Longevity Meme Newsletter, July 09 2007

July 09 2007

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.



- Fifth Annual Calorie Restriction Society Conference
- Seeking Longevity For All, the Human Thing To Do
- Discussion
- Latest Healthy Life Extension Headlines


For a good example of how to engage and assist the scientific community in advancing your cause, look no further than the Calorie Restriction Society. The annual conferences are replete with the scientists and science of calorie restriction research, mingling with those who practice calorie restriction (with optimal nutrition, of course) for its demonstrated health benefits and possible longevity benefits in humans. The conference this year will be held in November, in San Antonio, Texas:


"The fifth CR Society Conference (CR V) will be held in San Antonio Texas, November 7-11, 2007. The current roster of participating scientists includes Steven Austad, Rochelle Buffenstein, John Holloszy, Jim Nelson, Jay Phelan, Arlan Richardson, Walter Ward, and Bradley Willcox. We also will include presentations by members of the Society."

If you want to learn more about the CR Society and ongoing scientific research into the biochemistry of calorie restriction induced longevity in mammals, you might start with the many video presentations from the last annual conference:



To seek to provide the choice of healthy longevity for all who want it is an aspect of the better side of human nature:


"Helping to make life longer and better, one action at a time, is a core human ideal. There are no special cases, no magical transition point at which it's fine and dandy to write people off or justify their deaths. Healthy life extension flows quite naturally from the same mindset that helps neighbors and appreciates modern medicine. We all recognize that which is unpleasant in commonplace life, and it's only natural to work to remove that unpleasantness. ... Seeking equality of opportunity by helping people to overcome the limitations of their own personal human condition is a worthy goal today, and will be just as much so in a future of far greater opportunity. The foundation of opportunity is life - is being alive, and possessed of the vigor to take advantage of that fact. Without that, there is nothing. So I think we really have to start there, with aging, a great injustice blindly inflicted upon humanity by chance, physics and evolution. To not seek the cure for aging would be just as strange as to fail to seek a cure for cancer or Alzheimer's - it would be inhuman and unnatural for the species that helps its neighbors and appreciates the good things in life."


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/

Why Can't We Regenerate? (July 06 2007)
A video presentation from the TED conference back in 2006 has been doing the rounds over the past couple of days; it's worth your time, for all of being dated. "Alan Russellis a professor of surgery -- and of chemical engineering. In crossing the two fields, he is expanding our palette of treatments for disease, injury and congenital defects. We can treat symptoms, he says, or we can replace our damaged parts with bioengineered tissue. As he puts it: 'If newts can regenerate a lost limb, why can't we?' ... [he] leads an ambitious biomedicine program that explores tissue engineering, stem cell research, biosurgery and artificial and biohybrid organs. [He] studies regenerative medicine, a breakthrough way of treating disease and injury by helping the body to rebuild itself. He shows how engineered tissue that 'speaks the body's language' has helped a man regrow his lost fingertip, how stem cells can rebuild damaged heart muscle, and how cell therapy can regenerate the skin of burned soldiers. This new medicine comes just in time, Russell says -- our aging population, with its steeply rising medical bills, will otherwise (and soon) cause a crisis in health care systems around the world." That crisis has far more to do with socialism than aging - only under a socialist system can a greater need and greater ability to meet that need be turned into a disaster - but advancing medicine brings great benefits for those free enough to research and use it.

Critiquing WILT (July 06 2007)
Randall Parker notes one possible critique of WILT, Whole-body Interdiction of Lengthening of Telomeres as a strategy to eliminate cancer: "with a new report about telomerase enzyme [that] proposal seems problematic. According to this new result telomerase does not just lengthen the caps on the ends of chromosomes. ... If telomerase is keeping chromosomes stable then taking away telomerase could cause more things to go wrong sooner. I've never been enthusiastic about WILT because we need a cure for cancer for all our cells that do not already have telomerase knocked out in them. We have lots of cells all over our bodies that are getting older and at greater risk of becoming cancerous. Short of replacing our entire bodies WILT will not eliminate the risk of death from cancer. Fortunately, I expect cancers will become very curable. We'll develop immuno-therapies, gene therapies, cell therapies, and even nanobots that will seek out and selectively kill cancer cells." WILT is probably the least favorite part of present day SENS amongst those who support SENS; this is not an uncommon opinion. That is surprising in many ways, as WILT is no more ambitious than other SENS projects like allotopic expression of mitochondrial DNA.

