Longevity Meme Newsletter, December 24 2007

December 24 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.



- Is There a Potential Longevity Therapy in Mitoptosis?
- Our Folding@Home Team Closes In On Rank 200
- Choice and Freedom
- Discussion
- Latest Healthy Life Extension Headlines


Learning at least one new word every day is a good way to live - and you'll certainly do that if you make a habit of reading scientific papers. The life sciences have a language all to themselves. The new word for today is "mitoptosis":


"Mitoptosis is the programmed destruction of mitochondria in your cells, a process analogous to apoptosis, or programmed cell death. ... To cut a long story short, damaged mitochondria in a cell will breed more damaged mitochondria in that cell. Repeated over and over, this eventually causes a small but significant number of cells to export damaging free radicals throughout your body, causing great harm to health and life span over time. One focus of SENS and SENS-like research is to cut this process short at the 'damaged mitochondria' phase. Eliminate the damaged mitochondria aggressively and often, and that portion of the aging process is gone. Mitoptosis may be an existing mechanism that can be adapted to this end."

A longer description of the damage done to your healthy longevity by errant mitochondria can be found back in the Fight Aging! archives:


With more avenues that lead towards eliminating the contribution of mitochondrial damage to aging, we should be more confident that at least one will work out. At the present time, I'm aware of five or six different research strategies at various stages that aim to this end - all to the better.


The long-standing Longevity Meme Folding@Home team, volunteers contributing spare processing power to protein-folding simulations, is closing in on rank 200 in the grand leaderboard:


"The lower ranks are a tough slog, but the team has been doing well - growing and producing results. I have decided that the best thing to do to mark the passage of rank 200, rather than send out another round of Longevity Meme tchotchkes, is to donate a chunk of change to the Methuselah Foundation, where it can be put to good use in advancing longevity science. Here is my incentive for the team: pass rank 200, and stay beneath that level for a week, and I'll donate $1000 in support of Strategies for Engineered Negligible Senescence (SENS) research carried out by the Foundation."

Find out how to join the team here:



Ronald Bailey nails it:


"My vision of a future in which effective longevity treatments are available is one in which individuals get to choose to use them or not - no government gets to decide how long its citizens will be allowed to live. That would truly be tyranny. In the meantime, if Callahan chooses to go 'gentle into that good night' I wish him well of it, but his job is to warn us the dangers he sees arising from radically extended lives and that's all very well. He should allow the rest of us to ignore his advice and find out for ourselves whether he is right or wrong. Let us learn freely from trial and error as people always have done."

Freedom and choice are two vital portions of the fundament of a society worth living in. The freedom to be alive, and work on remaining that way, is the greatest of all freedoms - for without life, there is nothing: no possibilities, no human action, no building of a better world. We forget, in our comparative comfort, that to be able to choose to live another day in good health and do your part to move humanity into a better era is a luxury, considered in the grand scheme of human history. We should be champing at the bit to create more of that luxury.


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!




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/

Cell Fusion and Regenerative Therapies (December 21 2007)
Here is an interesting view of the mechanics of aging and regeneration in stem cells: "Harnessing cellular fusion as a potential tool for regenerative therapy has been under tentative investigation for decades. A look back the history of fusion experiments in gerontology reveals that [some] have demonstrated that fusion can be used as a tool to revoke cellular senescence and induce tissue regeneration. Recent findings about the role of fusion processes in tissue homeostasis, replenishment, and repair link insights from fusion studies of previous decades with modern developments in stem cell biology and regenerative medicine. We suggest that age-associated loss of regenerative capacity is associated with a decline of effectiveness in stem cell fusion. We project how studies into the fusion of stem cells with tissue cells, or the fusion between activator stem cells and patient cells might help in the development of applications that 'rejuvenate' certain target cells, thereby strategically reinstating a regeneration cascade."

One $25K SENS Matching Fund Down, One To Go (December 21 2007)
From the Methuselah Foundation: "A veritable stampede of generous donations flattened our first $25,000 matching challenge from Michael Cooper in something under a week. Well done! Strategies for Engineered Negligible Senescence (SENS) research will move that much further and faster for your efforts. Now Doug Arends has picked up the torch with another $25,000 matching challenge for SENS research. As before, when combined with Peter Thiel's $3 million matching fund, donations are tripled. Donate $100 and $300 will go to SENS research - so don't hold back!" If you haven't yet made a year-end charitable donation, here is a good place for it. The SENS research program, aimed at developing a foundation of biotechnology for rejuvenation through the repair of aging, is a bright spot of invention and determination in the biomedical research community. It deserves your support.

Resisting Early Mitochondrial Damage (December 20 2007)
This paper illustrates one the reasons why exercise is good for healthy longevity, diving into the mechanics of damage to mitochondria and its role in aging: "Mitochondrial dysfunction is commonly thought to result from oxidative damage that leads to defects in the electron transport chain (ETC). ... we highlight new research indicating that there are early changes in mitochondrial function that precede ETC defects and are reversible thereby providing the possibility of slowing the tempo of mitochondrial aging and cell death. ... Increased mitochondrial uncoupling - reduced adenosine triphosphate (ATP) produced per [oxygen molecule] uptake - and cell ATP depletion are evident in human muscle nearly a decade before accumulation of irreversible DNA damage that causes ETC defects. New evidence points to reduction in activators of [mitochondrial] biogenesis [and] to degradation of mitochondria allowing accumulation of molecular and membrane damage in aged mitochondria. The early dysfunction appears to be reversible based on improved mitochondrial function in vivo and elevated gene expression levels after exercise training." The more time you have before needing to benefit from the mitochondrial repair therapies of the future, the greater the chance those therapies will exist when you need them.

The Scientist on Engineered Organs (December 20 2007)
The Scientist looks at present initiatives in mass production of engineering autologous organs for transplant. Note the elephant in the room when people wonder why medical development is so challenging: if phase II trials go well, "the company will schedule a larger, Phase III trial. What happens then is still somewhat unclear. The FDA has never been asked to approve an autologous human organ. What safety criteria will it consider? What kind of quality control procedures and infrastructure will the company need to employ? 'It's not like we're stamping out a million pills a day. We have to custom-grow a new organ for every patient.' ... 'I think the task of trying to commercialize this type of custom-made organ for patients is pretty daunting.' From the beginning, the company interacted with the agency to educate it about how the technology works, scheduling 'at least five' pre-IND meetings. 'The FDA had to create new sets of standards for us,' Sender says. A handful of bladders is one thing; mass producing them is quite another. ... You can probably understand maybe doing one at a time, two at a time, three at a time.Now imagine having to grow thousands of organs a year. Or maybe thousands at one time." In a sane world, those laboring to bring benefits to humanity would just get on and do the job, absent the ball and chain of regulation for the sake of regulation.

Mixed Methods Versus Cancer (December 19 2007)
We've seen a lot of ingenuity in bioengineering attacks on cancer with viruses or the immune system. Here's an example of a mixed method - a little of both: "Researchers zeroed in on immature T-cells from bone marrow, programming them to respond to specific threats to the immune system while delivering a cancer-destroying virus to the tumor cells. To deliver the virus, researchers removed T-cells from a healthy mouse, loaded them with the virus and injected the T-cells back into the mouse. Researchers found that once the T-cells returned to the lymph nodes and spleen, the virus detached itself from the T-cells, found the tumor cells, selectively replicated within them and extracted tumor cells from those areas. ... In mice with lung cancer metastasis, cancer cells were significantly reduced in one-third of mice and completely eradicated in two-thirds of mice. Efforts to clear metastases from colorectal tumors were similarly effective. Lung and colorectal tumor cells were purged from lymph nodes. Also, the spleens of mice that had lung cancer developed immunity to the cancer after the treatment."

On the Hook (December 19 2007)
From Kevin Dewalt: "Person #1: 'Every day 100,000 people die a horrible death after a period of prolonged suffering. I want to stop this from happening.' Person#2: 'That may not be a good idea. It might lead to some unintended consequences.' ... I don't know about you, but the glaring next step in the debate between Persons #1 and #2 is as follows: Person#2 is on the hook to provide a very, very compelling reason to say why saving 100,000 lives a day is a bad idea. This brings me to the point of this post: Don't want to cure aging? The onus is on you - not us - to explain why. ... We may have an opportunity in the next several decades to develop treatments to end the suffering and death for 100,000 people EVERY DAY on this planet. If you think solving this problem is a bad idea, you had better come up with both some very compelling arguments and some facts to support your position. The onus is on you. And that, my friends, should end most of these discussions. So when you find yourself engaged into (yet another) one of these absurd discussions with someone who may be more eloquent, more educated, or better read than yourself, fear not because you have a safety net: The onus is on them to explain why we shouldn't reverse aging. It really is that simple."

