This year saw a demonstration showing noteworthy benefits to health and longevity from the targeted destruction of senescent cells in mice - an expected result for many researchers, but one that had yet to happen up to that point. Senescent cells, cell that have removed themselves from the cycle of proliferation, are an evolutionary response to the growing threat of cancer with age, but once in a senescent state they progressively cause harm to surrounding cells and tissue. The immune system destroys many senescent cells, but becomes much worse at this task - along with all its other duties - as time progresses because it suffers from its own age-related issues. As the numbers of senescent cells grow, so does their contribution to the physical failures and declines of aging.

But this entire portion of the basis for degenerative aging could be removed with a therapy that destroyed senescent cells sufficiently well. This is why the earlier mentioned demonstration of senescent cell destruction - and corresponding health benefits - in mice was a welcome advance. Unfortunately, the method used was based on some clever genetic engineering and while effective at eliminating senescent cells without harming other cells in the engineered mouse breed, it has little direct application to the development of human clinical medicine.

Meanwhile, the cancer and immunotherapy research communities are making great strides in developing many forms of nanoscale technology that can be coupled to a sensor and sent to destroy those cells that the sensor reacts with - and without harming any other nearby cells. Researchers have used nanoparticles, antibodies, viruses, and bacteria to home in on cells with specific surface markers or other characteristics, and there deliver some form of killing blow. The trick here is not so much the killing blow, as many of the successful demonstrations of targeted cancer cell destruction did no more than deliver old-style chemotherapy drugs - just in very small doses and on a cell-by-cell basis rather than flooding the whole body. That works very well to minimize side-effects and maximize harm to the cancer.

The point of this sidebar is that these technology platforms could be quickly repurposed to attack senescent cells, but only when there emerges a robust way of distinguishing between senescent and non-senescent cells. So now we watch with interest for published research that touches on that topic, such as this recent open access paper:

Changes in the shape of the nuclear lamina are exhibited in senescent cells, as well as in cells expressing mutations in lamina genes. To identify cells with defects in the nuclear lamina we developed an imaging method that quantifies the intensity and curvature of the nuclear lamina. We show that this method accurately describes changes in the nuclear lamina. Spatial changes in nuclear lamina coincide with redistribution of lamin A proteins and local reduction in protein mobility in senescent cell. We suggest that local accumulation of lamin A in the nuclear evelope leads to bending of the structure. A quantitative distinction of the nuclear lamina shape in cell populations was found between fresh and senescent cells, and between primary myoblasts from young and old donors. Moreover, with this method mutations in lamina genes were significantly distinct from cells with wild-type genes. We suggest that this method can be applied to identify abnormal cells during aging, in in vitro propagation, and in lamina disorders.

As an aside, you might recall that mutant lamin A is the culprit in progeria, and has been postulated to be a low-level contribution to normal aging as well. Expect to see more interest in progeria and potential therapies for that condition if more evidence emerges to link it to cellular senescence and ways to reliably distinguish senescent cells.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

A recent paper: "Birds generally age slower and live longer than similar sized mammals. For birds this occurs despite elevated blood glucose levels that for mammals would in part define them as diabetic. However these data were acquired in respiration states that have little resemblance to conditions in healthy tissues and mitochondrial [reactive oxygen species] production is probably minimal in healthy animals. Indeed mitochondria probably act as net consumers rather than producers of [reactive oxygen species]. Here we propose that (1) if mitochondria are antioxidant systems, the greater mitochondrial mass in athletic species, such as birds, is advantageous as it should provide a substantial sink for [reactive oxygen species]. (2) The intense drive for aerobic performance and decreased body density to facilitate flight may explain the relative insensitivity of birds to insulin, as well as depressed insulin levels and apparent sensitization to glucagon. Glucagon also associates with the sirtuin protein family, most of which are associated with caloric restriction regulated pathways, mitochondrial biogenesis and life span extension. (3) We note that telomeres, which appear to be unusually long in birds, bind Sirtuins 2 and 4 and therefore may stabilize and protect nuclear DNA. Ultimately these flight driven responses may suppress somatic growth and protect DNA from oxidative damage that would otherwise lead to ageing and non-viral cancers."