The Damage Underlying Parkinson's (July 05 2007)
From EurekAlert!: "In the vast majority of Parkinson's disease (PD) patients, the disorder arises not because of a genetic defect, but because some external insult triggers the death of dopamine-producing neurons. Now, researchers have reported progress in understanding the mechanism underlying that death ... a cellular switch called Cdk5 [regulates] yet another enzyme called Prx2. This enzyme [acts] to render harmless the chemically active reactive oxygen species that are produced inside mitochondria ... the loss of Prx2 activity also plays a role in human PD. They found reduced Prx2 activity in brain tissue from PD patients. ... our findings suggest that strategies to modulate Prx2 activity serve as beneficial targets for treatment of PD. This is of particular importance since Cdk5 is thought to have normal beneficial roles in neurons and modulating a relevant downstream target rather than Cdk5 directly may be a better therapeutic strategy with regard to this pathway." Interesting - recall that targeting antioxidants to the mitochondria extends life in mice, and recall the important role played by mitochondrial free radicals and reactive oxygen species in aging. More potential here than just a Parkinson's therapy, perhaps.

A Snapshot of Progress In Engineered Blood Vessels (July 05 2007)
Scientists are striving to construct complex tissue from scratch, for use in transplants for damaged or age-worn organs: "The research demonstrates the potential for eventually growing tissue-engineered vessels out of stem cells harvested from the patients who need them, providing a desirable alternative to the venous grafts now routinely done in patients undergoing coronary bypass operations. ... Although not yet strong enough for coronary applications, the UB group's tissue-engineered vessels (TEVs) performed similarly to native tissue in critical ways, including their morphology, their expression of several smooth muscle cell proteins, the ability to proliferate and the ability to contract in response to vasoconstrictors, one of the most important properties of blood vessels. The TEVs also produced both collagen and elastin, which give connective tissue their strength and elasticity and are critical to the functioning of artificial blood vessels. ... The TEVs were implanted into sheep and functioned normally for five weeks."

Some Aging Processes More Equal Than Others? (July 04 2007)
In response to a de Grey paper on aging, DNA damage and cancer I recently noted, Khrapko puts forward a different position: "In his pleasantly provocative opinion paper, Aubrey de Grey argues that (a) independent age-related deteriorative processes evolve to reach approximately equal importance for the aging process as a whole, but (b) this equality can be broken by 'protagonistic pleiotropies', i.e. when a process is contributing to more than one competing death causes. In particular, the fact that nDNA mutations are extremely efficient in killing by inducing cancer implies that these mutations should be irrelevant for non-cancer aging. In my opinion, (a) independent processes may not necessarily attain equal importance because of different inherent susceptibility of the corresponding genes or gene networks to evolutionary change. However, once this is taken in consideration, a refined evolutionary argument does imply that in protected environment, continuing lifespan extension will eventually make any age-progressive degenerative process a significant contributor to aging and (b) protagonistic pleiotropies may be ineffective in making degenerative processes."

Rethinking the Mitochondrial Theory of Aging (July 04 2007)
An interesting paper here, proposing that changes in gene expression have as much or more to do with rising levels of free radical damage with age than simple damage to mitochondrial DNA (mtDNA): "The Mitochondrial Theory of Aging postulates that accumulation of mtDNA mutations and mitochondrial dysfunction are responsible for generating aging phenotypes and limiting lifespan. Although widely accepted, this theory remains unproven because the evidence supporting it, while substantial, is largely correlative. Furthermore, recent experimental results in mice with accelerated rates of mtDNA mutagenesis have challenged the traditional formulation of the Mitochondrial Theory, perhaps warranting a reevaluation of some of its core principles. In this perspective, we summarize recent work suggesting that both the quantity and the quality of mitochondrial gene expression play a much greater role in the aging process than previously appreciated. We speculate that this form of mitochondrial dysfunction may operate independently or in concert with mtDNA mutations to promote age-related pathology and limit lifespan." Non-functional gene expression has the same effective result as a damaged gene - the proteins produced from the blueprint of that gene, essential to cellular machinery, are no longer made inside that cell.

Attacking Cancer With Stem Cells (July 03 2007)
Via EurekAlert!, another demonstration of the use of existing cellular mechanisms as a part of cancer therapies: researchers "have been able to derive mesenchymal stem cells from human adipose, or fat, tissue and engineer them into 'suicide genes' that seek out and destroy tumors like tiny homing missiles. ... Mesenchymal stem cells help repair damaged tissue and organs by renewing injured cells. They are also found in the mass of normal cells that mix with cancer cells to make up a solid tumor. Researchers believe mesenchymal stem cells 'see' a tumor as a damaged organ and migrate to it, and so might be utilized as a 'vehicle' for treatment that can find both primary tumors and small metastases. ... the researchers worked to find a less toxic way to treat colon cancer than the standard-of-care chemotherapy agent, 5-fluorouracil (5-FU), which can produce toxic side effects in normal cells. They expanded the number of mesenchymal stem cells in the laboratory and then used a retrovirus vector to insert the gene cytosine deaminase into the cell. This gene can convert a less toxic drug, 5-fluorocytosine (5-FC), to 5-FU inside the stem cells, and the chemotherapy can then seep out into the tumor, producing a lethal by-stander effect. ... tumor growth was inhibited by up to 68.5 percent in the animals, and none of the mice exhibited any signs of toxic side effects."

Blackburn On Telomeres (July 03 2007)
The New York Times interviews Elizabeth Blackburn on the topic of telomere science: "Telomeres are the protective caps at the ends of chromosomes in cells. Chromosomes carry the genetic information. Telomeres are buffers. They are like the tips of shoelaces. If you lose the tips, the ends start fraying. Telomerase is an enzyme. In cells, it restores the length of the telomeres when they get worn. As the ends of the chromosomes wear down, the telomerase comes in and builds them back up. In humans, the thing is that as we mature, our telomeres slowly wear down. So the question has always been: did that matter? Well, more and more, it seems like it matters. ... In my lab, we're finding that psychological stress actually ages cells, which can be seen when you measure the wearing down of the tips of the chromosomes, those telomeres. ... we looked at two groups of mothers. One had normal, healthy children. The other group had a child with a chronic illness. Physiological and psychological measurements were done on everyone. With the stressed group, we found that the longer the mothers had been caring for their chronically ill child, the less their telomerase and the shorter their telomeres."

Sirtuins and Neurodegeneration (July 02 2007)
Ouroboros looks at the role of sirtuins in relation to age-related neurodegenerative conditions: "Where questions are asked about diseases of aging, the discussion will eventually turn toward the great scourge of age-related neurodegenerative disease. Given that sirtuins have already demonstrated potential to positively impact the aging process in a wide range of animals, it seems logical to ask whether they might also have therapeutic or prophylactic potential against neurodegeneration. The answer may end up being murky, and rely on the specific details of the specific illness and sirtuin family member in question. Two recent papers have studied the effect of sirtuin expression (and pharmaceutical modulation of sirtuin activity) on neurodegenerative disease - and come up with two diametrically opposing answers. Why the dramatic difference in results? The answer could lie either in differences between the diseases studied or in the functions of the sirtuin family members that were targeted." There is a great deal more to learn if scientists are to successfully manipulate metabolism to good effect. There are faster paths to a future of greatly enhanced longevity.

Banging the Drum at Telomolecular (July 02 2007)
I'm seeing more press releases from Telomolecular of late. To me that suggests they are heading into the next round of funding. It never hurts to bang the drum: "Nanocircles (a nanotechnology developed at Stanford University) and vTert (Telomolecular's synthetic enzyme) are capable of repairing damaged and shortened telomeres. Researchers at Telomolecular believe they've found a way to deliver Nanocircles and vTert to chromosomes in living organisms, reversing diseases caused by that damage. The researchers envision the ability, eventually, to speed the healing process in humans, preventing or even curing cancer. ... In the laboratory, Telomolecular has regenerated aged tissues that remain permanently young and live thousands of times beyond their normal replicative life span. Duplicated in living animals, this process could cure a variety of diseases caused by critical telomere degradation." Longer lived tissues do not automatically translate to longevity of health - it's very specific to the situation at hand. I found the recent news relating to Telomolecular's licensing of mitochondrial repair technology to be much more interesting than these general interest releases, given research indicating links between mitochondrial damage and telomere shortening.



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