Biomedical gerontologist and radical life extension advocate Aubrey de Grey will be continuing his winter of conference appearances - after the Immortality Institute conference this coming weekend - by presenting at NEXT05 on November 25th 2005, at the IT University of Copenhagen, Denmark. You can find the program of speakers at the NEXT05 website, and I highly recommend you take the chance to hear de Grey speak if you are in the vicinity.

To get up to speed on de Grey's work and the case for major research projects aimed at extending the healthy human life span, you might want to start with the introduction to the Strategies for Engineered Negligible Senescence (SENS) at the Longevity Meme and move on to read through the SENS website:

SENS is a detailed plan for curing human aging. SENS is an engineering project, recognising that aging is a medical condition and that medicine is a branch of engineering. Aging is a set of progressive changes in body composition, at the molecular and cellular level, which are side-effects of essential metabolic processes. Many of these changes are eventually bad for us -- they are an accumulation of damage, which becomes pathogenic above a certain threshold of abundance.

...

the engineering (SENS) strategy is not to interfere with metabolism per se, but to repair or obviate the accumulating damage and thereby indefinitely postpone the age at which it reaches pathogenic levels. This is practical because it avoids both of the problems with the other approaches: it sidesteps our ignorance of metabolism (because it does not attempt to interfere with metabolic processes and their production of side-effects) but also it pre-empts the chaos of pathology (because it repairs the precursors of pathology, rather than addressing the pathology head-on).

Technorati tags: conference, life extension, SENS

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I had an interesting discussion yesterday with someone we shall describe, for the sake of brevity, as an investment scout for a venture fund. It was reassuring to see - once again - that the venture investment community, like other communities, has its share of pro-healthy life extension members. Like many of us, the scout wonders how best to speed progress towards longer, healthier lives within the present set of working constraints.

All in all, it was a good counterpoint to my personal focus on modern science and its many-faced relationships with the goal of extending the healthy human life span. I tend to move my attention away from areas in which there is a great deal of momentum and support - cancer research, or stem cell research in the past year, for example. My activities as a commentator and advocate would be largely superfluous for these branches of science, and certainly less effective than larger and more practiced groups. (I'm still eagerly awaiting this state of affairs to transpire for healthy life extension research - I'll be delighted to see more individuals and groups out there doing a better job than I am ... and yes, that was a challenge). For the investment scout, however, fields with momentum are the most promising; they generate more early stage companies and more successful later stage investment opportunities. In contrast, a field without momentum is probably at least five years from commecialization, it it heads that way at all - hence not all that interesting to most private investors because they have other, more rapidly maturing opportunities to choose from.

Giving high level venture investment advice is just common sense based on an extrapolation of what you know (and what you know about your own level of knowledge; anyone can give an opinion, but how useful is it?). Imagine yourself with $10 million and the constraint that you have to aim at a good rate of return - what fields would you invest in? The rate of return requirement immediately rules out most of the uses I would normally come up with, but I'm biased towards philanthropic approaches to early stage advocacy and education in healthy life extension - which may also go some way towards explaining why I must imagine my hypothetical investment money. In any case, here are my thoughts in brief:

• Commercialization of stem cell research is the obvious area of investment, whether in the US or not. It is a very active field, clearly going to bring enormous benefits to patients, advances our knowledge of cellular biochemistry and processes - which is a very good thing in and of itself - and addresses the first of the seven pillars of SENS.

• Companies working on calorie restriction mimetics and related forms of metabolic tinkering are currently a viable choice for investment, but I wouldn't choose to put money into this area. I think it's helpful work - which adds useful knowledge about our cellular processes, just like stem cell research - but it's just a stepping stone. Unlike stem cell research, it's also much less effective as a late-life therapy; to get the best benefit from a metabolic tweak, you would have to have it your entire life.

• Therapies based on repair or replacement of mitochondria will be hot in the next few years - the science is close to commercialization for at least one or two teams. A number of age-related diseases can plausibly be targeted by these therapies, allowing an approach through FDA and other regulatory hurdles, and they address another of the forms of age-related cellular damage noted in the Strategies for Engineered Negligible Senescence.

• Companies presently making the tools for the next generation of nanotechnology are a good investment if you want short term returns and long-term effects. The tools of non-medical ("dry") nanotechnology are in demand for present applications, but will be increasingly used as the basis for medical ("wet") nanotechnology over the next ten years. Bioinformatics, biotechnology and nanotechnology will converge to form the new discipline of nanomedicine - something a good deal more impressive than the drug delivery and diagnostics work that currently goes by that name. This convergence will be accomplished by groups who find ways to use the tools of dry nanotechnology to build truly advanced nanomedical applications, such as mass-produced nanomedical robots or superior artifical blood cells.
  

Technorati tags: investment, life extension, venture capital

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Some interesting news has surfaced from researchers working on uncovering the mechanisms of life extension through calorie restriction. From the Gerontology Research Group list (and via the transhumantech group) we have this:

Flachsbart and colleagues are reporting in Experimental Gerontology the result of a study many of us have been hoping to see. They assayed SNPs of SIRT1 in 1573 long-lived individuals (LLI) and find there is no association between longevity and any tested SIRT1 polymorphism or haplogroup. This does not rule out the possibility that lifespan-extending biochemistry or regimens (such as calorie restriction) might be acting through a separate pathway/mechanism in humans, as in yeast (reported by Kaeberlein and colleagues), or through another one of the other six sirtuins in humans. Consistent with this hypothesis Rose and colleagues have reported a weak association between polymorphisms of SIRT3 and male but not female longevity. This is unexpected since SIRT1 is probably the closer functional homologue of yeast Sir2 and C. elegans Sir 2.1 (since it is active in the nucleus and SIRT3 is active in mitochondria), and evidence has been pointing to SIRT1 being a regulator of lifespan in rodents. SIRT6 and SIRT7 might be even closer functional homologues to Sir2 since they are similarly localized within the cell: in heterochromatin and nucleoli. Association studies are probably underway for these two. Stay tuned.

The devil is in the details, as usual. As scientists close in on what makes calorie restriction work in humans, we may see calorie restriction mimetic drugs or therapies capable of reproducing modestly beneficial effects on metabolism and life span. As always, it should be noted that these sorts of metabolic tinkering are not the pathway to radical life extension - even if they work out, they are just a stepping stone to more effective anti-aging therapies capable of reversing age-related cellular damage.

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Is life good? Is being alive to find out a good thing? Is preventing suffering and death just as good? Does a value judgement even matter? Some people, when presented with the obvious moral imperative to healthy life extension, are apparently hazy on the answers:

I'm also not going to argue that extending the human life span is a bad thing. What I am going to do, though, is demand that some argument be put forth that it is a good thing.