Link: http://www.ncbi.nlm.nih.gov/pubmed/22198369

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Here is another of the many theories aiming to explain why women live longer than men: "One of the most significant achievements of the twentieth century is the increase in human lifespan. In any period studied, females live longer than males. We showed that mitochondrial oxidative stress is higher in males than females and that the higher levels of estrogens in females protect them against ageing, by up-regulating the expression of antioxidant, longevity-related genes. The chemical structure of estradiol confers antioxidant properties to the molecule. However, the low concentration of estrogens in females makes it unlikely that they exhibit significant antioxidant capacity in the organism. Therefore we studied the mechanisms enabling estradiol to be antioxidant at physiological levels. Our results show that physiological concentrations of estrogens activate estrogen receptors and the MAPK and NFKB pathway. Activation of NFkB by estrogens subsequently activates the expression of Mn-SOD and GPx. Moreover, we have demonstrated that genistein, the most abundant phytoestrogen in soya, reproduces the antioxidant effect of estradiol at nutritionally relevant concentrations by the same mechanism ... We conclude that estrogens and phytoestrogens up-regulate expression of antioxidant enzymes via the estrogen receptor and MAPK activation, which in turn activate the NFkB signalling pathway, resulting in the up-regulation of the expression of longevity-related genes."

Link: http://www.ncbi.nlm.nih.gov/pubmed/22188448

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

So what is the Methuselah Foundation up to these days? As you might know, the Foundation has administered the Mprize for longevity science since 2003: a multi-million dollar prize fund that encourages researchers to find ways to extend healthy life in mice - a good marker for technologies that may then be applicable to other mammals, such as we humans. Last year, the Foundation inaugurated a new prize, the NewOrgan prize that aims to spur greater progress in tissue engineering and the creation of functional new organs from a patient's own cells. This dovetails with the Foundation's investment strategy: helping to fund companies that focus on advanced tissue engineering, such as Organovo, and solving organ transplant issues, such as Silverstone Solutions.

The Methuselah Foundation sent out a sneak peek email yesterday with a pointer to the New Organ Mprize website and the first pledge drive with matching funds: this will be the big thing for the coming year. Here is the text:

Time for something new and personal.

In 2012, the next chapter for Methuselah and the journey for an enduring answer for millions will begin. We are excited to share this preview with our closest supporters and friends.

Introducing New Organ Mprize.

Think of a time when no one has to suffer and die waiting for an organ that never arrives. New Organ is creating the public prize that builds urgency for that future.

Sneak peek.

While we're finishing the campaign's site, we'd like to give you a preview of its homepage. We hope you like it as much as we do. Look for more pages in a few weeks.

Showing momentum.

Our goal is $200,000 by February 28th. To help achieve this and establish traction at launch, Organovo's Keith Murphy has pledged to match gifts up to $25,000.

Become a New Organ Founder.

We invite you to join us at the beginning. Let?s start New Organ with 25% of the job done. Kickstart the prize!

My yearly round of donations remain divided between the SENS Foundation and Methuselah Foundation - the two organizations to appear prominently on the Fight Aging! Take Action page. Both are worthy causes, consistently achieving a great deal more behind the scenes in networking and persuasion with the scientific and research funding communities than is apparent from the front end. A large fraction of the sea change in the aging research community in recent years can be attributed to the communities centered on these organizations.

Aiming to extend the healthy human life span has come to be a respectable goal in the scientific community over the past ten years. That wasn't always the case, and it's easy to forget just how much of a sea change has taken place since the [turn of the century].

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

We live in a world of oral fixation, or whatever equivalent post-Freudian term you'd live to use. It's not too hard to drawn the lines that lead unbroken from the magic of early human societies, insofar as it touched on beliefs regarding the consumption of various things, and the magical thinking of modern societies illustrated by the popularity of useless potions and pills. On the one hand tricksters cloaked as shamans, and on the other hand tricksters cloaked as marketing professionals pretending to use the methods of science. For every hot field of medical science, there are frauds out there somewhere selling edible goods to the credulous, trying to claim some of the mantle.of legitimacy enjoyed by the scientific community while practicing what is in effect an anti-science of belief and deception.

But back inside the real scientific community, we see the oral fixation at work in the amount and range of work on ingested substances. On diet, on tiny portions of diet, on the ingestion of specific substances beyond count, looking for results of significance. Funding for this sort of thing is evergreen, and I think that much of it is a grand waste. The path to longevity is not a freeway passing through the human stomach, but from the weight of research devoted to what we eat you might be forgiven for thinking otherwise. Would that these researchers were spending their time on something more useful, but the fixation of broader society on the mouth and what we put into it steers the strategic direction of research and research funding.

