Longevity Meme Newsletter, February 02 2009

February 02 2009

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 Argument From Great Suffering and Death
- Conveying the Simple Ideas
- A View of the Enhancement Debate
- Discussion
- Latest Healthy Life Extension Headlines


The death and suffering caused by aging far outstrips everything else that takes place in this world of ours - but, strangely, using this as an argument for greater support of longevity science doesn't seem to have much traction. Sadly, people will accept any situation, no matter how dire, if it is all they know: failure of progress is so often a failure of imagination.


"It is estimated that between the mid-14th century and mid-17th century, the 'Black Death' plague killed approximately 25 million people. This means that the current deaths caused by [chronic diseases of aging] in just one year outnumber the deaths caused by 3 centuries of the 'Black Death' plague. This clearly illustrates why the imperative to combat chronic disease is one of the greatest imperatives ever facing humanity. And since aging is the major cause of these afflictions, one of the greatest moral imperatives facing humanity today is to tackle aging itself so that we can avoid the unprecedented rise in chronic disease that is expected to befall the world's populations this century."


There are many levels of advocacy for increased funding of engineered longevity and other forms of applied aging research. In many ways, we still have a long road ahead in terms of conveying the simple ideas: that a) slowing and reversing aging are very plausible goals for the next few decades, and b) little is presently being done to make that a reality.


"The bad news is that despite all our advances in medicine, sanitation, and other relevant factors, [survival at old age] still tapers off around age 100. Average lifespan has increased, but maximum lifespan has not changed significantly. One reason may be that research to prolong maximum lifespan receives minuscule funding, especially compared with popular endeavors such as cancer research. Many people seem to feel that extending maximum lifespan would be 'wrong' (even at a time of rapidly declining birth rates in many nations) or 'unnatural' (even though our average life expectancy used to be around 40, and has improved through totally unnatural means such as antibiotics)."


As is sometimes pointed out, the debate over enhancing human performance is one and the same with the debate over engineering greater human healthy longevity:


"I suspect that the structure of arguments about cognitive enhancement will mirror those of future debates regarding lifespan extension. Both fields involve treatments that promise to improve or increase a parameter of human performance - one that varies to some extent within the natural population, but that seems fixed for a given individual. In both cases, human beings are 'fine' without the intervention - that is, we live comfortably (and, for the most part, happily) knowing that there is nothing much we can do to make ourselves smarter, and looking forward to our allotted threescore years and ten.

"Beginning from the premise that what isn't broken ought not be fixed, or that the 'natural order' of things ought not be meddled with, critics of both cognitive enhancement and lifespan extension may argue that neither sort of intervention in Normal Human Lives(tm) is warranted."


The highlights and headlines from the past week follow below.

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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/

Novel Telomere Extension Method Adds Longevity (January 30 2009)
This is an interesting paper. I would be almost inclined to think that the life extension effect has to do with the link between telomerase and mitochondrial damage, but that's very speculative at this point. For all we know, the treatment of mice might have led to accidental calorie restriction and extended life span by that method: "Telomeres become shorter after each cell division, which is one of the mechanisms of gradual ageing. Telomerase is the reverse transcriptase responsible for the extension of telomere length. It is well known that activation of telomerase in the most types of organism's cells is not enough for telomere length stabilization. The reason may be in the telomere 'caps', which cover telomere ends from telomerase action. This experiment shows that telomeres were elongated by the combination of hypoxia activated telomerase and a newly developed pharmacological method removing the telomere cap ... Rats from the control group died at the age 1 year 7 month - 1 year 8 month, which is typical for the Wistar rats from our sub-line. Rats from the experimental group died at the age 2 year 4 month."

Resetting a Damaged Immune System (January 30 2009)
Scientists can reboot a human immune system by destroying it and then transplanting new stem cells. This is a promising line of research given what happens to the immune system with aging, but the present focus is curing autoimmune disease: researchers "appear to have reversed the neurological dysfunction of early-stage multiple sclerosis patients by transplanting their own immune stem cells into their bodies and thereby 'resetting' their immune systems. ... [researchers] treated patients with chemotherapy to destroy their immune system. They then injected the patients with their own immune stem cells, obtained from the patients' blood before the chemotherapy, to create a new immune system. ... We focus on destroying only the immune component of the bone marrow and then regenerate the immune component, which makes the procedure much safer and less toxic than traditional chemotherapy for cancer ... After the transplantation, the patient's new lymphocytes or immune cells are self-tolerant and do not attack the immune system. ... In MS the immune system is attacking your brain. After the procedure, it doesn't do that anymore."

