LONGEVITY MEME NEWSLETTER
September 21 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.
- Learn More About the LifeStar Institute
- Inflammation as the Cause of Sarcopenia
- Latest Healthy Life Extension Headlines
We humans are largely irrational when it comes to aging and its consequences:
"Most people alive today will most likely develop, and die from, one of the chronic diseases of aging like cancer, heart disease or stroke. ... Retarding aging would help us delay all age-related disorders simultaneously, thus yielding healthy dividends that far exceed what a cure for cancer or AD or stroke could yield. So one of our top priorities should be to increase the health prospects of humans in late life. Thus aging research ought to be at the top of our priorities. ... but it isn't.
"Is the present generation of older folk going to quietly ride their degenerating bodies all the way down to the grave, or will they at some point take note of rapidly advancing capacities in biotechnology and decide enough is enough, perhaps giving rise to an energetic range of advocacy and investment groups?"
LEARN MORE ABOUT THE LIFESTAR INSTITUTE
The LifeStar Institute is a project of the Millard Foundation, whose founders have for some years been very interested in Aubrey de Grey's vision for the development of medical technologies of rejuvenation. One of the LifeStar Institute folk is presently taking questions and discussing the Institute's goals at the Imminst forums, and you can find links and discussion in this Fight Aging! post:
"It is our assertion that the science necessary to restore and maintain function against the degeneration of the aging process will get done. It is the 'when' that we are most concerned with, and with removing barriers so that the urgent need for therapies can maximally accelerate their development. Such barriers of course include funding and human resources, but moreover they are inherent in the way technology is developed after discovery - in the issues surrounding intellectual property and commercialization just to name a couple of critical areas. Indeed, the hardest part may not be the science, but making sure that the HUMAN components of the development equation are not the 'rocks in the road'."
INFLAMMATION AS THE CAUSE OF SARCOPENIA
Sarcopenia is the name given to age-related loss of muscle mass and strength, something suffered by all of us as we age. In recent years, evidence has gathered to implicate the rise in low-level chronic inflammation with aging as the root cause of sarcopenia:
Thus we might view sarcopenia as yet another of the consequences of an age-damaged immune system, which enters a dysfunctional state of spiraling inflammation as it fails with advancing years - though being overweight and carrying a lot of visceral fat will greatly boost your level of chronic inflammation long before your immune system starts its final decline. You'll find more on those sources of inflammation back in the archives:
Researchers have shown that a couple of different methods of reducing inflammation also reduce sarcopenia in rats. The method perhaps most applicable to long-term use in humans is the practice of calorie restriction:
"The study, using a rat model of life-time caloric restriction, showed that the diet reduces the amount of visceral fat, which expresses inflammatory factors that in humans cause chronic disease and a decline in physical performance and vitality across the lifespan. ... In addition, rats that ate a normal diet lost a significant amount of lean muscle mass and acquired more fat, while calorie-restricted rats maintained lean muscle mass as they aged."
The highlights and headlines from the past week follow below.
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LATEST HEALTHY LIFE EXTENSION HEADLINES
THE OXIDATION-INFLAMMATION THEORY OF AGING (September 18 2009)
An interesting paper: "The aging process is one of the best examples of the effects of a deterioration of homeostasis, since aging is accompanied by an impairment of the physiological systems including the homeostatic systems such as the immune system. We propose an integrative theory of aging providing answers to the how (oxidation), where first (mitochondria of differentiated cells) and why (pleiotropic genes) this process occurs. In agreement with this oxidation-mitochondrial theory of aging, we have observed that the age-related changes of immune functions have as their basis an oxidative and inflammatory stress situation ... Moreover, we have also observed that several functions of immune cells are good markers of biological age and predictors of longevity. Based on the above we have proposed the theory of oxidation-inflammation as the main cause of aging. Accordingly, the chronic oxidative stress that appears with age affects all cells and especially those of the regulatory systems, such as the nervous, endocrine and immune systems and the communication between them. This fact prevents an adequate homeostasis and, therefore, the preservation of health. We have also proposed a key involvement of the immune system in the aging process of the organism, concretely in the rate of aging, since there is a relation between the redox state and functional capacity of the immune cells and the longevity of individuals."