Here are a couple of examples:

Mediterranean diet gives longer life

Scientists at the Sahlgrenska Academy have now studied the effects of a Mediterranean diet on older people in Sweden. They have used a unique study known as the "H70 study" to compare 70-year-olds who eat a Mediterranean diet with others who have eaten more meat and animal products. The H70 study has studied thousands of 70-year-olds in the Gothenburg region for more than 40 years. ... The results show that those who eat a Mediterranean diet have a 20% higher chance of living longer. "This means in practice that older people who eat a Mediterranean diet live an estimated 2 3 years longer than those who don't", says Gianluca Tognon, scientist at the Sahlgrenska Academy, University of Gothenburg.

Are there differences in mortality among wine consumers and other alcoholic beverages?

Wine consumers, especially in comparison with spirits drinkers, have been shown to have higher levels of education and income, to consume a healthier diet, be more physically active, and have other characteristics that are associated with better health outcomes. However, epidemiologic studies have been inconsistent in showing that, after adjustment for all associated lifestyle factors, consumers of wine have lower risk of cardiovascular disease and mortality than do consumers of other beverages. A study based on the long-term follow up of a group of older Americans concluded that the associated lifestyle habits and environmental factors of wine consumers largely explained their better health outcomes.

We live in a world in which ingestion of alcohol has a greater and more active research community associated with it than is the case for serious efforts to develop the means to reverse aging. There will be more and greater publicity and funding generated by debates over tiny changes in life span and risk of disease through alcohol in the diet than there will be for the most important advance in longevity research this year, or any of the other high points in longevity science from the past twelve months. Sad but true. Real longevity science and biotechnology doesn't have much to do with sticking things into your mouth - it's largely low-level manipulation of cells and biomolecules - and in this world of oral fixation that's something of a disadvantage when it comes to publicity and support.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

An example of the sort of screening work presently taking place, in China in this case: "Damaged heart tissue is not known for having much inherent capacity for repair. But now, scientists are closing in on signals that may be able to coax the heart into producing replacement cardiac muscle cells. Using a zebrafish model system, researchers have identified a family of molecules that can stimulate stem cells to develop into beating heart muscle cells. ... Despite advances in modern medicine, management of myocardial infarction and heart failure remains a major challenge. There is intense interest in developing agents that can influence stem cells to differentiate into cardiac cells as well as enhance the inherent regenerative capacities of the heart. Developing therapies that can stimulate heart muscle regeneration in areas of infarction would have enormous medical impact. ... The zebrafish is an excellent model organism to study heart growth and development because there are established genetic approaches that permit visualization of fluorescent beating hearts within transparent embryos. After screening nearly 4,000 compounds, the researchers discovered three structurally related molecules that could selectively enlarge the size of the embryonic heart. The compounds, cardionogen-1, -2, and -3, could promote or inhibit heart formation, depending on when they were administered during development. ... Cardionogen opposes Wnt signaling to induce cardiac muscle cell formation. Importantly, the interaction of cardionogen with Wnt seemed to be restricted to specific cell types. ... Evaluating the potential of cardionogen on human adult and embryonic stem cells is the next logical step. This may ultimately aid in design of therapeutic approaches to enhance repopulation of damaged heart muscle and restore function in diseased hearts."

Link: http://www.eurekalert.org/pub_releases/2011-12/cp-hdy121611.php

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

A Rejuvenation Research paper: "As mammals age, the rate of neurogenesis in the brain declines with a concomitant reduction in cognitive ability. Recent data suggest that plasma-borne factors are responsible for inhibition of neurogenesis. When the circulatory systems of old and young mice are connected, the old mice experience increased neurogenesis and the young mice exhibit less neurogenesis, suggesting the importance of systemic circulating factors. Chemokine CCL11/eotaxin has been identified as a factor that increases with aging. Injections of CCL11 inhibit neurogenesis in young mice, an effect likely mediated by CCR3 receptors on neural stem cells. Identification of a specific factor that plays a causative role in stem cell dysfunction in aging is consistent with data showing that transforming growth factor-? (TGF-?) inhibits satellite cell-mediated repair. Together, these data suggest that the systemic milieu plays a critical role in the aging of adult stem cells. Because adult stem cells help maintain homeostasis by providing the possibility of replacing metabolically damaged differentiated cells, aging of the systemic milieu and stem cell niches may drive functional decline during aging. The identification of a specific systemic change suggests that aging is more amenable to therapeutic modulation than work on global metabolism-derived damage and cellular senescence implies."

