A most interesting report drifted into my sphere of notice today; a way of boosting life span in nematode worms. We are complex machines, built from a constantly recycling pool of component proteins built into intricate structures and systems; when proteins become damaged, that is wear and tear - grit in the works, the onset of aging, loss of function and the degenerations that lead to death.

Protein degradation and malfunction is a major cause of ageing and can be the result of attacks on proteins by other molecules. One of these processes, called glycation, involves the spontaneous attack by sugars on proteins. If glycation gets out of hand many proteins are degraded or destroyed – proteins which are important for the proper functioning of the body. Protection against glycation declines with age leading to increasing glycation damage with increasing age. A critical enzyme involved in protection against glycation is "Glyoxalase 1". Using a model nematode system, Professor Paul Thornalley (University of Warwick) and his collaborators at the University of Heidelburg have shown for the first time that by enhancing levels of glyoxalase I the glycation process can be diminished and life can be extended by up to 40%. Similarly, by decreasing amounts of the enzyme they have shortened the lifespan of the nematodes. Professor Thornalley will present the results at the Society for Experimental Biology's Annual Main Meeting on Sunday 1st April.

"This work shows for the first time that this enzyme also protects proteins against damage by oxidation and nitration", says Professor Thornalley. The enzyme works by converting the damaging reactive products of glycation derived from glucose into harmless compounds. "This implies that glycation promotes multiple types of protein damage in ageing"

You might be familiar with "advanced glycation endproduct" or AGEs, a class of damaging compounds that build up in the body over the years and that lead to some forms of progressive loss of function. As one might espect, the process of formation for these compounds starts with glycation - more glycation, more AGEs. In effect, AGEs are one portion of the root cause of aging. Scientists have shown promising results in animals with anti-AGE drug candidates (such as ALT-711) over recent years, but humans have very different types and proportions of AGEs than even other, shorter-lived mammals.

One can hope that the result quoted above will be repeated up the chain of animal models in the years ahead, and glyoxalase (or something similar, derived from this branch of research) will prove beneficial to humans. The odds are it'll end up in the same bucket as ALT-711 and a range of other compounds, however - a lot of different compounds are tested and fail for every one that even makes it to the "promising but near miss" category. It doesn't pay to get too excited about studies in nematode worms. Wait until the mice at least.

Technorati tags: biotechnology, life extension

Posted by Reason at 10:15 PM
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The Edmonton Aging Symposium is underway; congratulations are due to the hardworking volunteers who organized the event.

The degeneration which occurs with age was once thought to be the result of causes too complicated to ever understand and ultimately not amenable to medical treatment. However, new discoveries reveal common mechanisms involving the accumulation of damage are shared by most age-related diseases and that new technologies have the potential to repair that damage, restoring health and function to the aging body.

If you missed your chance to register and view the symposium presentations via streaming video, I'm sure it'll be available for purchase or download later. Given the attendees, I'm also sure we'll be seeing reports from the symposium soon enough, but here are a couple of articles from the mainstream Canadian press that surfaced today:

Conference hears of ways to repair aging bodies, restore health

International doctors and scientists met in Edmonton Friday to discuss how to repair the damage of aging.

The aging symposium looks at the types of damage that accumulate with age, what can be done to slow or repair it, as well as future therapies. Other sessions look at the economic costs to society of aging.

As millions of baby boomers worldwide approach their senior years, there is no better time to get the word out about new ways to live longer, said Kevin Perrott, a biomechanical engineer who is organizing the meeting.

Scientists try to answer age-old query: Should people live longer?

"If we all live to be 150, the hospitals would all be full and everyone would still say it certainly went by fast," says Daniel Callahan, from the Hastings Center, a bioethics research institute in Garrison, N.Y. "The only case for extending lifespans is that some people want it and that doesn't seem to be good enough."

At the symposium, Callahan will debate the ethics of "life extension" -- he has long attacked as "utopian" the arguments of those who say that science will find ways to keep elderly populations healthy. More importantly, he says, an older population will do nothing to solve today's social ills and could cause more problems. "I don't see it making any contributions at all to society beyond satisfying the wish of some individuals to live a long life. It's often said that the elderly have a wisdom to contribute. Well, I'm 76 and I don't notice that among people my age that we have any special wisdom," he says.

