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  • Bears, Osteoporosis and Data Mining the Living World
  • A Brief Glance at Stem Cell Politics and Research Timelines
  • Towards Dental Regeneration
  • What People Want, What They Say They Want, and How You Ask
  • Getting Started on Garage Biotechnology
  • Penetrating the Philanthropist Demographic
  • A Certain Immortality
  • Methuselah Foundation: Illustration and Design Volunteers Wanted
  • Two Old School Studies
  • Random Genetic Mutations, Mishaps, Copy Errors and Other Oddities
  • If My Cells Live Longer, I Live Longer ... Right?
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  • Pointing Out Sierra Sciences
  • Rejuvenation Research Journal Now Officially a Success
  • Dig Dirt From Around the World to Advance Anti-Aging Research
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    Friday, June 30, 2006

    Bears, Osteoporosis and Data Mining the Living World

    A great deal of biochemistry is going on out there in the world: odds are you'll learn something useful in relation to aging or age-related diseases - such as cancer - if you just know where and how to look. To pick one good example, a researcher has been investigating bear biochemistry for the past few years. This seems likely to provide some insight into methods to prevent osteoporosis - age-related deterioration of bone strength and density - in other mammals, such as we humans. A recent article at ScienCentral provides an update on progress since I last noted this research in 2004:

    Most of today's drugs for this disease aim to prevent bone loss. But Donohue argues that it may be more effective to increase bone formation.

    That's what hibernating black bears do. Donohue discovered this by analyzing the bending and breaking strength of a collection of black bear bones that was given to him by hunters. He found that while they do lose bone during hibernation, black bears grow new bone cells at an equal or faster rate. "And in fact their bending strength increases as a function of age, despite these annual periods of immobilization," Donohue says.

    ...

    levels of a hormone known to promote bone growth, called parathyroid hormone or PTH, actually increase during hibernation. He points to one study in people that found that a synthetic version of PTH increased bone mineral density in postmenopausal women.

    Donohue says that since the black bear version of the PTH gene is different from humans, understanding how it works could lead to better ways to treat or prevent osteoporosis in people. "We could develop those hormones or other growth factors synthetically, and then this could be used for drug treatments for osteoporosis in humans," he says.

    Donahue has synthesized the hormone in his lab and his next step is to sprinkle it on bone cells and watch for bone-forming activity.

    As the tools of biotechnology advance in capability and fall dramatically in cost, data mining the living world for existing solutions - or pointers to new solutions - to age-related medical conditions is ever more of an attractive proposition. In addition to those higher animals that avoid osteoporosis, others can regrow limbs, regrow damaged organs, or live healthily for centuries. In the grand scheme of things - a scheme that includes some truly strange and very different living creatures - the biochemistries of these overperformers aren't all that different from ours. Effective medical technologies will be built on this knowledge one day, and the cost-effectiveness equation for this research and development continues to tilt in our favor with each passing year of technological progress.

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    Posted by Reason at 9:10 PM
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    Thursday, June 29, 2006

    A Brief Glance at Stem Cell Politics and Research Timelines

    If you follow the machinations of those who spend their working lives striving to limit your access to new medical technologies, you'll no doubt know that a vote on stem cell research is coming up in the US Senate:

    A controversial bill that would lift federal restrictions on embryonic stem cell research is headed to the Senate floor for a vote next month along with two related bills favored by social conservatives.

    "We have been working a long time to bring this to the floor in an appropriate fashion," Senate Majority Leader Bill Frist, R-Tenn., said Thursday, nearly a year after his initial pledge to bring the bill to a vote.

    Research would no doubt be far more effectively directed and well-funded without the intervention of a government that enforces taxation, debases the currency, tramples over freedoms, willfully damages economic growth, and wastefully gluts itself upon the resources it takes. Debating government restrictions on the disbursement of tax dollars is one of those line items I prefer not to touch.

    A UPI article takes a broader view of the science and aspirations of researchers:

    Deepak Srivastava, director of the University of California at San Francisco's Gladstone institute of cardiovascular disease, told United Press International embryonic stem cells hold the greatest promise for regenerating heart tissue and could be in the clinic in the next several years.