Link: http://dx.doi.org/10.1089/rej.2011.1301

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

The latest Rejuvenation Research journal issue is available online. Down a way in the contents list, there's one page commentary on gender that can be read in its entirety provided you're fine with small print:

Life span [will be] limited even in biologically immortal individuals. Death can still occur from causes other than aging such as accident, extrinsic disease, murder, suicide, etc. Due to these factors, the statistical probability of extending life by eliminating aging has been estimated to range from as little as 700 years to a few thousand. Because women tend to take fewer risks than men, estimates for their survival are double those for men. Some authors speculate that because of future developments in medicine and technology, the risk for death can be even more significantly reduced, making it possible to extend human life for as much as 50,000 years. This estimate is obviously the extreme, but for argument's sake let's say it may be possible for cautious, biologically immortal individuals living conservative lifestyles to survive for 10,000 years or so before succumbing to a deadly contagion or catastrophic accident.

Which initially suggests that a world of ageless individuals would be largely a world of women - though by the time agelessness is a going concern, I'd imagine that ad hoc gender transformation and selection will also be practical going concerns. Which is not to mention options beyond the traditional male or female duality, or elective alteration of mental traits such as appetite for risk, decoupling the mind from its biological influences. It's entertaining to take narrow slices of the future and ask how things would change is that one slice stood alone, but the future is a monolith - we'll get the potential for all of these outcomes of biotechnology at once, not one at a time.

From where I stand, the technology needed to reduce risk for a standard issue human far enough to enable 50,000 years of life free from fatal occurrences would have to be some fairly advanced stuff - or at least that is so if the individuals in question intend to live free-range and interesting lives. Safety devices and autonomous watchdogs guided by strong artificial intelligences with millisecond reaction times and long planning horizons spring to mind. That sort of thing will be emerging within a hundred years at the present rate of development, but alongside will come the opportunity to stop being a standard issue human - a fragile package of tissue. The most robust way to reduce risk with the foreseeable high technology of the century ahead seems to be, to me at least, to transform the body rather than strive to protect it.

Your risk of fatality for any given activity is a function of your human physiology. Once the research and development community has achieved the goal of practical biotechnologies for the repair and reversal of aging, that will give us all a few hundred years of life in comparative statistical safety. Technological progress will continue across that long period of time, and I can't imagine that much of the toolkit needed for the next step in long-term risk reduction will remain beyond the human civilizations of the 2200s. Your own personal preferences for that next step will no doubt vary, but I would get my neurons replaced - slowly, one at a time over time, to ensure continuity of the self - with some form of much more robust, easily maintained nanoscale machinery.

...

Physical distribution of the self across many disparate locations is in fact the key point when it comes to considering risk over the long term. Locations have much the same issues with time, probability and bad events as people do. Meteorites happen, as do landslides, earthquakes, war, and volcanoes. The way to reduce your location-based risk dramatically is to spread out. You might imagine a wireless brain, using whatever the most robust communications technology of the time happens to be, scattered in a thousand separate machine bodies or vehicles across a continent, or even the whole planet.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Here is an interesting application of guided tissue growth, that focuses on blood vessels. A wide range of work is under way on blood vessel engineering and control of growth, as the ability to incorporate blood vessels into tissue in specific ways is essential to realizing the most important goals of tissue engineering: "A team of engineers has created a bandage that in just one week not only encourages new blood vessel growth but helps guide that growth as well. ... The ability to pattern functional blood vessels at this scale in living tissue has not been demonstrated before. ... The team [calls] the bandage a 'microvascular stamp.' Unlike similar bandages developed to help spur blood vessel growth, the stamp contains living cells that encourage damaged tissue to grow according to the stamp's pattern. At nearly a centimeter across, the stamp is made of porous material that enables small molecules to sneak through in addition to the larger growth factors. The team tested it on a chicken embryo; when they removed it from the surface a week later, a network of new blood vessels appeared in the pattern of the stamp's channels. Future applications could include not only healing wounds, but also redirecting blood vessels to grow around blocked arteries, and even improving the delivery of cancer drugs by repairing blood vessels that feed cancerous cells."

