy and influential) and Aubrey will be pitching billionaires.

Which billionaires should Aubrey de Grey be pitching for funding for his proposed Insitute of Biomedical Gerontology, or for a series of research prizes focused of repairing the biomolecular damage caused by aging? Or rather, at this stage, which billionaires should Aubrey and his supporters be considering for cultivation? We know that John Sperling and Larry Ellison have a strong interest in aging and longevity research, and have already devoted large sums of money to the cause. Does this make them better or worse candidates? The executive director of the Ellison Foundation is a skeptic when it comes to SENS, for example. While it would no doubt be possible to pitch Ellison directly in years ahead, it may not be as fruitful as pitching another billionaire who has not spent years forming an existing set of opinions on the topic.

Have thoughts on the matter? Comment away...

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From aging researcher Leonid Gavrilov, a pointer to a collection of articles on aging and longevity from the perspective of the Society of Actuaries. As a few minutes browsing will lead you to note, the present day process of determining mortality rates and statistics of aging is anything but easy or cut and dried. You might find the following PDF-format papers from the collection interesting:

The Great Debate on the Outlook for Human Longevity:

Several leading gerontologists are engaged in a spirited and even vituperous debate regarding the prospects for human longevity. The issue is what life expectancy will be just after mid-century in the industrialized countries, and, more particularly, in the United States in 2060. The debate on the future of life expectancy is closely linked to such issues as the possibilities for extending average recorded human life span, the existence of limits to human life span and life expectancy, the form of the trajectory of age-specific mortality rates at the highest ages of life and the utility of developing projections of mortality on the basis of causes of death

Search for Predictors of Exceptional Human Longevity:

Centenarians (people living to 100 and beyond) represent the fastest growing age group of the American population, with obvious implications for actuarial science and practice. Yet, factors predicting exceptional longevity and its time trends remain to be fully understood.

Actuarial circles seem fairly conservative with respect to healthy life extension, rather like a large portion of the gerontology community. If this selection of articles is any guide, most actuaries regard it as somewhat radical to suggest that current trends in human longevity may continue, never mind greatly accelerate due to funding of serious anti-aging medicine.

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Justin from Classical Values has penned a good post to explain and interpret for the layman some of the most recent research into manipulating mitochondrial DNA and the relevant background. What does it all mean and why is it important for the near future of healthy life extension? Get thee hence and read to find out.

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An interesting press release via the GRG list discusses a new way of producing glial-derived neurotrophic factor, or GDNF:

GDNF has been shown to protect dopaminergic brain cells, neurons that produce dopamine that becomes depleted in Parkinson's patients. GDNF has also been shown to have a beneficial role in protecting neurons in animal models of Amyotrophic Lateral Sclerosis (ALS) and Spinal Cord Injury (SCI).

Most of the current treatment of neurodegenerative diseases provide limited benefit to patients. Drugs for Parkinson's disease, which focus on dopamine supplementation, often cause prohibitive side effects. To overcome these problems, researchers around the world are intensively exploring novel cell- and gene-based therapies for replacement and augmentation of the lost neurons. Prominent among these novel therapies are attempts to deliver GDNF to the site of neuronal regeneration.

In the current BrainStorm-sponsored study at Tel Aviv University, biochemical and immunological methodology showed that human bone marrow mesenchymal stem cells may be uniquely differentiated into cells that resemble astrocytes, express astrocytic markers and produce significant levels of GDNF.

...

"Neurologists have long thought that GDNF can be used to preserve and maintain the integrity of dopaminergic neurons in Parkinson's disease. However, delivery to the appropriate location is a major challenge. Direct delivery of the protein has failed and there are current ongoing attempts at gene therapy. We believe that our approach, based on neural transplantation of stem cell derived GDNF producing cells, without any genetic manipulation, is preferable," said Prof. Eldad Melamed, Chairman of the Scientific Advisory Board.

In addition, "The use of a patient's own bone marrow stem cells to generate neural cells for replacement and support of a patient's damaged dopaminergic cells is a strategy that will avoid problems of immunological rejection," said Dr. Daniel Offen, Chief Scientist.

Make of that what you will; the good news I take away is that a variety of methods for attacking this class of neurodegenerative disease are currently under investigation. Diversity of study is always promising in the long term, and any progress towards curing or preventing neurodegeneration is a good thing. In the near future, probably within 10 years, you'll be able to replace failing organs with engineered tissue should your personal worst case medical scenario come to pass - but age-related damage to the brain has to be repaired in situ. Hence those of us interested in healthy life extension should also be interested in neuroregenerative work.

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For a splashy, high-power conference on the future of technology, TED Global 2005 has certainly left very little imprint in the media. Biomedical gerontologist Aubrey de Grey was one of the speakers this year, there to talk about the Strategies for Engineered Negligible Senescence and the future of healthy life extension research. You can find a non-Macromedia program of speakers elsewhere online - Peter Diamandis, Craig Venter, Kari Stefansson and Richard Dawkins are some of the other noteworthy folks.

One can hope that Aubrey spent his time turning his considerable charisma to forging potential relationships and cultivating donors. As opposed to, say, punting, that is ... as that post notes:

The attendees, while too engrossed to write, were still able to snap away… Including this one of extropian anti-aging beard-king Aubrey De Grey on a punt!

So come on people - there have to be some attendees out there in the wider blogosphere up to writing first hand reports of the bioscience topics to go with all those photographs.

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A great example of the need for caution and careful reading when following science in even the more reputable mainstream media can be found at the BBC. You might recall the buzz over recent work on mitochondria and aging that implies free radical damage is not as important a mechanism of aging as thought. The folks on the Gerontology Research Group list have suggested a wait and see approach - much the same as the line taken by Aubrey de Grey in this piece:

Dr Aubrey de Grey, an expert in ageing research at the University of Cambridge, said: "This is an important study, building on similar work by a couple of other groups over the past few years.

"It would be premature to say that these studies are conclusive with regard to the role of mitochondrial mutations in ageing, but they certainly imply that cell death, especially of stem cells, can make a big difference to the rate of ageing."

He said it was important to be cautious because it was impossible to be sure that something which shortens life if you accelerate it is also lifespan-limiting when it proceeds at its natural rate.

"Ideally, we would develop mice that had better mitochondrial DNA repair and maintenance and lived longer as a result, but we don't have that result yet."

The attention-grabbing header of the article - involving large quantities of orange juice, antioxidants and the dispelling of dearly held theories - is somewhat sensationalist, even if it may not appear as such to the casual reader.

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The dust has settled from the Methuselah Foundation charity auction for lunch with futurist and healthy life extension advocate Ray Kurzweil; congratulations to the lucky winner. I think that we can call it a win all round despite the uphill battle on the publicity side ... and we won't talk about just how long it took the combined technical genius of the Mprize volunteer crew, myself included, to figure out the details of how to run charity auctions on eBay through MissionFish. A humbling experience indeed. From Jay Fox:

The first main area of success was, of course, the money. The winning bid was $4,050.00, and when combined with Ray Kurzweil's generous offer to match up to $4,000.00, the total cash benefit to the prize was $8,050.00. When added to the cash already collected for the prizes, this would bring the total cash collected to nearly $160,000.00.

The second main area of success was public awareness and outreach. This multi-faceted area of success includes a doubling or more of the number of pages that link to the MPrize, a spike in traffic to the website, and at least one new membership to The Three Hundred, a group of dedicated individuals and organizations which pledge $1,000 a year for 25 years. These $25,000 commitments will help fund the first skirmishes in the coming War on Aging.

Please take a moment to recognize that a great deal of hard work goes into these fundraising events - the ongoing growth and success of the Mprize for anti-aging research is due to the commitment and dedication of volunteers and donors alike.

You can show your support for the fight to cure aging by donating to the Mprize fund. The amount doesn't matter; it is more important that you stand up and make a statement about your desire for the future - to enter a world of longer, healthier lives and working longevity medicine.

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ScienceDaily has a two part interview with Bruce Ames (part one, part two) of Juvenon - another portion of the wider healthy life extension community that sells old school products while discussing new school science. (A skeptic would say "hyping supplement sales with talk of mitochondria"). I would lump them into the same category as A4M or the Life Extension Foundation; heart in the right place, but basically health concerns rather than longevity concerns in all but rhetoric.

I have nothing against supplements: I use them, they're demonstrably good for your health in both the short and long term, but they are not the future of healthy life extension. Taking care of your health today is of course something you should do, but a focus on supplements to the exclusion of supporting research into developing working rejuvenation medicine is the path to aging and death - see some of my previous comments on this matter for a sense of where I stand on it all. Sadly, all too many people don't realize that there is anything beyond the very large, very vocal "anti-aging" marketplace as it stands today.

If you're big on mitochondria, selling vitamin supplements is not the way to support the future of healthy life extension. There are more than enough people out there selling vitamins; many of them are even responsible and do a good job. Protofection research and work on understanding the modes of mitochondrial damage and its cause and effect - now that's the way to go.

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Liberation Biology by Ronald Bailey is of course worthy of note, but I thought I'd point out this review from Science & Theology News:

Bailey addresses major issues in biotechnology: longevity, disease control, stem cell research, cloning, designer babies, agricultural biotechnology and mind improvement drugs.

Bailey openly dismisses bioconservative arguments, saying their "fears are vastly exaggerated; their ethical objections to biotechnological progress are largely misconceived; and the biotech revolution rather than diminishing human dignity and liberty will instead enhance and enlarge them." He takes leading bioconservatives to task, writing that the "future toward which the biotech revolution is taking humanity is in fact almost the exact opposite of the Brave New World."

The advance of biotechnology is indeed a liberation - a liberation first from sickness, then from degenerative aging, and finally from involuntary death. We are a thousand times better off than our ancestors for just the progress of the past century - and this is merely the beginning of a long, fascinating path of discovery and growth. More and better is to come, and those who oppose better medicine and longer, healthier lives should be denounced for the selfish fools they are.