    "There's a lot more that needs to be done in animal trials first before considering clinical trials ... but maybe within the next five years is a reasonable goal"

    ...

    Robert Lanza, vice president of medical and scientific affairs at Advanced Cell Technology in Worcester, Mass., said his company plans to get embryonic stem cell-derived therapies for heart disease in the clinic even earlier.

    "Optimistically, we plan to file an IND in 2008 for hemangioblasts derived from human embryonic stem cells," Lanza told UPI. "One of the lead applications would be cardiovascular disease," he added.

    Lanza said his company's first IND for a therapy derived from embryonic stem cell therapy could be filed late next year, but that would be for macular degeneration.

    To round off, Maclean's is running a profile of energetic researcher Hans Keirstead and his work on repairing spinal damage:

    someday -- maybe someday soon -- his work will restore mobility for those who are paralyzed with spinal injuries or stricken with multiple sclerosis. He has already made partially paralyzed rats walk again, using derivatives of human embryonic stem cells. The next stop -- as early as next spring -- is trying the same therapy in human trials.

    ...

    Critics have accused Keirstead of rushing ahead too fast, and of cozying up to biotech companies, but Keirstead is unapologetically entrepreneurial. If the purpose of the exercise is fixing spines, that means getting research out of the lab and into the market. With the cost of many human clinical trials for new therapies running about $500 million, that's not for the faint of heart. "Sorry if this sounds egotistical," he says, "but most scientists aren't as business savvy as I am."

    There could never be too many people in possession of this sort of attitude to the repair of failing human bodies. Progress in medical science requires people to get out there, work hard and succeed. This is the essence of the future, not the posturing of stuffed shirts and other government employees in Washington DC.

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    Posted by Reason at 9:32 PM
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    Wednesday, June 28, 2006

    Towards Dental Regeneration

    It's something of a historical accident that dentists stand in a somewhat separate cultural enclave of medicine; the forward edge of regenerative medicine for teeth is little different from that for other tissue these days.To pick one example, stem cells are a big deal in dental research:

    research has demonstrated that mixed populations of cultured post-natal tooth bud cells can be used to generate bioengineered dental tissues.

    Current research efforts focus on the identification and characterization of dental cell populations, scaffold materials, and design that can be most effectively used for tooth tissue engineering applications. Hoechst dye profiling and immuno-sorting methods were used to generate enriched clonal dental stem cell (DSC) lines. Expanded DSC and non-DSC lines are currently being examined, by both in vitro and in vivo methods, to define their potential to differentiate. Molecular and differentiation profiles will provide important characterizations of tooth bud cells, eventually to facilitate ongoing tooth tissue engineering efforts.

    Efforts to tissue engineer replacement teeth, or repair damaged tooth tissue in situ, appear to be proceeding at much the same rate as other stem cell medicine. The next decade should prove to be very interesting indeed, as many threads of regenerative research come to fruition and commercially available therapies.

    Meanwhile, intermediary technologies for regeneration are moving forward:

    Using low-intensity pulsed ultrasound (LIPUS), Dr. Tarak El-Bialy from the Faculty of Medicine and Dentistry and Dr. Jie Chen and Dr. Ying Tsui from the Faculty of Engineering have created a miniaturized system-on-a-chip that offers a non-invasive and novel way to stimulate jaw growth and dental tissue healing.

    ...

    "If the root is broken, it can now be fixed," said El-Bialy. "And because we can regrow the teeth root, a patient could have his own tooth rather than foreign objects in his mouth."

    ...

    Dr. El-Bialy first discovered new dental tissue was being formed after using ultrasound on rabbits. In one study, published in the American Journal of Orthodontics and Dentofacial Orthopedics, El Bialy used ultrasound on one rabbit incisor and left the other incisor alone. After seeing the surprising positive results, he moved onto humans and found similar results.

    There's no reason that effective stimulation of healing has to be achieved by the direct use of chemicals or biological cues, although that does seem to be the wave of the future. If mechanical or other forms of stimulation can be cost effective for the benefit they supply, then more power to those who are striving to understand the mechanisms and bring therapies to market.