Regenerating Spinal Cord Injury (January 29 2009)
Researchers are expanding the array of methods demonstrated to repair spinal cord injuries: "transplantation of stem cells from the lining of the spinal cord, called ependymal stem cells, reverses paralysis associated with spinal cord injuries in laboratory tests. The findings show that the population of these cells after spinal cord injury was many times greater than comparable cells from healthy animal subjects. The results open a new window on spinal cord regenerative strategies. ... The transplanted cells were found to proliferate after spinal cord injury and were recruited by the specific injured area. When these cells were transplanted into animals with spinal cord injury, they regenerated ten times faster while in the transplant subject than similar cells derived from healthy control animals. ... the presence of these stem cells in the adult human spinal cords suggests that stem cell-associated mechanisms might be exploited to repair human spinal cord injuries."

Gene Therapy Versus Arthritis: Small Steps (January 29 2009)
Via EurekAlert!: "Originally conceived as a means of treating genetic diseases, such as cystic fibrosis and hemophilia, gene therapy involves implanting a normal gene to compensate for a defective gene in the patient. ... This study helps extend gene therapy research to nongenetic, nonlethal diseases. Rheumatoid arthritis [RA] is an extremely painful condition affecting multiple joints throughout the body. Arthritis is a good target for this treatment because the joint is a closed space into which we can inject genes ... Evans has spent many years studying the molecules responsible for the breakdown of cartilage in patients with arthritis, identifying interleukin-1 as a good target. But, he adds, once he had this answer, another question was not far behind: How could he effectively reach the joints to block the actions of this protein? Gene therapy provided the answer. By implanting a gene in the affected joint, he was able to stimulate production of a human interleukin-1 receptor antagonist protein, which serves to block actions of the interleukin-1 protein. ... The idea is that by remaining in place, the new gene can continuously block the action of the interleukin-1 within the joints. In essence, the gene becomes its own little factory, continuously working to alleviate pain and swelling."

Linking General Health and Alzheimer's Risk (January 28 2009)
Another study confirms the link between diabetes and Alzheimer's risk, suggesting one again that Alzheimer's is a lifestyle condition for many, brought on by being overweight and not exercising over the years: "Diabetics have a significantly greater risk of dementia, both Alzheimer's disease - the most common form of dementia - and other dementia, reveals important new data from an ongoing study of twins. The risk of dementia is especially strong if the onset of diabetes occurs in middle age ... Our results [highlighted] the need to maintain a healthy lifestyle during adulthood in order to reduce the risk of dementia late in life ... the chances of a diabetic developing Alzheimer's disease may be even greater in real life than in the study, the researchers write. They identify several factors that might have led them to underestimate the risk of dementia and Alzheimer's among those who develop diabetes before the age of 65. Diabetes usually appears at a younger age than dementia does, the researchers note. Diabetes is also associated with a higher mortality rate, which may reduce the size of the sample of older adults. In addition, approximately 30 percent of older adults with diabetes have not been diagnosed. The results of the study implicate adult choices such as exercise, diet and smoking, as well as glycemic control in patients with diabetes, in affecting risk for Alzheimer's disease."

Ouroboros on Mitochondrial Antioxidant SkQ1 (January 28 2009)
Ouroboros weighs in on SkQ1 research: "Mitochondria produce rreactive oxygen species (ROS) as a byproduct of metabolism. These ROS are implicated in the mitochondrial free radical theory of aging (MFRTA) as the major cause of aging phenotypes. If the MFRTA is true, one could delay aging by removing these mitochondrially-produced ROS with enzymes or antioxidants. Although many antioxidant therapies for cancer and other age-related diseases have proved fruitless, these studies did not specifically target antioxidants to the mitochondria. One group recently did just that in mice with catalase, an antioxidant enzyme normally found in peroxisomes. By translocating catalase to the mitochondria, the scientists expanded the lifespan of the animals by five months. Such genetic manipulations such as these are not in the cards when it comes to preventing human aging. Therefore, other mitochondrial targeting strategies must be employed. Accordingly, Vladamir Skulachev's group synthesized an antioxidant attached to a positively charged ion, which they call SkQ1. This compound can readily pass through the cell membrane and travel to the mitochondrial intermembrane space, the only negatively charged region in the cell. There, SkQ1 will soak up any ROS formed by the electron transport chain. SkQ1 works similarly to the popular MitoQ, but does not have the pro-oxidant properties MitoQ is known to have at higher concentrations. SkQ1 is also better than MitoQ at inhibiting apoptosis induced by hydrogen peroxide."

