Longevity Meme Newsletter, October 18 2010

October 18 2010

The Longevity Meme Newsletter is a weekly email containing news, opinions, and happenings for people interested in aging science and engineered longevity: making use of diet, lifestyle choices, technology, and proven medical advances to live healthy, longer lives. This newsletter is published under the Creative Commons Attribution 3.0 license. In short, this means that you are encouraged to republish and rewrite it in any way you see fit, the only requirements being that you provide attribution and a link to the Longevity Meme.



- Video From the Immortality Institute 2010 Conference
- The Prehistory Leading to Gerontology
- Three Decades of Cryonics History
- Garbage Management and Cellular Immortality
- Discussion
- Latest Healthy Life Extension Headlines


The Immortality Institute held their 2010 conference in Brussels earlier this month: a mix of researchers and supporters presenting on longevity science. You'll find a couple of video records from the event are online already:


"That was absolutely a great event, with some of the most cutting-edge scientists in the field, presenting new facts, some of them not published yet, that will certainly change the face of the world in the next years or decades. I felt that scientists were really touched by this young dynamic generation that understands their work and supports them, and we could feel that this bridge between generations as well as between researchers and amateurs is bringing a lot of cohesion into this movement for life extension."


A Russian gerontologist recently posted some thoughts on aging research as a natural continuation of mankind's long, historical struggle against death. This struggle was, in fact, a large part of the motivation to achieve progress throughout human history: defeat hunger, defeat cold, defeat injury, then defeat disease - and now we must work to defeat aging. The translation is automated, so you'll excuse the quality:


"Unconscious fear of death occurs in a child already at birth. There he and the animals [are the same]. Fear of death plays an important biological role: along with the pain he wakes survival instinct that forces to avoid danger or flee from it. However, in humans, as a rational being, there is awareness of their own mortality. The child begins to recognize their mortality at the end of preschool age, and even earlier. Understanding of powerlessness in the face of death is inconsistent with fear of death and the unconscious desire to save his life. This contradiction [gives rise to two distinct psychological reactions] - adaptation or confrontation. ... Some psychologists [believe] that only [by overcoming] the fear of death, [does a] person starts to live a full and authentic life. Confrontation with the fact of mortality [is, or should be] a natural phenomenon for man. ... the desire to overcome the causes of death, along with a desire to improve the quality of life occurred in [antiquity] and became the principal engine of progress."


The cryonics movement is one of the oldest parts of the present day community of folk interested in engineered longevity. Alcor maintains a thirty year archive of Cryonics Magazine, which covers much of this span of time:


"The present day interest communities whose members advocate transhumanism, engineered longevity, cryonics, strong artificial intelligence, and advanced nanotechnology (in the sense of molecular manufacturing) didn't spring forth from nothing. They are an ongoing evolution that started with much smaller groups in the 70s and 80s, their growth and changing form spurred by the advent of the internet, web, and other advances in communication and distributed organization. Anyone with an interest in the formative history of our community would do well to browse the Cryonics Magazine archive. After all, many of the more interesting and pivotal folk involved in advocacy or research and development for transhumanist technologies - such as greatly extending the healthy human life span - have in some way touched upon the cryonics community."


Cells and single celled organisms can establish an immortal lineage - a fact which can be beneficial or harmful for we multi-cellular organisms. Think of the germ cells which carry the human lineage versus rampaging cancer cells, for example. The deep origins of aging are connected with the mechanisms by which cells achieve immortality:


"Over at the Scientist, you'll find an interesting researcher's perspective on a topic that's come up here a couple of times: the relationship between the mechanics of cell division, garbage management, and aging. In essence we might look back at the origins of cellular life and decide that aging was in some way an inevitable adaptation in bacteria and other single celled life, stemming from the need to manage their garbage load. A cell, after all, accumulates garbage in the form of malformed proteins and gunk that cannot be broken down. If allowed to build up indefinitely, that garbage will destroy the cell. In order to preserve a lineage, cells therefore practice garbage management when they divide: one daughter cell is given all the garbage, allowing the other to continue pristine.