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    Posted by Reason at 8:43 PM
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    Tuesday, June 27, 2006

    What People Want, What They Say They Want, and How You Ask

    From a post on the practice of calorie restriction last week, pointed out to me just recently:

    ABCNews reports a poll showing that 75% of women and 70% of men polled (lets not talk about the lack of information in "percentages" now...) are not interested in eating fewer calories to ensure living longer. In general, the poll respondents did not show overwhelming enthusiasm for an extremely long life; only 27% of women and 40% of men wanted to reach age 120. In that set of people, 44% said they’d be willing to eat one-third fewer calories in order to reach the goal. This means that 44% of 27% of 25% (or 2.97 of every 100) of women polled would consider giving up one-third of calories to live longer (and probably be thinner). Men were 1.5 times more interested. It seems that when offered a golden opportunity, we Americans prefer to pursue happiness in our bag of golden chips.

    What people say they want is often quite at odds with their actions. Ask those poor folk pulling their hair out in any corporate marketing department - surveys are a tricky tool.

    I'm inclined to think the apparent contradictions stem as much from the manner of asking as the nature of people to do say one thing and do another. Take that quoted poll above, for example. Given the widespread nature of the Tithonus error - the belief that living longer would mean being ever more frail and diseased - asking someone whether he would want to live to 120, providing no further context, is much the same as asking whether he would like to suffer for decades in increasing pain, frailty and disease. Not many takers there. Healthy life extension medicine will mean a longer healthy life; a postponement of disease and frailty by preventing or repairing the root causes of age-related degeneration. Tithonus is a mythical character, and will stay that way.

    The success of the "anti-aging" marketplace illustrates that people really do want to be younger for longer. So much so that they are prepared to pull the wool over their own eyes rather than face up to the harsh reality of present day limits to medical technology. People want easy solutions and quick answers right now - but such things don't exist.

    Calorie restriction is less popular than it might be because humans have a dreadfully short time preference - the lower regions of our brains value present food far more than the prospect of being alive and healthy decades from now. In effect, we've all evolved to screw the person we're going to be; good now, not so good when you have become that person.

    You don't have to let the lower parts of your brain run your life, however. The part of you that is you can ponder much more sophisticated time preference calculations. Look to the future of radical life extension via actuarial escape velocity, and weigh the chances of living into an era in which biotechnology will allow a healthy life of centuries or millennia - an era in which you eat whatever you like, insulated by the same advanced biotechnology that sustains your longevity.

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    Posted by Reason at 10:46 PM
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    Monday, June 26, 2006

    Getting Started on Garage Biotechnology

    In the 70s, a handful of knowledgeable computer hobbyists gathered in the Homebrew Computer Club. A mere three decades later, hundreds of thousands of far more empowered individuals around the world collaborate on the production of hardware and software designs to the betterment of all. They are a cultural force and infrastructure for change unto themselves. What better future to look forward to that one in which many hands are joined in ever more beneficial trade and progress?

    Today, the first biotechnology hobbyists are working their way through the same basics. As costs fall, the priesthood will dissolve and spread at the edges. Progress will accelerate - the long tail in any area of human endeavor has many hands and eyes, and a significant amount of funding power. More to the point, problems that traditional funds and organizations wouldn't touch will be open to new, less intensive, smarter approaches. This has all come to pass in the software world. It will also come to pass in biotechnology - which is simply a different form of programming in a wetter, much more complex operating system.

    On a related topic, this piece caught my eye the other day:

    A plan for a global database of all human gene mutations has been announced in Australia. The Human Variome Project could allow doctors to rapidly diagnose patients with rare genetic conditions and could ultimately lead to new treatments for diseases.

    About 100,000 human gene mutations have been discovered, but this total represents only about 5% of the predicted total number of mutations.

    I thought this interesting in light of recent research on the random nature of genetic mutations that accumulate with age. It won't be long now before complete genetic assays are a low-cost commercial product, something your doctor would order along with a blood test. What could one do for age-related genetic damage armed with the future technologies of genetic manipulation and replacement alongside a complete guide to the consequences of mutations?

    There is no practical way to complete a list of mutations - not to mention epimutations and other important errors in cellular biochemistry - and their meaning in combination given today's technology. There was no practical way to complete the human genome project when it launched either - but, thankfully, we live in an age of breakneck technological progress. It is, I think, important that scientists embark upon these sorts of projects early rather than late: the early work is rendered quaint soon enough, but it is essential in informing and driving necessary advances in infrastructure technologies.

    Soon enough, thousands, and then tens of thousands of biotech hackers will be joining in to assist efforts just like this one. Then it will all become most interesting - and we will all benefit greatly, just as we have from the blossoming of software development as a culture and infrastructure.

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    Posted by Reason at 9:42 PM
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    Sunday, June 25, 2006

    Penetrating the Philanthropist Demographic

    Today, a brief reminder that great, world-changing wealth still exists in the hands of comparatively few folk - enough that the realignment of even a modest fraction of the total will cause great changes across the entire space of non-profit and grant-using research organizations.

    "Brace yourself," Buffett warned with a grin. He then described a momentous change in his thinking. Within months, he said, he would begin to give away his Berkshire Hathaway fortune, then and now worth well over $40 billion.

    ...

    Buffett has pledged to gradually give 85% of his Berkshire stock to five foundations. A dominant five-sixths of the shares will go to the world's largest philanthropic organization, the $30 billion Bill & Melinda Gates Foundation

    Such dramatic realignments can only happen when effective control of wealth is very concentrated, and the purpose of wealth can be easily redefined. Such as, say, Berkshire Hathaway shares rather than an industrial conglomerate's manufacturing infrastructure. Large-scale wealth tends not to be fungible. Real wealth is tools, process and a cultural network of agreements with people actively engaged in the production of more wealth; everything else is a derivative of some sort.

    While great (and purloined) wealth flows through government channels, controlled by comparatively few individuals, that does not amount to effective control. When was the last time a government applied a single billion dollars to successfully changing the world? You can see an example of this sort of failure in progress - waste, conflict and a commons on the way to tragedy rather than real progress - in the California Institute for Regenerative Medicine today. Yet we can point to stunning examples in private or philanthropic investment and endeavor many times over in each passing decade. True responsibility, ownership and accountability for results make all the difference in the world.

    Back to the issue at hand: a reminder as to the scope of funds that are controlled by single or comparatively few individuals. Buffet may stand at the apex of wealth, but there are hundreds of billionaires in the world today. A decision by any one of them to enter the modern biotechnology arena with serious intent to defeat aging would change the landscape - just as those already in the pool have already accomplished. But today's progress is too slow, or too vested in conservative, limited-gain approaches, or undertaken with too few resources. If we are to live to see radical life extension, much more must be directed to this goal - as would be the case if more of the world's wealthy philanthropists found their way to our view of aging, biotechnology and the near future.

    One very wealthy individual has already placed a first million-dollar vote of confidence with the approach advocated by the Methuselah Foundation and biomedical gerontologist Aubrey de Grey - and many thanks to you for that, whoever you are. What if the wealthy of the world were to repeat this vote of confidence a thousand times over in the course of a decade? A billion dollars could build the large-scale research infrastructure that develops robust rejuvenation in mice, the first step towards the the defeat of aging in humans. Ageless, healthy, biotech-repaired mice, living a life that could be brought to humans with further investment: there would be the world changed. And cheap at the price!

    Resources for research must come from somewhere if we are to escape our fate of suffering and death by aging. We must explain our goal; educate the public; raise widespread support; motivate the scientific community. We have made good, strong progress in the past few years - but a long road lies ahead. As a community, we have yet to successfully engage and persuade the wealthiest and most conservative of philanthropists, seeking support for modern, aggressive bioengineering approaches to the problem of age-related degeneration.

    We can do this. We must do this. Too many lives, too much suffering is at stake to fail.

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    Posted by Reason at 6:41 PM
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    Saturday, June 24, 2006

    A Certain Immortality

    The work of Leonid Gavrilov and Natalia Gavrilova on the influence of birth order and mother's age on longevity is receiving press attention again. Earlier actuarial studies showing that birth order correlates with life expectancy is explained by the mother's age relationship - younger mothers seem to mean a greater life expectancy for the children.

    The chances of living to the ripe old age of 100 -- and beyond -- nearly double for a child born to a woman before her 25th birthday, Drs. Leonid Gavrilov and Natalia Gavrilova reported. The father's age is less important to longevity, according to their research.

    In a previous study, the husband and wife research team of Gavrilov and Gavrilova identified birth order as a possible predictor of an exceptionally long life. They observed that first-born children, especially daughters, are much more likely to live to age 100.

    But their latest research suggests that it is the young age of the mother, rather than birth order, which is significant to longevity.

    This can be tied in with the researchers' reliability theory of aging - younger mothers are producing children with a lower initial load of cellular or genetic damage. This is a conceptual framework for thinking about the processes and advance of degenerative aging; it poses many more questions than it answers, says nothing about the underlying biochemistry, and exists to guide future research.

    The research serves as a reminder that a certain immortality runs through humanity and its biochemical components: for all that we suffer age-related degeneration - and frailty, pain and death as a result - we produce healthy, youthful children with each new generation. Our cellular biochemistry contains the potential to rejuvenate and repair itself: children are the demonstrable proof that decay and entropy are not inevitable. We must progress as fast as possible to understanding and developing the means by which our present decay as individuals can be arrested, and our healthy life spans greatly extended.

    The threads of immortality that wend their way through humanity as a whole - and the ongoing daily demonstration of the effectiveness of our biochemistry to turn back time - form a romantic notion. But you can't enjoy romance when you're dead and buried, nor when you're suffering unto death. Via science, we are capable of better and more practical approaches to the toll of degenerative aging than hiding our heads in the sands of romantic appreciation.

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    Posted by Reason at 7:27 AM
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    Friday, June 23, 2006

    Methuselah Foundation: Illustration and Design Volunteers Wanted

    Are you a skilled professional in the area of graphics, illustrations, prints or design work? Are you in a position to volunteer time over the next few months - enough time to get a good job done - to one or more projects aimed at advancing advocacy for healthy life extension research? If so, the Methuselah Foundation would like to hear from you.

    A number of high-impact Foundation projects presently underway - and yet to be revealed on the Foundation website or to the wider public - would benefit greatly from the attention of professional, skilled artists, illustrators and graphic designers. If you would like to add your stamp to the developing future of longer, healthier lives and widespread public support for healthy life extension research, now is the time to speak up.

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    Posted by Reason at 9:41 PM
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    Thursday, June 22, 2006

    Two Old School Studies

    A pair of studies presented at a recent neuroendocrinology conference have been doing the rounds of the science press: just the facts can be found at EurekAlert!, and an article with more commentary at the Post-Gazette. With no disrespect intended to the authors, both come across as something of a look back to the old school standard of progress prior to the bioinformatics boom: uncover a single relationship between a compound or molecule and health, then ponder on the possible significance. Nowadays, I think we're starting to expect somewhat more from research groups: metabolic pathways, complete understanding of relevant mechanisms, and the first steps towards a therapy all delivered in a nice package.

    The first of the two studies investigates the use of a growth hormone stimulator to somewhat mitigate the consequences of muscle loss with aging; as for some previous work, it found benefits:

    Aging is characterized by a progressive decline in muscle mass, strength and exercise capacity, often leading to frailty and the inability for living independently. Since growth hormone (GH) secretion also declines with age and many age-related changes resemble those seen in GH deficiency, the researchers are investigating the potential physical and endocrine effects of stimulating GH in older adults.

    In this controlled trial involving 395 men and women aged 65 to 84 with mild limitations in their physical functioning, participants received either placebo or various oral doses of the growth hormone stimulator (GHS) capromorelin ... GHS at any dose prompted an acute GH peak and an increase in overnight GH secretion – increases that were sustained throughout a 12-month treatment period. The GHS treatment also was associated with a 1.4 Kg increase in lean body (muscle) mass and an improvement in tandem (heel-to-toe) walking at 6 months and in stair climbing at 12 months.

    However, a weight of work still exists to show that there are potentially serious side effects; scientists do not yet fully understand the biochemistry and its variance between individuals. Growth hormone could have any number of unpleasant side-effects that are masked in the short term by the benefits of additional muscle, loss of fat and enabling increased exercise. Growth hormone for anti-aging use should not be illegal - for all the same reasons that taking any risk with your own body should not be illegal, providing it harms no-one else - but it's definitely a case for caveat emptor and careful research.

    Compare this with the weight of evidence for the long-term, side-effect-free benefits of exercise, losing excess fat or calorie restriction, for example. As I've noted before, growth hormone seems very much like a drug for a few specific age-related conditions - the condition in this case being a frailty that prevents the use of the three methods mentioned above to maintain health as best as possible. Like many other drugs with wide-ranging effects on metabolism, growth hormone and growth hormone stimulators are poorly characterized, poorly understood, and the research is very much in flux.

    Like calorie restriction, exercise, and losing excess fat, growth hormone therapies are short term, stop-gap measures that will not significantly extend your maximum life span - to 150 or beyond, say. No amount of tinkering with your metabolism at this level can achieve the goals of radical life extension or a defeat of aging. We must not lose sight of the fact that much more impressive technology will be needed - our primary effort should be to support the advance of suitable research to this end.

    The second study illustrates a simple relationship:

    A protein derived from fat tissue may be an important determinant of longevity, suggests a study of 133 women, including 25 aged 100 to 102, whom researchers found had notably higher levels of adiponectin circulating in their blood. Adiponectin is a peptide that has anti-inflammatory properties, helps keep vessels clear of fatty deposits and plays an important role in metabolism, particularly of lipids and glucose. Insufficient levels of adiponectin are thought to contribute to obesity, insulin resistance, diabetes or the formation of lipid deposits in the arteries, collectively known as symptoms of metabolic syndrome.

    To restate my ealier point, this is one of those results that we would nowadays expect to be accompanied by much more "how," "why" and "what this means." Correlation is not causation, and so results like this are largely fuel for speculation and little else in the absence of further investigation into the underlying biochemistry. The obvious speculation would be the same as that for the ratios of LDL and HDL cholesterol in the blood of centenarians - the people who are lucky enough to have a metabolism with this characteristic tend to live longer. Which is no great advance in knowledge - just the first sight of a long road - without an accompanying explanation as to why this might be so.

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    Posted by Reason at 9:48 PM
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    Wednesday, June 21, 2006

    Random Genetic Mutations, Mishaps, Copy Errors and Other Oddities

    A short walk throught the realm of DNA and genetic biochemistry today - never a dull moment here. You'll find an interesting letter at Nature on the growth of random changes (copy errors, oddities, mutations and other odds and ends) in your DNA. In science-speak, this accumulation of error is a stochastic process; somewhat random, somewhat determined by the state of your biochemistry today. The longer you live, the more genetic errors you will carry with you - and errors in your biological machinery inevitably mean that the machinery isn't working so well anymore.

    The accumulation of somatic DNA damage has been implicated as a cause of ageing in [animals]. One possible mechanism by which increased DNA damage could lead to cellular degeneration and death is by stochastic deregulation of gene expression. Here we directly test for increased transcriptional noise in aged tissue by dissociating single cardiomyocytes from fresh heart samples of both young and old mice

    ...

    Although gene expression levels already varied among cardiomyocytes from young heart, this [variance] was significantly elevated at old age. We had demonstrated previously an increased load of genome rearrangements and other mutations in the heart of aged mice.

    ...

    These results underscore the stochastic nature of the ageing process, and could provide a mechanism for age-related cellular degeneration and death in tissues of multicellular organisms.

    One of many mechanisms, sad to say. Researchers will need to significantly impact all of them to hit radical life extension or superlongevity - but incidental gains in fighting age-related disease along the way will not be negligible.

    What we should be viewing with concern is the evidence of destruction of information: it's not unlike what happens to most magnetic storage media from the past two decades. Bits get flipped as time passes, and given long enough you lose the original data. In the case of your genome, the damage is less extensive but still worrisome.

    Loss of data is much more expensive to understand and repair than other forms of damage; you're losing the very knowledge needed to guide you to the solution. It seems clear that gene therapies and related technologies are progressing rapidly towards safe, global changes and wholesale replacement of damaged portions of DNA. But what to replace in the case of pervasive, widespread random damage? It's by no means an impossible task, but it's a far more ambitious goal than curing a disease by changing a single gene.

    Will it be easier if the aged patient thought to have a less damaged tissue sample cryogenically stored fifty years earlier? Maybe, or maybe bioinformatics will be at the point at which sorting out the loss of information safely will be trivial. Given the present (rapidly decreasing) cost of tissue storage, it seems almost sensible insurance against some of the possible future economics and science of healthy life extension medicine.

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    Posted by Reason at 9:03 PM
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    Tuesday, June 20, 2006

    If My Cells Live Longer, I Live Longer ... Right?

    There are any number of interesting studies and technology demonstrations that extend the life span of individual cells by one means or another. If your cells live longer, you live longer, right?

    Well, no, sadly.

    Consider this thought: if everyone in your city drove twice as fast, all the extra efficiency would make the local economy grow more rapidly. Right?

    But wait - driving twice as fast only really works to save time and improve efficiency under some circumstances. What about residential areas and curvy roads? Can these cars even drive twice as fast all the time without falling apart and causing all sorts of other problems? Doesn't fast driving cause more noise and wear on the roads? Does it cost more to drive fast than the time saved adds to your income? Plus which there are always going to be people for whom driving fast is never going to translate into efficiency: they'll be at the beach or in the bar. I'm pretty sure that a large chunk of the economy has no relationship to how fast people are driving, in any case.

    Your body is a complex system, and as such its properties - such as health and life span - are not necessarily directly related to the properties of its individual components. Like a city or an economy, your body is a process in motion, with more hidden depths than the mere sum of its parts might suggest. In many cases, tissue and organs have evolved to operate most effectively with a high turnover rate of individual cells, for example. Changing that is somewhat like trying to downgrade a precision engine. Damaged cells need to be removed from the system, and cancer is the ultimate expression of cellular longevity.

    There are no doubt subsystems within your body that would benefit greatly from extended cellular longevity; specific tissues in which longer cell life spans would in some way put off the local advance of age-related degeneration. A number of groups are aiming at just this sort of goal in telomere research, attempting to produce therapies for specific, localized age-related conditions. For the most part, however, "extended cellular longevity" seems to mean "lots and lots of cancer." From the standpoint of the present scientific consensus, would take a challenging array of supporting biotechnologies to change this situation.

    So, no, a focus on cellular longevity is not the way to be looking at present day research with an eye to applications in healthy life extension. Instead look at cellular damage and its repair: some classes of damage do indeed shorten the life span of individual cells, but that is not the reason why treating this damage is important. After all, some forms of age-related damage lead to cells lingering for too long, cluttering up the joint, or actively proliferating longer than is safe and damaging the body. Rather, we would benefit from medical technologies capable of repairing this damage because it has been demonstrated to contribute to the degeneration of biological systems within the body.

    This is the way to go: identify the components, identify the damage, prevent or repair the damage. Whether it involves cellular life span along the way is somewhat irrelevant - we care about our healthy life spans.

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    Posted by Reason at 9:56 PM
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    Monday, June 19, 2006

    Comments Requested on Superlongevity and Boredom

    Mark Walker is requesting comments on an early draft of a paper on superlongevity and boredom. Take a look and see what you think:

    As usual, comments welcome. Here is the abstract:

    "Superlongevity" may be thought of as doubling (or more) the human lifespan through the use of technology. Critics have argued that superlongevity will inevitably lead to boredom, while proponents have denied this claim. Rather than attempting to resolve the debate through theoretical speculation, I argue that allowing persons to become superlongevitists can be construed as an experiment to decide this issue. Further, the moral benefits of conducting the experiment greatly outweigh the moral costs of not running the experiment.

    A conclusion I wholeheartedly endorse. Run the experiment!

    The idea that a far longer, healthier life somehow implies a doom comprised of boredom - and that this renders the whole exercise pointless from the outset - is one of those oddly widespread and utterly silly kneejerk objections to healthy life extension:

    Even active, inventive, happy people often assume that longer healthy lives will bring boredom through repetition, however. Ask someone you know how long it would take them to run out of new things to do and become bored if they could live in good health forever. Your friend will give you an outrageously low number of years, I'll bet. If you stop to think about it - rather than just going on instinct - you'll soon realize that you are never going to be any more likely to become bored of life than you are right now. There is simply too much to do, too many different things