Link: http://news.cnet.com/8301-27083_3-57346717-247/high-tech-bandage-spurs-blood-vessel-growth/

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

From the New Atlantis, a tour of some of the disturbing views of those who are opposed to enhanced longevity, and in favor of government force used to set limits to life: "Age-retardation technologies are the 'killer app' (so to speak) of enhancements - so deeply and self-evidently appealing that they would seem to sell the whole project of enhancement on their own. Nonetheless, there are those who oppose them. For example, Leon Kass, the former chairman of the President's Council on Bioethics (PCBE) under President Bush, has asserted, 'the finitude of human life is a blessing for every individual, whether he knows it or not.' And Daniel Callahan, co-founder of the Hastings Center, has declared, 'There is no known social good coming from the conquest of death.' Callahan added, 'The worst possible way to resolve [the question of life extension] is to leave it up to individual choice.' When asked if the government has a right to tell its citizens that they have to die, Johns Hopkins University political scientist Francis Fukuyama answered, 'Absolutely.' ... In addition to these concerns, Schaub suggests that 'a nation of ageless individuals could well produce a sclerotic society, petrified in its ways and views.' Daniel Callahan makes a similar argument in a debate with life-extension advocate Gregory Stock, in which he claims, 'I doubt that if you give most people longer lives, even in better health, they are going to find new opportunities and make new initiatives.' Stock goes so far as to help his interlocutor with the hoary example of brain-dead old professors blocking the progress of vibrant young researchers by holding onto tenure. But that seems more of a problem for medieval institutional holdovers like universities than for modern social institutions like corporations. ... In fact, the available evidence cuts against concerns about 'a hardening of the vital social pathways.' Social and technological innovation has been most rapid in those societies with the highest average life expectancies. Yale economist William D. Nordhaus estimates that increases in longevity in the West account for 40 percent of the growth in gross national product for the period 1975-1995. Why? Not only do people work longer, but they work smarter - long lives allow for the accumulation of human capital. ... We do not know what immortality would be like. But should that happy choice become available, we can still decide whether or not we want to enjoy it. Besides, even if the ultimate goal of this technological quest is immortality, what will be immediately available is only longevity. The experience of longer lives will give the human race an opportunity to see how it works out. If immortality is a problem, it is a correctable one. Death always remains an option. Let us turn on its head the notorious argument by Leon Kass that our initial repugnance to biotechnological advances should make us wary of them. Put the other way around, the near-universal human yearning for longer, healthier lives should serve as a preliminary warrant for pursuing age-retardation as a moral good."

Link: http://www.thenewatlantis.com/publications/the-case-for-enhancing-people

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

It is a truism that, in general, people who look ahead to the future both greatly overestimate predicted progress in the near term of twenty years or less and greatly underestimate predicted progress across longer timeframes. One might argue that this is due in part to most memorable predictions being made about industries and technologies in the early stages of an exponential curve - not much happens for many years as people experiment, persuade, bootstrap support and funding, and then a lot happens in a comparatively short period of time after someone hits the big time, gets it right, and the mainstream wakes up to the latest new new thing. But that's an oversimplification; there are many factors at work here, such as the many variants of hopeful but ultimately self-deluding optimism in the advocacy and technology development communities.

So it is a useful exercise to temper our own predictions of what lies ahead with a look back at earlier well-thought-out and detailed predictions of past progress, to see where they fell down. Here's an example via New Cryonet, written in 1987, and making a set of predictions that, in many cases, have yet to come to pass despite being fairly reasonable - we are not as far along as we'd like to be:

Fairly predictive tests for Alzheimer's disease, schizophrenia, depression, some malignancies, heart disease, and most of the rest of the major killers and disablers will probably be in place by 2000 to 2010. Many if not most of these ailments will be assessable in terms of a very sophisticated genetic risk profile which it will be possible to generate in infancy or childhood (or in utero).

...