"This works out well for single celled organisms - after all, they can just write off the occasional daughter lineage turned into a garbage disposal mechanism. It isn't so helpful for the multi-cellular organisms that later evolved. Now the garbage-cluttered cells can't just be written off: they're still present in the organism, being broken, inefficient, and gradually messing up the cellular environment. The ugly realities of cellular garbage gives rise to the garbage catastrophe in aging, and related issues, such as the age-related failure of garbage recycling mechanisms that have evolved to deal with multi-cellular existence."


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!




From Spectroscopy Now: "Eat less and you could live longer. That's the view held by an increasing number of people around the world, with the Calorie Restriction Society one of the main standard bearers. ... Following this diet brings about a reduction in the white adipose tissue mass and this has been proposed as a principal factor in longevity. Aging itself tends to have the opposite effect, increasing adipose tissue stores and insulin resistance and this is where clarification is needed. What are the effects of CR and how do they relate to those of aging? ... [researchers] studied the protein profiles of white adipose tissue of rats. One set was maintained on a 40% CR diet from age 12-24 months, with a second age-matched set fed ad libitum (AD). Proteins were extracted from the white adipose tissue ... a total of 133 proteins were found to be differentially expressed between the CR and AD animals. Many of the CR-induced changes were unaffected by age, implying that CR does not simply arrest or reverse age-associated changes. The influences of the two processes appear to operate under different mechanisms. ... [some] protein expression changes induced by CR gave improved protection against oxidative stress by halting the age-associated reduction in the levels of several antioxidant enzymes and decreasing the levels of stress-induced proteins. ... Both CR and aging also changed the expression of proteins involved in the cytoskeleton, iron storage and energy metabolism ... In the long term, the results could also lead to the identification of novel biomarkers of aging and possible targets for mimetics of CR that could provide the same outcome, an extended lifespan, without having to follow a rigorous and controlled diet."

Maria Konovalenko looks at the work of researcher Ana Cuervo: "the current challenges in the field of aging are two-fold: To continue and complete the molecular dissection of the factors that contribute to aging and to promote the translation of these novel findings into interventions to improve the health-span of the aging human population. ... Dr. Cuervo identified certain defects that lead to decreased activity of chaperone-mediated autophagy (CMA) with age and how to correct and improve cellular function. Dr. Cuervo theorized that the decrease of autophagy could be a determining factor in why some older organisms are unable to fight off cell abnormalities. Her research looked at the breakdown of the various autophagic pathways as the body ages and if restoring these pathways would jumpstart normal cellular activity. ... CMA is involved in at least 30% of the body's cell degradation processes and upon studying this pathway, Cuervo determined that the LAMP-2A protein acts as a vital receptor in the pathway. In recent experiments, livers in genetically modified mice 22 to 26 months old (the equivalent of octogenarians in human years), that were injected with the LAMP-2A protein, cleaned blood as efficiently as those in animals a quarter their age! By contrast, the livers of normal mice in a control group began to fail."

Researchers continue to catalog the parts of our cellular machinery that are affected by longevity-enhancing changes in metabolism, such as the practice of calorie restriction: "Metallothionein (MT) is a low molecular weight protein with anti-apoptotic properties that has been demonstrated to scavenge free radicals in vitro. MT has not been extensively investigated within the context of aging biology. The purpose of this review, therefore, is to discuss findings on MT that are relevant to basic aging mechanisms and to draw attention to the possible role of MT in pro-longevity interventions. MT is one of just a handful of proteins that, when overexpressed, has been demonstrated to increase mouse lifespan. MT also protects against development of obesity in mice provided a high fat diet as well as diet-induced oxidative stress damage. Abundance of MT is responsive to caloric restriction (CR) and inhibition of the insulin/insulin-like signaling (IIS) pathway, and elevated MT gene expression has been observed in tissues from fasted and CR-fed mice, long-lived dwarf mice, worms maintained under CR conditions, and long-lived daf-2 mutant worms. The dysregulation of MT in these systems is likely to have tissue-specific effects on aging outcomes. Further investigation will therefore be needed to understand how MT contributes to the response of invertebrates and mice to CR and the endocrine mutations studied by aging researchers."