This is only to be expected, I suppose, in a varied world that includes attitudes like those put forward by Leon Kass or similarly minded folk. Yet it never ceases to amaze me that people require a justification for individual choice. Make no mistake, choice is precisely what the future of healthy life extension is all about; it is the creation of a choice - whether to age, whether to suffer, whether to die - where no choice previously existed. In this respect progress towards real, working anti-aging medicine is no different from every other aspect of technological progress - we are all transhumanists, expanding the bounds of the possible, discarding bad old limitations.

There should never be any argument over whether people can collaborate to make a choice for their own lives and bodies - the most basic of property rights, the necessary foundation of a truly free society - and there needs to be no further justification than "we want to and we are capable."

Technorati tags: bioethics, libertarian, life extension

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I've talked about Dr. Weil's current advertising blitz and his aging apologism fairly recently. The topic seems worthy of more discussion, in light of position statements like this:

Weil calls anti-aging advocates "false prophets who are putting out a message that aging is reversible or that we can stop it."

"I think those are very wrong ideas," he says during a recent interview at his Vail ranch, about 30 miles southeast of Tucson. "Aging is a universal natural process, and I think if you set yourself up in opposition to it, you're in a very wrong relationship with nature."

Anthrax is completely natural too, but I'm sure Dr. Weil isn't so accepting of that - or maybe he would be if modern science didn't have it under control. Living in caves and dying at age twenty due to parasites and disease is also absolutely the natural human condition - everything from shaped sticks and controlled fire onwards is not. Arguments to nature are a very bad way to support any point of view in this modern age, and especially points of view that advocate the avoidable suffering and death of billions of people over the course of future decades.

We cannot presently make major inroads in the fight against age-related degeneration; there is no such thing as a proven therapy prevent or repair age-related damage and thus extend healthy life span by decades. Yet. (Although it is certainly the case that you can make decades of difference one way or another to your eventual life span through choice of life style and preventative health strategies). Dr. Weil is in a position in which it benefits his bottom line to claim that anti-aging medicine is impossible, since his business is competing with the reputable and less reputable arms of the anti-aging industry. However, he also benefits from completely ignoring or disparaging the growing scientific consensus that aging is reversible and can be defeated in the future - he's selling to customers in the here and now and certainly wouldn't thrive if they all donated that same money to real healthy life extension research or the Mprize for anti-aging research.

So don't listen to the Dr. Weils of the world. They may be well-meaning, but they're still trying to get you to give up, lie down and die rather than seize the endless possibilities offered by the future of healthy life extension medicine.

Technorati tags: aging, anti-aging, life extension

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I'm not exactly an advocate of metabolic tinkering as anything more than a stop-gap measure for healthy life extension research - in absence of anything better in the immediate pipeline. It's quite unclear as to the sort of extension of life span you could engineer in humans or other primates simply by tweaking metabolic controls, even though a 50% increase in life span with minimal side effects seems like a very reasonable near future goal for mouse studies these days. Arguments over the effectiveness of calorie restriction on life span in humans could equally be extended to other methods of metabolic control, for example. If we could even manage a decade or two in humans via these methodologies, with a nice reliable technology platform to back it up, that would be great - but I don't think we should be devoting all our resources to metabolic manipulation. It just doesn't have much of a future beyond this optimization, and we want to see much larger gains in healthy life span. To achieve those gains, we have to move beyond optimizing metabolism into repairing or preventing age-related cellular damage or more advanced technologies.

With that all said, however, it's nice to see that research groups armed with modern biotechnology are up to delivering a continual stream of information regarding the mechanisms of metabolism and longevity. From the latest interesting research:

The longevity-promoting effect of reducing CLK-1 activity that was initially observed in C. elegans is conserved in three different genetic backgrounds of mice. In 129Sv/JxBalb/c mice for instance, reducing activity of the gene mclk1 (mouse clk-1) results in a prolongation of lifespan of about 32%. The inactivation of mclk1 gene, which encodes a mitochondrial enzyme, decreases reactive oxygen species (ROS) levels, the toxic molecules that damage proteins, lipids and DNA, and this likely explains this increase in lifespan.

Commenting on his study, Professor Siegfried Hekimi said: "Increased lifespan can be considered a marker for a physiological condition in which oxidative stress is reduced. Extrapolated to the pathophysiology of human diseases partially decreasing CLK-1 activity by pharmacological means should limit oxidative stress and consequently, prevent or slow the development of common age-related degenerative diseases such as Alzheimer's disease, Parkinson's disease or atherosclerosis. Such new therapies may also be beneficial to treat more acute diseases where oxidative stress is also significantly increased such as ischemia-reperfusion injury."

It's both amusing and saddening to watch commentaries such as the one above completely avoid any mention of human healthy life extension even in circumstances where you would think it was unavoidable. This is the atmosphere in which modern gerontology takes place; age-related disease is bad, but no-one must ever say anything about extending life spans.

A life extension of 32% is a good figure for mice - it's in the same ballpark as other life-extending genetic tweaks thought to work by reducing free radical populations. Or calorie restriction for that matter. As always, I eagerly await studies of the healthy life span of mice that possess all of the presently known life-extending genetic modifications.

Technorati tags: life extension, science

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An update to the $20,000 Strategies for Engineered Negligible Senescence (SENS) Challenge can be found at MIT Technology Review editor Jason Pontin's blog:

Contrary to Mr. Bartlett's story, we have received a number of interesting responses to the challenge - and a group of biologists is, I know, preparing a large, detailed critique of SENS. We still lack a review panel, however, who will review the critiques.

Good to hear that progress is being made; we all win when the research community comes forth to engage in scientific debate on the points, merits and problems of SENS - as it has largely avoided doing to date. Open, honest debate is how we move forward in the process of gaining support for the development of real, working anti-aging medicine - by putting more minds to work on developing the best possible selection of paths forward and persuading more scientists and funding organizations to get the research done.

Pontin also makes a helpful clarification to the SENS Challenge rules:

The full text of any critique can be of any number of words, but any submission should include an abstract of 750 words. In fact, that had always been the spirit of the Challenge ("The form of the submission must be a core document of no more than 750 words, although additional footnotes, citations, and references can be of any length"), but I was perhaps less than clear in my expression.

A substantiative critique of SENS on merits and points of science is exactly the sort of step forward that this challenge is designed to elicit if it is in fact met. Having researchers discussing SENS on the record allows advocates of directed healthy life extension research the open scientific debate they want. The desired end result is a clear, rapid path to working anti-aging medicine that is supported by a large portion of the scientific community, whether it be SENS, a revised version of SENS, or something completely different.

