LONGEVITY MEME NEWSLETTER
November 13 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.
- An Update on the Longevity Dividend Initiative
- Methuselah Foundation Seeks Development Officer
- Latest Healthy Life Extension Headlines
AN UPDATE ON THE LONGEVITY DIVIDEND INITIATIVE
For those who have been waiting, slides and video from the September 12th Longevity Dividend event in Washington D.C. are now available online. Researcher S. Jay Olshansky had this to say:
"The event in D.C. on the 12th of September went extremely well. Senator Craig kicked off the meeting using the language of the Longevity Dividend to suggest that health care spending will swamp the budget unless we pursue this initiative. Several of us met with Senator Harkin personally after the meeting to discuss the idea. He subsequently asked us for language to place in the appropriations bill, which we did. We're now drafting a follow-up to the Longevity Dividend calling for a paradigm shift in the way at which we look at aging and disease. It's important that we begin using the language of the Longevity Dividend to keep up the momentum."
Links, background information and my commentary can be found at the following Fight Aging! post:
The video and slides are over at the Alliance for Aging Research website, one of the backing organizations:
METHUSELAH FOUNDATION SEEKS DEVELOPMENT OFFICER
As you may know, the Methuselah Foundation has been expanding its named administrative positions of late in recognition of the growing number of core volunteers:
The Foundation is also actively seeking a well-connected and effective fundraiser in the Bay Area, California:
"The Methuselah Foundation seeks a singularly outstanding Development Officer to secure major donations from the entrepreneurial, technology and venture capital communities in the Bay Area. The mission of the Foundation is to devise new approaches to combating and eventually reversing the diseases and debilities caused by aging. Following two recent substantial financial contributions, the Foundation is poised for significant acceleration in 2007, both in realizing its slate of research projects and in continuing to develop its prize-driven model, the Mprize. Working with the senior management of the Foundation, you will plan, launch and manage a new fund raising program designed to strategically and systematically develop the major gift pipeline."
I know a good many of you folk are well connected in your own right: feel free to slide this notice into your personal networks. It's a wonderful opportunity for the right sort of person.
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
LATEST HEALTHY LIFE EXTENSION HEADLINES
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/
End Results Versus Root Causes (November 12 2006)
The huge regulatory burden placed on new medicine ensures a disproportionate amount of effort goes into finding multiple uses for any given drug. In addition, present regulation forces a focus on patching up the end result rather than addressing the root cause. Here, EurekAlert! notes some progress on the end result known as atherosclerosis: two drugs "decreased inflammatory proteins produced by macrophages, a type of white blood cell. These inflammatory proteins can make the atherosclerotic plaque unstable. ... researchers also measured dramatic decreases in LDL and total cholesterol in the macrophages. ... And the drugs prevented macrophages from turning into foam cells inside arterial walls, which is a key component of the buildup of plaque." But this doesn't address root causes, such as the growth in oxidized LDL resulting from mitochondrial damage and free radical buildup with age. Until medical science can economically focus on root causes, it will continue to be a very expensive, inefficient way of buying a little time.
Another Targeted Cancer Therapy (November 12 2006)
(From ScienceDaily). Given the tools and the knowledge of modern biotechnology, there are a great many potential targeted approaches that can defeat cancer. This one uses an otherwise harmless engineered chemical that becomes toxic in the presence of cancer. Researchers "had developed a protoxin, named PRX302, by modifying an inactive molecule, proaerolysin (PA). They engineered PRX302 to be activated by prostate-specific antigen (PSA) - a protein made in higher than normal levels by prostate cancer. Once activated, they hoped that it would target and kill prostate cancer cells specifically. ... This represents a different kind of 'targeted' therapy, in that it seeks to use a protein made by the cancer to destroy itself. ... Initial tests in the lab and in animals revealed that when the protoxin was injected into cancerous prostate tissue, it had a significant effect ... A phase I clinical trial is in progress now for men with locally recurrent prostate cancer after definitive radiation therapy."
From the Hillblom Foundation Meeting (November 11 2006)
Chris Patil of Ouroboros reports from the latest Hillblom Foundation meeting: "most of the scholars represented were studying either some aspect of pancreatic islet biology or a neurodegenerative disease. Basic biologists of aging per se were fewer and further between, though there were a couple of excellent worm talks from Andy Dillin from the Salk, and Laura Mitic from the Kenyon lab at UCSF. Probably the most exciting talk at the meeting was from Irvin's Charlie Glabe, whose lab is developing antibodies targeted at amyloid Abeta oligomers (increasingly, the form considered likely to be the primary pathologic species in Alzheimer's disease [AD]). ... Passive immunization, in which a patient is given the antibody directly, rather than immunized against the toxic molecule and left to develop their own antibodies, seems to be the main direction for immunologically based AD treatments."
