Longevity Meme Newsletter, April 17 2006

April 17 2006

The Longevity Meme Newsletter is a weekly e-mail containing news, opinions and happenings for people interested in healthy life extension: making use of diet, lifestyle choices, technology and proven medical advances to live healthy, longer lives.



- 2nd Immortality Institute Book: Call for Abstracts
- Too Damn Optimistic, I Say
- The Latest Rejuvenation Research
- Discussion
- Latest Healthy Life Extension Headlines


The Immortality Institute volunteers are gearing up for a second book to follow the success of "The Scientific Conquest of Death." If you haven't read the Institute's first book of essays yet, you can do so for free online - and a hard copy for your coffee table isn't that much more than free:


The Institute leadership has issued a call for abstracts with a deadline of June 30th. You can learn more about the project and the sort of submissions requested by following the links below:



Too much optimism can be as much a failure mode as too little; if you're over-optimistic on timelines and capabilities of future healthy life extension medicine, then you are less likely to feel the urge to materially contribute to that future. Free riding is an easy choice if it's "obvious" that what you want will happen anyway. If everyone thinks that way, then nothing gets done and we all suffer and die:


I'd be optimistic myself if a scientific healthy life extension infrastructure as dedicated, large and advanced as that for cancer or Alzheimer's research actually existed. But it doesn't, and the scientific and advocacy communities have barely even started on the long road to building such a thing. The process could have been started a generation ago, but it wasn't. It may not get off the ground this generation.

I see signs of overconfidence in the younger supporters of healthy life extension; that is good if it drives action, but complacency would be the death of all of us if it spread. We have a chance, a shot at radical life extension. We have to contribute, all of us, or it will slip from between our fingers.



The latest issue of Rejuvenation Research is out. Find some of the highlights - such as the latest from the team working on those regenerating MRL mice - in the following Fight Aging! post:


Personally, I'm skeptical that MRL-like (or engineered salamander-like) mechanisms in mammals could, on their own, net you something approximating physical immortality, as seen in lower animals like the hydra. Mammalian regeneration - even impressive, standout, amazing mammalian regeneration - comes from the actions of stem cell populations, and stem cells in mammals have a sell-by date due to the accumulation of genetic mutations. After a certain point, you're looking at cancer and ever more cancer, no matter how well you can regenerate.

But there's much more to look at as well, such as telomeres in Bristlecone Pines and a closer look at the dysfunctional aging immune system - and what could be done to fix it up. You'll find the Rejuvenation Research issue here:



The highlights and headlines from the past week follow below.

Remember - if you like this newsletter, the chances are that your friends will find it useful too. Forward it on, or post a copy to your favorite online communities. Encourage the people you know to pitch in and make a difference to the future of health and longevity!


Founder, Longevity Meme



To view commentary on the latest news headlines complete with links and references, please visit the daily news section of the Longevity Meme: http://www.longevitymeme.org/news/

More Linking: Diabetes and Cancer (April 16 2006)
Inflammatory conditions can already be linked to cancer and obesity is linked to inflammation and diabetes. Medical News Today here notes another biochemical linkage: a study "has defined the function of p110 alpha, the flag-ship molecule of the eight member PI3K family, which is one of the most frequently activated pathways in cancer. ... p110 alpha controls the action of insulin and other key hormonal signals that play roles in growth, diabetes and obesity. p110 alpha is frequently mutated or overexpressed in cancer, and the results of the present work imply that cancer cells hijack a key signalling pathway to fuel their energy needs and drive their proliferation and survival. The current work has far-reaching implications, given that several million of people are affected by metabolic disorders, and every year, several hundreds of thousand new cancer cases with mutations in p110 alpha are diagnosed."

Recategorizing Aging (April 16 2006)
The concept of "normal aging" or "normal wear and tear" doesn't hold up well to the advance of biotechnology. Most age-related conditions were once thought to be "normal aging" and thus not worth devoting resources to - and I'd wager that almost all of what is left of "normal aging" is a mass of unidentified conditions. Medical News Today has an example of recategorization at work: "Heart valve disease is caused not by a 'wear and tear' phenomenon, but by an inflammatory process likely triggered by high cholesterol that stimulates certain cells to reprogram into bone cells in the aortic valve and cartilage cells in the mitral valve ... Common wisdom in the medical community has always been that thickening of the mitral valves was part of the aging process as deposits of calcium, a mineral found in the blood, built up on the valves. Therefore, research has never focused on preventing the problem."

Biomedical Tests, Attitudes to Research (April 15 2006)
Randall Parker makes an interesting point here: "Imagine you could be told two or three or four decades in advance what you are going to die from. Imagine a doctor could tell you that you will die from pancreatic failure 20 years from now barring the development of stem cell therapies or bioengineering technologies for growth of replacement organs. Would it change your attitude toward the urgency of medical research? I've been predicting for some years that advances in biomedical testing will lead to the ability to predict occurrence many diseases decades in advance and that this will change public attitudes toward biomedical research funding. ... Since advances in testing are happening and will continue to happen for decades to come I'm predicting a growth in the size of interest groups in support of the development of stem cell research, gene therapy, growth of replacement organs, and other cures for diseases." Food for thought.

More On Human CR Studies (April 15 2006)
The Record examines some of the present day studies of calorie restriction, health and aging in humans: "We're hoping to learn more about whether calorie restriction can alter the aging process. ... low-grade, chronic inflammation seems to mediate aging. Overweight and obese people tend to have higher levels of inflammation than lean people, so it makes sense that losing weight might increase average lifespan by lowering the risks of some age-related diseases, such as diabetes and atherosclerosis. But in animal studies, not only did more of the animals live longer, the maximum length of a rat's or mouse's life also increased. ... It's going to be many years before we know whether calorie restriction really lengthens life [in humans], but if we can demonstrate that it changes these markers of aging, such as DNA damage and inflammation, we'll have a pretty good idea that it's somehow influencing the aging process at the cellular level."

Project 2's Rhesus Monkeys (April 14 2006)
As noted at wisbusiness, it takes a long time to run a study on calorie restriction (CR) and aging in primates: "A calorie-restriction experiment that began in 1989 with a group of rhesus monkeys under the care of the Wisconsin National Primate Research Center is entering the 'golden years' of the study, and the monkeys are showing no signs of slowing down. ... The monkeys in the oldest group are now about 25, being equivalent to 60-year-old humans ... How well are these calorie-restricted monkeys aging compared to their control group counterparts? They are doing exceedingly well ... showing no obesity, better blood glucose control and, based on studies from the other projects funded by the grant, fewer cellular defects and less muscular atrophy."

Big Numbers, Stem Cell Politics (April 14 2006)
(From the New York Times) Eliot Spitzer, an excellent example of the sort of person best kept far from the reins of power, is pulling out large sums - of other people's money - for stem cell research as a campaign bulletpoint: "his administration would push for a $1 billion bond to pay for stem cell and other medical research. Mr. Spitzer, the state's attorney general, said the money for research on stem cells and other promising treatments would be the 'centerpiece' of the state's health care policy if he were elected." This is an amplified reflection of public funding proposals underway many other US states; for better or worse, a state-funded infrastructure to rival cancer research institutions is clearly in the making.

FuturePundit On Xenotransplantation (April 13 2006)
Xenotransplantation - a path to an industry capable of mass-producing replacements for age- and disease-damaged organs - has been in the news more often of late. We can hope that this is the result of a rising tide of new advances. Via FuturePundit: "Revivicor's pigs have been genetically modified to not produce alpha-1-galactose sugar which causes human immune rejection. Much more could be done along those lines to make pig organs more like human organs in order to enhance compatibility. This strikes me as a direction that ought to get huge amounts of funding. ... Every day that goes by your organs all get one day older and closer to failure. If we start trying a lot harder now many of us could get youthful organs transplanted from pigs when our own organs get old and start to fail. Time's a wasting. Time is wasting our body parts and making them slowly break down. We ought to develop the means to repair and replace old human body parts."

New Scientist on Bioprinting (April 12 2006)
From the New Scientist, a look at the application of inkjet printing technologies to biotechnology and tissue engineering: "droplets placed next to one another will flow together and fuse, forming layers, rings or other shapes, depending on how they were deposited. To print 3D structures, Forgacs and his colleagues alternate layers of supporting gel, dubbed 'biopaper', with the bioink droplets. To build tubes that could serve as blood vessels, for instance, they lay down successive rings containing muscle and endothelial cells, which line our arteries and veins. ... We can print any desired structure, in principle ... Other tissue engineers have tried printing 3D structures, using modified ink-jet printers which spray cells suspended in liquid ... Forgacs and a company called Sciperio have developed a device with printing heads that extrude clumps of cells mechanically so that they emerge one by one from a micropipette. This results in a higher density of cells in the final printed structure, meaning that an authentic tissue structure can be created faster."

On Tissue Engineering (April 12 2006)
The Sydney Morning Herald examines the present state and near future of tissue engineering: "The holy grail for tissue engineers [is] to develop 'smart' scaffolds for each particular organ that could be placed into the appropriate body cavity so they recruit the right cells to build up the desired tissue and develop a blood supply. ... Every surgeon would like to have scaffolds, sitting on a shelf in their packages, that are designed for specific uses, for example, breast regeneration ... Growing complex organs such as the kidney - with more than 25 different types of cells arranged in an intricate structure - this way will be very difficult. But it may be possible within a few years to grow a particular component of the organ that a patient needs."

Targeting Cancer With Nanoparticles (April 12 2006)
Medical News Today looks at the work of one of many groups developing targeted cancer therapies using the latest nanoscale engineering techniques. The researchers use "tailor-made tiny sponge-like nanoparticles laced with the drug docetaxel. The particles are specifically designed to dissolve in a cell's internal fluids, releasing the anti-cancer drug either rapidly or slowly, depending on what is needed. ... to make sure only the correct cells are hit, the nanoparticles are 'decorated' on the outside with targeting molecules called aptamers, tiny chunks of genetic material. Like homing devices, the aptamers specifically recognize the surface molecules on cancer cells, while avoiding normal cells." Killing cells is easy. Killing just the right cells is very hard - but scientists are making good progress.

Skin Grafts From Stem Cells (April 11 2006)
Via RxPG News, a report of tissue engineered skin used in place of skin grafts: "A Singapore company has used stem cells to help victims of serious burns and other wounds grow fresh skin ... While some more research work has to be done to test the new treatment, Dr Ivor Lim of the Singapore-based Cell Research Corporation said, 'the procedure has allowed three patients so far to do away with painful skin grafts'. ... The treatment involves growing stem cells on synthetic scaffolds and transferring them onto the patients' wounds. ... In case of stem cell treatment 'the healing rate has been as fast as with a conventional skin graft, with no complications or rejection. It would also be a help for patients who are so badly wounded they do not have enough skin for a graft.'"

BBC News on Regenerating MRL Mice (April 11 2006)
The BBC News has a good popular science article on the enhanced regenerative capabilities of MRL mice - something that has impressed scientists for a while now: "The MRL mouse has been used in research for years - mostly as a model for autoimmune diseases because the genetic mutations they carry mean they have a lupus-like disease. ... This animal has an unusual ability to show cell proliferation and lack of scarring which I think are two key elements to why we don't regenerate. ... She believes that one of the factors that blocks regeneration in most mammals is a membrane that forms as the body starts to repair itself. ... When the team looked at the formation of the membrane in the ears of MRL mice, they found that it did form initially, but disappeared soon after and then cell growth begins. ... [the researchers] are now looking to see if they can breed mice have the regenerative capabilities but do not carry autoimmune disease."

Regrow Your Own (April 10 2006)
From the New York Times, an article on efforts to replicate the regenerative powers of lower animals, such as salamanders: "Stem cell therapy has long captured the limelight as a way to the goal of regenerative medicine, that of repairing the body with its own natural systems. But a few scientists, working in a relatively obscure field, believe another path to regenerative medicine may be as likely to succeed. ... it is the solution that nature itself has developed for repairing damaged limbs or organs in a wide variety of animals. ... The salamander can regenerate its limbs, its tail, its upper and lower jaws, the lens and the retina of its eye, and its intestine. The zebra fish will regrow fins, scales, spinal cord and part of its heart. Mammals, too, can renew damaged parts of their body. All can regenerate the liver. Deer regrow their antlers ... the machinery for regeneration must be a basic part of animal genetic equipment, but the genes have for some reason fallen into disuse in many species."

Mitochondrial DNA and Aging (April 10 2006)
The Scientist reports on new support for the mitochondrial DNA mutational theory of aging: "Pigmented neurons in aged human substantia nigra -- the main site of neurodegeneration in Parkinson disease -- contain very high levels of mitochondrial DNA (mtDNA) deletions ... Neurons with the most mtDNA deletions showed defects in cellular respiration, which the authors say may lead to common symptoms of aging, such as the mild Parkinson-like symptoms often observed in older people. ... I think our result in nigra is the most convincing case so far. ... These aged cells often possessed extremely high levels of deletions -- many showed more than 60% deleted mtDNA, which is considered the phenotypic threshold above which respiratory function of the cell becomes impaired." A good job that researchers are already working on ways to replace age-damaged mitochondrial DNA.



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