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The long Chronicle of Higher Education article on biomedical gerontologist Aubrey de Grey and his tireless efforts to speed the development of working anti-aging medicine is a good read. I recommended forwarding the link to all the healthy life extension skeptics and wavering supporters in your address book. Here are some of the better quotes:

de Grey is a serious, thoughtful, sincere, prolific, even brilliant researcher and thinker who seems to have devoted every last ounce of his intellect to conquering the single biggest medical menace facing mankind. Along the way, he has acquired plenty of supporters and detractors — and gained the respect of some of the top scientists in the world.

...

It may seem surprising that someone of Dr. Atala's stature was a featured speaker at an on-the-fringe conference. Although he declines to pass judgment on Mr. de Grey's more-extreme prognostications, he clearly respects him. "Aubrey is highly visionary and very selfless in his approach," Dr. Atala says. "It takes people like Aubrey to say 'Hey, look at this again. Maybe there is another way to do this.'"

...

Perhaps the biggest celebrity at the conference was Woo Suk Hwang, a South Korean researcher who has shocked the scientific world in the last few years with his laboratory's achievements. ... And yet there he was [at SENS 2], along with dozens of other well-regarded scientists who study anticancer therapies, immune-system disorders, or cellular aging. There were also less-mainstream researchers who look at topics like how to preserve tissue cryogenically. It was a strange hodgepodge of scientists who would probably never meet otherwise.

...

In 1995, after having absorbed a great deal of genetics, Mr. de Grey moved on to gerontology, a subject that had always intrigued him. For two months he immersed himself in the literature. He emerged with an insight into the mechanics of mitochondrial mutations, wrote a paper on what he thought, and submitted it to a respected journal.

It was accepted. He was off to a good start.

...

"Aubrey's always arguing against people who tell him he's crazy," says Graham Pawelec, a professor of experimental immunology at the University of Tübingen in Germany. "I have never heard him lose an argument." ... "In 10 years, we will have proof that we can cure these seven things and therefore beat aging," says Mr. Pawelec, who spoke at the conference on "immunorejuvenation" in the elderly. "All of my mainstream colleagues will be up there saying Aubrey was right. And then the general public will believe it."

...

"There are people who say that if Aubrey says it must be right then it must be wrong." At the same time, despite his criticism, Mr. Finkelstein has some appreciation for Mr. de Grey's role as provocateur. "I like him," he says. "He ruffles feathers. He has the balls to say stuff."

The question is whether that stuff will prove to be true. Gregory M. Fahy, a biologist and vice president and chief scientific officer of 21st Century Medicine, a biomedical research company, was very skeptical at first. While they still do not agree on everything, Mr. Fahy has been largely won over. And, like Mr. Finkelstein, he respects Mr. de Grey for his courage in the face of ridicule. "If you think you're right, you have to stand up and say what you believe even if people think you're nuts," says Mr. Fahy. "Now, if they prove you're nuts, you have to shut up. But that hasn't happened yet."

On Tuesday November 1st at 1pm EST, the Chronicle will be holding a live, online discussion with Aubrey de Grey. Mark your calendars!

Technorati tags: life extension, science, SENS

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Is there such a thing as centenarian envy? Do many people read articles about gung-ho, active centenarians and scheme on how to do just as well in later life? I suspect envy could be a powerful motivator in this case, especially now that the mainstream media has come into the habit of linking centenarians with aging and longevity research:

Right now, most Americans say they don't want to live that long. A USA TODAY/ABC News Poll of 1,000 adults released today shows that Americans, on average, would like to live to be 87 years old, up from the current life span of nearly 78. Just a quarter of the people who responded to the poll said they want to live to be 100 or older.

If researchers could make it possible to live to 120, most Americans would take a pass. Their reasons: Most worry that they'll become disabled by health problems and end up being a burden to their families.

But old age, as Murray illustrates, doesn't always translate to disability or even disease. And scientists already have made some progress toward provocative, futuristic therapies that would slow the aging process itself.

Research by Richard Weindruch at the University of Wisconsin-Madison and others, for example, suggests that an extremely low-calorie diet, one right on the edge of starvation, pushes the life span of mice and other animals to an extreme. If people get the same benefit, some might live beyond 120, about the longest the human body is thought to be able to last today.

Other advances on the horizon include genetic research to identify those genes that might one day protect people from heart disease and other age-related killers.

The National Human Genome Research Institute, one of the National Institutes of Health, last week announced plans to use its gene-sequencing capabilities to search for the genetic roots of diseases that have long eluded scientists.

And scientists at the University of Utah and other research institutions believe that telomeres - long segments of repeated "junk" DNA on the ends of chromosomes - might hold the same key to human longevity that they do to the life of an individual cell. The Utah team linked shortened telomeres to higher death rates from heart disease and infections, speculating that telomere-lengthening drugs could add years to a human life.

Attitudes towards aging and living longer are very shaped by the Tithonus error, as the survey mentioned above demonstrates - far too many people have no enthusiasm for healthy life extension precisely because they think it that a longer life necessarily means more infirmity and disease. Nothing could be further from the case, of course; all successful efforts to repair or prevent age-related cellular damage will contribute to extending your healthy years and postponing age-related degeneration.

Can centenarian envy overcome the widespread Tithonus error in popular culture, leading to greater support for healthy life extension research and a future of legitimate, working anti-aging medical technology? We can hope so - and it certainly can't hurt to see more of this sort of article in the press.

Technorati tags: advocacy, aging, anti-aging, life extension

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A recent study on the life expectancy and mortality rate of people retiring at different ages shows some correlation between continuing to work and longer life:

Researchers have disproved the theory that people who take early retirement enjoy longer lives as a result. In fact, those who stop working at 55 have nearly double the death rate of those who continue to work on until they reach 65, a study suggests.

...

Poorer health forcing some to retire early may be a factor, say the authors.

...

However, this would not entirely explain the differences they found, neither would factors such as sex and socioeconomic status.

Of interest are the effects on health and longevity not already accounted for by existing poor health forcing an early retirement. It's entirely possible that the study authors failed to account for more subtle effects of individual rates of age-related degeneration leading to a retirement decision, but it seems equally likely that "use it or lose it" effects are taking place, both physically and mentally. Stay working, and you are more likely to benefit from whatever exertions you are making in the course of your employment.

Enforced retirement ages in many countries are already quite clearly a monsterous, unethical consequence of entitlement and wealth transfer schemes - and the dangerous mindset of positive rights and enumerated freedoms underlying it all.

There is an even bigger issue here, and it concerns nothing less than the essence of liberty. It is best brought out by considering the distinction, originally due to the British philosopher Isaiah Berlin, between negative and positive freedoms. A negative freedom is a freedom from, whereas a positive freedom is a freedom to. For instance, freedom from being forced to get your neighbor ice cream is a negative freedom; freedom to get your neighbor ice cream is a positive freedom.