For proponents of life extension, the idea of keeping people alive without keeping them healthy is irresponsible. However, they think funding research that might help people live longer, healthier lives is vital to stave off the rising costs associated with caring for aging populations. Many also believe that extending lifespans is in line with society's core values.

"If you judge by what people do to improve their health, they value their lives highly," says Gregory Stock, director of UCLA's medicine, technology and society program. "So adding to your period of vitality is something that most people would certainly do. If there was a pill that would do that, it's clear that everyone would take it."

Stock will face off against Callahan in a debate over public funding for life extension. He argues that scientists must take risks, even if the ultimate outcome of their research is still unknown.

It has long struck me that some of the more vocal opponents of healthy life extension simply don't enjoy being alive all that much. Couple that to the strange delusion that people like you and I must wait for the elite to approve our actions and intents, and there you go. Rather sad, really.

Technorati tags: aging, conference, life extension

Posted by Reason at 9:16 PM
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The latest Charlie Rose show, which can be watched online at Google Video, takes a look at the modern mainstream of longevity research. By the guest list - including Cynthia Kenyon, Richard Weindruch, Robert Butler and Jay Olshansky - you might correctly guess that the focus will be in Longevity Dividend territory: modest gains, modest ambitions, the history of the past decade of genetic manipulation of longevity, calorie restriction research of the sort performed by Sirtris Pharmaceuticals, and the manipulation of metabolism to slow aging.

If you wander over to the Immortality Institute, you'll find an ongoing discussion on the show:

Well I thought it was very informative.

They talked about a lot of the research going on into longevity and aging. It was a round table discussion and they had a lot of experts sitting around (and one by satellite). They covered a lot of ground throughout the hour, but some of the things that they hit on were Caloric Restriction (and the results of study in worms, mice, monkeys, and humans so far), Resveratrol (and why it works, plus a word of warning to be cautious about the stuff you buy because of not knowing the quality of what you are buying, which could cause other problems), the effects of lengthened lifespans on society (which they all felt would be a net positive), genetic research and the results that have been shown in animals, plus a lot of other things I am probably forgetting.

I found it very interesting, and would urge all ImmInst members to watch the program if and when they get a chance. They were all very standard researchers that appeared, so there were no claims of immortality or indefinite lifespans or anything like that, but it was very interesting to see and hear what some of the top scientists in aging related fields are working on and think about some aging related issues.

...

The worst quotes of the show award goes to (starting at about the 45 minute mark):

Charlie Rose: "Nobody is arguing we could have a way to become immortal are they?"
One of the panel: "No, No, No. Nobody here is making that argument."
Charlie Rose: "Although there are some people that talk about it."
One of the panel: "There is a school out there that does."
Charlie Rose: "What is that school called?"
*everyone laughing*
One of the panel: "The radical school."
*laughing some more*
Charlie Rose: "Yeah...right"

...

I'm glad there are two "schools" as it's going to take a lot of funding and there will be many possible solutions to the problems of aging. I see it boiling down to :

School A: Metabolic Tinkerers. Focus is to slow aging and maximize qaulity - Sinclair, Olshansky, et al.

School B: Radical Engineering via Damage Repair, Gene & Stem Cell Therapy, etc (SENS). Focus is to rejuvenate and maximize both quality and quantity - de Grey, SENS et al.

If you don't stretch for the greater goals, you won't attain them. if you're not working towards the best possible result, you certainly won't get there. If we want to see significant progress towards true rejuvenation within our lifetimes - enabled by the march of science towards methods of repairing the cellular damage of aging - then we'd better step up and help to support the growth of SENS-like research programs.

Repairing aging is better than slowing aging, and doesn't look like it will take much longer, or be any harder. So why take the obviously worse route? Sadly, the obviously worse route is the dominant path for that part of the modern gerontology community willing to work towards healthy life extension. This must change in the years ahead.

