It seems Second Life is even more popular post-grey goo; no such thing as bad publicity. Mark your calendars: Anders Sandberg will be giving a presentation on healthy life extension in the virtual space:

It is not a coincidence that the oldest remaining literary epic is the one about king Gilgamesh’s search for the herb of immortality: the dream of eternal youth is as old as mankind. But what has so far mainly been wishful dreaming is increasingly becoming medical and demographic reality. Today life is routinely extended and ageing slowed in lab animals. We live in a rapidly greying society where the average lifespan, health and vigor would have seemed nearly divine to king Gilgamesh, whose subjects had a life expectancy at birth around 25 years. As researchers increasingly see ageing as something mutable - and hence potentially treatable - we have to start considering how to deal with the changes it will cause in society and our lives.

Extending lifespans is something many do not take seriously. It is in the realm of wishful thinking, science fiction and health gurus. But if one is concerned about the current demographic trends and the somewhat long-term future, then one ought to at least consider progress in extending lifespans as one possibility to take into account. In his report “Keep on raging against ageing” Anders Sandberg, research director Eudoxa and transhumanist par excellence, will make a moral and scientific case for life extension.

As for a number of other transhumanists of a more philosophical bent, Sandberg has come to be a part of the new Future of Humanity Institute. The transhumanist community builds as it goes, a sort of diffusive expansion into the broader world, and one that produces interesting secondary reactions, vortices and calcifications. Such is the evolution of most movements from a small core community with an intense, pinpoint vision, out to dilution, evolution, change and a widespread acceptance of ideas once too radical for adoption.

Twenty years from now, it will be hard to explain to the young folk just how ridiculed and shunned was the concept of scientific research to extend healthy longevity - and it will be our shame that we and those who came before advanced this cause too slowly to benefit the billion who will die between now and then.

Technorati tags: advocacy, life extension, presentation

Posted by Reason at 10:15 PM
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An aging body has changed in many ways, and not just in those obvious to visual inspection. The typical old body is identifiably different from the typical middle-aged body at the level of cells, genes and biochemistry: biochemical processes, gene expression, levels of molecular damage, cellular behaviors, cellular populations, and so on.

Some of these differences are clearly causally linked - a wide range of age-related changes can often be shown to be caused by a lesser number of underlying changes. For example, damage to mitochondria leads to oxidization of low-density lipoproteins (LDL), which in turn leads to detrimental changes involved in atherosclerosis, which is the principal cause of coronary heart disease and other forms of cardiovascular disease. Most modes of biochemical wear and tear contribute to a wide range of recognized age-related conditions and frailty.

One role of aging research should be to explore these linkages, so as to better characterize the core of aging; what, really, are the essential changes of aging when all the chains of failure have been cut back to their root causes?

The other role of aging research - a role that continues to be woefully underserved - is to develop the means to prevent and repair changes associated with aging. This is where the engineering and scientific viewpoints tend to diverge. Scientific culture aims for full understanding prior to action; engineering culture aims for enough information to enable working, reliable tools and outcomes. Strong, long-lasting bridges and large buildings existed long before the tools and knowledge to completely understand strategies for architecture and construction. Similarly, an engineering approach to aging could make meaningful inroads in extending our healthy life span prior to a complete scientific understanding of all the complex change that comes with the passing of years and the workings of our bodies.

At root, what the engineer proposes is to fix all observed change. Science is essential to this goal - it reduces the problem space down to one that can be tackled in a short enough timeframe by identifying root causes. Science then provides the knowledge needed to build the tools - modern biotechnology in this case - to do the job. But you have to recognize the point at which there is enough information to set forth and engineer results; this point is usually far in advance of complete understanding.

Don't know whether a characteristic change between an aged body and a youthful body is harmful? Work to fix it anyway. The worst that can happen at the end of the day is you'll make an aged body even more like the youthful body next door, but gain little in the doing of it.