In the liberal-political tradition, the essence of liberty consists in an open-ended horizon of negative freedoms. Man is deemed free to do as he pleases as long as he does not infringe on the (equally valued) liberty of others. By contrast, in the socialist tradition, a man's liberty is conceived as essentially a bundle of positive freedoms. We are free to do whatever the government allows us to do. The government may make generous allowances, but unless it does, we have no freedoms we can rightfully call our own.

I don't think that we need any further utilitarian justifications for their abolishment to make the case. If you are willing to work, how is it in any way right and proper for you to be prevented from doing so by government employees?

Technorati tags: libertarian, longevity, retirement

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The latest edition of Better All The Time from the Speculist gives an enthusiastic nod to the Mprize for anti-aging research:

Read it again carefully: When aging in mice is shown to be 'treatable' the funding necessary for a full-line assault on the aging process will be made available. That means that right now there is almost $2 million in prize money waiting to be awarded to the scientist who figures out the best way to make you live longer.

Research prizes work - that's a soundly demonstrated truth. Harness the human urge to competition, and great things can be achieved. Our hope is that the Mprize will do for serious anti-aging research what the X Prize has accomplished for the private aerospace industry: invigoration, legitimacy, increased funding, and a base on which to grow.

A great deal of work remains in the scientific quest for therapies capable of repairing the cellular damage caused by aging - and the longer it takes, the worse off we all are. If you are prepared to invest money for your financial future, and few of us are not, then you should certainly consider donating to the Mprize to help ensure that future biomedical science can provide you with a longer, healthier life!

Technorati tags: activism, anti-aging, life extension

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There has been a flurry of promising news and progress of late in the fields of stem cell research and regenerative medicine. This is a good thing, needless to say; visible progress towards cures for many presently fatal age-related conditions is very welcome. As the Strategies for Engineering Negligible Senescence (SENS) remind us, however, even the mature regenerative medicine of ten or twenty years in our future will only provide part of a solution to age-related degeneration. Loss of functional tissue - the problem solved by regenerative therapies - is only one of the seven general classes of age-related damage outlined in SENS.

Technorati tags: regenerative medicine, SENS, stem cell research

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By way of a reminder, the 13th Foresight Conference on Advanced Nanotechnology will be starting this weekend in San Francisco. If you look at the program, you'll see that biomedical gerontologist Aubrey de Grey is speaking this Saturday and Sunday on the use of nanotechnology in the future of healthy life extension. The event is also a chance to hear Ralph Merkle discuss the nuts and bolts of advanced nanomedicine.

You'll find much more on this topic over at the Longevity Meme and in the Fight Aging! archives.

UPDATE: You'll find a timely interview with Christine Peterson of the Foresight Nanotech Institute over at the Speculist.

Technorati tags: conference, life extension, nanomedicine, nanotechnology

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Barring poor luck, it seems unlikely that I will die from cancer. I may be greatly inconvenienced by cancer, financially at the very least, but not killed. I take the same view of Alzheimer's - the scientists and researchers tackling these age-related conditions are well established, well funded and making progress. We may not be anywhere near as close as we'd like to a cure for cancer, but the institutions of cancer research are in place and ready to benefit from falling costs and increasing capacities in biotechnology. I feel confident that these diseases will indeed be reduced to the status of obscure threat or minor chronic condition within the next twenty years - the momentum is there. As an example of the sort of basic research that encourages optimism, here we have a recent advance in immunotherapies for cancer:

Research in Immunology and Cancer (IRIC) of the Universite de Montreal, has succeeded in developing a new approach to eradicate malignant melanoma tumours in mice. The findings of Dr. Perreault and his research team are reported in an article just published in the online edition of Nature Medicine, and soon to be published in the print edition of the publication.

In brief, the method developed by Perreault consists of administering T-lymphocytes – cells whose function it is to recognize and destroy abnormal cells – from a healthy mouse donor to mice with cancer. These lymphocytes are pre-immunized against a specific antigen (H7a) present in host mouse cancer cells. Although the target antigen is found in some of the host's healthy cells, the treatment does not cause any side effects because the anti-H7a lymphocytes cluster almost exclusively around the tumour site where they are attracted to the molecule VCAM-1 present on the blood vessels that irrigate the tumour. The T-lymphocytes produce interferon gamma and perforine/granzyme to eradicate cancerous cells.

"We are very pleased with the insights yielded to date from this research project which our team initiated in 2003, explains Dr. Perreault. Thanks to another five-year grant from the Canadian Cancer Society, we have moved on directly to explore the cancer-curing potential of this immunotherapeutic method in the treatment of human melanoma. We may be only a few years away from testing the application on human beings. The prospect of this work leading to the development of an effective, nontoxic and non-invasive therapy against certain types of cancer for broad clinical use is exciting for every basic research students, scientist and doctors working on this project."

Barely a month goes by without an equally promising advance from cancer researchers; this state of affairs is the end result of a long history of hard work by patient advocates, scientists and activists. It makes you wonder just what we would be seeing from biomedical gerontology in terms of progress towards working healthy life extension therapies if the field were funded and supported to the degree it deserves.

Technorati tags: biotechnology, cancer

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It's always good to wake up to the news that my favored charitable cause has gained another respected donor organization. From Dave Gobel, news of another large lump sum for the Mprize for anti-aging research:

The Scott B. and Anne P. Appleby Charitable Trust has donated:
$20,000 for the Longevity Mprize
$20,000 for the Rejuvenation Mprize
$15,000 for [Methuselah Foundation] directed purposes including expenses for Aubrey de Grey

The Mprize fund is within $100,000 of the end of year goal of $2 million in pledges - only four more members of The Three Hundred and we'll be there. Congratulations to the Methuselah Foundation volunteers on the results of their hard work, and many thanks to the many donors who have stepped forward to make a committment to the future of healthy life extension medicine.

Technorati tags: activism, anti-aging, life extension

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I'm not made happy by the necessity of animal research in medicine; we all have a little of the paradise engineer in us. In my case, I think that we have something of an obligation to work towards extending relief from suffering to those beings not as intelligent as ourselves. But animal research is necessary, very much so if we are to move as rapidly as possible into an era of radically extended healthy life spans. This will continue to be true until we can adequately simulate almost all of what we need to find out - a point I've made before:

In the not so distant future, biotechnology will come to look much like present day software development. This is somewhat inevitable, given the falling cost of computing power. While a great deal of the newest biotechnology is powered by advances in computational technology, ultimately everything bio will benefit. Most currently real world experimental techniques - rather than just a select few - will become cheaper to carry out in simulation. Why spend millions keeping racks of mice when you can spend hundreds of thousands on reliable, tested software to do the same job - software that will become cheaper by an order of magnitude with each passing decade.

