Longevity Meme Newsletter, August 07 2006

August 07 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.



- The Longevity Dividend is on the Move
- On Compression of Morbidity
- Discussion
- Latest Healthy Life Extension Headlines


The big-tent Longevity Dividend initiative of scientists and advocates S. Jay Olshansky, Daniel Perry (of the Alliance for Aging Research), Richard A. Miller, and Robert N. Butler (of the International Longevity Center) is moving forward. You can read more at the following Fight Aging! post:


"We suggest that even a relatively small deceleration in the rate of aging would yield the equivalent of simultaneous major breakthroughs involving every major fatal and non-fatal disease and disorder associated with aging. As a way to follow through with our recommendation, we are planning an event on Capitol Hill on September 12, 2006. At this event there will be U.S. Senators from both sides of the aisle, Nobel Laureates, representatives of national and international health organizations, and scientists - all of whom will be advocating an investment in the pursuit of the Longevity Dividend."

Olshansky et al are presently seeking endorsements from the scientific and health advocacy communities. As I'm sure long time readers will recall, I have my issues with anything involving politics and taxed funds, as well as with the scope and detail of the Longevity Dividend's scientific side:


But you make your own minds up; these folk are set on their course, and a rising tide tends to raise all boats. All in all, I'd rather have them advocating the plausibility of very moderate healthy life extension than remaining silent on the topic. Mainstream gerontology is being forced - by advocacy, by the results of the latest research - to move with the times, and this should be cause for celebration. It illustrates to all who care to listen that the scientific debate is now "how much more healthy life, and how soon."

Via the Methuselah Foundation blog, we have these words from chairman Aubrey de Grey:


"I'm very strongly in support of the Longevity Dividend initiative. I'm especially pleased that, in the consensus document that the original authors are now circulating for expert endorsements, there is no repetition of the dismissal of SENS that appeared in the original paper in The Scientist. Another important improvement is the diminished emphasis on the idea that compression of morbidity is a plausible consequence of progress in gerontology research, a stance that I believe is on balance not supported at all by available data. All in all this initiative is as big-tent as can be. If anyone can pull this off, these people can."


Researchers who aim at a compression of morbidity are seeking to reduce or even eliminate late life frailty, disease and incapacity - but with no expectation of extending healthy life span. The benefits of medical science would then translate into nothing more than a shorter time of incapacity before death; a great improvement over the present day, but very disappointing to supporters healthy life extension!

Fortunately, the framing principles of the reliability theory of aging and longevity, amongst other work, would seem to suggest that compression of morbidity is impossible. In other words, any successful efforts to alleviate age-related suffering will also extend healthy life span.


In this viewpoint, all manifestations of aging - disease, frailty, degeneration and death - are the results of accumulated damage. Our bodies are complex machines, and all the normal intuitions regarding machinery and slowly accumulated damage apply here too. The best way to prevent age-related degeneration is to prevent or repair that damage, but this will also extend healthy life span. You can't have one without the other, and a good thing too! For a layman's explanation of the science behind this view, you should peruse the Strategies for Engineered Negligible Senescence (SENS) website:


A final argument against the view of compression of morbidity is to simply take it to its logical extreme, to compress infirmity down to zero. How could one completely eliminate age-related frailty, disease and degeneration with no extension of life span? What exactly would people be dying of?


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/

Funding For Synthetic Biology (August 06 2006)
As this release shows, the field of synthetic biology has found its feet; the level of recognition, support, collaboration and ongoing work has risen to the level at which centers are being founded. "Funded by a five-year, $16 million dollar grant from the National Science Foundation (NSF), the Synthetic Biology Engineering Research Center, or SynBERC, is gathering pioneers in the field of synthetic biology from around the United States ... Synthetic biology is the design and construction of new biological entities such as enzymes, genetic circuits and cells, or the redesign of existing biological systems. The field builds upon advances in molecular, cell and systems biology and seeks to transform biology in the same way that synthesis transformed chemistry and that integrated circuit design transformed computing." To me, the significance of this field lies in the new capabilities that could be directed to repair age-related cellular damage in our existing biology. Protofection - replacement of age-damaged mitochondria - is an early example of this sort of capability. We'll be seeing much more in the years ahead.

An Introduction to p53, Cancer and Aging (August 06 2006)
A long article from the Times Online looks one present focus of modern cancer and aging research: "The [p53] gene keeps cancer at bay, and scientists are racing to find a wonder drug to harness its power. If they get it right, we'll live longer, healthier, cancer-free lives. ... [aging and cancer are] two sides of the same coin, sharing a common mechanism in which the scales can be tipped either way. In other words, that wrinkled skin, thinning bones and failing organs may be the price we pay in the long run for holding cancer at bay. ... The clinical implications are clear. People are beginning to ask, 'Can I manipulate the system to get the best of both worlds?' ... Drugs to manipulate the p53 system to protect against cancer and slow down ageing at the same time are even further over the horizon, but scientists working to understand this relationship are making some sensational discoveries."

Longevity, Evolution, Mitochondria (August 05 2006)
Good basic science in this paper, relating biochemistry, evolution and mechanisms for longevity: "The amino acids sequences of the mitochondrial DNA-coded peptides of placental mammals evolved at different rates in different branches of the mammalian phylogenetic tree. ... Mitochondria generate reactive oxygen species (ROS) that appear to constrain the life span of many species. Therefore, I tested the hypothesis that the evolution of mammalian longevity drives the accelerated evolution of mitochondrial DNA-coded peptides. ... It is suggested that, in mammals, adaptive selection of mutations that decrease the rate of production of reactive oxygen species, [directly or indirectly], increases longevity." Longevity need not be selected for directly. Reliability theory suggests that gains in health and function during youth selected for in this manner will incidentally lead to increased longevity - less oxidative damage leads to a longer life. You can learn more about evolutionary theories of aging and longevity at Fight Aging!

Understanding Embryonic Stem Cells (August 05 2006)
EurekAlert! reports on an important advance in understanding just what makes an embryonic stem cell an embryonic stem cell: scientists "have found that the DNA of human embryonic stem cells is chemically modified in a characteristic, predictable pattern. This pattern distinguishes human embryonic stem cells from normal adult cells and cell lines, including cancer cells. ... Our results suggest that therapeutic cloning of patient-specific human embryonic stem cells will be an enormous challenge, as nuclei from adult cells will have to be epigenetically reprogrammed to reflect the specific DNA methylation signature of normal human embryonic stem cells. This reinforces the need for basic research directed at understanding the fundamental biology of human embryonic stem cells before therapeutic uses can be considered." Informed commentary on the difficulty of creating embryonic stem cells from adult cells is a big step up from not knowing how to do the job.

Progress in Cancer Vaccine Research (August 04 2006)
From EurekAlert!, a long overview of recent advances towards cancer vaccines: "for the first time, the prospect of eradicating a specific cancer through vaccination is possible. ... researchers are working on the next era of vaccines designed to treat cancer that has already developed. These vaccines don't rev up the human immune system to attack an invading microbe, but prime the system to go after a unique biological tag found only on tumor cells. ... Hypothetically, once the immune system has been sufficiently stimulated, it would be able to find and destroy every single tumor cell throughout the body ... It could do this without destroying healthy tissue. That's the goal we strive every day for. ... This is an exciting time in cancer research, given our increased understanding of the molecular nature of cancer and the immune response." The defeat of cancer is a very necessary step on the road to radical life extension.

On Zebrafish Regeneration (August 04 2006)
From PLoS Biology, research into the regenerative capabilities of zebrafish: "Injured mammalian hearts cannot regenerate; instead, they scar. ... By contrast with mammals, newt and zebrafish hearts regenerate after amputation. The molecular mechanisms underlying this phenomenon have not been characterized in newts because of a lack of genetic tools. Recently, we and others showed that zebrafish fully regenerate myocardium after 20% [amputation of the ventricle]. ... zebrafish hearts regenerate by cardiomyocyte proliferation, whereas fin regeneration involves the formation of a blastema, a mass of proliferative, pluripotent progenitor cells ... we hope to elucidate the molecular mechanisms underlying heart regeneration in lower vertebrates. We have identified genes that serve as regulators during heart regeneration ... these genes represent promising candidates for future therapeutic approaches in regenerative medicine."

How To Improve An Immune System (August 03 2006)
Research into the nuts and bolts of the human immune system shows that increased understanding of any process can lead to potential improvements: "researchers followed T cells as they spent time in the thymus then moved to the body. ... regulatory T cells learn what to protect while in the thymus and that everything the cells learn may not be good
... The findings mean, essentially from the beginning, some people may have regulatory T cells less skilled at keeping the immune system from attacking their bodies and/or too skilled at protecting invaders. It also means one day physicians might steer early education of regulatory T cells in the thymus as a way to vaccinate children against diseases such as lupus, arthritis and type 1 diabetes. Or, they might add regulatory T cells to improve the mix in people who already have some bad [cells]." Your immune system becomes less effective with age due to a bad mix of T cells - strategies of this nature may work to rejuvenate the aging immune response.

To Add Decades to Our Life Spans (August 03 2006)
As a follow up to the wisdom of actuaries on the near future of healthy life expectancy, Reuters sent a reporter to chat with biomedical gerontologist Aubrey de Grey: "Ultra-long lifespans are so far the stuff of science fiction, [but] it is no longer just a dream that people may live decades longer than they do now, de Grey said. The gerontologist said that while some people are skeptical, or even hostile, to the idea that the average lifespan will lengthen, scientific advances are likely to make this a reality. As a result, lifestyles will change. ... decades-longer lives may change traditional patterns of family life, careers, retirement, education and child-raising and force radical changes to pensions. ... These are things that people with expertise with financial planning need to take on board now." Not to mention the rest of us as well - don't expect other people to look after your future health and financial stability. It's up to you to craft the best possible future for yourself.

Examples of Aging Research in Rats (August 02 2006)
Via Ouroboros, an example of the impressive rate at which scientists are producing papers on the biomechanisms of aging in rodent species. "calorie restriction preserves the oxidative capacity, though not the levels of respiratory proteins, in skeletal muscle mitochondria. Dietary restriction was also found to delay the increase of T-kininogen, an immune suppressant previously reported to be a biomarker of aging in the rat, as well as the age-related loss of muscle mass termed sarcopenia ... the protein profile of [sarcopenia is] distinct from that of acute injury-induced muscle atrophy. In other words, in muscle at least, we can begin to distinguish between aging per se and simple 'wear and tear' via a molecular measurement."

The Actuaries Know (August 02 2006)
(From the Times Online). Of all the people in the world, actuaries have the greatest immediate financial incentive to truly understand the likely future progression of healthy life extension medicine. Vast sums are at stake, which is why archly conservative actuarial culture is actually not too far behind the leading edge of mainstream science in terms of futurism. "For more than 80 years the Continuous Mortality Investigation (CMI) has supplied mortality tables that showed how lifespans were lengthening and how they might continue to improve. Yesterday, the CMI acknowledged after the release of its latest set of tables that there was so much room for error it was no longer sensible to offer a single set of predictions. It said that projections of future mortality had not been done with the latest tables 'because of the uncertainty surrounding future improvements.'" Recent actuarial conference presentations make for interesting reading.

Timelines For Regenerative Therapies (August 01 2006)
The common wisdom on widespread availability of stem cell based regenerative therapies for age-damage tissue is repeated in this CNN article: "stem cell therapies for degenerative disorders afflicting major organs such as the heart and liver could be available within 10 years. ... What we're going to see is one or two patients being helped in some way and people are going to hail it as the end of Parkinson's and Alzheimer's. But it's going to be a slow process. We hear an awful lot of hype about what stem cells can do but in reality there's still a lot of work to do ... the pace of progress would depend on increasing the number of suitable cells made available to scientists - and warned that a great deal of 'fundamental research' still had to be done before stem cell applications were ready for clinical trial." The first of the first generation autologous and transplant stem cell therapies are moving ahead successfully today, but sophistication, reliability and better economics take time.

On Inflammation and Disease (August 01 2006)
Via Scenta, a popular science piece on the bugbear of chronic inflammation: "When an infection occurs, immune cells flock to the area and secrete large amounts of highly reactive chemicals to combat the invader. But these inflammatory chemicals also attack normal tissue surrounding the infection and damage critical components of cells, including DNA. During chronic inflammation, the damage may lead to mutations or cell death and even to cancer and other diseases. [Researchers] have discovered that the DNA damage produced by one of these inflammatory chemicals, nitrosoperoxycarbonate, occurs at unexpected locations along the DNA helix. The finding counters the prevailing theory about where the DNA damage occurs and may shed light on new ways to diagnose and combat inflammation ... We need to understand the mechanisms of inflammation in order to make new drugs that will break the link between inflammation and disease and to develop predictive biomarkers."

Vav and Alzheimer's Mechanisms (July 31 2006)
Via Medical News Today, a great example of the degree to which researchers are unravelling the biochemical mechanisms of Alzheimer's disease (AD): "Oxidative damage has long been suspected as playing an early critical role in AD. Because the events that trigger the beginnings of AD are still unknown, [researchers] began targeting research on the reaction between the [amyloid beta] plaque and immune cells. ... researchers found that the microglia had the appropriate immune response that the plaque was harmful, but then the protein Vav was found to be a component in oxidative damage since elimination of the protein resulted in reduced free radical production. ... by understanding this biological component in the disease process, it holds the potential to 'push back the severity of the disease.'" Other groups have shown that even excessive amyloid can be prevented from causing neurodegeneration - perhaps there's an effective therapy to be made from breaking the chain from amyloid to oxidative stress to neural cell death.

To Rapidly Build a Kidney (July 31 2006)
This press release from Yahoo! News notes an ongoing research program aimed at the rapid tissue engineering of whole kidneys from a patient's own cells: "Using principles of 'tissue self-assembly' (cells coming together to form actual tissues such as a kidney, heart, lung etc.) and stem cell research, scientists involved with the MUSC Bioengineered Kidney Project are testing the possibility of creating a new kidney from a patient's cells. ... While other researchers are trying to grow kidney tissues slowly, the essence of [this technological approach] is rapid directed tissue self-assembly, which is based on exploration of the tissue fusion phenomenon." This program has been running for a while - we'll see what comes of it. Reading between the lines, this release something of a positioning piece for funding; nothing wrong with that, and it is helpful to see intent and goals as they are expressed in the field, but don't mistake it for actual results.



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