As it turns out, the list of root causes (changes that occur with aging) looks to be small, especially when considering the fact that gerontologists have divided the world of the failing human body into thousands of named medical conditions. I'm sure most of you are familar with the list from the Strategies for Engineered Negligible Senescence, an engineering-oriented proposal and young research program to extend the healthy human life span by reversing changes that occur with aging:

Some tissues lose cells with advancing age, like the heart and areas of the brain. Stem cell research and regenerative medicine are already providing very promising answers to degeneration through cell loss.

We must eliminate the telomere-related mechanisms that lead to cancer. de Grey suggests selectively modifying our telomere elongation genes by tissue type using targeted gene therapies.

Mitochondrial DNA is outside the cellular nucleus and accumulates damage with age that impairs its critical functions. de Grey suggests using gene therapy to copy mitochondrial DNA into the cellular nucleus. Other strategies for manipulating and repairing damaged mitochondrial DNA in situ were demonstrated for the first time in 2005.

Some of the proteins outside our cells, such as those vital to artery walls and skin elasticity, are created early in our life and never recycled or recycled very slowly. These long-lived proteins are susceptible to chemical reactions that degrade their effectiveness. Scientists can search for suitable enzymes or compounds to break down problem proteins that the body cannot handle.

Certain classes of senescent cell accumulate where they are not wanted, such as in the joints. We could in principle use immune therapies to tailor our immune systems to destroy cells as they become senescent and thus prevent any related problems.

As we age, junk material known as amyloid accumulates outside cells. Immune therapies (vaccines) are currently under development for Alzheimer's, a condition featuring prominent amyloid plaques, and similar efforts could be applied to other classes of extracellular junk material.

Junk material builds up within non-dividing, long-life span cells, impairing functions and causing damage. The biochemistry of this junk is fairly well understood; the problem lies in developing a therapy to break down the unwanted material. de Grey suggests searching for suitable non-toxic microbial enzymes in soil bacteria that could be safely introduced into human cells.

You'll find one of these classes of change mentioned today at Ouroboros:

I currently work on a phenomenon known as cellular senescence, which is a permanent growth arrest caused by telomere dysfunction (e.g., the critically shortened telomeres that arise after many cell divisions) and also by other kinds of stress (particularly genotoxic damage).

One of the active controversies in this sub-field of biogerontology is, somewhat paradoxically, whether it’s part of biogerontology at all: While senescence certainly arises as cells get older in culture, and while there’s a good story to be told about how senescent cells could contribute to age related decline in tissue function, it’s not yet fully clear to what extent the phenomenon actually plays a role in physiological aging of intact animals.

Research scientists will keep investigating. In the meanwhile, given that the buildup of senescent cells accounts for a significant fraction of some tissues in later life, the engineers should already be looking at potential fixes. It's not hard to think of approaches to reversing the acculumation of senescent cells in this day and age of targeted therapies for discriminating cell destruction and other advanced biotechnology under development:

Getting rid of cells is a much simpler job than most of the other things we have to do as part of SENS. In the case of fat, it's possible to use simple surgery, but that's unnecessarily invasive. There are two main other ways: we can inject something that makes the unwanted cells commit suicide but doesn't touch other cells, or we can stimulate the immune system to kill the target cells. Both approaches involve making use of distinctive molecules on the surface of the target cells: luckily, different cell types tend to have different things on their surface, so this shouldn't be too hard. But it hasn't been done yet, and not enough people are working on it -- it needs much more attention.

Sadly, comparatively little funding is directed towards any of this, and the engineering side garners far less than the better established investigative community. That will have to change, and the way it changes is the same way it changed for other growth fields in science: the bootstrapping of advocacy and progress side by side, within and without the scientific community.

Technorati tags: advocacy, life extension, medical research

Posted by Reason at 7:21 PM
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Having completed phase I trials of calorie restriction in humans, the CALERIE research program is moving on into phase II:

Dr. William Wong, professor of pediatrics at Baylor College of Medicine's USDA Children's Nutrition Research Center in Houston, was awarded a $2.2 million grant from the National Institute of Aging to help determine if a reduction of calories can increase longevity and decrease the risk of chronic disease. Previous animal studies suggest this is the case.

Wong's lab will serve as the central doubly labeled water lab to support the NIA's Comprehensive Assessment of Long-term Effects of Reducing Intake of Energy, or CALERIE, study.