More Blood Vessel Engineering (December 18 2007)
As I might have remarked once or twice, the efficient construction of blood vessels is a crucial infrastructural goal for the field of tissue engineering. Further progress absolutely depends upon it: "The work focuses on vascular tissue, which includes capillaries, the tiniest blood vessels, and is an important part of the circulatory system. The team has created a surface that can serve as a template to grow capillary tubes aligned in a specific direction. ... The surface is patterned with ridges and grooves that guide the cells' growth. ... The cells, known as endothelial progenitor cells (EPCs), not only elongate in the direction of the grooves, but also align themselves along the grooves. That results in a multicellular structure with defined edges, also called a band structure. Once the band structures form, the researchers apply a commonly used gel that induces cells to form three-dimensional tubes. Unlike cells grown on a flat surface, which form a network of capillary tubes extending in random directions, cells grown on the nano-patterned surface form capillaries aligned in the direction chosen by the researchers."

Modest Inroads Into Reducing Mitochondrial Damage (December 18 2007)
As Wired notes, the old school drug development community is making some inroads into altering the level of age-related damage suffered by mitochondria, and thereby improving health. This is small potatoes compared to what will soon be possible, but inroads are inroads: "The drugs target mitochondria, the cellular power generators that provide our bodies with chemical energy. Over time, mitochondria accumulate damage, causing cells and eventually tissues to malfunction and break down. Some scientists believe that such seemingly disparate diseases as cancer, Parkinson's, Alzheimer's, diabetes and heart disease - all of which become more common with age - share a mitochondrial root. Fix the mitochondria, and you might fix aging itself. Preliminary research suggests that mitochondria-rejuvenating drugs are capable, at least in lab animals, of halting these diseases and extending longevity." Unfortunately, more than just repairing mitochondria is required to sort out aging - a number of other classes of age-related biochemical damage are also important and must be addressed.

Another Strategy for the Aging Immune System (December 17 2007)
One of the reasons the aging immune system fails in its job is the reduction of naive T cells, ready to tackle new threats. One approach to tackling this problem is to eliminate the cause - that too great a fraction of the immune system's limited resources is uselessly devoted to CMV-targeted memory cells. Another approach is outlined here: make more naive T cells available. "Throughout our lives, naive T-cells divide very slowly in our bodies. This helps maintain sufficient numbers of naive T-cells while we are young. As we age, naive T-cells are lost and the remaining ones speed up their division to make up for the losses in their numbers. Interestingly, after a certain point, this actually causes the numbers of naive T-cells to dwindle over time. Our data shows that once the number of naïve T-cells drops below a critical point, the rapidly dividing naive cells are very short lived. Based on this finding and other information, research suggests that some of the aging Americans may be better protected against disease by finding a way to jumpstart production of new naive T-cells instead of through revaccination. ... Even a slight boost in the number of these important T-cells could protect an aging person against disease for several years."

Fresh Eyes on the Buck Institute (December 17 2007)
It's always interesting to see community institutions from a fresh perspective. Here, Anne C. discovers the Buck Institute for Age Research: "I'm tremendously pleased to see that the Institute exists, and I really like their up-front focus on improving the health of the elderly. ... The notion of 'strategic aging' as described here is actually quite similar to the SENS paradigm on which the Methuselah Foundation is basing its research objectives. Of course everyone is going to get old someday (it's one of those inevitable consequences of being born), but there's no fundamental reason why getting old should have to lead to painful, fatal illness. The notion of 'strategic aging' recognizes that people's health needs change as they age, and that it makes much more sense to address these changing needs proactively than wait until a person sits at death's door. This proactive approach is becoming more and more of a realistic one, and if all goes well, it will hopefully become the default paradigm within a few decades or so." I'd have placed the Institute in that part of the research community that has yet to come around to the importance of repair over metabolic tinkering in addressing aging - which I consider far more important a division than intent.



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