CRITICIZING THE MITOCHONDRIAL FREE RADICAL THEORY (September 18 2009)
Via Ouroboros, a look at researchers who declare the mitochondrial free radical theory of aging (MFRTA) over and done with: "MFRTA recently turned 50, and consequently has received a lot of attention lately; q.v. this review and this retrospective by Denham Harman, the originator of the theory. The thesis of most pieces seems to be that the theory hasn't been demonstrated to explain the bulk of age-related decline, but that there's still life in the idea. In contrast, the authors of this review argue that the relevant experiments have been performed and that the theory has been falsified - in other words, we've done our scientific duty and it's now time to move on. I doubt very much that this article will put a permanent end to the controversy. Data reported fairly recently have breathed new life into oxidative theories in general and the MFRTA in particular. While these authors contend that the CLK-1 mouse mutant contradicts the underlying mechanisms of the MFRTA, other recently reported work on this pathway supports the claim that inhibiting mitochondrial respiration delays aging, a key prediction of MFRTA. Furthermore, if mitochondrially generated oxidative radicals are truly not playing a causative role in aging, it becomes much harder to explain how mitochondrially targeted antioxidants can extend lifespan in mammals."
AN INTERVIEW WITH MEREDITH AVERILL AND PAUL MCGLOTHIN (September 17 2009)
h+ Magazine interviews calorie restriction (CR) practitioners Meredith Averill and Paul McGlothin, noted for their work to spur the scientific community into greater human studies of CR: "McGlothin says he 'had the good fortune' to come into contact with one of the country's leading internist, who is a calorie restrictor. It was through this physician that McGlothin and Averill both became smitten with CR practice and science and surrounded themselves with a team of doctors in an attempt to sort out fact from fiction in the practice. They also initiated the first CR study of humans, accomplished with MetaMetrix Clinical Laboratory in 2001. Subsequently, they formed a partnership with Drs. Luigi Fontana and John Holloszy at the Washington University in Saint Louis School of Medicine. ... His work in testing CR results led to his being named Research VP of the CR Society, where he works with scientists to plan studies. ... We want everything we do to be backed by solid scientific research and testing. That is why we helped set up the first longitudinal study of calorie-restricted humans. Now, for the past seven years, we and a cohort of other calorie-restricted humans have been thoroughly tested by teams of scientists headed by Drs. Luigi Fontana and John Holloszy at the School of Medicine at Washington University in St. Louis."
A POLITICAL THEORIST ON LONGEVITY SCIENCE (September 17 2009)
This piece from In Search of Enlightenment is just as applicable to the level of attention given to longevity science by ordinary folk: "Aristotle would scoff at the insularity and specialization of contemporary political theory. While concerns for the good of humans do populate debates in the field (some more than others), that concern is peripheral rather than central. The neglect of science and technology, for example, easily illustrates how wide the gap is between debates in political theory and the real world. If you were born 200 years ago you probably wouldn't live to see your 30th birthday. If you are born today you will most likely live long enough to suffer from one of the chronic diseases of aging in late life (after age 60). We have more than doubled the life-expectancy of humans in just 200 years. And yet the significance of the advances that made this possible - like the sanitation revolution, vaccinations, material prosperity, changes in behaviour, etc. - go largely unnoticed by the political theorist. Such 'macro-level' considerations typically aren't on the radar of theorists because we tend to form our theories and principles on the basis of micro-level considerations (e.g.: 'Look, the Jones's have more money than the Smith's do. Is this inequality in one small dimension of their life prospects fair if it is the result of 'brute luck'?'). So, how does one go about linking political theory to aging research? This is my project."
A PROFILE OF LEONARD GUARENTE (September 16 2009)
Aging researcher (and competitor in the Mprize for longevity science) Leonard Guarente is profiled at the MIT News: "After winning tenure at MIT in 1986, biology professor Leonard Guarente did some soul-searching. He had made his mark by studying gene regulation in yeast, but that field was getting overrun with researchers, and he wanted to pursue a riskier project, where success would have a dramatic scientific impact. ... With the help of some bright graduate students who arrived in his lab in 1991, he hit on the idea of looking for genes that control aging in yeast. At the time, it was a plan with little prospect for success: Few scientists believed that aging might be controlled by a single gene (or small group of genes). Guarente turned that view around - and pioneered a new field of study - with his discovery of so-called longevity genes, which dramatically boost the lifespan of yeast, worms, mice and potentially humans. The human version of the gene, known as SIRT1, is now the target of several drugs in development to treat the diseases of aging, including diabetes, Alzheimer's and cardiovascular disease."
ON THE REVIVAL OF CRYONICS PATIENTS (September 16 2009)
Over at Depressed Metabolism, Aschwin de Wolf has assembled a list of literature on how we expect cryosuspended people to be restored in the future. The general class of technologies required are fairly well understood, and a lot of thought has gone into the processes and machineries that must be developed: "There is a growing literature that discusses the technical aspects of revival of cryonics patients. [This list] of the published literature was compiled by Ralph Merkle and Robert Freitas and published as an appendix of their article on molecular nanotechnology in Cryonics Magazine 2008-4." Much of the list is available online for interested readers, such as Merkle's technical feasibility outline: "This paper considers the limits of what medical technology should eventually be able to achieve (based on the currently understood laws of chemistry and physics) and the kinds of damage caused by current methods of freezing. It then considers whether methods of repairing the kinds of damage caused by current suspension techniques are likely to be achieved in the future."