...

The phase 2 CALERIE clinical trial will study the effects of cutting calorie consumption by one-fourth. Wong's lab will use the doubly labeled water method to establish the participant's caloric need, which will then be decreased by 25 percent in participants assigned to the treatment group.

The study will follow two groups for two years with participants coming in periodically for follow-up doubly labeled water studies.

As is often left out in articles on the subject, the practice of calorie restriction is a matter of engineering your diet to lose the empty calories - those that were not contributing essential nutrients. In other words, eat less of a better diet. Expect to see more news articles of the following variety in early 2008 as the results start to firm up for publication.

It's very clear that calorie restriction has a powerful, protective effect against diseases associated with aging ... We don't know how long each individual actually will end up living, but they certainly have a much longer life expectancy than average because they're most likely not going to die from a heart attack, stroke or diabetes.

The real benefit from this sort of broader study - and that sought by the present fundraising efforts of the Calorie Restriction Society - is to better characterize the differing responses to this sort of dietary choice in different people. Given that people show a range of responses to more or less everything else the world can throw at them, I would expect response to calorie restriction will vary as well. How wide is this range? Is there even a small number people in the world who might react poorly to calorie restriction by way of their genes, rather than due to illness or other medical conditions? Only broader usage and measurement will tell.

I'm sure this will also further boost interest in potential calorie restriction mimetic drugs presently under investigation; the actual practice of calorie restriction seems unpopular in certain quarters. Oh well - their loss.

Technorati tags: calorie restriction

Posted by Reason at 8:19 PM
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Into every well-organized life a little entropy must fall, and hence here a post with little direct relevance to science and healthy life extension.

A note to those who are wondering why the latest Longevity Meme Newsletter is not in their in-box - well, I'm wondering much the same thing myself. It seems the mailserver ate it, and then the secondary mailserver ate the backup mail batch that was to replace it. Puzzlement all around, and I'm working it through with the ISP.

UPDATE: Seems that a few people did get it, multiple times even. A very strange situation, and apologies to those folk.

Meanwhile, comments here at Fight Aging! are suspended until I can work up a better protection against denial of service style runs of comment spam - such as the one that took down the entire server earlier today. This "mandatory upgrade" version 3.33 of Movable Type has some serious flaws that were not present in the 2.* versions, one of which is acute vulnerability to these sorts of attacks.

Work, work, work.

Posted by Reason at 6:21 PM
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If you want a taste of present opinions and debates within the scientific community on any given topic, run a search of the past couple of months of publications at PubMed. It helps to have general background knowledge of the field in question, not to mention an appreciation for the nature of science and research at the leading edge, but there's always something new to learn. Here are some of the results obtained by searching on "aging longevity" and "molecular damage aging":

Theories of biological aging: Genes, proteins, and free radicals.

Traditional categorization of theories of aging into programmed and stochastic ones is outdated and obsolete. Biological aging is considered to occur mainly during the period of survival beyond the natural or essential lifespan (ELS) in Darwinian terms. Organisms survive to achieve ELS by virtue of genetically determined longevity assuring maintenance and repair systems (MRS). Aging at the molecular level is characterized by the progressive accumulation of molecular damage caused by environmental and metabolically generated free radicals, by spontaneous errors in biochemical reactions, and by nutritional components. Damages in the MRS and other pathways lead to age-related failure of MRS, molecular heterogeneity, cellular dysfunctioning, reduced stress tolerance, diseases and ultimate death. A unified theory of biological aging in terms of failure of homeodynamics comprising of MRS, and involving genes, milieu and chance, is acquiring a definitive shape and wider acceptance. Such a theory also establishes the basis for testing and developing effective means of intervention, prevention and modulation of aging.

A very dry way of jumping right on in to say that a SENS-like approach is a sensible next step if you buy in to a reliability theory view of aging - i.e. that aging is no more nor less than an accumulation of varied forms of molecular and cellular damage in a complex biological machine, and that we can work to understand and find ways to repair that damage. By repairing the damage, we prevent and reverse aging.

Speaking of SENS, it's not surprising that Aubrey de Grey shows up in any such search of PubMed:

Foreseeable pharmaceutical repair of age-related extracellular damage.