This is a novel formulation of aging, though I don't think it has any great impact on the justification for repair strategies such as SENS: "In the past, it has been assumed that all the biological and medical changes that occur in old age are deleterious. It has therefore been concluded that treatment and prevention of such changes in old age should increase healthspan and delay death. However, accruing epidemiological and clinical trial evidence in older humans suggests that this is not the case. Some studies have shown that antioxidants and hormone supplements increase mortality, whereas high blood pressure, obesity, and metabolic syndrome are often associated with improved outcomes in very elderly people. Perhaps, some of these supposedly detrimental changes accompanying old age are in fact evolutionary adaptations to prolong life after reproduction in humans. Indeed, a form of reverse antagonistic pleiotropy or adaptive senectitude might be occurring. Some common biological and medical changes in old age might actually enhance longevity and represent novel targets for improving health in older people."

Via EurekAlert!: scientists "report a new experimental compound that can improve memory and cognitive function in ageing mice. The compound is being investigated with a view to developing a drug that could slow the natural decline in memory associated with ageing. ... the team has identified a preclinical candidate that they hope to take into human trials within a year. ... memory loss has been linked with high levels of 'stress' steroid hormones known as glucocorticoids which have a deleterious effect on the part of the brain that helps us to remember. An enzyme called 11beta-HSD1 is involved in making these hormones and has been shown to be more active in the brain during ageing. ... the team reports the effects of a new synthetic compound that selectively blocks 11beta-HSD1 ... Normal old mice often have marked deficits in learning and memory just like some elderly people. We found that life-long partial deficiency of 11beta-HSD1 prevented memory decline with ageing. But we were very surprised to find that the blocking compound works quickly over a few days to improve memory in old mice suggesting it might be a good treatment for the already elderly. ... The effects were seen after only 10 days of treatment."

Ben Goertzel reports on the recent Personalized Life Extension conference at h+ Magazine: "It was a pretty sophisticated crowd with an attitude both radical and down-to-Earth - the general feeling was something like 'We all pretty much believe that "longevity escape velocity" is likely to happen sometime this century, due to a combination of scientific and technological advances, so if we can just live long enough into the century, we may be able to live centuries or millennia or longer. So now the question is: What can we do, in practice, and so increase the odds that we do live long enough to see the really radical life extension technologies emerge?' Or to put it in Ray Kurzweil's terms: how can we live long enough to live forever? If Kurzweil is right, then in 2045 or so, technology will have advanced far enough that involuntary death will be an unlikely tragedy. In that case, what really matters is to keep our meat-bags chugging till that wonderful date. Whether the precise date is really 2045 or not, the concept still has value. Aubrey de Grey has called it 'the Methuselarity' - the date at which, if you live that long (by hook or by crook), cascading improvements in life extension technology will likely keep extending your lifespan forever."