Financially attractive experiments using simulated animal (or human) tissue or bodies don't just require stable software platforms and falling costs of processor power; they also require a large foundation of research and data. You have to make sure that your simulation reflects reality through a suitable (and invariably painstaking) program of analysis of and checking against reality. One of the first steps on this road - albeit a largely inadvertent step, made with different and more immediate goals in mind - is underway in Europe:

In Venice this weekend, scientists launched a £100 million EU programme to breed millions of genetically engineered mice. The aim is to recreate all the main human ailments - diabetes, heart disease, cancer and mental illness - in the mouse. In doing so, the genetic and environmental roots of these conditions will be exposed and new paths to the creation of drugs and treatments revealed.

...

The EuroMouse programme will involve using a strain of mouse known as the BL/6 or Black Six. These are already used extensively in laboratory experiments and are completely inbred. Each male is an exact clone of all other Black Six males, and similarly for females, no matter if used in an Australian or an Austrian laboratory.

From their populations of Black Sixes, EuroMouse scientists will take embryos, delete or modify one of the genes in them, and then put the genetically engineered embryos back into mice wombs to create a new population, one that has a single mutant gene inside each member.

This process will then be repeated for each of the mouse's 20,000 genes. 'Eventually, this will give us 20,000 strains of mice, each with a different mutated gene,' added Birney.

Each mouse strain will then be observed to see how this mutation manifests itself in the animal's appearance and behaviour. Thus, scientists will find out what each mouse gene does and, from that, what each corresponding human gene does.

This type of project has already been accomplished for yeast; these breeding projects and the resulting analysis is an important part of the groundwork for the future of much more efficient, rapid and effective simulated experiments in medical research.

Technorati tags: science

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My eye was caught - hard to avoid noticing if you spend any time perusing health websites - by Dr. Weil's latest round of combined business advertising and health advocacy. The good doctor is an excellent example of the sort of health advocacy that also serves as an apologism for degenerative aging. The latest Time cover story is a good example of the sort of commentary I have in mind. "Degenerative aging - what a thing! It's just great to slowly lose your faculties, capabilities, and ultimately your life, if you only go about it this way." I exaggerate, but the real thing isn't much better. Whatever we might like to tell ourselves, age-related degeneration is not good, never good:

Without action now, your future will be one of pain and suffering, of the slow destruction of your body and mind. Aging is not noble. It is not romantic. It is a slow and increasingly terrible disease - no one goes quietly or with dignity.

I realize that it is simply human nature to justify to yourself the general excellence and correct nature of the slowly heating pot of water you happen to find yourself in - it seems to be a helpful adaptation when you can do nothing about the situation. But the years in which "nothing can be done" was true for aging are now past and gone; it is quite clear that patient advocacy for directed, serious anti-aging research could have startlingly effective results over the next 20 to 30 years.

Keep this in mind the next time you read commentary from a health advocate. They may be talking good sense on general health matters, but at the same time most tend to romanticize, accepting and excusing the ugly realities of aging. That's not a good message.

Technorati tags: advocacy, aging, anti-aging, health

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Something a little more mathematical and abstract today; via the Gerontology Research Group and transhumantech mailing lists, here are some interesting comments on the relevance to aging of the slope of the Gompertz curve:

In keeping with my prevailing status as angry young man of gerontology I think it is time I commented on the use of the Gompertz slope as a measure of the rate of aging. Let's be quite clear, this idea rests on a generalisation that is broadly true across natural species (ones that have not been manipulated by biotechnology to live longer) but that we have absolutely no reason to believe will be true for ones that have been thus manipulated, and in particular for humans that are receiving future medical care. This generalisation is that the mortality rate doubling time (which is just ln(2) over the Gompertz slope) is pretty accurately a constant multiple (across species) of the life expectancy -- around 1/10 of it. In other words, survival curves for different species are rather well superimposable just by altering the scale on the x-axis. (This is the same statement because the maximum slope of the survival curve is essentially a constant multiple of the Gompertz slope in populations exhibiting a negligible Makeham term, and we are generally considering such populations if we look at vertebrates in captivity with state-of-the-art husbandry, or at humans in the West.) It is therefore of very little scientific (let alone biomedical) value to say that when an intervention lowers the Gompertz intercept but not the slope that it has not slowed aging: one could just as well say that it has indeed slowed aging but has also lowered the variability of the rate of aging within the population. The example I used in my latest editorial in Rejuvenation Research is that if you take two populations with somewhat different Gompertz intercepts and identical Gompertz slopes, and you then compute the Gompertz parameters of the population made by combining these two populations into one, it will have a lower slope (a longer mortality rate doubling time) than the component ones do. If that doesn't make a mockery of using the slope as a measure of the rate of aging, I don't know what would.

You'll find a little more exposition on the use of Gompertz slopes in the middle of a recent post at Longevity First. As for most topics in gerontology, discussions on the validity of Gompetz slopes as a measure of aging have extended over many years. Here is the abstract for a paper from 2001, for example:

The Gompertz transform of the distribution function for the age at death expresses mortality in a form R = R_0e^[alpha] t where R_0 is the mortality at time zero and [alpha] is the rate of increase of mortality, frequently taken as the rate of ageing. The slope of the line [alpha] is frequently used as a measure of the rate of ageing. It is argued that it is incorrect to use [alpha] in this way. To support this contention, a paradox is produced whereby selection for longevity increases [alpha], which could lead to the absurd conclusion that selection for longevity increases the rate of ageing.

Technorati tags: aging, science

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When affluence causes problems, it's a strong sign that the system is broken. Such is the case in wealth transfer schemes such as social security in the US or pensions in Europe; the affluence in question is the increasing length of healthy, productive life span. What a mess has been fashioned whereby longevity begats problems!

Belgium was shut down Oct. 7 by a general strike. Unions didn't want the retirement age lifted from 58 to 60. Yet Belgium, like many rich nations, has little choice. People are living longer and too many will soon be drawing benefits. In Britain, too, unions threaten a national work stoppage over a plan to raise the retirement age for public-sector workers to 65 from 60.

In America, poll-conscious politicians haven't raised the age for receiving full Social Security in a couple decades. (For workers born in 1960 and later, the age will rise from 65.5 by about two months a year until it reaches 67 in 2027.) Yet the first baby boomers hit 60 this year, and that generation - 78 million strong - can't possibly have their pension and medical costs subsidized by fewer, younger workers.

The culture of entitlement combines with the leverage provided by ever-growing government to make problems where none should exist. Humans are selfish, jealous creatures, but competition, rule of law, strong property rights and the requirements of responsibility can make virtues of these urges, harnessing them in service of progress. Sadly, there's all too little of that going on these days - it's a battle in many countries simply to gain the liberty from repressive laws to work as you would like in later life.

The institutions of retirement must change, indeed will change as medical technology adds ever more healthy years. The key to removing the entirely artificial "problems" of increasing human longevity is very simple: freedom. Freedom to work if healthy, freedom to voluntarily provide for the frail either directly or by supporting medical research, and freedom from forced wealth transfer to those older, and on average wealthier, than yourself.

These are things to bear in mind when planning for your long term future. It's not just health and savings - it's ensuring that medical progress and prosperity will continue in the face of what most modern nations are becoming.

Technorati tags: libertarian, politics

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It is interesting to note that the medical research community in highly regulated countries - the UK in this case - is still in the process of trialing adult stem cell therapies for heart damage:

The first part of the study will involve 300 patients whose hearts are failing because of heart disease or a previous heart attack.

A second arm will involve 200 patients whose hearts are failing specifically because of dilated cardiomyopathy - a heart muscle disorder.

And a final element will involve 200 patients who have just had a heart attack.

Some patients will have stem cells extracted from bone marrow in their hip and injected into their major coronary arteries or directly into their heart.

Others will receive injections of growth factor drugs to try to cause stem cells to spill out of their bone marrow and into their blood without the need for the operation.

You might recall that even trials of this sort of work were blocked in the US by the FDA until successful tests were conducted in South America. Meanwhile, today, the same class of stem cell treatment for heart disease discussed above is commercially, responsibly available to the paying public in Thailand.

Centralized, unaccountable, state regulation of medicine and medical research is simply incompatible with rapid, effective progress - it leads to greater levels of death and suffering than would otherwise be the case. Entities like the FDA and its overseas counterparts must be dismantled, and the process of accountability in medical research left to the free market in reviewing and rating concerns - i.e. those that will actually do a good, cost-effective job.

Technorati tags: stem cell research

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This news is most interesting:

"To date gene therapy has relied upon vectors that randomly insert genes into the cell's genome," explains Savio L. C. Woo, PhD, Professor and Chairman of Gene and Cell Medicine at Mount Sinai School of Medicine and corresponding author on the study. "The technique we developed identifies a specific sequence which only occurs in a few places in the mammalian genome. These sequences occur between genes so there is no danger of the insertion of the gene damaging existing genes in the cell.

"Because the genes are inserted permanently, a few applications would suffice to permanently correct a disease."

The key word here is "permanently." Genes inserted using existing methodologies don't stick around for long: gene therapy under those conditions is more analagous to courses of medication in that the patient's biochemistry is altered for a limited period of time only. Now, however, permanent correction is a possibility. That's a big step forward in the potential quality and effectiveness of gene therapy - it opens the door to comparatively low cost therapies for any condition that could be cured by adding a new gene or an additional working copy of an existing gene. We're one step closer to being able to reconfigure an adult human genome for therapeutic benefit - what interesting times we live in!

UPDATE: You'll find a discussion thread on this advance over at the Immortality Institute forum.

Technorati tags: biotechnology, science

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Humans live a long time compared to other mammals of a similar mass. Not long enough my tastes, but this distinction of longevity has spurred a great deal of scientific investigation and theorizing over the years. In recent work, Joao Pedro de Magalhaes suggests an association with evolutionary optimization of mitochondrial function:

A gradual optimization of mitochondria - the cells' powerhouses - may have occurred in the human lineage, which could be associated with the evolution of human longevity and intelligence.

...

Humans are not only the smartest primates but have the longest lifespan, and hence these results could indicate a gradual optimization of mitochondrial proteins in the lineage leading to humans as a means to delay certain forms of neurodegeneration. "It has long been argued that longevity and intelligence evolved together in the lineage leading to humans," says de Magalhaes. "In fact, some nonhuman primates develop neurodegenerative changes at considerably earlier ages than what is typically observed in human patients. Mitochondria have been associated with neurodegenerative diseases, including the genes whose human disease-causing allele was found to be the normal allele in some nonhuman primates, and the mitochondrial genome has been linked to aging. So the general pattern of these results could indicate a selection on the human mitochondrion associated with the higher human intelligence and extended lifespan. Still," de Magalhaes warns, "we will need more detailed studies to prove this hypothesis."

The evolutionary value of delaying the onset of neurodegenerative conditions would be much the same as that proposed in the grandmother hypothesis - capable elders increase the survival rate of their descendants.

Technorati tags: aging, science

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The sixty-sixth member of The Three Hundred signed up today, bringing the grand pledge total from these generous everyday philanthropists to $1.65 million - all in support of the realization of working anti-aging medicine, technologies capable of preventing and reversing the root causes of age-related degeneration. Because the Mprize is a research prize, these funds will be multiplied by the alchemy of competition and the human drive to succeed - the X Prize saw 16 dollars raised by competitors for every dollar in the prize, to pick one recent example.

Back when the Mprize volunteers were stalled chasing member number fifteen for Dave Gobel's clever fundraising concept, it was by no means clear that we'd be where we are now. But thanks to persistence, hard work and help from many quarters, here we are - sixty-six members to the Three Hundred and accepting six-figure donations to the Mprize fund. Onwards and upwards!

Technorati tags: activism, advocacy, life extension

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Via the Extropy-Chat list, John Grigg pointed out a C-SPAN interview with Sherwin Nuland:

I watched Dr. Sherwin Nuland (considered one of the three finest M.D. authors in the west) on C-Span and the subject of life extension came up in the interview. He felt "compressed morbidity" or the reduction & management of age-related breakdown until the very end of life was what we should be aiming for, and not life-extension (anything beyond 120 years in his view).

The reliability theory of aging suggests that any effort to compress morbidity will ultimately produce healthy life extension: all age-related degeneration is the consequence of acculumated cellular damage. Efforts to prevent and cure age-related disease will prevent or repair some of this damage, thus extending life span. Quite aside from this consideration, one has to look askance at this rather odd end goal: to aim at accomplishing an arbitrary healthy life span and then just let everyone die rather than continuing to explore the infinite possibilities offered by advancing medical science.

Nuland said he had recently spoken with Aubrey de Grey and went on about de Grey's plans for greatly extending lifespan (which he said were somewhat vague and not fully worked out yet) with a tone that was surprisingly almost friendly or at least neutral. The doctor calmly stated he disagreed with de Grey's goal of a human lifespan around 5-10,000 years. lol I wondered why de Grey had the arbitrary figure of 10,000 years as his finishing line. Why not 100,000 years?

This projected goal for human life span comes from a consideration of the fatal accident rate in a world in which death and disablility due to aging have been conquered. You'll find a further elaboration on this figure in Chris Lawson's The Tithonus Option is Not an Option. None of Aubrey de Grey's projections and goals are in any way arbitrary; you should take a look at his Strategies for Engineered Negligible Senescence website for much more information.

As with many doctors, Nuland wants to maximize life expectancy rather than expand lifespan. I did find it interesting that he said Leon Kass (who he claims to admire for his academic achievements) was too far right of the spectrum, while he himself was "just right."

You may recall that Nuland was the author of the rather obnoxious Technology Review article on Aubrey de Grey's work. He's in much the same boat as Leon Kass when it comes to healthy life extension technologies, but without the calls for government intervention to block their development and use.

Technorati tags: life extension, SENS

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From Zack Lynch's Brain Waves, a good example of the way in which conservative forecasts based on simple extrapolation of trends fail to account for the reality that is the future:

Twenty percent of us, according to a Rand Corporation study, are going to get cancer or another rapidly debilitating condition and we'll be dead within a year of getting the disease. Another 20 percent of us are going to suffer from some cardiac or respiratory failure. We'll suffer years of worsening symptoms, a few life-threatening episodes, and then eventually die.

But 40 percent of us will suffer from some form of dementia (most frequently Alzheimer's disease or a disabling stroke). Our gradual, unrelenting path toward death will take 8 or 10 or even 20 years, during which we will cease to become the person we were. We will linger on, in some new state, depending on the care of others.

To the end of this, we should mentally add "provided that nothing in medicine and research changes greatly." You should add that endpoint to most reports on the future of health and longevity (with a few enthusiastic exceptions). Excepts like the above are not predictions; rather, they are warnings, just as any serious consideration of your own personal future in the absence of advanced medicine should be a warning. This will be our fate unless we do something about it - and there is much that we can be doing! Folk like you and I can make a great deal of difference by advocating, supporting and encouraging medical research into cures for age-related disease and strategies to prevent the root causes of degenerative aging.

The future is what we make of it - and that is just as true for medical progress, health and longevity as for anything else.

Technorati tags: advocacy, medicine

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Two reports on new stem cell research caught my eye today. Neither promises immediate leaps forward in regenerative medicine this week or next, but both should be of interest to those who follow the underlying science.

Neural Stem Cells Are Long-lived:

New studies in mice have shown that immature stem cells that proliferate to form brain tissues can function for at least a year — most of the life span of a mouse — and give rise to multiple types of neural cells, not just neurons. The discovery may bode well for the use of these neural stem cells to regenerate brain tissue lost to injury or disease.

...

In terms of using neural stem cells for therapeutic purposes and to regenerate tissue, it's important that they can continue to proliferate, and that these stem cells can make different cell types. ... If these stem cells do produce cells that contribute to injury repair, it is fairly easy to infuse growth factors to coax these stem cells to do more in repairing injury.

Researchers have been making real progress of late in identifying, manipulating and culturing neural stem cells. Robust brain regeneration is high on my personal laundry list of things I'd like to be solved well before I'll have need of it - we can envisage many ways of dealing with a failing heart, up to and including cloning and transplanting a replacement organ or building mechanical substitutes, but the options for the aging brain are much more limited.

Stem Cell Subtype Aids Lung Patients:

High levels of a stem cell subtype called endothelial progenitor cells (EPCs) in the blood may improve the survival rate of people with acute lung injury, a deadly form of lung failure.

A study of 45 patients with acute lung injury by researchers at Grady Memorial Hospital in Atlanta found that patients with higher levels of EPCs had better survival rates. Patients with an EPC colony count of 35 or more had a death rate of 30 percent, compared with 61 percent for patients with an EPC colony count of less than 35.

That's a pretty impressive demonstration of the degree to which your survival depends on the effectiveness of your stem cells. Different people have more or less effective personal regenerative toolkits, but all those toolkits become steadily less effective with advancing age and accumulated cellular damage. How much of a difference will it make to the onset of age-related conditions when medical science can rejuvenate your stem cells?

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This post is a slight diversion from the normal topics of interest here, but not by too far. You may be familiar with the work of Robert Freitas on the future of nanomedicine, and you may have read his essay "Death is an Outrage" at the Longevity Meme. Robert Freitas and Ralph Merkle's latest collaboration - like the Nanomedicine volumes, part of the groundwork for the future of nanotechnology - is now available for free online:

With 200+ illustrations and 3200+ literature references, [Kinematic Self-Replicating Machines (KSRM)] describes all proposed and experimentally realized self-replicating systems that were publicly known as of 2004, ranging from nanoscale to macroscale systems. The book extensively describes the historical development of the field. It presents for the first time a detailed 137-dimensional map of the entire kinematic replicator design space to assist future engineering efforts.

To be able to build nanomedical machines capable of acting as blood cells or repairing damaged DNA, then we have to know - in detail - how to build nanomachines, period. So if you want an idea as to what the future of advanced nanotechnology in medicine will hold, and how fast it's coming along, you have to keep your eye on the dry nanotechnology field. Each new advance will be incorporated into medical devices and new technologies before you know it.

For a more gentle introduction to the future of radical life extension via medical nanotechnology, you might want to read Chris Phoenix's "Nanotechnology and Life Extension."

Technorati tags: life extension, nanomedicine, nanotechnology

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Here's a little slice of recent scientific history for today via GRG mailing list. The capabilities of biotechnology continue to improve, and scientists are mapping and understanding ever more of the complex web of human biochemistry and genetics. As this process continues, I think we'll see many more proposals along the lines of the conclusion to this PDF-format scientific paper from 2004 on angiotensin I-converting enzyme (ACE). The authors connected this particular small component of human biochemistry to a range of age-related conditions and concluded:

Genomic epidemiologic data, increasingly supported by clinical outcomes results, strongly suggest that overactivity of angiotensin I-converting enzyme (ACE) may underlie most age-related diseases. Angiotensin II, the main product of ACE, is a pleiotropic hormone, capable of serving as a neurotransmitter, growth factor, angiogenesis factor, vasoconstrictor, pro-thrombotic agent, and cytokine. So it is perhaps not surprising that the ACE DID genotype is associated with several major psychiatric diseases, most cancers except prostate cancer (where the DID genotype is actually protective), most cardiovascular diseases, most autoimmune diseases, and even infectious diseases like tuberculosis and HIV.

...

For example, calorie restriction prolongs life-span in a number of species. With less fuel consumption, mitochondrial electron transport and production of ROS are decreased. sACE overactivity as a cause of aging is entirely consistent with this model, since angiotensin II stimulates mitochondrial electron transport, oxygen consumption, and production of ROS. Chronic angiotensin II signaling leads to mitochondrial hypertrophy and proliferation. Eventually, angiotensin II leads to mitochondrial dysfunction, with increased uncoupling of electron transport from A TP synthesis, and increased production of ROS. Inhibition of ACE in old animals restores mitochondrial function.