DECIPHERING THE GERMLINE-LONGEVITY LINK (September 15 2009)
Researchers are making progress in understanding exactly how germline cells are linked to longevity in flies and nematodes: "In Caenorhabditis elegans and Drosophila melanogaster, the aging of the soma is influenced by the germline. When germline-stem cells are removed, aging slows and lifespan is increased. The mechanism by which somatic tissues respond to loss of the germline is not well-understood. Surprisingly, we have found that a predicted transcription elongation factor, TCER-1, plays a key role in this process. TCER-1 is required for loss of the germ cells to increase C. elegans' lifespan, and it acts as a regulatory switch in the pathway. When the germ cells are removed, the levels of TCER-1 rise in somatic tissues. This increase is sufficient to trigger key downstream events, as overexpression of tcer-1 extends the lifespan of normal animals that have an intact reproductive system. Our findings suggest that TCER-1 extends lifespan by promoting the expression of a set of genes regulated by the conserved, life-extending transcription factor DAF-16/FOXO."
DISABLING MITOCHONDRIAL GENES FOR LONGEVITY (September 15 2009)
Researchers make flies live longer by interfering with components of the mitochondrial energy-generating machinery: "Mitochondria have long been proposed to play an important role in the aging process. In the nematode Caenorhabditis elegans, genes important for mitochondrial electron transport chain (ETC) function stand out as a principal group of genes affecting life span. However, it has been suggested that this may be a peculiarity of nematode biology. In the present study, we have used an in vivo RNA interference (RNAi) strategy to inactivate ETC genes in Drosophila melanogaster and examine the impact on longevity. ... RNAi of five genes encoding components of mitochondrial respiratory complexes I, III, IV, and V leads to increased life span in flies. ... Our data suggest that the role of mitochondrial ETC function in modulating animal aging is evolutionarily conserved and might also operate in humans. Furthermore, our findings suggest that the longer life span of flies with reduced ETC gene expression cannot simply be attributed to reduced energy production leading to decreased 'rate of living.'"
SEEKING THE CURE FOR AGING (September 14 2009)
The Telegraph notes the recent SENS4 conference: "Cranks and crooks have been peddling immortality potions since before the dawn of history. All manner of bizarre antidotes to ageing have been tried, including the drinking of mercury salts and the eating of diced monkey testicles. Immortality, it would seem, has long been inextricably entwined with lunacy. But that may be about to change. Earlier this month, 200 scientists descended on Queens' College Cambridge to discuss ways of radically extending human lifespan - and even achieving immortality. The Strategies for Engineered Negligible Senescence (SENS) conference, drew together researchers from disciplines as diverse as tissue engineering, artificial intelligence, law, demographics and politics. 'Most people fail to understand how fast medical science is advancing in this area,' says the conference organiser Dr Aubrey de Grey, editor-in-chief of the journal Rejuvenation Research and co-founder of the SENS Foundation. 'Conventional medical progress has ensured that a child born today can expect to live 120 to 150 years. I think it's possible for them to live far longer. If we make the right breakthroughs in the next 25 years, then there is a 50:50 chance that people alive today could live to be 1,000 years old."
STUPID ARGUMENTS AGAINST LIFE EXTENSION (September 14 2009)
From Anders Sandberg: " I comment on a Times article that claims life extension will make us worse off because 1) it would be bad for society, and 2) because the finiteness of life give it value. These are bad arguments that seem to crop up again and again. Arguing that we shouldn't do X because of bad social consequences hinges on the assumptions that we can accurately predict these social consequences to be bad, that we cannot fix them in a reasonable way and that their badness will always outweigh the good X could do. The assumptions in the case of life extension are very debatable, since we actually do have data about how societies handle longer lifespans and it suggests that they do adapt nicely and become happier. Maybe an extremely rapid shift would be wrenching, but again that would also correspond to a large number of people who would otherwise have died now not dying often horribly. Trying to find some social effects that can outweigh the badness of 100,000 deaths a day is hard, and I have not seen any convincing argument along these lines. ... the 'death gives life meaning' argument [sounds] deep, but nobody would consider 'divorce gives love meaning' or 'bookworms give libraries meaning' profound or even accurate. The meaning of love is to be found in the deep positive emotions and relations, not in their breakdown or ebb. Similarly life has a meaning based on that it is lived, not any boundary condition."