Longevity Meme Newsletter, June 19 2006

June 19 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.



- Digging Dirt for SENS Research!
- Diving in On Telomere Research
- Discussion
- Latest Healthy Life Extension Headlines


It's that time of year again; flush with new resources, researcher John Schloendorn wants you to send him soil samples from around the world to help advance LysoSENS research. Follow the link below for details:


"When was the last time you really looked down at the ground you walk upon? The soil from your backyard - or the next street over, or a nearby graveyard, or the park across the way - could contain the key to advancing real anti-aging science: bacterial enzymes capable of repairing biochemical damage that accumulates with time and leads to age-related disease."

Researchers in this program - the first Strategies for Engineered Negligible Senescence (SENS) research to be funded through the generosity of Methuselah Foundation donors - are searching for bacterial enzymes capable of safely breaking down harmful biochemical byproducts that build up in our tissue and contribute to a range of age-related diseases.

This is where folk like you and I come in: in order to have the best possible chance of success, Schloendorn needs as diverse a set of soil samples as possible. So get out there and get digging! A big step forward for anti-aging research might be lurking right beneath your feat - but you'll never know unless you send in a sample.

If you would like to financially support LysoSENS research - and I encourage you to do so once you've sent in a soil sample or two - you can donate directly at the MPrize website by following the link below and clicking the "Fund SENS Research" button:



A fair few privately funded groups are presently working on the manipulation of telomeres with the intent to address age-related conditions, or some of the root cause of aging itself:


There seems to be as much of a research impetus here as there is to decode the biochemistry of calorie restriction, but with less of a profile - or perhaps I just haven't been paying enough attention. That's always plausible; far more good science is taking place than any one person can reasonably be expected to follow closely.

The telomere theory of aging is been pretty much shot full of holes in recent years; while shorter telomeres are associated with a high risk of age-related disease (and cancer most of all), lengthening shortened telomeres is most likely not going to provide a blanket extension to healthy longevity:


"This longitudinal study of the elderly and oldest old does not support the hypothesis that telomere length is a predictor for remaining lifespan once age is controlled for. ... This sounds like shorter telomeres are not good, but the sum of all other progressive age-related cellular damage is worse."

The science is still intriguingly uncertain, however. For example, and remembering that about half of all scientific papers are wrong, take a look at some results that contradict half of my commentary above:


The proper attitude is to lean back and enjoy the battle to find the truth - the miracle of the scientific method is that it succeeds in enabling we unreliable humans to sift nuggets of truth from a vast desert of unknown lies. This foaming uncertainty of work in progress means that sink or swim, today's telomere research ventures will contribute positively to our knowledge of the biochemistry of aging. Judging from progress over on the calorie restriction side, we should be expecting tangible results within the next five years.


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/

First Embryonic Stem Cell Therapy (June 18 2006)
After good results in animal studies, researchers are aiming for human trials of an embryonic stem cell (ESC) therapy for spinal injuries. "Via the New Scientist: I'm confident that we will be in the clinic next year with the first human ESC-derived product ... Geron's plan is to treat people that have acute spinal injuries with oligodendrocyte progenitor cells grown from human ESCs. Oligodendrocyte cells support neurons in the brain and spine by sheathing them in myelin, a fat that helps neurons to transmit signals. Spinal 'crush' injuries often cause a loss of myelin, and so destroy the capacity of nerves to transmit signals. Previous experiments carried out by Geron in rats with damaged motor nerves suggested that oligodendrocyte progenitor cells injected into the spine can redress this, helping to restore movement." A thought for the day: if the FDA didn't exist, this therapy would already be in the clinic and at a far lower cost.

Update on Reliance Life Sciences (June 18 2006)
(From DNA India). The Indian group Reliance Life Sciences is a well-backed portion of a large conglomerate, and is forging ahead with stem cell research for regenerative medicine - Indian bureaucrats haven't developed anything as monumentally harmful to progress as the FDA in the US. "RLS also has plans to introduce therapies for cardiac and nerve-related diseases like Alzheimer's and Parkinson's. ... They are under pre-clinical stages and we are awaiting approval for human trials from the department of biotechnology (DBT) ... The efficacy of the therapies for neuro-degenerative diseases like Parkinson's and Alzheimer's has been successfully identified in pre-clinical trials ... The stem cell therapy developed by Reliance for the treatment of cartilage damage associated with osteoarthritis is under research studies and will soon enter the pre-clinical studies."