Various molecular and cellular alterations to our tissues accumulate throughout life as intrinsic side-effects of metabolism. These alterations are initially harmless, but some, which we may term "damage", are pathogenic when sufficiently abundant. The slowness of their accumulation explains why decline of tissue and organismal function generally does not appear until the age of 40 or older. Aging is thus best viewed as a two-part process in which metabolism causes accumulating damage and sufficiently abundant damage causes pathology. Hence, a promising approach to avoiding age-related pathology is periodically to repair the various types of damage and so maintain them at a sub-pathogenic level. Some examples of such types of damage are intracellular and others extracellular. Several types of intracellular damage are highly challenging--sophisticated cellular and genetic therapies will be needed to combat them, which are surely at least 20 years away and maybe much more. Extracellular damage, by contrast, generally appears more amenable to pharmaceutical repair which may be feasible in a shorter timeframe. In this article, the major types of age-related extracellular damage and promising avenues for their repair are reviewed.

One form of extracellular damage is the accumulation of advanced glycation endproducts, or AGEs. This is the sort of purely chemical problem that could be addressed by the existing pharmaceutical research and development infrastructure, within the present very limiting regulatory straitjacket, and more rapidly than many other aspects of aging that will require new technologies or research communities to be developed.

Moving on, we find another confirmation of one of the steps in the present form of the mitochondrial free radical theory of aging, which describes how mutated mitochondria take over cells and turn them into exporters of damaging free radicals - and how those free radicals lead to age-related disease and damage to other systems in the body.

Mitochondrial DNA damage and the aging process-facts and imaginations.

the accumulation of acquired mutations to functionally relevant levels in aged tissues seems to be a consequence of clonal expansions of single founder molecules and not of ongoing mutational events.

The clonal expansions of damaged mitochondria occur because some types of damage prevent the cell from flagging that particular mitochondrion for destruction in the lysosome. When it comes time to repopulate after a cycle of tearing down old mitochondria, the new ones are cloned from the old - after a few cycles of this, the bad non-recycleable mitochondria take over the cell ... and then matters go south from there. Hence "clonal expansion" - the population of bad mitochondria in a cell expands through cloning.

If you're up for something a little more dense, here is more on naked mole rat biochemistry; in essence it recapitulates what has been said in the popular science press - naked mole rats produce lots of free radicals, but don't appear to be suffering anywhere near the same level of consequences to cellular components, health and life span that other rodents do.

Comparison of endothelial function, O2-{middle dot} and H2O2 production, and vascular oxidative stress resistance between the longest-living rodent, the naked mole rat, and mice.

Vascular aging is characterized by decreased nitric oxide (NO) bioavailability, oxidative stress, and enhanced apoptotic cell death. We hypothesized that interspecies comparative assesment of vascular function among rodents with disparate longevity may offer insight into the mechanisms determining successful vascular aging. ... Interspecies comparison showed there is a negative correlation between H(2)O(2)-induced apoptotic cell death and [maximum life span]. Thus endothelial vasodilator function and vascular production of reactive oxygen species do not correlate with maximal lifespan, whereas increased lifespan potential is associated with an increased vascular resistance to proapoptotic stimuli.

One theory advanced is that it has to do with the proportionality of various species of lipid, the biochemicals in which such damage is most consequential to your heath. It seems that naked mole rats have more of the resistant lipids and less of the easily damaged lipids.

Lastly, a reminder that senescent cells are most likely not good for you:

The second type of supernumerary cells, senescent cells, accumulate in quite large numbers in one tissue, the cartilage in our joints. They also accumulate elsewhere, but in much smaller numbers; however, these may still be important by being actively toxic. They aren't able to divide when they should, and they also secrete abnormally large amounts of some proteins.

Accumulation of senescent cells in mitotic tissue of aging primates.

Cellular senescence, a stress induced growth arrest of somatic cells, was first documented in cell cultures over 40 years ago, however its physiological significance has only recently been demonstrated. Using novel biomarkers of cellular senescence we examined whether senescent cells accumulate in tissues from baboons of ages encompassing the entire lifespan of this species. We show that dermal fibroblasts, displaying markers of senescence such as telomere damage, active checkpoint kinase ATM, high levels of heterochromatin proteins and elevated levels of p16, accumulate in skin biopsies from baboons with advancing age. The number of dermal fibroblasts containing damaged telomeres reaches a value of over 15% of total fibroblasts, whereas 80% of cells contain high levels of the heterochromatin protein HIRA.

If a function or population within the body differs between youth and age, then that is something researchers need to look at: is a root cause or consequence of aging? If the former, then we should aim to do something about it.

Technorati tags: aging, biotechnology, medical research, science

Posted by Reason at 2:56 PM
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Quiet if you're avoiding the rush, that is. A couple of items caught my eye, or otherwise came to my attention - such as by being the one to post it. That first then; a group photo from the Methuselah Foundation core volunteers meeting in Boston earlier this month. If you'd like to put faces to the names, go and take a look.

If all the folk who have helped and donated over the past few years were at the meeting, there wouldn't have been room on the pier - a great many people indeed have helped to make the Methuselah Foundation grow and succeed. Thank you all!

If you would like to see the Methuselah Foundation's initiatives - aimed at turning ever more of the scientific community to the defeat of aging - continue to grow, then the best ways to help are to offer your time and talents, and contribute to meeting Peter Thiel's $3 million matching grant for SENS research.

Moving on, I'm sure you've noticed that the work of Leonid Gavrilov and Natalia Gavrilova on the relationship of maternal age (and thus also birth order) to longevity is back in the press:

It turned out that first-born children were 1.7 times as likely as their siblings to live to be 100. An even stronger predictor of longevity was how young their mother was when they were born. Those whose mothers were less than 25 years old were twice as likely to survive beyond a century.

While the researchers aren't certain why this should be, they suspect younger mothers are less likely to have acquired latent infections during their life that could damage the health of the fetus. Younger mothers may also have better-quality eggs. "If the best, most vigorous maternal ova cells are used first - very early in life - this could explain why particularly young mothers produce particularly long-lived children," Gavrilov says.

As I pointed out earlier this year, this raises a great many questions:

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.

It will be interesting to see what the underlying mechanisms turn out to be - but I doubt they will be anything other than yet another advertisement for the merits of working rejuvenation technologies. We really need to get moving on the development of ways to effectively turn back and repair the accumulation of cellular damage that causes aging.

Next, a couple of good posts from Randall Parker on reasons for - and examples of - the accelerating trend of cost-effectiveness and capabilities in biotechnology:

Stem Cell Regulatory Circuitry Mapped

While I sometimes write posts about promising individual stem cell treatments no one announcement of a promising treatment or even a dozen such announcements will amount to much of a breakthrough given our current deficient state of knowledge on how cells work. The real breakthroughs that will provide us with the most power to produce treatments are going to come from the development of knowledge on how cells control their differentiation (i.e. how cells specialize to become heart muscle cells or liver cells or other specialized types). So this announcement is much more important than the average report about stem cell advances.

Once scientists understand the complex circuitry governing cell differentiation the next set of real important breakthroughs (though mostly invisible to the general public) will come. Scientists will seek to intervene in those cellular circuits and to do so they will develop techniques to tweak those circuits in highly precise and controlled ways.

Cells in the embryonic state are several state changes away from any other state such as muscle cell or artery lining cell or liver cell. Once we have detailed knowledge of the circuits that control cell state the need for embryonic stem cells will go way down. It will become possible to start with a cell in any state and tweak it to shift into any other state.

One Third Of MIT Engineers Work On Biology Problems

Biology used to advance at a snail's pace because its tools were so primitive. The influx of talent from semiconductor engineering and other engineering disciplines has greatly sped up the rate of progress in the field and promises to speed it up by orders of magnitude in the future. The field of microfluidics chases the idea of highly automated and cheap labs on a chip.

Imagine a chip made using semiconductor processes that has lots of reaction vessels and miniature tubes and valves, all digitally controllable. No more pipettes. No petri dishes. No lab techs making mistakes from the tedium. Software will be able to carry out long experimental sequences. Computer programs with limited domain-specific artificial intelligence will even be able to generate hypotheses and carry out experiments. That's where the world of biology is going.

Lastly, Phil Bowermaster discusses the intersection of popular culture, attraction to mortality, and the mindset that welcomes it; something that seems very embedded in the story forms and myths our culture is built upon and propagates anew.

The Hard Stuff

Or let's put it another way. If we can all agree that an average lifespan of 70 years possesses a poignancy and urgency that a 500-year lifespan might not, shouldn't we also agree that an average lifespan of 30 years would be even more beautiful and meaningful? Isn't it time we started rolling back the clock on sanitation, nutrition, medicine, and public safety so that people can lead more beautiful / meaningful lives?

No. I didn't think so.

...

Our ancestors of a couple centuries ago who had those poignant and urgent 30-year lifespans also struggled with figuring out the meaning of life. As do we. As will our offspring.

But the nice part is, they’ll get more time to work on it.

If we (personally, as younger individuals) don't make it into an era of radically extended life spans and advanced medicine, it'll be in no small part because we did ourselves in by failing to work and produce results when we could have succeeded.

Technorati tags: activism, biotechnology, life extension

Posted by Reason at 4:51 PM
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Attila Csordás has hit on a good meme with this short interview question and answer format on aims and means for healthy life extension. A couple more can be found over at the Pimm blog, such as with David Kekich, one of the first donors to the MPrize for anti-aging research, and brain behind the Maximum Life Foundation - an ongoing search for a self-sustaining healthy life extension research funding engine.

Maximum Life CEO David Kekich: the investment strategy of life extension

I have basically committed all my professional efforts to help reverse aging within the next 25 years. My commitment was a by product of watching my parents relatives slowly deteriorate and die off due to aging related conditions. Life extension was also a strong interest of mine since my late 20’s, about 35 years ago. My total commitment happened as a result of a productivity and goal reaching exercise designed to show how much productive time I had left to accomplish my goals. My conclusion was, I needed to live longer.

Maximum Life’s James Clement: what can a lawyer do for life extension?

The vast majority of the public still thinks that extreme life extension is science fiction. Blogs and websites can help educate them as to how close we really are to ending the suffering of disease and aging. Every day, 100,000 individuals die from aging related disease. If we are to put an end to this travesty as soon as possible, we need to motivate the public to make this a priority of our society.

Life extension interviews: Nick Bostrom and the philosopher’s point of view

I’m in favor of research into anti-aging medicine for precisely the same reasons that I’m in favor of cancer research, heart disease research, and diabetes research: because it might prevent or cure disease and save lives.

...

If you put your effort into building awareness and support, try not to talk exclusively to other life extension supporters, but also reach out to other audiences. Speak up; don’t let negative attitudes to healthy longevity go unchallenged.

You might know Nick Bostrom as the author of the truly excellent Fable of the Dragon-Tyrant - if you haven't yet read it, shame on you. Get thee hence and do so this very instant.

Technorati tags: interview, life extension

Posted by Reason at 9:53 AM
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The latest issue of the rather glossy McGill University magazine Headway contains a couple of popular science articles on Alzheimer's research and the advance of technology for the repair of neurons.

The Mind Thief :

"We believe that we've identified one of the very early markers of Alzheimer's disease," she says.

The missing piece in the puzzle might be an elusive enzyme produced in aging human brains that, in its active form, systematically kills neurons. Known as Caspase-6, this protein destroys other proteins that are known to be involved in learning and memory. "If those proteins are being chopped up by our enzyme, it may be that this is what leads to the very first signs of cognitive impairment," LeBlanc says. After a dozen years of studying samples of donated brains and tissue cultures in the lab, LeBlanc hopes next to search for elevated levels of Caspase-6 in the cerebrospinal fluid of Alzheimer's patients - and then identify specific inhibitors of the enzyme that could stop the disease.

A range of new and interesting lines of research are presently underway in the Alzheimer's research community. Along the way, they are building a foundation of technology and knowledge for the next generation of brain medicine. This is a very good thing; assuming that tissue engineering and cancer research proceed much as we expect over the next few decades - and assuming similar levels of progress in dealing with damaged mitochondria and the aging immune system - then the brain begins to look like the complex sticking point for healthy life extension.