More Differentiation Progress (November 11 2006)
ScienceDaily notes another small step forward in learning how to control cellular differentiation to advance the capabilities of regenerative medicine. "Smooth muscle cells (SMCs) are a crucial cellular component of many parts of the body, including blood vessels, the intestines, and the lungs. SMCs in the blood vessels are involved in several causes of heart disease and understanding how SMCs are generated is important for designing therapies for such diseases. It is also knowledge that could be used to engineer tissues in the laboratory, for example new blood vessels for use in bypass surgery. ... [researchers] show that SMCs can be generated from multipotent adult progenitor cells (MAPCs) isolated from the bone marrow of rats, mice, pigs, and humans. ... This study therefore identifies a model system for studying the effects of potential therapeutics on SMC development and SMCs. It also describes a potential source of SMCs for engineering tissues."
Organization at Alcor (November 10 2006)
Since organization seems to be the topic today, here is a long update from the cryonics provider Alcor: "Earlier this year, Alcor engaged in some long-term organizational planning. The result was the drafting of a three-year plan for development. ... It considered strategic positioning and facility improvements that would be necessary to transitioning Alcor from a small start-up into an organization that is capable of surviving successful outreach and mass marketing. ... We still have a lot of work to do, but we have a good staff that is fully capable of handling the load. We're pleased with the progress that has recently occurred, and we intend to keep the momentum going ... Needless to say, we're excited about the current direction Alcor is headed, though we're fully aware that there is still a tremendous amount to do. We hope you'll stay tuned and see how this all develops"
Methuselah Foundation Seeks Fundraiser (November 10 2006)
Organization is underway at the Methuselah Foundation, which "seeks a singularly outstanding Development Officer to secure major donations from the entrepreneurial, technology and venture capital communities in the Bay Area. The mission of the Foundation is to devise new approaches to combating and eventually reversing the diseases and debilities caused by aging. Following two recent substantial financial contributions, the Foundation is poised for significant acceleration in 2007, both in realizing its slate of research projects and in continuing to develop its prize-driven model, the Mprize. Working with the senior management of the Foundation, you will plan, launch and manage a new fund raising program designed to strategically and systematically develop the major gift pipeline. You will have responsibility for increasing annual and periodic, unrestricted or directed support for the Mprize fund and SENS research program through the solicitation of donations, typically in the range $5,000 - $100,000." If folks could pass this along into their networks, I would be appreciative.
Underlying Mole-Rat Science (November 09 2006)
To follow on from recent interest in the mechanism of longevity in naked mole-rats, here is a paper that looks at the biochemistry: "Underlying causes of species differences in maximum life span (MLS) are unknown, although differential vulnerability of membrane phospholipids to peroxidation is implicated. ... membranes of longer-living, larger mammals have less polyunsaturated fatty acid (PUFA). ... Both species had similar amounts of membrane total unsaturated fatty acids; however, mice had 9 times more docosahexaenoic acid (DHA). Because this n-3PUFA is most susceptible to lipid peroxidation, mole-rat membranes are substantially more resistant to oxidative stress than are mice membranes ... suggesting that membrane phospholipid composition is an important determinant of longevity." So there you go; mole-rats have just as many free radicals as their short-lived peers in other species, but may be vastly more resistant because their metabolism uses tougher biochemicals. Less damage means less aging - and thus a longer, healthier life.
Mass Producing Bioartificial Organs (November 09 2006)
It's good to see people paying more attention to the challenges of scaling and commercializing promising new medical technologies. From the MIT Technology Review: "The bioartificial kidney is one of the most promising examples to date of a bioengineered medical device. The innovative, external device passes blood through a cartridge of human kidney cells. ... But scientists now face a challenge that may be as great as designing the device itself: turning a successful academic invention into a mass-produced medical device. ... Both Humes and Lysaght liken the problem to that faced twenty years ago by researchers working with recombinant proteins, such as human insulin. Scientists could successfully make the proteins in the lab, but it took several years to figure out how to scale up that process for broad medical use. Lysaght says he's confident the same will be true for tissue-engineered products once people recognize the extent of the problem."
Discussing Overpopulation, Longevity (November 08 2006)
The Speculist gives some space to discussion of the old canard of overpopulation; some people like to use it as an argument against healthy life extension. Interestingly, Randall Parker appears to fall into the "something must be done" school. But Malthusianism of any sort has always been wrong; a good example of the way in which most people find it hard to grasp the nature of change and consequences of human action. "The level of technology necessary to deliver radical life extension will give us other solutions. We'll get cheaper energy, more efficient desalinization for potable water, and - most importantly - exponential improvements in computation. Areas of wilderness that have are presently uninhabitable will be opened up. When space elevators become a reality many could take up residence in space. People might even choose to live virtually - essentially taking up no space."
Report From Wonderfest (November 08 2006)
The Stanford Wonderfest was held recently, and the prospects for extending healthy life span were discussed: "'There is a lot of evidence that maximum lifespan can be extended,' said Thomas Rando, associate professor of neurology and neurological sciences at Stanford, noting that the increase in life expectancy over the last few centuries gives reason to remain hopeful. 'Historically, there has been a huge change in how long we live.' ... Rando, who investigates the regenerative properties of muscle stem cells, predicted that stem cell research would likely have a greater impact on health than longevity. 'People think that stem cells can help us live to 150 or 200. But I am more convinced that the whole value of stem cells will be to help us age healthier than make us live longer.'" As Judith Campisi points out in the article, we're going to have to beat cancer if we want to benefit from all the other bioscience that could extend our lives.
Preventing Heart Attack Damage (November 07 2006)
One of the next advances in first generation autologous stem cell therapies is to bring them to the patient faster - try to prevent damage rather than repair it further down the line, in other words. From the Times Online: "There have been a couple of clinical trials in Germany to demonstrate that the technique is safe. In these trials, the bone marrow cells were given late, some time after the heart attack, in order to repair the muscle. We believe that if we give it immediately, it can prevent damage. We will show whether it works in acute heart attack - and the treatment will involve no extra stay in hospital and virtually no extra cost. ... There is good animal evidence in rats and mice that it will work. There are no drugs involved, and nothing to patent, so if the treatment works it will be available to all who can benefit, without extra cost."
CR Science Isn't Simple (November 07 2006)
The present day science of metabolism is far from simple and clear-cut, and especially so in fields making dramatic process. This NYT article on calorie restriction (CR) research is illustrative of this point; one has to be careful parsing out their claim of no proof for the health benefits of human CR, given there are studies that show these benefits - but there are no multi-thousand member, multi-decade studies, for example. You always have to ask what is meant by "prove" in popular science pieces. From the article: "A new class of drugs is looming on the horizon that could, if they live up to their promise, avert heart disease, diabetes, cancer and neurodegenerative disorders. By suppressing the common killers of age, the drugs, sirtuin activators, could significantly prolong both health and lifespan. But is the promise a mirage or a serious possibility?"
Small Steps Towards Restored Sight (November 06 2006)
Medical News Today notes that researcher seek "to equip cells of the retina with photoswitches, essentially making blind nerve cells see, restoring light sensitivity in people with degenerative blindness such as macular degeneration. ... The researchers demonstrated in 2004 that they could turn cultured nerve cells on and off with this optical switch. Since then [they've] injected photoswitches into the eyes of rats that have a disease that kills their rods and cones, and have restored some light sensitivity to the remaining retinal cells. ... Their group, centered around the optical control of biological function, will develop viruses that can carry the photoswitches into the correct cells ... We plan to develop the tools to create a new layer of optically active cells for the retina."
Unusual Genes Versus Osteoporosis (November 06 2006)
Learning from rare human genetics is a frequent theme in modern biotechnology and medicine; here, The Scientist looks at what might come from one rare condition: "His bone density was eight times higher than average for a man his age ... He's had several failed hip replacements because they can't screw the prosthesis into his bone. It's too hard. ... As it turned out, [osteoporosis researchers] had already zeroed in on exactly the same mutation while studying a Nebraska family with unusually dense bones. They'd identified 21 family members with the condition. ... None of those people, ranging in age from 3 to 93, had ever had a broken bone ... Many questions [remain] unanswered, but [scientists] are hopeful that clinical trials of osteoporosis treatments stemming from their work could begin within five years." As is often the case, there is a potential enhancement here - who wouldn't want stronger bones as a preventative measure?