On Growth Hormone Again (June 17 2006)
Via Yahoo! Sports, a fairly sensible article on growth hormone, the darling of the most disreputable, irresponsible end of the "anti-aging" marketplace. As I usually note when on this topic, growth hormone treatments appear to have legitimate uses for some conditions and injuries. It is certainly not the case that there is anywhere near a gold standard of evidence for general anti-aging use, however - compare the wide-ranging disagreements between possible results, benefits and damage to health resulting from growth hormone studies with the strong agreement and far more impressive results for the practice of calorie restriction, for example. Many organizations have a great deal of money vested in convincing you to buy growth hormone products, whether or not the science is there to back up their claims, and regardless of whether it will help or harm your health. It should always be your choice to try or not, but be appropriately skeptical.

More On Lamin A and "Normal" Aging (June 17 2006)
More on what researchers have learned from studying the biochemistry of progeria can be found at the Journal of Cell Biology: "Aging looks and feels like it is multifactorial: everything falls apart independently. ... [but] multiple hallmarks of cellular aging can be reversed by eliminating one aberrant splicing product of lamin A. The lamins form a structural cage on the interior surface of the nucleus. Lamin A has a long tail that is first farnesylated and then chopped off. In [progeria] an aberrant splicing event creates a lamin A that gets farnesylated but not cleaved. ... normal cells also have a small amount of this aberrant splice product. Although neither the splice product nor its protein product accumulate to higher levels with age, their effects do. As in [progeria] cells, older cells have decreased heterochromatin and other nuclear markers, and increased markers of unrepaired DNA damage. Many of these changes were reversed by an oligonucleotide that eliminated the aberrant splice product."

Towards Liver Regeneration (June 16 2006)
(From the Seattle Times). Researchers are making progress towards regenerative medicine capable of repairing the liver: "the scientists were able to both isolate the liver stem cells and grow them into basic liver and bile-duct cells. ... It's so far the best work on the characterization of stem cells in the human liver. ... UW researchers then maintained the cells in special lab cultures for up to six months, and at various times infused them into mice with about half of their livers destroyed. The immune systems of the mice were suppressed to prevent rejection of the human cells. ... It was a delight when we saw these cells were capable of [partially] repopulating the damaged liver ... we gained tremendous understanding of human embryology, cell origins and how the liver is put together. That kind of knowledge is absolutely crucial for future research." Researchers are making similar progress for many other types of tissue in the body, setting the stage for a blossoming of regenerative medicine for age-related tissue damage in the years ahead.

Making Your Stem Cells Work Harder (June 16 2006)
Research noted at EurekAlert suggests that stem cells could be manipulated into working much harder to produce replacements for damaged tissue. Scientists "have identified an important mechanism that regulates how many new cells are produced by each intestinal stem cell. ... As many serious disorders cause a reduction in the production of new cells, scientists are keen to develop drugs that stimulate the process, which in turn could help the body to cure itself. ... Understanding how cell production is regulated increases our chances of producing drugs able to stimulate the endogenous production of new cells ... He hopes that the new findings can be used to develop drugs that stimulate, for example, the formation of new nerve cells to treat conditions such as stroke and Parkinson's and skin cells to facilitate the healing of wounds."

Better Calorie Restriction Press (June 15 2006)
From NBC11, another reminder that more scientific investigation of the practice of calorie restriction and its health benefits is turning skeptical, ignorant press attention into more educated, supportive press attention. "Studies prove that in animals, calorie restriction works. Monkeys, rodents, even fish sometimes live up to twice as long when they're forced to eat less. The initial human research suggests that even exercise can't compete with cutting calories when it comes to living longer. The calorie cutters in the studies had almost zero heart-attack risk. They had the blood pressure and cholestorol levels of a teenager, even when they were in their 50s." Scientists are still the arbiters of truth in our culture - and rightfully so. We should remember this in our efforts to advocate greater funding for directed anti-aging research: the more science that is funded, the more ammunition flows back to advocates to aid in advancing the debate.

Slow Progress on Nanog, Pluripotency (June 15 2006)
Researchers are making slow but steady progress towards creating pluripotent cells from adult cells - to recapture the regenerative utility of embryonic stem cells on demand. Via Forbes: "Nanog was first identified in 2003. It is a protein that acts in embryonic stem cells [and in the early embryo] to keep cells pluripotent. ... At the moment, it is not yet feasible to turn an adult cell into an embryonic stem cell simply by introducing Nanog ... Many other molecular players are likely to be involved and [there] is still much more work to be done to unravel the whole process of reprogramming [cells] ... Stem cell research is arguably one of the most exciting fields of biomedical research today, but, as with all scientific endeavors, it advances step by step, at times apparently gently, but always surely."

New Approach to Gene Therapy (June 14 2006)
An interesting new approach to gene therapy is outlined at the New Scientist: "Take an artificial chromosome containing the gene to correct a serious disease, put it in a stem cell, and transplant into the body. That is the future of gene therapy, according to Mitsuo Oshimura of Tottori University in Japan. Oshimura's team has now proved that the concept works by correcting a genetic defect in mouse stem cells." A diversity of approaches to engineering our DNA is a good thing: greater diversity leads to faster, greater success. The road that starts with correcting single gene defects leads to technologies capable of repairing all the random age-related damage to our DNA - restoring our genomes to pristine condition and turning back the clock on one of the root causes of degenerative aging.

Alzheimer's and Calorie Restriction (June 14 2006)
(Via Newswise). Most research funding is tied to repairing specific diseases or the end-stage results of accumulated cellular damage that we call disease. There's money - and greater effectiveness - in prevention, but inefficiency is the way that the present over-regulated medical system leans. So we see a lot of "forest for the trees" research, such as this study. It is clearly a step on the way to pushing calorie restriction (CR) mimetics as a therapy for end stage Alzheimer's disease (AD) - rather than, say, the practice of CR as one of the best preventative measures you could be employing to avoid Alzheimer's. From the article: "caloric restriction through promotion of SIRT1 (a molecule associated with brain longevity) may initiate a cascade of events like the activation of alpha-secretase which can prevent AD amyloid neuropathology. ... the study demonstrates a mechanism by which dietary caloric restriction might benefit AD."

More on Long Term CR in Monkeys (June 13 2006)
A long-running study on calorie restriction and healthy longevity in rhesus monkeys has been funded out to 2011: "The idea that fewer calories can extend lifespan and improve health has a long experimental history. ... rhesus macaques in the Wisconsin study [offer] perhaps the best window into a phenomenon that is the only proven dietary way to extend lifespan. ... The animals on a restricted diet exhibit 70 percent less body fat, and the fat tissue itself [is] very different from the fat tissue in the control animals, those allowed to eat freely. His group has also observed that the animals that eat less have less insulin in their bloodstreams and less insulin resistance ... So far, we've had complete protection from type 2 diabetes. Normally, 30 percent of the animals in a research colony will exhibit type 2 diabetes. ... 90 percent of the animals who began the study on a reduced diet are still alive, while only 70 percent of the animals allowed to eat freely have survived to this stage."

On DNA Repair Mechanisms (June 13 2006)
PLoS Biology has published an introduction to DNA repair mechanisms and some of their implications. A portion of degenerative aging - not to mention cancer - is caused by a buildup of DNA damage. This is a problem that must be solved along the way to working healthy life extension medicine: "You probably weren't thinking about your body's DNA repair systems the last time you sat on the beach in the bright sunshine. Fortunately, however, while you were subjecting your DNA to the harmful effects of ultraviolet (UV) light, your cells were busy repairing the damage. The idea that our genetic material could be damaged by the sun was not appreciated in the early days of molecular biology ... it was assumed that DNA is fundamentally stable since it carries the blueprint of life. However, more than 50 years of research have revealed that our DNA is under constant assault by sunlight, oxygen, radiation, various chemicals, and even our own cellular processes."

The Long Life Family Study (June 12 2006)
The LEF News reprints a piece on the Long Life Family Study, soon to start and seeking participants: "Over the next several years, hundreds of families from Pittsburgh, Boston, New York and Denmark with multiple members alive and functioning in their 80s, 90s or beyond will be interviewed and have blood samples drawn. Researchers say it may be the most extensive aging study yet, with hopes of uncovering not a fountain of youth, but a sea of information on what contributes to healthy aging. ... 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." Successful aging is something of a contradiction in terms, but these studies serve a useful purpose: it is still more efficient to find starting points for biochemical investigations into longevity and metabolism this way.

Towards Controlled Stem Cells (June 12 2006)
From Scientific American, news of another step towards the control - and possibly creation - of embryonic stem cells: scientists used short hairpin RNA (shRNA) "to sequentially turn on and off various genes within embryonic stem cells from a mouse. The shRNA, delivered by a virus, allowed the researchers to determine whether a given gene helped control stem cell differentiation. ... the scientists found 10 likely candidates [and] engineered versions of these genes that could be turned on and off by the presence of the drug doxycycline to uncover their specific effects. Seven of the identified genes proved to be potent regulators of a stem cell's ability to split and then renew itself. Without them, the cell rapidly became specialized, losing its unique pluripotent status."



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