We're going to have to become very good at maintaining and repairing the brain at the cellular and sub-cellular levels; fortunately, the first steps towards the technologies required are already underway.

Bridge Over Troubled Neurons:

The orb is a latex bead, micrometres in diameter, coated with the organic compound polylysine; the organic blob is a neuron. Lucido and Colman, a Canada Research Chair, believe the image captured on that slide was the cell attempting to form a synapse - an active communication - with the bead.

Get that cell communicating with some man-made electronics, and it could be possible to create a bridge between severed nerves and muscles up to a metre away - light years in neuronal terms. The possibilities are breathtaking - malfunctioning glands linked to artificial regulators, severed spinal cords repaired, stroke victims rehabilitated.

Technorati tags: biotechnology, medical research, neuroscience

Posted by Reason at 12:17 PM
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It's pleasant to see that the fine art of the snooty anti-science piece is being kept alive even in this age of research breakthroughs and new knowledge every other week. No sense in moving forward - or advancing your own personal store of knowledge on a topic - when you can pad out a few thousand words with cheap shots and an exhortation upon the limits of what you know. On this theme, I thought I'd point out a couple of articles.

This first one is a determined defense of avoiding the opportunity to extend an enjoyable, healthy life via calorie restriction (CR). I'll say this for the somewhat snarky NYM piece last month - at least the author got out there, did the research, and tried the practice of CR. You'll have a watch a brief advertisement to read this Salon piece:

A distorted sense of self-satisfaction, while on the whole a cheerier disorder than outsized self-loathing, can still be troubling, especially when it is the result of having forsaken eating habits that many people would love to be able to enjoy. When Matt Lauer introduced "Today's" CR segment by dramatically asking, "Could food itself be the problem?" it was hard not to wonder how insane we've become to devote airtime (larded with food commercials, no less) to demonizing something that people all over the world do not have enough of. Is it so that people who can afford organic scallops can live to be 150 while everybody else dies their regularly scheduled death?

As I said, cheap shots, either calculated or ignorant; some people seem to make a fair living by turning out that sort of thing, however. It takes a certain distasteful point of view to stand behind the idea that only the rich are capable of putting in a little effort to plan their diet, and that CR is therefore some hitherto unseen form of class warfare. Equally distasteful: that simple reporting from the world of science has context based on your preferences for socioeconomic organization. But enough of that.

On the plus side, there are plenty of resources online that people can use to learn about calorie restriction and the research backing it. There really is no such thing as bad publicity in an era of search engines, and the calorie restriction community is a gateway to other communities and initiatives aimed at the development of more effective means to extend healthy life span. If you're interesting in calorie restriction, you should also be interested in the Longevity Dividend project, SENS, the Methuselah Foundation, and so forth.

The more the merrier, and even dumb articles mean that more folk will come to realize that aging is not set in stone. From that realization will come the support and understanding needed to grow the healthy life extension community and build a larger funding base for serious research aimed at putting a halt to aging.

The second article I wanted to link to today concerns the state and future of stem cell science, and is a touch more subtle in its attack. You'll always see articles of this nature as the first wave of research and commercialization in a new field fades into the second wave. Most of the early companies fail or dramatically reduce their stated goals - this is very much par for the course in biotechnology and medical research, or indeed any other field. The early investors take a high risk, but the potential rewards are great indeed, so in they dive. Equally par for the course are the solomn analysts come to pronounce on the corpse; most such dirges look pretty silly a decade later.

In short, yes, stem cells do have the potential to turn into more specialized cells (that is what we mean by a stem cell). But after eight years of trial and error, scientists have not yet shown that they know how to nudge or coax or direct any given cell in a desired direction -- for example, into the dopamine producing cells that are needed to combat Parkinson's disease.

"It looks hard to me, so we'll never make the progress we'd like!" If I had a dime for every time I've seen some variety of that sentiment ... well, I'd have a fair-sized pile of dimes. Meanwhile, progress continues: tools become cheaper, capability per dollar increases.