Technorati tags: aging research, life extension, video

Posted by Reason at 8:21 PM
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In response to the last Longevity Meme Newsletter, Ian Clements emailed:

Thanks for another newsletter.

But why are you so down on small improvements? Re: Patching, Regulation, Trial and Error (March 24 2007)

I say: thank goodness for the trial-and-error brigade, a foundation of human progress over the ages.

...

Incidentally, I fail to see why you enthuse over the also relatively small improvement to teeth yet are scathing about possibility of reducing Parkinson's. Because even tho' the former falls within a regeneration/rejuvenation paradigm, it is further from implementation than the latter.

The answer to this question is, at root, that I am far less impressed by old-style drug development based on search-and-trial methodology than I am by work that is an exploration of a new space, builds upon new knowledge of biochemical mechanisms, and as a result returns more knowledge to the general pool for others to use. Modest gains with no follow-on, to my eyes, forms a worse deal than modest gains with ramifications.

The resources poured into the above mentioned studies of the Parkinson's drug that may bring only a modest improvement lead to a dead end - you have the drug, for whatever incremental benefit it brings, and nothing else. It does not enable any wider parallel or following work in a meaningful way. I see this as an example of everything that is wrong with the present mainstream of drug research and regulation - the entire setup leads to mediocrity, a suppression of more ambitious approaches.

Researchers are for the first time testing to see if creatine, a nutritional supplement popular with weightlifters, might hold Parkinson's at bay. ... Creatine is one of several over-the-counter supplements being investigated as a Parkinson's treatment.

There is no real attempt to understand mechanisms - only to test on the basis of screening and see how the results turn out. This black box science, all too recently all that could practically be done, is now positively archaic and wasteful in this age of biotechnology. We can do better, and by virtue of being able to better, we should do better. To progress just a little is just as much a failure in this environment as the absence of progress.

The tooth enamel research, on the other hand, for all that it is just as small a step in and of itself, is everything that the creatine study is not.

Now that dental epithelial cells can be propagated in culture, the next step will be to achieve the same success with their partners in tooth formation, the dental mesenchymal cells. Further development of this technique will be aimed toward production of tissue to replace damaged or missing enamel, and ultimately, regeneration of whole teeth

It builds upon known mechanisms, returns new knowledge to the fold, and will help a wide range of other projects in regenerative medicine by the fact of its existence. It is an example, as Ian Clements points out, of research taking place within a more effective paradigm.

That, at least, is my view of matters. Your mileage may vary - and we still live in a society in which you can direct your resources to support the research you value the most. Discussion is good, but setting forth to help make a difference is better.

Technorati tags: medical research

Posted by Reason at 7:54 PM
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The Calorie Restriction Society is making available DVDs of the last three Society conferences, held in 2003, 2004 and 2006.

There are two DVDs for each conference (Volume 1 and Volume 2). Each stores about 7 hours of video, for a total of about 14 hours of video for each conference. This allows essentially all the talks at each conference to fit onto the two DVD set. The DVDs are packaged in a slim plastic case, which takes up very little space. They use the DVD-R media type and the VCD encoding format which play on most (more than 90%) of DVD players, and essentially all computers with a working DVD ROM drive.

You can find a list of the contents by following the links below:

• CR-IV (2006 Conference) DVDs
• 2004 Conference (CR-III) DVDs
• CR-II (2003 Conference) DVDs

There is a strong emphasis on the science of calorie restriction and its effects on health and longevity throughout; the members of the CR Society have always fostered strong ties with the research community. The 2006 conference features presentations from Luigi Fontana, Aubrey de Grey, Edward J. Masoro, Caleb Finch, Steven Austad and Steven Spindler, for example - quite the array of researchers with interests in aging, longevity and calorie restriction.

Technorati tags: calorie restriction

Posted by Reason at 8:59 PM
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I have a deep and abiding interest in the development of a cure for cancer, or better still, an absolutely effective method of prevention. This should be true of anyone who plans for longevity. Live long enough and you'll meet a fatal cancer with your name on it - unless something is done about that unfortunate fact in the intervening time.

Cancer researchers are hard at work on a number of very promising strategies for eliminating cancer with near-perfect targeting. If you couple that with a methodology of detection sensitive enough pick up the first few hundred cancer cells as they develop, and at a price point to run all the time, then that might make a good method of prevention - at least until we can engineer our aging biochemistry to stop generating cancers in the first place. But first things first.

I noticed a couple of items regarding the use of the immune system as a cancer therapy; targeting is still the name of the game, but the biotechnology that actually kills cancer cells is home grown rather than developed in a lab.

Targeting tumors the natural way:

The new tumor targeting strategy [cleverly] harnesses one of the body's natural antibodies and immune responses. "The killing agent we chose is already in us," says UW-Madison chemistry professor Laura Kiessling, who led the work with postdoctoral researcher Coby Carlson. "It's just not usually directed toward tumor cells."

In a series of cell-based experiments, the researchers' system recognized and killed only those cells displaying high levels of receptors known as integrins. These molecules, which tend to bedeck the surfaces of cancer cells and tumor vasculature in large numbers, have become important targets in cancer research.

...

"What we've shown is that you don't need a receptor that's found solely on tumor cells," she says. "You just need one that's found in significantly higher numbers on cancerous cells than on normal ones."

Immune response to cancer stem cells may dictate cancer's course:

Although stem cells hold incredible promise in the fight against certain diseases, in cancer they're anything but helpful. In fact, mounting evidence is showing that a tumor's growth and spread may depend on "cancer stem cells," which comprise only a very small subset of the tumor. Now, a new study by Rockefeller University scientists shows that immunity to cancer stem cells may help protect people with a precancerous condition from developing the full-blown disease, and that these cells could be an important target for cancer vaccines.

...

This immune response, which correlates so closely with clinical outcome, appears to be targeting the cancer stem cells rather than the bulk tumor cells in myeloma - something that gives researchers hope for a completely new approach. "In immunology for the longest time, we've tried to focus on targeting bulk tumors. But maybe we should be targeting stem cells," Dhodapkar says. "You need to target the roots to really kill the tree, but what we've been doing is trimming the branches and it hasn't worked."

If, ten or twenty years from now, as seems likely, we have access to robust cancer therapies and even more robust methods of detecting cancer early, will that be enough? Will that keep someone cancer free between 60 and 120, for example? It's an interesting question, given that the chances of contracting new cancers are an accelerating prospect with each passing year.

The risk of cancer in any tissue increases with age - and as for most failing machines, quite dramatically so in later life. This stems from underlying changes in biochemistry and the simple rules that determine failure rates in machinery based on gradual wear in component parts - possibly the shortening of your telomeres, possibly damage to stem cells, possibly something else, possibly all of the above. Is it good enough to have a good after-the-fact cure on hand when the risk of occurance is increasing enormously with each passing year? Is there a point past which a good therapy is just overloaded by sheer weight of new cancer bursting from your cells, and where does that point occur?

Food for thought.

Technorati tags: cancer research

Posted by Reason at 8:20 PM
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The succinct version of the actuarial viewpoint on limits to the healthy human life span is as follows:

• limits to life span presently exist
• these limits are increasing at a modest rate, something like 1 year every 5 years
• there appears to be no ceiling to life span in the future

This viewpoint is derived from an examination of mortality rates in various population groups over time, but still comes to the same answer as a consideration of the operation of our biology from first principles, such as the reliability theory of aging and longevity. Our bodies are enormously complex machines and, like all machines, the life span and failure rates are determined by the degree and capabilities of maintenance.

So: more knowledge, better medicine and better biotechnology means longer, healthier lives. This will happen slowly as a matter of course, since better medicine reduces the rate at which damage accumulates over a lifetime. It could happen much faster if we put our minds to it and there was a much greater level of support for moving directly and deliberately to extend healthy life span by the most efficient means possible.

Here is the abstract for another recently published paper giving support to the actuarial viewpoint outlined above; hopefully you recall a little of statistics lessons from past years. If not, then skip to the last line and the explanation below:

Increase in common longevity and the compression of mortality: The case of Japan

This study shows a strong increase in the modal age at death (M) in Japan over a period of 50 calendar years, accompanied by a clear decrease in the standard deviation of ages at death above M (SD(M+)) until the 1990s for men and the mid-1980s for women. For the most recent periods SD(M+) appears to have stopped decreasing, even though M has continued to increase linearly. This stagnation in SD(M+) has been accompanied by stagnation in q(M). The number of deaths at M (d(M)) and the number of deaths at and above M (d(M+)) have increased, but significantly more slowly since the period 1975-79. Since the 1980s an acceleration in the increase of M+kSD(M+), our indicator of the longest life durations, has been essentially due to the pause in SD(M+). Our data do not suggest that we are approaching an upper limit in human longevity.

Translated for those of us far past our school days: the most common age of death is increasing with no signs of slowing down. If there was a compression of mortality - in other words, if medicine was only succeeding in pushing all our life spans ever closer up to some absolute limit - then we would see the distribution of ages at death compressed down into a smaller span of years. However, this distribution of age of death for the longest lived people continues to expand ahead in years. Compression of mortality is not what we are seeing here, but rather something much more like the scenario of better maintenance leading to longer-lasting machinery.

This bodes well for the future, should we get our act together and push harder for the development of better medicine aimed at the repair of damage that causes aging.

Technorati tags: aging, statistics

Posted by Reason at 1:40 PM
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Nitric oxide (NO) is everywhere you look, assuming you're looking at changes in human biochemistry with aging, and the resultant degenerations and diseases of the body. I ran across one example not too long ago: nitric oxide is a part of the control mechanism for blood vessel dilation (vasodilation), located in the blood vessel lining, or endothelium, amongst other things. We know that a range of age-related conditions are related to degradation in the flexibility of blood vessels, and it seems this has more to do with damage to the control mechanisms, rather than incapacity of the tissue:

Endothelial dysfunction, often demonstrated by the loss of the endothelial cell’s ability to cause vasodilation in response to appropriate stimuli, is one of the earliest events in the development of atherosclerosis. This has led to intense investigation of the factors affecting both the production and the degradation of NO, the endothelium-derived relaxing factor and a primary mediator of endothelial function. Reactive oxygen species (ROS), particularly superoxide anion, are well known to inhibit NO, and therefore the mechanisms by which endothelium regulates production of ROS are also of high interest. In this issue of The American Journal of Pathology, Zhang et al demonstrate regulation of such events by a mitochondria-specific thioredoxin, which reduces oxidative stress and increases NO bioavailability, thus preserving vascular endothelial cell function and preventing atherosclerosis development.

Another good reason to damp down the production of reactive oxygen species is the way they damage mitochondrial DNA, leading to even more ROS being produced and exported into the body at large:

Cholesterols, such as low-density lipoproteins (LDL) are used everywhere in the body and travel widely. If ROS reacts with nearby LDL - and there will always be nearby LDL - to form damaged, oxidized cholesterol, that damaged cholesterol can then be incorporated into and further damage biochemical processes throughout the body. For example, its effects on our arteries is well known. In conditions with elevated concentrations of oxidized LDL particles, especially small LDL particles, cholesterol promotes atheroma formation in the walls of arteries, a condition known as atherosclerosis, which is the principal cause of coronary heart disease and other forms of cardiovascular disease.

The body is a fascinating, complex, roiling sea of mechanisms and chemicals, many of which have evolved into use in multiple mechanisms and delicate balances between too much and too little. Nitric oxide seems to be important to stem cell activity, for example:

In the body, nitric oxide occurs naturally. It helps the repair cells move out of the bone marrow where they are made, and it opens blood vessels and improves the uptake of oxygen.

...

"We went on to show that actually what's happening is nitric oxide is affecting the skeleton, or scaffold of the cell, and by adding nitric oxide we're able to rearrange the scaffold," Segal said. "When we rearrange the scaffold, the cells are able to migrate. The benefit of this is that when cells have improved movement they are able to repair the endothelium (the lining of the blood vessels) better and perhaps prevent atherosclerosis."

Moving on, calorie restricted mice produce more nitric oxide - one of many pieces of the puzzle surrounding the mechanisms for the benefits to health and longevity provided by calorie restriction.

The results showed that mice that were fed 30% to 40% fewer calories produced more nitric oxide than those who followed an unrestricted diet. Calorie restriction also caused the mice to increase production of another chemical messenger that stimulated production of new mitochondria (the main energy source in cells) and increased oxygen consumption and expression of a protein previously shown to play a role in calorie restriction's effect on life span. These beneficial effects of calorie restriction were not found in mice that lacked the enzyme necessary to synthesize nitric oxide. Therefore, researchers say the findings suggest that nitric oxide may play a critical role in calorie restriction's effect on longevity.

Lastly, for this selection at least, suggestions that nitric oxide - like most chemicals in the body - isn't always a good thing:

An enzyme [iNOS] that triggers the production of nitric oxide (NO) - a gas that helps immune cells fight off invading pathogens - accelerates the formation of brain lesions in Alzheimer's-prone mice ... For nearly a decade, researchers have known that iNOS was present in the brain lesions of patients with Alzheimer's disease, but nobody had addressed whether its presence was making the disease worse. Nathan and colleagues now show that Alzheimer's-prone mice that lack iNOS live twice as long and develop fewer brain lesions than iNOS-expressing mice.

It all depends on context and circumstance - but a far greater level of understanding of our biochemistry will certainly lead to better ways to extend and improve health and longevity.

Technorati tags: aging, medical research

Posted by Reason at 9:12 PM
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The latest Rejuvenation Research is available online, and microglia are the order of the day, it seems. Microglia are a component of the immune system, scavenging debris and defending the central nervous system. What is their role in the degenerations of aging, and what is there to be done about it?

Evidence That Aging And Amyloid Promote Microglial Cell Senescence

Advanced age and presence of intracerebral amyloid deposits are known to be major risk factors for development of neurodegeneration in Alzheimer's disease (AD), and both have been associated with microglial activation. However, the specific role of activated microglia in AD pathogenesis remains unresolved. Here we report that microglial cells exhibit significant telomere shortening and reduction of telomerase activity with normal aging in rats, and that in humans there is a tendency toward telomere shortening with presence of dementia. Human brains containing high amyloid loads demonstrate a significantly higher degree of microglial dystrophy than nondemented, amyloid-free control subjects. Collectively, these findings show that microglial cell senescence associated with telomere shortening and normal aging is exacerbated by the presence of amyloid. They suggest that degeneration of microglia is a factor in the pathogenesis of AD.

Cellular Therapy Using Microglial Cells

Recent insights into the function and dysfunction of microglia may inform future therapies to combat neurodegeneration. We hypothesise how different aspects of microglial activity including migration, activation, oxidative response, phagocytosis, proteolysis, and replenishment could be targeted by novel therapeutic approaches. A combined approach is suggested, encompassing opsonization and anti-inflamatory strategies in conjunction with an engineering of microglial precursors. Xenoproteases for bioremediation could be used to enhance intracellular and extracellular proteolytic capacity. The capacity of microglial precursors to cross the blood-brain barrier and to home in on sites of neural damage and inflammation might prove to be particularly useful for future therapeutic strategies.

One of the names attached to this second paper is John Schloendorn, who works on bioremediation research funded by donations to the Methuselah Foundation. "Xenoproteases for bioremediation could be used to enhance intracellular and extracellular proteolytic capacity" means "let's adopt some useful biochemicals from bacteria that can help microglia clean up cellular debris by degrading harmful metabolic byproducts." Our metabolism generates damaging chemicals as a side-effect of its operation. When these build up with age, they damage the workings of our cells - and thus damage the workings of our bodies. So why not try to help the body out by removing the source of damage?

Given that many types of bacteria consume human remains - and also consume the damaging biochemical junk that builds up in and between our cells - it stands to reason that researchers can find the basic components of biochemical tools in those bacteria that will enable us to safely decompose damaging chemicals while we're still alive. Given that some fraction of aging is due to the buildup of these compounds, that should benefit us greatly.

Shifting topics, here is another interesting paper; it doesn't sound like a practical line of research to me, but it's still an intriguing idea. A popular science article from yesterday is somewhat more informative for the layman than the abstract of the paper:

Food containing heavy isotopes of hydrogen, carbon and nitrogen could slow down the aging process. That's the claim of Oxford-based researcher Mikhail Shchepinov, who suggests that seeding key biological molecules with deuterium or carbon-13 could drastically reduce oxidative damage or even avert it altogether.

Reactive oxygen species (ROS) are a staple of ageing research, as they are believed to cause cumulative damage to biomolecules such as DNA, proteins, and lipids. Typically, breaking a carbon-hydrogen bond is the rate-limiting step of these reactions. But if the carbon or hydrogen atoms involved were replaced by a heavier version of the same element (13C or D), the reaction will be slowed down due to a well-established phenomenon known as the kinetic isotope effect.

...

Heavy water (D2O) is toxic to higher organisms, but Shchepinov argues that isotopes would only be incorporated in the sites that need to be protected from oxidation. 'Ideally, they will slow down the oxidation reaction so much that they will never be released to take part in other reactions. If some of them do break free, they will only occur in small concentrations,' he said.

As for the other folk quoted in the article, I'm dubious - it seems to me that the level of technology required to target the isotopes reliably (and keep them targeted) would enable far more effective methdologies of repairing rather than preventing oxidative damage.

Technorati tags: biotechnology

Posted by Reason at 9:32 PM
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At some point, 20 to 30 years from now, advances across the board in medical engineering will lead to artificial organs that are better, safer and more reliable in every respect than those you can grow (or regrow, with the help of regenerative medicine) youself. Blood, immune systems, bones, muscle, kidneys and so on - everything is open to improvement. Just as the room-sized computers of the 1960s have given way to handheld devices vastly more powerful and reliable at a fraction of the cost, so too will today's cutting-edge (but still large and cranky) life-support devices give way to low-cost artificial organs inside you - organs which will fail far less often than their organic counterparts.

It will be interesting to see how increasingly sophisticated engineering measures up against the increasing capabilities of regenerative medicine in the years ahead, but a great deal of work lies betweeen here and 2030. A couple of articles I noticed today give a hint of the progress underway, present challenges, and the progress yet to come:

Nanotechnology could lead to improved implant devices:

Unfortunately, in many cases these metal alloys with a life time of 10-15 years may wear out within the lifetime of the patient. They also might not achieve the same fit and stability as the original tissue, and in a worst case, the host organism might reject the implant altogether. While available implants can alleviate excruciating pain and allow patients to live more active lives, there often are problems getting bone to attach to the metal devices. Small gaps between natural bone and the implant can increase over time, requiring the need for additional surgery to replace the implant. In the quest to make bone, joint and tooth implants almost as good as nature's own version, scientists are turning to nanotechnology.

...

Rather than just experimenting by trial and error, scientists are aiming to intelligently design implant surfaces to control protein interactions important for subsequent cell adhesion that may provide answers to those problems which have plagued current orthopedic implants.

The devil is in the detail, and you have to start with the basics. If you want to integrate compact new biotechnology into the body, replacing damaged or aging organs with machinery that will eventually function far more efficiently than the original, you have to ensure that the interface between the two sides is far better than was possible in the past.

An insight into the rewarding world of biomedical engineering:

The phrase ‘engineers make a difference’ is used in virtually every branch of engineering, and no doubt the structural, civil, chemical and other engineers would all argue that they make the biggest difference of all. But there is one branch of engineering that has a direct affect on our lives that the other disciplines cannot. Biomedical engineering helps to relieve pain, repair damage, improve the quality of life, deliver faster, non-invasive diagnoses - and more.

...

Regardless of the branch of biomedical engineering, one of the biggest challenges is the patient interface. Colin Hunsley explains: “For a routine hip replacement, the surgeon will select modular components to build up a joint that will suit the patient. However, for some reconstructive surgery there may be a requirement to use rapid prototyping technologies to create prosthetics that are unique to the patient. We also have to be aware of biocompatibility, as the human body can be a harsh environment for many engineering materials; and, conversely, the body will reject most materials. Various surface treatments have been developed to help overcome this, but the latest developments seek to go beyond a material or device being merely tolerated by the body; rather the aim now is to create something that will function with the human body as well as - if not better than - what it replaces.”

In the future, everyone who cares to look after themselves will be a little bit cyborg. It'll be simple common sense. Why settle for a cranky old natural human immune system when you can buy one far better and more durable? Why stick with version 1.0 kidneys when the hybrid bioartificial models filter out chemical byproducts of metabolism that accumulate to damage your body in old age? The decades ahead are golden - well worth sticking around to see.

Technorati tags: medical engineering

Posted by Reason at 9:05 PM
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A couple of items of interest showed up in my wanderings today. Firstly, Bruce Klein notes his modest profile in the recently released "How to Live Forever or Die Trying":

Bruce Klein founded The Immortality Institute (Imminst) in 2002 as a non-profit organisation with the aim of ‘conquering the blight of involuntary death’. ... Klein was thirty-one when I met him at Imminst’s conference at the Georgia Tech Conference Center, Atlanta, in November 2005. The conference turned out to be a snapshot of the immortalist front line. It is a movement that is part cult and part serious science. But all were united by the fervency of their belief in the rightness of the project of extending life and by their vehement rejection of deathism and scepticism.

The world "cult" is thrown around all too easily these days; I can only think that it is a symptom of the absence from public view of human activities that truly deserve the label. Strive to support the development of cures for age-related disease and you're a patient advocate. Strive to support the repair of the root causes of all age-related disease - via the same scientific processes and methods, I might add - and you're a cultist, hairstyle and clothing choices open for comment. Such blind, irrational creatures, we humans; I consider a wonder that anything of ambition is ever accomplished. A larger excerpt can be found elsewhere online; see what you think of the rest of it.

Why? Because, says Klein, ‘oblivion is the issue’. He says: ‘I came to a point about five years ago where I realised I can’t do all of this unless I’m alive . . . The thing that human beings, I think, are evolved to do is put the issue of oblivion to one side. What I try to do is address that problem with writings, with film scripts and the thing is not only to address it but to provide a solution, the solution of infinite life span.’

He speaks, as does everybody in this business, of the 150,000 people who die in the world every day, 100,000 of them from the diseases of old age. For him, this is not acceptably explained as the natural order of things, rather it is a disaster to which we are called to respond.

‘I call it the Silent Tsunami, every day more than 100,000 people die quietly and acceptingly, saying their time has come or some other euphemism. But, with a real tsunami, they say this is a tragedy, we must do things to prevent this in the future.’

Switching topics, we have some thoughts on calorie restriction from a member of the community who thinks that the arguments for significant human life extension via this methology are plausible:

Think of the differences in human longevity, from person to person. One person can live decades than another. Isn't that AMAZING?! Calment lived DECADES longer than the average person... Her aging was much slower than the average person. There are centenarians that live to old age and centenarians that survive to old age. Calment lived and survived to old age with luck, genetics and possibly lifestyle factors. But it shows you just how much of a degree there can be between how much longer one can possibly live.

...

The huge difference between when the average person dies, and when the oldest human ever documented lived is huge, spanning over 40 years? That’s a remarkable reduction in the rate of aging. Aging must have been slowed in her, and damn right, CRON will slow the aging for us. To what degree is up for debate. But I would bet that our average life expectancies will be up their with those lucky few who survived to extreme old age without the help of calorie restriction.

There is a very good weight of science backing the fact that calorie restriction will do very good things for your health and resistance to the more common aspects of age-related degeneration today. But will that add a couple of years to your life, ten years, or how long? Good question, but look at exercise as a comparison - the difference between fit and unfit is large once you make it into later life. Just as for staying fit with exercise, you'd be a fool not to look into calorie restriction, given the impressive health benefits demonstrated in human studies.

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