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Researchers see Alzheimer's as a two-protein disease: amyloid plaque - target of attempts to produce an Alzheimer's vaccine - on the one hand and neurofibrillary tangles on the other, both somehow related to or responsible for neurodegeneration. One particularly interesting thread of Alzheimer's research involves exploring the theory that these neurofibrillary tangles are not in fact a root cause of mental degeneration associated with the disease. You can find a high level overview of the basics over at Nature:

The brains of people with Alzheimer's and some 50 other forms of dementia are known to have certain characteristic features, including messy bundles of fibres in nerve cells called neurofibrillary tangles. But no one has been sure whether the tangles are a cause or symptom of dementia.

Mice engineered to massively overproduce a protein called tau tend to grow more of the tangles and display the same problems with memory and learning as humans with dementia. Researchers think that it is a certain version of the tau protein, rather than a simple over-abundance, that leads to the tangles.

It has been speculated that these tau proteins, rather than the tangles, kill nerve cells.

...

They trained mice to navigate a maze partly submerged in water, and watched for signs of memory loss. By the age of three months, mice genetically engineered to express 13 times too much tau protein couldn't remember the route to dry land, and had developed tangles in their brains.

But surprisingly, when the researchers turned off the switch promoting tau expression, the mice began to gain back some lost memory.

Most promising. Progress towards understanding and defeating the most common neurodegenerative diseases is a vital part of healthy life extension science. After all, the worst case scenario for the future of your heart and other organs is that they will have to be replaced wholesale with new, healthy tissue grown from your own cells. This isn't an option for the brain - so we had better develop very effective means of in situ repair.

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I have it on good authority that Jay Fox will be - briefly - on tonight's edition of the Daily Show in a segment on "The Fountain of Youth." So respect the sacrifice in pride he is making for the wider cause of healthy life extension advocacy and tune in.

Don't forget to watch the Daily Show with John Stewart, tonight (Wed., July 13) at 11 PM EDT on Comedy Central. I've been told I will be on for about 30-45 seconds. No idea if my plug for the MPrize made it to the final cut. Anyway, have a good laugh at my expense.

We shall see if all publicity is good publicity...but join the discussion at the Immortality Institute forum and have your say on the matter.

UPDATE: Ah, the vagaries of media scheduling.

The segment on "The Fountain of Youth", in which I will appear, and which was originally scheduled to air tonight, has been rescheduled. It is tentatively scheduled for Monday, July 18th. Tentatively.

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With all the spume and nonsense online and in the media regarding embryonic stem cell research, it's actually quite hard to find a sane, well-written, scientific article that explains just why embryonic stem cell research is important. The staff over at blog.bioethics.net seem have found a good example, even if it is rather diluted by discussion of funding and politics:

My laboratory is studying embryonic stem cells in hopes of making blood stem cell transplants safer and more widely applicable. A critical part of the strategy is using somatic cell nuclear transfer to generate stem cells that are customized to the specific patients I mentioned earlier, kids with leukemia, immune deficiency, and sickle cell anemia. We hope to correct the genetic defects in these patient-specific cells, direct their differentiation into blood, and transplant kids with these genetically matched autologous cells. This strategy is already working in mice, and we are eager to translate this work into humans. The current Federal funding policies have held us back.

Although it is true that no one has to date been treated with cellular therapies based on human embryonic stem cells, I can assure you that mouse embryonic stem cells have had a major impact on medical research. Over the past 25 years, mouse embryonic stem cells have been used to create models for scores of human diseases, including cancer, heart disease, obesity, and Alzheimer's. Research discoveries based on these models has led to new drug development and therefore touched countless lives. As for the criticism that no one has been cured with embryonic stem cells, the field of human embryonic stem cell research is a mere 7 years old, so it is premature to expect successful cell therapies to have already been delivered to patients. I believe it is only a matter of time before human embryonic stem cells are used in drug development research and become the basis for important new cell therapies.

As further evidence of how human embryonic stem cells enable unique opportunities to study disease, consider research on Fanconi's anemia. Kids with Fanconi's anemia suffer bone marrow failure, and often develop leukemia. Scientists have tried to model this disease in mice, but the mice do not develop bone marrow failure, and the adult blood stem cells from Fanconi's patients cannot be maintained in culture. Recently, a team from the Reproductive Genetics Institute of Chicago isolated a human embryonic stem cell line that carries a Fanconi�s gene mutation. This cell line could enable us to study the uniquely human aspects of Fanconi's anemia.

Read the whole thing - there's a lot more.

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I noticed a post yesterday discussing a comparatively recent theory of programmed aging (which you may recall was mentioned here last year). The author, I think, hits on one reason why the prospect of aging as a genetic program - rather than a complex, messy process of decay - is attractive to those of us thinking about healthy life extension:

It seems easier to tweak the programming in a computer than to try to replace part after part in an old car that is steadily collapsing.

Sadly for would-be genetic tinkerers, the Reliability Theory of Aging and messy, complex, unprogrammed decay looks to be a much more likely model for degenerative aging in mammals.