Tune up your nonsense filters; these sorts of things come in cycles, and it looks like it's that time again.

Technorati tags: calorie restriction, stem cell research

Posted by Reason at 8:32 PM
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The thing about trends is that they exist right up until the point at which they don't; they are best used as tools to corral the boundaries of uncertainty, and never as the basis for firm predictions. In the case of healthy life extension - and the medical research trends driving it - the worst thing that could happen would be for everyone to look at the trends, think "great, job well done, we're on course!" and then fail to contribute to further progress.

A trend is not a beast with a life unto itself. A continuing trend only continues because research is funded, people are hard at work, results are achieved, and support for progress is growing.

A reminder on the trends that make us feel better about the prospects for later - and longer, healthier - life can be found over at the Longevity Meme. Hopefully they don't make us feel as though we can coast by without helping make these trends a continuing reality. In light of that post, I thought it worth pointing out a Scientific American piece from last week entitled "Trends in Research, Business and Policy":

[Alzheimer's] treatments might one day be based on a synthetic protein fragment Robert P. Hammer of Louisiana State University has developed to disrupt formation of the plaques believed to provoke massive brain cell death in Alzheimer's patients. The plaques are aggregations of fibers that form when individual amyloid-beta peptides begin abnormally sticking together. Hammer also tweaked building blocks of amyloid-beta, synthesizing a non-sticky version of the amino acids that permit amyloid-beta proteins to bind to each other. Adding the engineered fragments to a test tube of normal amyloid-beta blocked the proteins' ability to form fibers, even after four months' exposure. If it does the same in human brains, tens of millions of Alzheimer's sufferers might finally be liberated from a deadly burden of poisonous plaque.

...

The promise of stem cells was again reaffirmed by an experimental therapy to treat patients with lupus - a disease in which the patient's immune system targets the body's own tissue. A group led by Richard K. Burt of the Northwestern University, Feinberg School of Medicine, removed stem cells from the patient's bone marrow. Drugs then wiped out the population of white blood cells before the stem cells were returned to the body, where they formed new white blood cells that were less likely to make damaging antibodies. In a study of 48 patients, half did not have the disease after a period of five years.

...

Although we may not be able to re-grow limbs as salamanders do, the human body does have intrinsic regenerative power, and the discipline of tissue engineering has discovered ways to exploit it. Biodegradable scaffolds made of both natural and synthetic fibers can be seeded with cells that come together to form sheets that mimic the body's natural matrix of soft tissue.

...

The exorbitant cost of deciphering a person's genome dropped sharply in 2005, from $20 million to roughly a tenth of that amount. DNA sequencing technology using off-the-shelf equipment devised by George M. Church at Harvard Medical School and collaborators at Harvard and Washington University in St. Louis may help realize the federal goal of reducing that price to $1,000 by 2015, which experts say would make it practical to decode an individual's genes for routine medical purposes.

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Conventional wisdom specifies that the central nervous system--the brain, spinal cord and eye--cannot heal in adults. Once injured a patient remains impaired for life. Experiments with animals have demonstrated regrowth of injured nerve fibers. But these techniques often need to be applied at or before injury. The standard thinking no longer holds. Larry I. Benowitz at Children's Hospital Boston and his colleagues found a molecule that triggers better nerve regeneration than any other studied-and one that that proves effective when applied days after injury. The scientists discovered that a protein, oncomodulin, is secreted in damaged eyes by immune cells known as macrophages. They found that oncomodulin, when given with compounds that enhance its activity, can increase nerve regeneration fivefold to sevenfold in rats with injured optic nerves.

The trend in biotechnology and medicine is onward and upward, at an accelerating pace. The burning question is whether this trend can be sustained and harnessed in the direction of enabling healthy longevity by repairing the root causes of aging, and not just patching up diseases one by one.

Technorati tags: life extension, medical research

Posted by Reason at 9:04 PM
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To follow up on comments on the culture of Alzheimer's research linked over at the Longevity Meme, I thought I'd point out some of the folk working hard to inject new ideas and theories into the field. You don't have to look far; quite a few interesting lines of research have reached the popular science websites in just the past few days: