Longevity Meme Newsletter, June 05 2006

June 05 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 MPrize Hits $3.5 Million
- Rank 300 For the Folding@Home Team
- Discussion
- Latest Healthy Life Extension Headlines


Good news from the Methuselah Foundation: the addition of the 92nd member of The Three Hundred has pushed the grand total of cash and pledges in the prize fund just past $3.5 million. That's not even counting more than $500,000 in additional donations to Foundation expenses and LysoSENS research.


This progress is good news for all of us who believe in taking action to build a better future - one that includes working anti-aging medicine, and excludes age-related disease, frailty and suffering. With each additional dollar, the MPrize and Methuselah Foundation become more empowered to sway public opinion and research plans, and enhance the legitimacy of the fight to cure aging.

The perception of legitimacy is the root of large-scale funding for any scientific endeavor. We must never forget that the biggest task ahead is the creation of a research infrastructure and scientific community to rival cancer research in size and determination. The first steps are barely being taken:


So much more has yet to be accomplished if we are to defeat age-related degeneration.


If you can't bring yourself to donate to the MPrize for anti-aging research, you should at the very least take the few minutes necessary to donate the time your computer sits idle to advancing medical research: the Folding@Home project makes that easy.


The members of the Longevity Meme folding team have worked their way up to rank 300 - and there will be mementos to pass around when we hit rank 200. So join up and help out!



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/

Update on Myostatin Gene Therapy (June 04 2006)
It wasn't all that long ago that scientists linked myostatin to muscle growth, and started to think about therapies for age-related muscle loss and injuries. Here, more news on that research via EurekAlert: "researchers injected mice with a gene therapy vector containing myostatin propeptide - a protein that blocks the activity of the muscle-growth inhibitor myostatin - three weeks prior to experimentally damaging the mice's skeletal muscles. Four weeks after skeletal muscle injury, the investigators observed an enhancement of muscle regeneration in the gene-therapy treated mice compared to the non-gene-therapy treated control mice. There also was significantly less fibrous scar tissue in the skeletal muscle of the gene-therapy treated mice compared to the control mice. ... we expect that gene-therapy treated cells will continue to overproduce myostatin propeptide for at least two years."

On Premature Cellular Senescence (June 04 2006)
How much of degenerative aging is due to the acculumation of senescent, no longer functioning cells? More in some tissues than others, such as skin, it seems. "Cellular senescence is considered an essential contributor to the aging process and has been shown to be an important tumor suppression mechanism. In addition, emerging evidence suggests that senescence may also be involved in the pathogenesis of stem cell dysfunction and chronic human diseases. Under these circumstances cells undergo stress-induced premature senescence, which has several specific features." As this review paper points out, developing a technology to turn off programmed senescence would simply result in much more cancer - the process serves an important purpose in shutting down potentially dangerous cells. The problem needs a better solution, more likely focused on convincing the body to recycle these cells rather than leaving them to degrade the performance of tissue.

The Life Lost to Excess Fat (June 03 2006)
The Life Extension Foundation News quantifies the life - and health - lost to even a modest amount of excess fat: "Simply put, overweight people die younger. On average, they lose as many years to their excess weight as smokers lose to their cigarettes. It stands to reason, doesn't it? With all the health problems that we know are caused or worsened by excess weight, it is to be expected that those who carry an excess would die sooner than those who don't. ... Dutch researchers studying Americans found that there's a lot to lose for those who don't lose their extra pounds. ... Among those subjects who were overweight but not actually obese, the study showed that 40-year-old female nonsmokers lost 3.3 years of life due to their excess weight. In this weight class, the 40- year-old male nonsmokers lost 3.1 years of life expectancy." This is in addition to the life lost because you are not practicing calorie restriction, and the costs of suffering age-related disease - it all adds up, and could be avoided.

Viral Gene Therapy Squashes Cancer (June 03 2006)
Impressive progress is being made with gene therapies in the laboratory, as demonstrated by this item from EurekAlert: "researchers have used gene therapy to either completely abolish or significantly inhibit tumor progression in a mouse model of ovarian cancer ... They treated some of the mice immediately with a genetically engineered vaccinia virus containing a gene coding cytosine deaminase, a suicide gene, and delayed treatment of other mice for 30 or 60 days. ... The researchers found complete inhibition of tumor growth in the mice that were treated immediately with gene therapy and significant tumor inhibition in the 30- and 60-day delayed treatment mice." Scientists can now target abnormal cells with great specificity based on their biochemistry, but the real economic barrier for this sort of treatment is the enormous variety in that biochemistry for cancer cells.

Never Too Late For Exercise (June 02 2006)
EurekAlert delivers another pointed reminder of the necessity of exercise for healthy longevity. Calorie restriction may be strictly better, but you're only hurting yourself by not keeping up with the exercise: "Continuing to lead an inactive lifestyle leads to a gradual decline in many important markers for cardiovascular health. ... The good news is that a small amount of physical activity can make a big difference in reducing the risks for developing such conditions as heart disease, stroke or diabetes. Our findings demonstrate that while the cost of choosing a sedentary lifestyle can be high, switching to an active way of life can be beneficial at any time." You only have the one shot at living healthily into the era of meaningful anti-aging medicine - why risk missing out on a long, exciting future by failing to keep up with the health basics today?

On Hormesis and Healthy Longevity (June 02 2006)
Via the Life Extension Foundation News, a short article on hormesis and its effects on our health and longevity. As for so many complex aspects of our environment and biochemistry, researchers presently know too little to offer specific recommendations: "Small doses of 'stressors' normally considered dangerous to health can actually boost the body's self-repair system, and as a side-effect preserve youth, experts believe. ... In recent years, it has been shown to extend lifespan in yeast, fruit flies, worms and rodents. If the results of such studies also apply to people, it means hormesis could extend average human lifespan to 90. Average lifespans in the UK are now around 75 for men and 80 for women. Stressors seem to kick-start natural repair mechanisms, including the enzymes that patch up damaged DNA. As the repair systems fix damage normally caused by ageing, the body is rejuvenated. ... Exercise and calorie restriction may both promote longevity partly through the stress they cause."

Exploring the Cancer-Aging Link (June 01 2006)
EurekAlert shows one of many ongoing investigations into the biochemical roots of the relationship between aging and cancer: "Proteins which prevent cancer in humans by ensuring that cells don't divide if they have chromosomal damage have been shown to determine lifespan in the nematode worm C. elegans. ... checkpoint proteins, traditionally thought only to be functional in cells that divide, are also active in cells that no longer divide. The fact that the proteins appear to have dual functions opens a new way to study the connection between aging and cancer.
... variations in checkpoint proteins in humans may place some individuals at risk for cancer, but protect them against other age-associated diseases; or conversely, set a genetic course for a shorter life which would be free from cancer. ... We think there are many more checkpoint proteins - in worms, in complex animals, in humans. Some may be more attractive than others for developing therapies for cancer and aging."

35th AGE Annual Meeting Starts (June 01 2006)
As Kevin Perrott notes, the 35th American Aging Association (AGE) annual meeting gets underway tomorrow. "The broad theme selected for the AGE 2006 meeting is Interventions in Aging and Age-related Diseases: The Present and the Future. ... The first day is comparison of caloric restriction (CR) in model organisms which I think will be a very helpful in integrating what is known about CR into a more coherent picture of what it might mean for its effectiveness in humans. There are more than a couple of Mprize researchers making presentations so it should be particularly interesting. Day two is focusing on the role of mitochondria in aging and the mechanisms behind sarcopenia and osteoporosis. Day three continues in the same fashion of discussing the physiological basis for aging syndromes of the skin and immune system. ... All in all another busy weekend of information sharing and some great opportunities to talk with some of the major players in aging research today."

State of Werner Syndrome Research (May 31 2006)
Accelerated aging conditions are teaching us more about the biochemistry of normal aging; progeria is yielding its secrets, and Werner syndrome will most likely soon be next: "If WRN function is lost (as exemplified in cells from Werner patients), problems with replication and DNA damage processing arise, probably resulting in an increased number or persistence of strand breaks. In turn, these events lead to chromosomal and telomeric abnormalities or activate checkpoints that bring about early senescence or increased apoptosis. Thus, elevated cancer incidence associated with Werner syndrome is due to increased chromosomal changes, while the accelerated aging characteristics probably stem from telomere dysfunction leading to accumulation of non-functional senescent cells or excessive apoptotic cell death over time. More research is needed to determine whether these specific DNA-dependent mechanisms contribute to development of aging characteristics in normal individuals."

Better Than Exercise (May 31 2006)
Another take on recent human calorie restriction (CR) research arrives via EurekAlert: "both calorie restriction and endurance exercise protect [mice and rats] against many chronic diseases including obesity, diabetes, cardiovascular disease and some types of cancer. However, the research has shown that only CR increases the animals' maximum lifespan by up to 50 percent. These animal studies suggest that leanness is a key factor in the prevention of age-associated disease, but reducing caloric intake is needed to slow down aging. ... [this human study] suggests that CR has some specific anti-aging effects that are due to lower energy intake, rather than to leanness ... Primary aging determines maximal length of life. Secondary aging, on the other hand, refers to diseases that can keep a person or an animal from reaching that expected lifespan. ... By slowing primary aging, CR may increase maximal lifespan." But don't skip the exercise - add both exercise and CR to your lifestyle and reap the benefits.

A Switch For Blood Vessel Growth (May 30 2006)
Better control over the growth of blood vessels, or angiogenesis, is required for continued progress in tissue engineering. It could be a novel avenue for regenerative medicine. Reversing blood vessel growth will be most useful in fighting the growth of cancer in the body. Here, Medical News Today reports on progress towards that control: scientists have discovered "a switch inside blood vessel cells that controls angiogenesis ... Angiogenesis is an important natural process that can be both good and bad for the body. It restores blood flow after injury [and] increases circulation in a damaged heart. But, it can also nourish cancer tumors and damage delicate retinal tissues when uncontrolled. ... Understanding this process opens a whole new avenue for treatment of angiogenesis-related diseases. For instance, drugs could be designed to decrease [a switching enzyme] in cancer patients or those with proliferative diabetic retinopathy or macular degeneration, or designed to increase it in a damaged heart."

Stem Cells Inside the Heart (May 30 2006)
(From the New Scientist). Present first generation stem cell therapies for heart damage involve obtaining stem cells from elsewhere and introducing them to damaged heart tissue. As it turns out, there is an existing population of heart stem cells that might be used instead: "Leri and her colleagues have now removed tiny numbers of cardiac stem cells from people undergoing heart operations, grown them in the lab and then transplanted them into the damaged hearts of rats and mice. The results are promising, says Leri, and may eventually give better heart-healing results than bone-marrow derived stem cells. ... We think that these are the cells that normally provide new heart tissue and will most likely be better suited for repair of diseased hearts." Scientists have been finding stem cell populations throughout the body in past years - this will hopefully speed the maturation of early regenerative therapies.

Indian Stem Cell Heart Therapies (May 29 2006)
Express Pharma examines the present state of first generation stem cell therapies in India: "Hurkisondas hospital, under the guidance of Shah has treated seven to eight patients with stem cells so far ... Four patients have been re-studied after a period of six months and we have found that their cardiac indices have improved ... Stem Cell Research centre located at Manipal Hospital is actively involved in stem cell research and currently focussing on both adult and embryonic stem cells. Currently, Phase I clinical trial for safety and efficacy studies of bone marrow derived mesenchymal stem cells is going on [for] myocardial infarction ... [the All India Institute of Medical Sciences] too has conducted a study on 35 cardiac patients, who have been injected with stem cells and have been monitored at six, 12 and 18 month intervals. ... Six months later, 56 percent of the dead muscle area injected with these cells had shown improvement. After eighteen months, this went up to 64 percent."

A Look At Korean Public Funding (May 29 2006)
Via The Korea Times, an update on public funding for stem cell research in South Korea for those who like to keep up with such things: "The Korean government Monday set up a plan to channel roughly 430 billion won ($454 million) of taxpayers' money into stem cell research over the next decade. ... The big budget earmarked for the stem cell sector will be spent both on adult and embryonic stem cells ... Included in specifically targeted areas are a study of the stem cell's differentiation mechanism, establishment of a clinical test database and a system to set up stem cell banks." This compares in size and timeline to existing and proposed state funded programs in the US - and will no doubt be just as inefficient as every other government program, sad to say.



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