...

In summary, population morbidity and mortality should be significantly reduced, and longevity enhanced, by widespread use of an ACE inhibitor or ARB. The only caveat is that white men taking an ACE inhibitor or ARB will need to check their PSA at least once a year.

The authors may have been overreaching, although the mitochondrial connection is especially interesting in light of what we presently know, but I think we'll be seeing more of this sort of review and proposal in the future. Understanding a system implies understanding how to fix and improve that system - and an increased understanding is certainly one of the things we need in the fight to cure aging.

Technorati tags: life extension, science

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New medical technologies have a way of becoming commercially available for veterinarian use long before we humans have a shot at it. This is largely because the veterinary world has no real equivalent to the destructive influence of the FDA (and its overseas cousins). New medical technologies for use with animals are developed and commercialized in an environment that - even though overregulated - more readily rewards effectiveness, time to market, a good grasp of risks involved and economic viability. The entrenched interests in human medicine, as in all centralized, largely unaccountable systems, have become dangerously ineffective. Hence dolphins gain access to reconstructive tissue engineering and stem cell therapies, as do horses:

For the past three years, Prof Roger Smith and his team at the Royal Veterinary College in North Mimms, Herts, have recovered stem cells from bone marrow and used them to treat more than 160 horses.

About a third of National Hunt racehorses injure the digital flexor tendons at the back of the lower leg. In the new treatment, a damaged tendon is rapidly "repopulated" by flexible new tendon tissue, rather than leathery scar tissue that naturally forms over a period of up to 18 months.

About 70 per cent of treated horses have returned to racing form - more than double the percentage that would be expected had they received conventional treatment.

Something must be done about the oppressive regulatory regime in Western countries that slows commercialization, blunts the incentives for success, reduces effectiveness and increases costs for human medicine. If good, working regenerative medicine is possible in dolphins and horses, then it is certain possible in people.

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Governments large enough to interfere in any aspect of life produce this effect: any comparatively small group can leverage its resources through government (by buying politicians or legislation, by steering tax dollars or fiat government funds) to produce a far greater effect that its members would otherwise be capable of. We see this happening for progress in medical research on a constant, ongoing basis; it is hampered and slowed by the actions of successful influence groups who oppose technological progress, either deliberately (no embryonic stem cell research or therapeutic cloning) or incidentally (let's run everything by centralized control). On the other side of the coin, you can see the same process going on for pro-research groups. Both sides waste resources profligately on steering notoriously inefficient government efforts rather than getting things accomplished themselves - it becomes an arms race, a race to the bottom in wasting donated resources to fight over taxed or fiat resources, rather than simply utilitizing donated resources directly. The lesson you should take away from a recent Virginia Postrel article on opposition to progress has nothing to do with right or left, corporations or activists, despite her framing of the issue:

You can't say the same for the antibiotech left. In liberal Canada, in fact, the law defines cloning expansively. Future procedures that might avoid religious objections would still be illegal. The goal is to stop certain research altogether.

That may sound strange to Americans. To many liberal Democrats reproductive choice and scientific progress are touchstone values. But they aren't the only values on the activist left. For many environmentalists, most famously Bill McKibben and Jeremy Rifkin, tampering with genetic nature is inherently wrong. How you do it is a minor detail.

Some feminists object to egg donation, paid or unpaid, for research or conception. "It presupposes an instrumental attitude toward one's own body and that of others" and begins to impose a "social obligation on the female body," notes German feminist Ingrid Schneider.

Genetic research also offends egalitarians. They fear that the rich will benefit first or that money for research will come from social programs. Social justice, argues Marcy Darnovsky of the Center for Genetics & Society in Oakland, Calif., "means not just 'no designer babies,' but also 'no designer medicine.'"

These intellectual influences are stronger in Europe (and Canada) than in the U.S. But two equally threatening ideas do crop up frequently among mainstream Democrats: that commerce taints medicine (those evil drug companies!) and that any activity that has social consequences ought to be centrally regulated.

The real problem is not that some people dislike progress and are willing to try and convert or impose upon others - there will always be people like that. In a free world, they would be able to buy their own land and live as they like, and their influence would only scale by their numbers. Rather, the problem is that leverage of the enormous, unaccountable resources of modern governments a) allow otherwise marginalized anti-research, anti-progress groups to greatly damage our prospects for health and longevity and b) drag pro-research groups into what is ultimately a wasteful, less efficient employment of resources. The problem isn't people, it's the concentration of power.

It is precisely this concentration of power - and the political battles that come with it - that compels patient advocates, supporters of regenerative medicine, healthy life extension research and other proponents of freedom in medical science to generate widespread public support for their common cause. Widespread support has other merits and benefits, but it is a needed defense in a world in which your efforts can be greatly harmed by an errant, misdirected government.

Technorati tags: politics, medical research

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Frank Rummel has another of his SENS 2 reports up for your reading pleasure. This time, the focus is on progress towards copying mitochondrial genes into the cellular nucleus - this is one of biomedical gerontologist Aubrey de Grey's proposed strategies for mitigating age-related cellular damage. Mitochondrial DNA is essential to the functioning of our cells, but is damaged much more readily than nuclear DNA; this damage is implicated as a cause of a range of age-related degenerative conditions.

Dr. de Grey says,"Rather than fixing mitochondrial mutations, we can obviate them. We can make copies of those 13 genes and put these copies into the chromosomes in the nucleus. Then, if and when the mitochondrial DNA gets mutated so that one or more of the 13 proteins are no longer being synthesised inside the mitochondria, it won't matter -- the mitochondria will be getting the same proteins from the nucleus."

This is exactly what Dr. Weiner has done; the frst case of one of these 13 mitochondrial proteins in particular having the gene for making it expressed in the nucleus rather than in the mitochondrial DNA. More details can be found in Professor Weiner's abstract of his SENS 2 presentation entitled "Factors that might affect the allotopic replacement of a damaged mitochondrial DNA-encoded protein".

...

Professor Weiner cautioned me that they had worked with the easiest case of the 13 mitochondrial component proteins, and that the remaining 12 would be much more difficult to solve because they are so difficult to get at. In very simple terms, working with the 13 is complicated by the fact that simply pulling aside what surrounded what you are trying to get at jeopardized the very thing you were trying to get at due to the complexity of all the interactions involved.

But still, that's a promising step forward. Another strategy for dealing with damaged mitochondrial DNA is to replace it with fresh, new, undamaged DNA - a more conventional task of repair for those of us familiar with everyday machinery. At least one group has achieved early success in developing the tools needed to perform this repair, using a technique called protofection.

Technorati tags: science, SENS

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