The quality of automated translation for Norwegian is apparently lagging behind that of more widely used languages, but here is an earthy men's magazine piece on biomedical gerontologist Aubrey de Grey: "There are trees that can live for 5,000 years, and there is evidence that some bacteria have survived for 25 million years. And a small freshwater creature, [called] hydra, does not seem to age at all. They can die [through accident or violence] but [if left alone] will most likely live forever. Old age - which [de Grey believes] is the worst humanitarian crisis of all time - will never kill it. Then it's different with us humans. 100,000 of us die of old [age] every day. ... We are experiencing something that is equivalent to 30 World Trade Centers [each] day, and nobody does a damn thing about it, says de Grey. ... de Grey's great a-ha experience came at four in the morning in June 2000. De Grey had twisted his head back and forth over the old age problem, and now he was jet-lagged in a hotel in Manhattan Beach in California and let the mind drift. Then it hit him: Instead of trying to understand the problem [of aging], it's easier just to fix it. ... de Grey took out pen and paper and wrote down everything in the body that need to be fixed to prevent physical and mental [degeneration]. Surprisingly enough, this list only on nine points, and today it is down to seven. And since then he has worked with a step-by-step treatment for old age, called Strategies for Engineered Negligible Senescence or SENS shortened. He has a dedicated laboratory with researchers who are under the supervising eyes of de Grey, and if it was not [for lack of funding] they believe [that] we will have eternal life [in a laboratory mouse] in a decade."

A report by Ben Best can be found at Depressed Metabolism: "On the first weekend of October, 2010 I was an invited speaker at 'Applied Cryobiology – Scientific Symposium on Cryonics held in Goslar, Germany ... The meeting was the first effort by the German Society for Applied Biostasis (DGAB) to create a milieu for scientific discussion of cryonics-related issues as well as to elevate the scientific status of cryonics and bring more scientists into the field. DGAB hopes to have another such symposium in two years. ... The symposium was originally to be held mainly in German, but there were twice as many attending (about 50) as had been anticipated - and so many were from outside Germany that the organizers decided to have all sessions in English. Although many of the participants had impressive scientific backgrounds, they were overwhelmingly people with a personal interest in cryonics. The organizers struggled to get speakers with scientific credentials, but many of those who would have been otherwise interested and qualified did not want to risk their careers by participation." As is the case for other facets of longevity-related research and development, such as the Strategies for Engineered Negligible Senescence, cryonics has a good scientific foundation, but much of the scientific community - especially in cryobiology - reject and shun it for reasons that have nothing to do with science.

Research suggests that changes in messenger RNA (mRNA) translation - a step in the complex process by which proteins are built from the blueprint of a gene - are important in the metabolic determination of longevity. This appears to be one of the ways in which the TOR gene, and thus rapamycin, influences longevity: "Appropriate regulation of mRNA translation is essential for growth and survival and the pathways that regulate mRNA translation have been highly conserved throughout eukaryotic evolution. Translation is controlled by a complex set of mechanisms acting at multiple levels, ranging from global protein synthesis to individual mRNAs. Recently, several mutations that perturb regulation of mRNA translation have also been found to increase longevity in three model organisms: the budding yeast Saccharomyces cerevisiae, the nematode Caenorhabditis elegans and the fruit fly Drosophila melanogaster. Many of these translation control factors can be mapped to a single pathway downstream of the nutrient responsive target of rapamycin (TOR) kinase. [This suggests] that mRNA translation is an evolutionarily conserved modifier of longevity and [could] influence aging and age-associated disease in different species."

This open access PDF editorial is illustrative of the mainstream scientific examination of human longevity. Demographic studies lead to genetic studies - to identify long-lived populations and then the genetic roots that make them different: "It is now evident from various socio-demographic studies that a greater portion of the population survives into old age, above the seventh decade of life. Projections for Europe estimate that in 1995 13.3% of the population was over the age of 65, whereas by 2015 this figure is expected to rise to 16.3%. However, the factors that promote living after the seventh or eighth decade of life remain unknown. Therefore, a question may arise: what is the 'formula' that allows some elders to avoid chronic diseases, such as cancer and cardiovascular disease? ... Clearly, longevity is a complex attribute determined by factors, such as exposure to disease, variability in sleeping patterns, smoking habits, physical activity and diet, that have a direct effect on longevity, in addition to their indirect emotional and cognitive influence on physiological pathways." This sort of work will continue for many decades, with little sense of urgency and equally little effect upon our lives. It is a world removed from the engineering approach to extending life span advocated by the SENS Foundation, amongst others.



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