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From Rafal Smigrodzki - via the Extropy chat list - excellent news on progress made by the research group he works with:

Today our team confirmed our previous preliminary data showing that we can achieve robust mitochondrial transfection and protein expression in mitochondria of live rats, after an injection of genetically engineered mitochondrial DNA complexed with our protofection transfection agent. A significant fraction of cells in the brain is transfected with this single injection even though we so far did not optimize the dose.

This achievement has important implications for medicine: protofection technology works in vivo, and should be capable of replacing damaged mitochondrial genomes.

For those new to mitochondrial research and its relationship with aging and rejuvenation science, you can find more on Rafal's work here at Fight Aging! and details on the importance of repairing mitochondrial DNA damage at Aubrey de Grey's Strategies for Engineered Negligible Senescence (SENS) website. In short, this merits celebration! We're going be hearing much more about the repair of damaged mitochondria in the years ahead, firstly to cure specific age-related disease, and then to tackle general age-related damage to the mitochondrial genome.

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Author Damien Broderick pointed to an almost Kassian article on healthy life extension recently. After some economic commentary and sweeping misjudgements of human nature, we hit the punchline:

It is, I suppose, just conceivable that Broderick may be right about the theoretical possibility of indefinitely prolonged life. However, human nature is less malleable than human physiology and ill-adapted to immortality's challenges. I also have my doubts about whether, if offered the everlasting option, all that many of us would take it.

After all, well-adjusted people tend to develop a serene acceptance of finitude. Then again, the sense of an ending is all that makes some lives, especially very long ones, bearable in the meantime.

One would hope that it goes without saying that this is rank and outright nonsense, just like the screeds put out by the likes of Leon Kass. I have nothing against people who want to age and die - but I suspect that they haven't really thought through or otherwise correctly grasped just how much suffering and pain is involved. We humans aren't really all that good at empathy or looking ahead; if we were, you can be sure that we would be far further ahead in medical research.

People eager to inflict death and suffering on others are a different kettle of fish, however. By the standards of this writer, everyone who seeks to cure disease or relieve suffering in the world is maladjusted. I don't really have any comment to make on that - I think it stands on its own as a shining example of foolishness. I have to say that I am continually surprised by the pro-death-and-suffering contingent. It's human nature, I suppose; any set of terrible ongoing circumstances, no matter how ugly and horrific, will give rise to people who attempt to accept and justify it.

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As you may know, the Methuselah Foundation - home of the Mprize for rejuvenation and longevity research - is currently auctioning a celebrity lunch with Ray Kurzweil, to be held at a mutually convenient time and location. The auction has been running for a few days now, with healthy bidding between the Immortality Institute full members group and a number of other folks.

Kurzweil is a fascinating individual - a great example of what you can accomplish if you put your mind to it. He has been doing a fair amount of heavy lifting for the popularization of healthy life extension in the wake of his book Fantastic Voyage, co-written with Terry Grossman. Whatever I may think about supplements boosterism and topics such as the timescale of technology progress, Kurzweil's efforts have benefited the wider community of healthy life extension advocates. A world in which more respected, influential people are talking seriously about greatly extending the healthy human life span is a world in which actually achieving this end becomes easier. I would certainly put in a bid for lunch myself were I not involved in some of the volunteer work related to the auction.

The celebrity lunch auction will run through to the end of the Thursday 14th - if you are considering a bid, you have the weekend to think about it and get together five like-minded friends. Lunch with Ray Kurzweil would certainly be something to talk about for a while, and the proceeds are going to the best of causes.

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I'm pleased to note that Jay Fox managed to wrangle his way into an interview on the Daily Show, probably to air sometime in the week beginning July 11th. This brave endeavor was accomplished under the theory that there is no such thing as bad publicity, and a certain loss of pride and posture for Jay is worth the attention it will bring to the Immortality Institute and healthy life extension in general. As he notes:

Even if only 1 out of 100,000 viewers of the show becomes interested enough in what we do to become Full Members at some point in the coming weeks or months, then that could mean dozens of new Full Members of ImmInst, representing $2,500 a year in membership dues to help us do projects like the books or the documentary or the conference. As embarrassed as I am to be made the butt of multiple jokes on national television, I'm very optimistic about how this will benefit ImmInst in the short term, and enough short term successes can lead to long term victory in the scientific conquest of death.

By the sound of things, the interview will be par for the course for the Daily Show, so we shall see how it all turns out - and congratulations to Jay for pulling this off.

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Via the Gerontology Research Group mailing list, an early reminder of the Eighth International Symposium on Neurobiology and Neuroendocrinology of Aging in July 2006 - in Austria, so an event for those with a travel budget. The list of confirmed presentations and speakers is interesting even at this early date, including as it does "Genetic control of longevity in C.elegans" and "Mitochondrial DNA and aging."

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We all have our thoughts on - and hopes for - the timeline for healthy life extension (and radical life extension). Here are some from Stephen Gordon at the Speculist:

Last year I speculated that a simple form of life extension therapy would be available within a decade. With less than nine years left to go, I stand by this prediction.

Aging is a very complicated problem. But age therapy is coming soon because the beginning of the answer to aging will be much simpler than a more complete solution that addresses all seven of Aubrey de Grey's age problems.

As Aubrey de Grey has repeatedly pointed out, we don't have to have a complete solution to benefit. In fact, we might live to see a complete solution to the age problem if we live to see the first true therapy for aging. This "bootstrapping" idea means that the time we gain from the first age therapies might help us live to benefit from second-generation therapies, second-generation therapies bootstrap us to the third generation, etc.

I think this is overly aggressive as a timeline for widespread availability of therapies, given the problems caused by regulation and increasing socialism within medicine. I do expect to see some very impressive lab work taking place in 2014 - especially if we research advocates do our job.

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Michael Rae is Aubrey de Grey's research assistant and a man who writes a mean post (and a great article) once he gets going. Here is a good example on the Mprize, aging research and other related topics, made in response to Matt Piles on the Calorie Restriction Society mailing list. I'll let him take it from here:

Matt Piles wrote:
> Michael wrote:

>> Solution: don't get biologically old ;). Keep your
>> Calories low; speculatively, also keep your long-chain PUFA and
>> dietary cholesterol intakes low; and be a luddite
>> in the engines of aging by giving till it
>> hurts to the MPrize .
>
> Actually in my view this would be a huge waste of
> money. Especially if it hurts...... Aubrey de Grey
> grossly misunderstands what motivates biology
> researchers. The analogy with the Ansari X-Prize for
> example is false. In contrast to aerospace engineers,
> gerontologists can easily get *tons* of money from the
> government.

That depends on which "gerontologists," and what exactly they want to do with the money. The NIA curretnly has a budget of just over US$1 bn. Of this, more than half now goes into Alzheimer's disease (plus the amount invested separately by NIMH, NB); much of the rest of its budget goes into other specific diseases; and a large chunk also goes to geriatric (ultimately, palliative) medicine and to "social gerontology" (ie, how to set up social structures to support the frail elderly).

Richard Miller has pegged the total NIA budget actually allocated to the biology of aging at "somewhere between six and ten million dollars a year" [1] -- a blip that would hardly be missed in the US biomedical research budget.

Even this gives an overoptimistic picture of the funds available for INTERVENTION, because almost all gov't-funded biogerontology expenditure is going into curiosity-driven descriptive studies -- trying to tease out the metabolic origins of aging -- and not into intervention-oriented work. Even most CR work, after the failure of the (relatively) massive Biomarkers of Aging study's flop, is oriented toward its impact on specific diseases, or toward testing theories of aging causes, or trying to figure out its human extrapolability, and not into actually doing something about aging as a disease in need of biomedical solution.

I actually asked Huber Warner, the outgoing director of the NIA, why the NIA wouldn't put more money into intervention-oriented work at the last AGE conference. After first either greatly misunderstanding, or trying to politely duck, this question by talking about the difficulties of so-called "accelerated aging" models, he ultimately gave a response that made Aubrey smile in the way that a police officer who's just extracted a confession of a horrible crime must smile. Because Warner's response appeared to confirm key elements of the nasty "vicious circle" that Aubrey has long held to be holding back serious work on anti-aging biomedicine. He said that they receive very few applications for such work, and that the NIA's internal "peer" review process tends to shoot most such proposals down. As I have written in my previous, major post on the MPrize:

Also, gov't funded researchers are not exactly at liberty to pursue whatever they want. They have to write up proposals to explain exactly what they want to do, and exactly why. And here, a nasty vicious circle gets started. Because the people doing the funding decisioins, while they are scientists, are (in their capacity as funding allocators) first and foremost bureaucrats, with political masters. Crazy-sounding (to politicians, or to their electorate) schemes to "engineer negligible senescence" are deadly to a political or bureaucrataic career. Ironically, because of its less cut-and-dried nature, similar bureaucracies in the arts (eg. the NEA in the 'States) are actually more insulated from their political masters, because they can defend the allocation of funds to (say) an exhibition of crucifixes smeared with an assortment of bodily exudae on freedom of expression grounds, and because art is by its nature in the eye of the beholder; neither defense clearly applies for scientific work.

So scientists continue to pursure relatively modest, uninspiring projects, and to couch their work in modest, uninspiring terms. "We're not looking for a cure for aging. We'd just like to learn how to delay some of the diseases of aging so that Granny can be more comfortable in her old age."

This reinforces the impression, in the mind of the electorate, of a scientific consensus that real intervention in the aging process is impossible at this time. This reinforces the pressure on politicians not to have government funding 'wasted' on such work. Which reinforces scientists playing it safe. And 'round and 'round ...

So how do we break out of these self-perpetuating systems?

In the post in question, I say: the Prize.

Despite his rivalry with de Grey, Richard Miller (unsurprisingly) agreees about the basic structure of the logjam:

"Scientists and their patrons -- even those who have legitimate research interests in interventional gerontology -- do not wish to be seen hanging out with [purveyors of useless nostrums]. Perhaps for these reasons, discussions of research on life span extension are carefully skirted in political discourse at the [NIH] and among similar custodians of public funding. One can sometimes get away with cautious circumlocutions ("we do research on the causes of late-life illnesses"), but to be safe, it is clearly better to focus on how to "add life to years" and how "to learn the secrets contributing to a healthy old age." A president who publicly committed the government's resources to research on extending peoples' life span would be deemed certifiable." (2)

He also lists several less important reasons. Having had a lot more close interaction with the biogerontology establishment in the couple of years since the first SENS conference (reminder: SENS 2 is coming this September -- yeah!!), and especially since early this year when I began formally working as Aubrey's research assistant -- I must now, depressingly, add one more factor: most biogerontologists really aren't actually INHERENTLY interested in their field of study. They are simply intelligent people with enormous curiosity and the skills to do science, who like to exercise their brains and beakers, and who will pursue whatever project that they can get funded that allows them to do so. They got into biogerontology because, as grad students, someone had a grant doing aging-related work, and they just kept pursuing the resulting trajectory -- or, they repackaged their existing work as being in some sense or another "aging research" because the field has recently become somewhat sexier, and perhaps their old niche was not (or was too crowded).

But most biogerontologists would be just as happy to be working in almost any other field of biology: they feel no particular existential urgency about their own aging, nor about the grey holocaust that surrounds them, and would be completely satisfied to simply spend their days teasing apart metabolic pathways and playing with the latest visualization tools for the rest of their careers (which are, of course, doomed to be cut short by the ongoing, progressive, intrinsic degeneration of their bodies and brains -- oops, don't think about that ... focus on your gels ...). They feel no particular urge to damn well DO SOMETHING ABOUT the molecular rot whose progression they so painstakingly document.

This isn't all of them, of course: Richard Miller, Mark Lane, and many of the people who have actually done lifespan calorie restriction (CR) studies (a vanishing breed, alas) are much more conscious of the horrors of biological aging -- and optimistic that something can be done about it -- than their peers. I think, unfortunatley, that the work that most of these folks either are doing, or WOULD be doing if they could somehow beg the farthings, is devoted to a very poor strategy for developing genuine anti-aging biomedicine: the development of CR mimetics and other methods of perturbing the metabolic processes that CAUSE aging damage, instead of work to UNDO the damage itself.

By comparison, the Nationall Cancer Inst gets US$4.7 bn per annum, and almost all of the research dollars (ie, what isn't gobbled up by bureaucracy, outreach, etc) go into work that the researchers have successfully argued will plausibly ultimately result in cures. And it's much more likely that these researchers recognize the seriousness of their work: many of them have watched someone they love suffer and/or die of cancer, and while eveyone has relatives that have suffered and/or died of aging (and everyone has the disease themselves), the nigh-universal state of false consciousness and quietism about the aging plague extends to most biogerontologists as well.

We need to create an independent incentive system, and/or a pump-priming supplement to the existing one, and/or to mobilize the public to demand that the government put money into interventive biogerontology research on a scale proportional to its actual impact on morbidity and mortality -- ie, a scale far exceeding that awarded to the NCI. (As a ballpark: per 1985 figures, the average 50-yr-old woman would gain 2.7 years of life from the utter ERADICATION of cancer from human experience; an effective CR mimetic that could be administered in childhood would gain her over 30 yrs, or more than ELEVEN TIMES as much (2) -- including by greatly reducing the incidence of cancer. Yet it's cancer that gets most of the money: as another ballpark, something like 470 times as much per annum).

The MPrize goes a long way toward addressing all of this.

> And The Methuselah Foundation is viewed
> with suspicion in some circles and even as a bit of a
> joke. Look at Spindler's Web site.
> He doesn't mention that he won one of the Methuselah
> Foundation's prizes.

Well, first, in a real sense he HASN'T won one of the prizes. He was given the inaugural award -- the baseline, against which the first Rejuvenation Prize winners will be judged. This came with no funding at all.

Second, Spindler himself does appear to think that the MMP is a good strategy:

While he concedes that the fruits of his research—in the form of drugs and other biological interventions that could slow aging in the human population—are not likely to appear for several years, Spindler sees tremendous promise in the burgeoning field of anti-aging research. Ventures like the Methuselah Mouse Prize and the research it spurs will help turn skeptics into believers, erasing the public perception that his line of work involves a hopelessly quixotic search for some bogus fountain of youth.

Third, and most important: the impact of the Prize on actual research agendas can't be expected to be much as yet, nor a winner in the near future to trumpet hir results too much, for the simple reason that the Prize is as yet too small. The total pledged pot is now ~US$1.3 million, but most of this is in pledges such as the "300" commitment http://www.mprize.org/index.php?pagename=thethreehundred ; the prize amounts actually available for dispersement are:

Longevity Amount 60,065.84
Rejuvenation Amount 90,329.68

... of which only a percentage will actually accrue on winning, since one only gets a fraction of the prize money available for the Prize in which one is entered, depending on the magnitude by which one exceeds the existing record (see http://www.mprize.org/index.php?pagename=structure ). Even the full $150K would not cover a single mouse lifespan study; a mere slice of said jackpot clearly is not a significant incentive.

To determine if something is a good bet or investment, you take the value of the anticipated reward, subtract the cost of the wager/investment, and multiply by the odds of its occurrence, and compare the result with a similar analysis of all the other things one might do with the wager (including sticking it in one's pocket). The course of action with the greatest result is the rational course of action. If the reward is, as in this case, LESS than the investment risked, and the odds are not overwhelmingly favorable, it's a bad bet.

So as yet, no one is actually gambling. The contestants to date are signed up either for ideological reasons (Bartke) or for publicity (Sinclair) or because Aubrey is just so gosh-darned congenial (Weindruch; probably Leeuwenburgh). When the Prize jumps up by an order of magnitude or two, we can expect a genuine horse race, both because it will actually begin to be a good bet, & becaue the horse race itself will be good enough publicity to make being in the competition valuable to private companies.

> Ergo De Grey's charts about how motivation can be
> altered with the prestige of the prize may be based on
> an utterly false assumption about the prestige of the
> prize.

First, I'm not sure to what chart you refer: the only attempt to estimate the impact of the Prize that I've seen has actual *dollars*, and not prestige, on the X-axis:

http://www.mprize.org/index.php?pagename=lifeline

(Note that I don't take the specific dollar values terribly seriously: it's PAINFULLY back-of-the-envelope. But it does give an accurate impression of HOW it's likely to work based on the history of research prizes).

Prestige as such is not the major reason why the Prize will ultimately succeed. Rather, the Prize will help create radically long-lived mice (and through them, humans) because it will have an award that is actually large enough to (a) keep an academic lab or biotech startup going, and (b) generate excitement and publicity on a scale that (i) is of use to such ventures -- as advertising for private firms (note the enrollment of both Sirtris' Sinclair and Elixir's Guarente), and as a grant magnet for academics -- and that (ii) will rouse the public's anticipation of progress, break their quietism, & spur them to make political and economic demand for a real cure for aging. From a sheer publicity POV, the Prize has been doing very well of late -- but the real effect on the research agenda will come when there really are millions on the table.

And indeed, to the extent that prestige IS a factor, the prestige of a prize is itself in large part a function of its cash value: think about prizes in science or literature, and how much attention tracks dollar value (often explicitly in the media: the XYZ Prize is "the richest prize for Canadian short story writers," "the largest award for an English-language novel," etc. Furthermore, for the political reasons mentioned above, many biogerontologists will shy away from being associated with any efforts to actually intervene -- *now* -- in aging, until the previously-described loggerhead is broken, and the Prize is just too small a juggernaut, as yet, to smash thru'.

To again quote Miller: after listing numerous other political and institutional obstacles to work on genuine anti-aging interventions (the length of time needed to do lifespan studies; the profitability of existing -- yet ineffective and/or unproven -- "anti-aging" "treatments;" active opposition to interventive biogerontology by the Kass gang; etc -- he concludes that "the obstacles blocking the development of the hypothetical discipline of applied gerontology are at this point about 85% political and 15% scientific, and *they will not be overcome by biologists alone*."

I doubt that Miller would publicly endorse the Prize, mostly because of the ongoing feud between him and Aubrey about the proper strategy through which to pursue anti-aging interventions (rather than about the moral imperative to do so -- a subject on which they are in vigorous agreement). However, I suspect that in the secrecy of his own heart he thinks it's a great idea. The MPrize is exactly in a position to deal with this latter side of the equation -- & once it becomes big enough, with the side that is dependent on the scientists and their institutions (academic and capitalist) as well.

> The best thing to do is invest in the right private
> sector research companies,

First, as explained in the previously-linked post and elsewhere, there is a perverse set of anti-incentives keeping VC from seriously pursuing interventive biogerontology. And indeed, thus far, companies originally set up to do so (most prominently, Geron, Elixir, and Sirtris) have all eventually gone into panicked retreat at the behest of impatient financiers, redirecting the intellectual property and reserve of knowledge and skills built up during the initial pursuit of real anti-aging therapies into the development of drugs for specific diseases. Investment in such firms won't work unless $ are specifically tied to doing real anti-aging research. The Prize addresses this because its structure ensures that it only pays for actual life-extending therapies -- and only *successful* therapies, at that.

And second, the problem here is where to put that money even when such companies are available as investment options. Bakcing a losing horse does not help the other horses win a race of this kind. If one is Bill Gates, one can afford to invest in a hell of a lot of horses in hopes of getting just one across the finishing line, but for the rest of us, splitting our investment dollars across several firms with promising-sounding ideas isn't likely to actually push forward the date of their success, even if they actually do turn out to have a viable therapy in the making (tho' if one were right one would at least make oneself a tidy sum). The Prize uses a structure which has historically mobilized private investments in the goal valued at at least ten times the size of the prize itself -- and again, the money only goes out when someone actually pulls off the stunt.

> and to write to the NIA.

Yes, please do! Indeed, there are many ways that one can push forward the day when humans will receive the first radically life-extending biomedical therapies; many of them are here:

http://www.gen.cam.ac.uk/sens/how.htm

... and here:

http://www.longevitymeme.org/projects/

The question is how to get a much wider public doing all of this -- how to extend the political agitation and serious market for genuine, radical anti-aging biomedicine by turning the goldfishbowl of committed life extension fanatics into a big tent of soccer moms who become increasingly unwilling to just go about their (brief) lives watching their parents (and increasingly, their peers and themselves) slowly slide further and further into the yet-implacable maw of biological aging -- physical and mental decay, loss of function, suffering, and ultimately, death -- with every turn of the planet's axis.

Donating to the MPrize is, IMO, the most effective way for any individual who isn't obscenely wealthy to waken the sleeping masses, and to leverage hir very limited dollars directly into the incentive systems governing academics and venture capitalists alike.

REFERENCES

1. http://www.sagecrossroads.org/Default.aspx?tabid=57

2. Miller RA. Extending life: scientific prospects and political obstacles. Milbank Q. 2002;80(1):155-74. PMID: 11933792 [PubMed - indexed for MEDLINE]

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As Jay Fox notes, the Mprize for anti-aging medicine is making great progress. The prize exists to promote scientific research in the field of rejuvenation and longevity medicine - scientists are close to being able to make large gains in both mouse and human healthy life span, but this can only happen with much greater levels of funding and public support.

The first item of news, which happened to little fanfare so far, unfortunately, is that the Mprize recently celebrated its 50th member of The Three Hundred. In fact, as of now, there are 52 members of the 300, representing 1.3 million dollars in long-term commitments towards the prize. It doesn't sound like much, but when I first became aware of the Mprize, about 13 months ago, there were only 13 members, one fourth of the number today, representing only $325,000 in long-term commitments. So the prize has grown very rapidly in the last 13 months.

More importantly, 13 months ago the Mprize had only collected about $60,000 in cash so far, give or take. Thanks to a roughly $3,000 donation by a very special person, the Mprize just broke the $150,000 mark in cash collected.

Amongst these donors are famous names and organizations, such as Ray Kurzweil, William Haseltine of Human Genome Sciences, the X Prize Foundation, the Foresight Foundation, and others - but the important contributions come from everyday folks like you and I, demonstrating that there is broad support for progress towards healthy life extension medicine.

As you may know if you've been reading the Longevity Meme daily news, the next Mprize event kicks off this coming Tuesday 5th - an auction for a celebrity lunch with Ray Kurzweil, all the proceeds going to the Mprize fund. Round up six friends, pool your money and make a bid when the auction goes live!

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In an excellent piece published at EMBO Reports, biomedical gerontologist Aubrey de Grey expands on past comments on the lack of scientific and public debate over a cure for aging.

A perennial complaint in biogerontology, and one whose legitimacy I would be the last to dispute, is that public funding for ageing research is far lower than it should be. Such funding has roughly kept pace with biomedical research spending as a whole, but much more is warranted because postponement of ageing would have a far greater impact on public health and healthcare spending than postponement of any or all of the major age-related diseases. Here, I discuss whether our obstinately modest funding is due, as most of my biogerontologist colleagues evidently feel, to a failure on our part to communicate the scientific and biomedical realities to our political paymasters, and is therefore best rectified by continuing to repeat the arguments we have used for decades until they sink in. I argue that it is instead because those arguments are genuinely weak. I then discuss whether our neglect of more effective justifications for greater investment in biogerontology research is because we overlook key components of the trade-offs that determine funding policy, or whether the problem is the failure of most biogerontologists to maintain an open mind concerning the scientific options. I conclude that it is for both those reasons. Thus, our field is passing up the opportunity to elevate itself to its rightful level of public appreciation and investment, with the result that much longer healthy lives are being denied those who will die before 'real anti-ageing medicine' arrives unless we start working harder towards it now.

As usual, Aubrey de Grey goes on to make detailed points and suggestions - many of which will be familiar to those who have read his past thoughts on the topic. He has made a convincing scientific case that - with adequate funding, public support and directed research programs - the research community knows enough to get started and is within decades of technologies that can greatly extend the healthy human life span. New medicine to address the root causes of degenerative aging would greatly reduce the staggering ongoing toll of suffering, disease and death that claims tens of millions each year.

The scientific path ahead towards healthy life extension technologies is as clear as the future of science ever gets. The problems all lie in matters of funding, scientific and public support and understanding. This is why activism, advocacy and education are vitally important, both within and without the scientific community.

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A long post from Randall Parker will no doubt be of interest to those who were following the back and forth over weight and life span not so long ago.

Brace yourselves for a study which produced results which are, to say the least, counterintuitive. A group of Finnish researchers found in an epidemiological study on twins that those overweight people who intended to lose weight who lost weight were most at risk of dying over the study period. (the higher the hazard ratio the greater the risk of dying).

...

But don't rush to conclusions. Epidemiologist Meir Stampfer of the Harvard School for Public Health says epidemiology studies of the effect of weight on mortality need to correct for a number of problems.

I take all of this to indicate that not becoming overweight in the first place is a good thing - but then you knew that already, right?

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