Calorie Restriction Improves Memory (January 27 2009)
Another metric by which to measure the more rapid impacts of calorie restriction upon health: "The participants [underwent] memory tests before and after going on the diet. At the end of three months, the calorie-restricted group increased its scores by about 20 percent, while the performance in the other groups did not change. ... in addition to showing a boost in memory, the study also suggests that the same underlying mechanisms uncovered in animals could be at work in humans too. The researchers found that people who cut calories had improvements in several indicators of metabolic health, such as blood levels of insulin and C-reactive protein, a marker of inflammation. In fact, the rise in cognitive test scores correlated with lower insulin levels. In animal studies, high insulin levels and low-grade inflammation - products of being overweight and of high calorie intake - have been shown to hamper cognitive function. ... limiting calories in mice boosts a molecule in the brain called BDNF, which has a key role in memory. Regular exercise, along with calorie restriction, also boosts the growth of new brain cells in mice. ... the current results [suggest] that those pathways from animal studies might also work in humans."

Fashionable Pessimism and Enzymatic Slime (January 27 2009)
A lengthy post at Existence is Wonderful looks at the intersection of modern pessimism in the transhumanist community and advocacy for radical life extension: "sometimes I feel like I'm caught in the middle between, on the one hand, well-meaning folks (who might very well be contributing plenty from a scientific and fundraising standpoint to longevity research) who nonetheless see superlativity critique as pessimistic or irrelevant, and other folks (such as Jones and Carrico) who in my assessment seem to have very astutely identified particular problems in public technology discourse (including that surrounding biogerontology) as it presently stands." It has become somewhat fashionable for the transhumanist mainstream to be more concerned with existential risk than with progress these days and to disparage visionary viewpoints as "superlativity" or similar. In that the community reflects the spirit of the times - it's environmentalism's shadow cast large, an infection of the mind brought over from the vast number of people who deeply fear change or wish a return to an imagined idyllic past. I can't see this ending well, given that the change of progress is exactly what transhumanism is all about.

General Interest Article on Sirtris (January 26 2009)
A good example of the very diluted, delayed way in which news of progress in aging research makes its way into the mainstream from CBS News: "Dr. Westphal says we all may soon be taking a drug that just might beat the clock, a simple pill that could delay the inevitable. 'Our goal is to prevent and forestall many of the diseases that strike us as we reach 50, 60, and 70. All with one pill.' Asked if he's suggesting that it's some kind of a rejuvenation drug that would turn a 70-year-old into a 35-year-old, Westphal tells Safer, 'That might be pretty hard to do. But I think if we're on a train heading one direction, we can slow down that train. I think we can slow down these genes that control the aging process.' That quest to put death on hold began in 2003 when Westphal met David Sinclair, a biochemist at Harvard who was studying the genetic components of aging. 'Five years ago I met David. And he had shown that you could extend life span in yeast. That's pretty exciting,' Westphal recalls. Yeasts are one thing. Human beings are more complicated. So Sinclair focused on a gene present in almost all life forms: the sirtuin gene. It's normally inactive, but when it is active, Sinclair believes it triggers a survival mechanism that extends life. Convinced that something in nature could activate that gene, Sinclair randomly tested thousands of compounds and got a hit: resveratrol."

Breakdown of Barriers in Old Cells (January 26 2009)
Via EurekAlert!: "We still have a very poor understanding of the mechanisms behind cell aging. It has been known for some time that the gene expression profile of an aging cell changes and somehow is linked to age-related diseases, but no one really knows why. Our work could provide an explanation for why we observe age-dependent defects in cells ... Like guards controlling access to a gated community, nuclear pore complexes are communication channels that regulate the passage of proteins and RNA to and from a cell's nucleus ... Do they turn over in nondividing cells, or do they remain in place for the life of the cell? Because most of the cells in our body are not actively dividing, the answer would have implications for aging and age-related diseases. ... Many of the neurons in the cortex area of the brain are as old as we are; they are nondividing for a very long time. ... What they found was that in aging cells, one of the proteins composing the scaffold structure becomes damaged, and the permeability barrier deteriorates; molecules that should be restricted to the cytoplasm invade the nucleus. ... Because some cells live for a long time, the accumulation of damage in the long-lived nuclear pore complexes can impair their function and have important consequences for cell homeostasis and survival. It may also play a significant role in the aging process."



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