Longevity Meme Newsletter, May 08 2006

May 08 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.



- Video of Aubrey de Grey at TED2006
- Google Health, Coming Soon
- Chapter's End
- Discussion
- Latest Healthy Life Extension Headlines


The latest addition to the Methuselah Foundation's growing collection of multimedia is the presentation given by biomedical gerontologist Aubrey de Grey at TED2006 earlier this year. While TED events are becoming much less cloistered out of necessity - try keeping anything away from the public sphere these days, let alone the contents of a conference packed with blog-owners, artists and internet technologists - it's still pleasing to see that the Foundation volunteers garnered agreement to have the video released. You'll find links to various hosting locations at Fight Aging!:


Thank you to those who helped out with conversion, uploading and all the other time consuming work that comes with large multimedia files. Quite a few other interesting videos reside in the multimedia section of the website of the MPrize for anti-aging research; you should take the time to browse while you're there:



Google will soon be launching a set of refinements to assist searches on medical information, infrastructure, diseases, trials and conditions. I think that many of the readers of this newsletter will find it a useful improvement for research both personal and professional; see this Fight Aging! post for a few notes:



As I'm sure many of you know, the Extropy Institute formally dissolved this week. Many of us found our way to our present positions in the healthy life extension community via our interaction with the Institute and the salons it sponsored:


Given the growth of the healthy life extension community over the past couple of years, this may be a look back at hoary old subcultural history for many of you - but I can think of few better accolades than becoming irrelevant to the movements you helped get off the ground. Perhaps the only step up from that will be to see younger folk utterly fail to appreciate or understand that their ongoing, large-scale scientific fight to cure aging and abolish age-related frailty was once a ridiculed idea, relegated to the fringes. That would be pleasant indeed - but we have much work to do in order to reach that point:



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/

Short Telomeres and Dementia, Or Not (May 07 2006)
Via the Doctor's Guide, news of a study on telomere length and dementia: "Despite previous mixed reports, telomere length cannot be used to predict dementia, according to the largest longitudinal study ... The telomere hypothesis of aging is based on the notion that telomere shortening with each cell division, and therefore with age, results in cell senescence ... This thus led to the 'telomere hypothesis of dementia,' that asks whether telomere shortening contributes to the genesis of certain age-related diseases, such as dementia ... [but] telomere lengths in both the dementia and nondementia patients showed no significant decline with age. ... There was no association between telomere length and change in cognitive status." It would be wonderful progress to find a simple association between known mechanism and disease, but this is rare indeed amidst the vast complexities of human biochemistry.

Further Insight Into Type 2 Diabetes (May 07 2006)
Type 2 (age-related) diabetes can usually be avoided through smarter lifestyle choices, but further insights into biochemical mechanisms and genetic risks associated with diabetes will lead to therapies to help people who did not make these choices. From EurekAlert, news of a gene that "likely influences the ability of the pancreas to recruit a type of cell essential for constructing the walls of blood vessels. The beta cells of the pancreas, which are the critical insulin producing cells of the organ, are found clustered together in structures called islets and are nourished by a complex network of small blood vessels. If there are changes in this gene [the] blood vessels within islets may not form properly. ... The hope is this will open up scientists' thinking to realize that there are other cells of importance (in diabetes) beyond beta cells."

Popular Mechanics on Living Longer (May 07 2006)
A Popular Mechanics article takes a look at what the near future holds in terms of upgrades for we humans; biomedical gerontologist Aubrey de Grey is one of the featured scientists: "There's a difference between working on aging and working on a specific age-related disease. Curing one age-related disease might extend life by five or 10 years, but an awful lot of people who would have died from it will die of something else instead. Even if we fix only four or five of these things very well, we probably won't get more than an extra 10 or 20 years of life because the things that we can't fix will still be accumulating. ... Depending on funding, it will take another 10 years or so to get to the proof-of-concept stage in the lab. I'd say we have a 50/50 chance getting these therapies all working in humans 15 years after that."

How p53 Controls Cancer Rates (May 06 2006)
The gene p53 is central to biochemical processes governing cancer and aging. From EurekAlert, more on how p53 controls DNA damage: "The body's solution to minimizing mutations is to have no fewer than ten different 'careless' [DNA replication] enzymes. Although this may seem paradoxical - intuitively, more careless enzymes should mean more mutations - each of these enzymes is tailored to deal with certain specific types of DNA damage. This specialization is what keeps the level of mutation, and thus the cancer risk, low. But the existence of this variety of specialist enzymes implies precise regulation of the system - otherwise copying by the careless enzymes might get out of control and lead to an unhealthy proliferation of mutations. ... The main components in this system are the proteins p53 and p21. ... if the functioning of p53 or its relative, p21, is harmed, the activities of the careless enzymes can go into overdrive, leading to more mutations."

The Damage Done by Patents (May 06 2006)
Via the Paramus Post, an examination of some of the damage done by patents. "Along similar lines, San Francisco-based Athena Neurosciences holds the patent on a gene associated with Alzheimer's disease. Athena will not allow any laboratory except its own to screen for mutations in that gene. ... Doctors and laboratories across the country face a lawsuit if they try to determine whether one of their patients carries this genetic predisposition to Alzheimer's disease, even though testing can easily be done by anyone who knows the sequence of the gene, without using any product or device made by the patent holder." So one company patent holder blocks or exacts a toll on any and all work the rest of the world might do to improve this technology. The bottom line: restrict competition and you restrict progress. Industries without patents are far more dynamic than those stifled by them, in which short-termists profit at the expense of everyone else.

Mitochondria and Sarcopenia (May 05 2006)
This paper from Aging Research Reviews discusses current scientific thought on the connection between accumulated damage to mitochondrial DNA and sarcopenia, the progressive loss of muscle mass and function with age: " Many key theories on aging describing the mechanisms underlying sarcopenia are now focused on the mitochondria because of their dichotomous role in controlling life and death processes within myocytes. ... Evidence supports that apoptosis occurring in aging skeletal muscle may be due, in part, to the progressive decline in mitochondrial function and the resulting energy depletion within the cell." Damaged mitochondria seem to play an important role in many of the conditions and failure modes relating to age-related degeneration - methods to repair or prevent this damage will be most welcome.

A Step Towards Replacement Lungs (May 05 2006)
Via BusinessWire, news of early stage progress in engineering lung tissue for regenerative therapies and similar applications: "The growth of functional three dimensional organ structures begins with proof of concept studies showing that organ subunits can successfully be generated. This work takes us a step closer to realizing this goal which we hope will be applicable to all organs in the future ... a combination of 3-D cell growth on a [hydrogel] support and the addition of tissue-specific growth factors can induce functional lung tissue development. In a paper entitled, "Engineering Three-Dimensional Pulmonary Tissue Constructs," the authors report on their success in creating pulmonary tissue with appropriate lung tissue morphogenesis, architecture, and branching, as well as specific gene and protein expression."

Standing Up To the FDA (May 04 2006)
(Via Marginal Revolution). It is pleasant to see someone within the present establishment standing up to FDA bureaucrats and what they stand for - suppression of freedom, removal of choice in medical treatment, and the systematic destruction of incentives for research and investment in new medicine. "A right of control over one's body has deep roots in the common law. The venerable commentator on the common law William Blackstone wrote that the right to 'personal security' includes 'a person's legal and uninterrupted enjoyment of his life, his limbs, his body, [and] his health,'...barring a terminally ill patient from use of a potentially life-saving treatment impinges on this right of self-preservation." We are all terminally ill; we are all suffering age-related degeneration that will ultimately kill us. Government obstruction of freedom of medical research must cease if we are to see significant advances in the future of healthy life extension medicine.

Gathering Data on Longevity (May 04 2006)
More studies are underway with the aim of gathering raw data on patterns in the genetics and biochemistry of aging: "An $18 million National Institute on Aging study examining families with longevity patterns gets under way in the next few weeks ... Over the next several years, hundreds of families [with] multiple members alive and functioning in their 80s, 90s or beyond will be interviewed, and have blood samples drawn. ... Given that these individuals pan out to be models of successful aging and have abilities to escape or delay age-related disease, or escape or delay disabilities, we want to find out how they do that ... and we don't believe it's because of any one single factor. ... the interest is not just in those who live a long time, but in those who do so with vigor." A point of contention in the gerontology community is that scientists already know enough to be working towards meaningful anti-aging medicine - not just gathering more data.

No Therapeutic Cloning in Australia (May 03 2006)
A few years ago, stem cell politics in Australia took the turn for the worse that was - and still is - threatened in the US and much of Europe. The Scientist looks at the present state of affairs: "The Australian government has come under pressure this week to respond to proposals that national laws should be amended to allow somatic cell nuclear transfer (SCNT) for research purposes. The changes, recommended late last year by a government-commissioned independent review, would permit therapeutic cloning under strict controls. But scientists fear the government will ignore the advice and decide to keep the current ban." Ultimately, the problem is not politicians - who are only more cruel, venal and callous than you or I because they have brought upon themselves the means and opportunities to be so - but that power has been centralized, ripe for abuse. In whose hands should your future health and longevity lie - yours, or those of bureaucrats who care nothing for your well-being?

More On Parkinson's, Mitochondria (May 03 2006)
From Forbes, a nice follow-on to recent research on mitochodrial DNA damage in parts of the brain associated with Parkinson's, and oxidative stress in Parkinson's: "Our study, using Drosophila [fruit fly] model, revealed that two distinct gene products, Parkin and PINK1, converge in a common pathway in maintaining mitochondrial integrity and function in both muscles and dopamine neurons. This clearly suggests that mitochondrial failure is the central mechanism in the pathogenesis of Parkinson's disease. ... If we can find drugs that can rescue these mitochondrial functions, that would be a much better drug than the current therapies that are targeted on dopamine replacement."

Killing Cancer With Autophagy (May 02 2006)
(From EurekAlert). Cancer researchers are turning out some impressive technological demonstrations these days, building on ten years of rapid advancement in biotechnology. "An engineered virus tracks down and infects the most common and deadly form of brain cancer and then kills tumor cells by forcing them to devour themselves ... The modified adenovirus homed in on malignant glioma cells in mice and induced enough self-cannibalization among the cancer cells - a process called autophagy - to reduce tumor size and extend survival ... This virus uses telomerase, an enzyme found in 80 percent of brain tumors, as a target. Once the virus enters the cell, it needs telomerase to replicate. Normal brain tissue does not have telomerase, so this virus replicates only in cancer cells."

Aging and Group Selection (May 02 2006)
Via ScienceBlog, an argument for aging as an evolutionary adaption rather than a tradeoff: "Aging is taken to be an adaptation, but one that benefits the community, not the individual. This is 'group selection,' and most theorists have been skeptical that evolution can work this way. ... Mitteldorf claims that population crashes constitute an exception to this rule. Animal communities can't afford to go consuming food and reproducing as fast as possible - they would end up starving their own children. This leads to a mechanism of group selection that is swift and ruthless. Aging has evolved as one way to limit population growth. Mitteldorf calls it the 'Demographic Theory of Aging.' It is the first theory to regard aging as an adaptation since August Weismann abandoned his ideas in the 1890's." Given the level of scientific backing for the present consensus view of evolution and aging, Mitteldorf has an uphill road ahead.

Reminder: Singularity Summit at Stanford (May 01 2006)
The Singularity Summit at Stanford will start on May 13th, and seems a worthy use of your time: "What, then, is the [technological] singularity? It's a future period during which the pace of technological change will be so rapid, its impact so deep, that human life will be irreversibly transformed. Although neither utopian or dystopian, this epoch will transform the concepts that we rely on to give meaning to our lives, from our business models to the cycle of human life, including death itself. Understanding the singularity will alter our perspective on the significance of our past and the ramifications for our future." To understand the consequences of exponential growth in the real world is to see the seeds of radical life extension in today's rapidly advancing biotechnology infrastructure, even allowing for plausible limits to the steepness of the upward curve.

Alzheimer's as Feedback Loop (May 01 2006)
Most age-related conditions take place within feedback loops, if only the one in which progressive inability to exercise causes further physical decline. Via EurekAlert, a look at the biochemistry of Alzheimer's in this way: "mitochondria appear to be a site where significant disease progression takes place ... We believe that the disease produces mutant [amyloid precursor protein] and beta amyloid which in turn impacts mitochondrial function. This results in increased production of hydrogen peroxide, resulting in a progression of the disease and higher levels of beta amyloid. In other words -- this model appears to be a vicious cycle where damage to brain cells increases and in fact feeds upon itself." Present Alzheimer's research seems very much a case of blind men and the elephant - but scientists are close to understanding the whole shape of the disease.



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