Tissue rejection will be amenable to treatment in almost all cases by highly selective destruction or inhibition of certain parts of the immune system without the negative consequences of today's immunosuppressive drugs. Monoclonal and synthetic antibodies carrying toxins or regulatory molecules will be used to turn off or destroy the fraction of immune cells which initially respond and proliferate when a transplant is carried out. More widespread transplantation of tissues will be undertaken, including transplantation of limbs and scalp. Xenografts will be used increasingly in the mid to late 1990's and it will not be uncommon for people to have pancreatic tissue from bovine or porcine sources and perhaps hearts, lungs, and livers from other animals. Expect the first workable transplants to be from great apes (chimps, gorillas, orangutans), with porcine and bovine grafts coming later.

...

By the early decades of 2000, significant rejuvenation and geroprophylaxis of skin, bone, immune, and other "high turn- over" tissues will be possible as the natural regulatory molecules which control these systems are understood and applied. Expect several significant synthetic compounds to be discovered with these kinds of properties as well. There will be the possibility of profound improvement in personal appearance and general health as these agents enter the marketplace. By the early years of the 21st century the first generation of compounds effective at "rejuvenating" (i.e., restoring some degree of normal maintenance and repair to existing brain cells) the central nervous system will be available. These drugs will work by turning on protein synthesis and stimulating natural repair mechanisms.

Many of the specific predictions in the article were in fact demonstrated in the laboratory to some degree, and were technically feasible to develop as commercial products by the year 2000, and in some cases earlier but at much greater expense. Certainly there are partial hits for many of the predictions by 2010, in the sense of it being possible, somewhat demonstrated, or in the early stages of being shown to be a practical goal. Yet the regulatory environment in much of the developed world essentially rules out any form of adventurous, rapid, highly competitive development in clinical medicine - such as exists in the electrical engineering, computing, and other worlds. We are cursed therefore with the passage of many years between a new medical technology being demonstrated possible and then attempted in the marketplace ... if it ever makes it to the marketplace at all. This must change if we are to see significant progress.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

A study here shows that calorie restriction reduces levels of mitochondrial damage that accumulates with age - that damage being thought of as a contributing cause of aging - but in different levels in different tissues and different species: "The hypothesis that life-span extension by caloric restriction (CR) is contingent upon the attenuation of macromolecular oxidative damage was tested in two different strains of mice: the C57BL/6, whose life span is extended by CR, and the DBA/2, in which CR has relatively minor or no impact on longevity. Mice were fed ad libitum (AL) or restricted to 40% lesser food, starting at 4 months of age. Protein damage was measured as protein-linked adducts of 4-hydroxy-2-nonenal (HNE) and malondialdehyde (MDA) in skeletal muscle mitochondria at 6 and 23 months of age. Protein-HNE and -MDA content increased with age in C57BL/6 mice and CR significantly attenuated these augmentations. ... DBA/2 mice exhibited little effect of age or CR on protein HNE/MDA content in skeletal muscle mitochondria. In contrast, protein-HNE levels in liver mitochondria showed a significant increase with age in AL-fed mice of both strains, and CR caused significant attenuation of this damage. Overall, results indicated that the age-related increase in protein oxidative damage and its abatement by CR are genotype- and tissue-specific, and not a universal phenomenon."

Link: http://www.ncbi.nlm.nih.gov/pubmed/22182424

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

An open access paper that suggests that producing therapies for the characteristic loss of muscle mass and strength with age - known as sarcopenia - may be more challenging than we'd like it to be: "Several age-related changes occur in skeletal muscle including a decrease in myofiber size and number and a diminished ability of satellite cells to activate and proliferate upon injury leading to impaired muscle remodeling. Although the molecular mechanisms underlying sarcopenia are unknown, it is tempting to hypothesize that interplay between biological and environmental factors cooperate in a positive feedback cycle contributing to the progression of sarcopenia. Indeed many essential biological mechanisms such as apoptosis and autophagy and critical signaling pathways involved in skeletal muscle homeostasis are altered during aging and have been linked to loss of muscle mass. Moreover, the environmental effects of the sedentary lifestyle of older people further promote and contribute the loss of muscle mass. There are currently no widely accepted therapeutic strategies to halt or reverse the progression of sarcopenia. Caloric restriction has been shown to be beneficial as a sarcopenia and aging antagonist. Such results have made the search for caloric restriction mimetics (CRM) a priority. However given the mechanisms of action, some of the currently investigated CRMs may not combat sarcopenia. Thus, sarcopenia may represent a unique phenotypic feature of aging that requires specific and individually tailored therapeutic strategies."

Link: http://impactaging.com/papers/v3/n12/full/100409.html

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm