Fight Aging! Newsletter, September 5th 2011

September 5th 2011

The Fight Aging! 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 Fight Aging!



- Thoughts on 100 Plus
- Perhaps Cryonics Needs a Luxury Line
- Creating People: Necessary, but Not Very Nice?
- Mixing Old and Young Blood is Informative
- Discussion
- Latest Headlines from Fight Aging!


100 Plus is a recently published book on the topic of longevity science and advocacy for building longer human life spans:

"To my eyes, the book is essentially a fast overview of the last ten years of science, debate, important subjects, and noteworthy people in the aging research and longevity advocacy communities. A survey of the historical and mythological roots of present day attitudes serves as a springboard into a fast look at some of the important lines of medical research and development - SENS, tissue engineering, longevity genes, and so forth. Then it's off to observe the squawking of Malthusians and their resource-based objections to engineering greater human longevity, followed by a side-trip into philosophical discussions of longevity, and then a soujourn in the realm of economics to talk seriously about how the length of life shapes society. The book is rounded out by a glance at some of the present cast of vocal movers and shakers in the longevity advocacy and research communities: Aubrey de Grey of the SENS Foundation, David Gobel of the Methuselah Foundation, Peter Thiel, Ray Kurzweil, and a range of others in that same broad network - people willing to stand up, set forth, and make efforts to do something about aging.

"100 Plus is, I think, a good book to give to the average fellow in the street who would be flattened and slain by the attempt to read Aubrey de Grey and Michael Rae's Ending Aging. That book is where the meat is - but 100 Plus is a Cliff's Notes for the current state and direction of longevity science and the advocacy community supporting it. That is a useful thing: a person reading 100 Plus will wind up in roughly the same place as a casual reader of the high points of Fight Aging!"


It is possible that the cryonics industry might benefit from a company or product line aimed at people who can afford to pay a million dollars for their cryosuspension:

"While you might not think of it as such, given the $100,000+ sticker price on a cryosuspension ordered at short notice, cryonics is actually a service priced for the mass market: people who can plan enough to regularly put aside a little for the long term. Most customers pay for cryonics through life insurance, which when started in middle age is no more than a very modest monthly payment - less than your car payments, perhaps less than your car insurance payments. There is nothing wrong with that per se, but the industry isn't overcoming the barriers to growth. The most reliable way of pushing through a barrier to growth is investment: large sums of money poured into marketing, research, development and so forth.

"There are two sources of capital for investment: investors and your customers. ... Obtaining funding from early customers is a time-honored tradition in many businesses [as] the early customers tend to be wealthy and pay high prices for their early access to a product. The money they provide pays off the debts of prior research and development and funds ongoing growth - this is a part of the process in many industries by which products start out as a costly luxury item and later become a mass-market commodity that is both far cheaper and far better.

"Cryonics seems to have skipped the costly luxury item stage in its existence, which is both interesting and possibly a liability for the industry in the long term. One might envisage some form of Cryonics Platinum organization that offers $500,000 or $1 million packages for folk like Simon Cowell, Ted Williams, politicians, and other multimillionaires who can both afford it and have use for the additional services, security, process management, and cachet that a higher price point can supply. I have no idea whether such a thing is viable, but I don't see any obvious purely economic reason as to why it wouldn't be. It's really little different in structure than, say, the business of long-term leasing of luxury yachts or private jets and their crews. Something to think about."


The human condition is something of an unpleasant hole that we're digging out way out of slowly, generation by generation. It looks like we're near the top, but it's still a valid question as to how ethical it is to knowingly create new people who have a chance of suffering through death by aging:

"Less us ponder the subject of having children in the face of the existence of aging coupled with the possibility of progressively defeating aging - perhaps to the point where some of us alive today will escape age-related death by the skin of our teeth. Or perhaps not if we don't get our act together here and now. Evidently we need to have children in order to have the chance of incrementally defeating aging by building ever better versions of a biological repair kit to reverse ever more of the damage that causes degeneration and death. This task is one of decades, long enough that it may be today's researchers who start the job, but it'll be younger hands that finish it - their children and grandchildren. Yet creating people is somewhat like drafting them into a war and a human condition that they didn't ask for: 'There's a task we need you for, son, you and the rest of your generation. We may or may not manage to complete it, but we certainly won't without your help - and if we don't get this done, we're dead all too soon, a slow death, heavy on the pain and suffering. We'll be dragged away first so you get to see the end in all its horror, with plenty of sleepless nights to think it over before it happens to you as well. Oh yes, and most people don't see the need for any of this work and think the pain and suffering and death is just dandy. So that's the deal, a raw one all round - welcome to the asylum, son. No need to thank me.'"


Researchers are continuing to learn from the mixing of young blood with old mice and old blood with young mice:

"Stanford University School of Medicine scientists have found substances in the blood of old mice that makes young brains act older. These substances, whose levels rise with increasing age, appear to inhibit the brain's ability to produce new nerve cells critical to memory and learning. ... An early step in the Stanford team's study involved connecting the circulatory systems of pairs of old and young mice via a surgical procedure, so that blood from the two mice comingled. "This way, we could examine the effects of old mice's blood on young mice's brains, and vice versa. ... We saw a threefold increase in the number of new nerve cells being generated in old mice exposed to this 'younger' environment." ... In contrast, the young members of old/young mouse pairs exhibited fewer new nerve cells in the dentate gyrus than did young mice untethered to elders."

A part of aging is the steady decline in stem cell activity and generation of new cells necessary to maintain tissues. Some parts of aging are a sort of wearing away as the processes of cell proliferation slow down and stop keeping pace with day to day damage. This is theorized to be an evolved response that balances life span between risk of cancer on one side, due to increasing DNA damage and other disarray, and risk of death due to unrepaired tissue on the other. As cancer detection and therapies become better, we would want to prevent or reverse this decline in stem cell activity and cell generation for tissue repair - and researchers are now cataloging key control mechanisms that might be altered with designed drugs.


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!



Friday, September 2, 2011
An open access review paper in PDF format that discusses some of the fine details of current research into the mechanisms by which calorie restriction slows aging. This work is aimed at establishing a level of understanding sufficient to produce calorie restriction mimetic drugs that also slow aging: "The molecular mechanisms of aging are the subject of much research and have facilitated potential interventions to delay aging and aging-related degenerative diseases in humans. The aging process is frequently affected by environmental factors and caloric restriction is by far the most effective and established environmental manipulation for extending the lifespan of various animal models. However, the precise mechanisms by which caloric restriction affects lifespan are still not clear. Epigenetic mechanisms have recently been recognized as major contributors to nutrition-related longevity and aging control. Two primary epigenetic codes, DNA methylation and histone modifications, are believed to dynamically influence the chromatin structure resulting in expression changes of relevant genes. In this review, we assess the current advances in epigenetic regulations in response to caloric restriction and how this impacts cellular senescence, aging and potential extension of a healthy lifespan for humans. Enhanced understanding of the important role of epigenetics in control of aging through caloric restriction may lead to clinical advances in the prevention and therapy of human aging-associated diseases."

Friday, September 2, 2011
An interesting discovery, and one more benefit of exercise: "researchers have found one more reason to exercise: working out triggers influential stem cells to become bone instead of fat, improving overall health by boosting the body's capacity to make blood. The body's mesenchymal stem cells are most likely to become fat or bone, depending on which path they follow. ... The exercising mice ran less than an hour, three times a week, enough time to have a significant impact on their blood production ... In sedentary mice, the same stem cells were more likely to become fat, impairing blood production in the marrow cavities of bones. ... The composition of cells in the bone marrow cavity has an important influence on the productivity of blood stem cells. In ideal conditions, blood stem cells create healthy blood that boosts the immune system, permits the efficient uptake of oxygen, and improves the ability to clot wounds. Bone cells improve the climate for blood stem cells to make blood. But when fat cells start to fill the bone marrow cavity - a common symptom of sedentary behavior - blood stem cells become less productive, and conditions such as anemia can result. ... Some of the impact of exercise is comparable to what we see with pharmaceutical intervention. Exercise has the ability to impact stem cell biology. It has the ability to influence how they differentiate."

Thursday, September 1, 2011
A mainstream press article on exercise and aging: "As we age, our bodies change in ways that challenge athletic ability. But exercise also can slow down - and in some cases even prevent - some of the physiological ravages of time. ... A lot of things that we thought were just inherent to the aging process and were going to happen no matter what don't really have to happen if you maintain an appropriate lifestyle. ... How much can exercise slow down the ravages of aging? Potentially a lot. It will partially, but not completely, prevent arterial stiffening with age and completely prevent the dysfunction of the arterial lining that develops with age ... Exercise, it turns out, is probably as powerful as any other kind of prevention strategy or treatment that has been assessed so far. ... . For 21 years, researchers at Stanford University have studied the effects of consistent exercise on 284 runners 50 and older. In a 2002 article [they] reported that - 13 years into the study - a control group of 156 similar people who exercised much less on the whole than the runners had a 3.3 times higher death rate than runners as well as higher rates of disabilities. In a 2008 [study] they reported that after 19 years, 15% of runners had died, compared with 34% of the control group. After 21 years, runners had significantly lower disability levels than non-runners; their death rates from cardiovascular events, cancer and neurologic disorders were much lower than in non-runners - 65 of the runners had died of cardiovascular, neurologic and cancer events compared with 98 deaths in the control group."

Thursday, September 1, 2011
News of another step towards the availability of autologous stem cell therapies in US clinics: "Using a patient's own bone marrow stem cells to treat acute stroke is feasible and safe ... The trial was the first ever to harvest an acute stroke patient's own stem cells from the iliac crest of the leg, separate them and inject them back into the patient intravenously. ... In order to bring stem cells forward as a potential new treatment for stroke patients, we have to establish safety first and this study provides the first evidence in addressing that goal. Now we are conducting two other stroke cell therapy studies examining safety and efficacy, one of which can be administered up to 19 days after someone has suffered a stroke. ... Of the 10 patients enrolled in the study, there were no study-related severe adverse events. ... Although the study was not intended to address efficacy, the investigators compared the study group with historical control patients ... In that comparison, the study team found a number of patients who did better compared with controls. However, [that] type of analysis has limitations." The US medical development community is years behind Korean and even Brazilian researchers in this work, who were testing bone marrow stem cells for stroke in humans back in 2004 and 2005. That sort of delay, and the financial costs accompanying it, are some of the consequences of the regulatory policies of the FDA.

Wednesday, August 31, 2011
Via EurekAlert!: "When the body fights oxidative damage, it calls up a reservist enzyme that protects cells - but only if those cells are relatively young, a study has found. [Biologists] discovered major declines in the availability of an enzyme, known as the Lon protease, as human cells grow older. ... Lon protects the mitochondria - tiny organisms in the cell that convert oxygen into energy. The conversion is never perfect: Some oxygen leaks and combines with other elements to create damaging oxidants. Oxidation is the process behind rust and food spoilage. In the body, oxidation can damage or destroy almost any tissue. Lon removes oxidized proteins from the mitochondria and also plays a vital role in helping to make new mitochondria. ... To fight the oxidant, young cells doubled the size of their Lon army within five hours and maintained it for a day. In some experiments, young cells increased their Lon army as much as seven-fold. Middle-aged cells took a full day to double their Lon army, during which time the cells were exposed to harmful levels of oxidized proteins. Older cells started with a standing Lon army only half as large and showed no statistically significant increase in Lon levels over 24 hours." It is worth noting that the age of individual cells and the age of a person don't have much to do with one another except in some long-lived tissues where the same cells operate throughout life. But you might recall that mitochondrially-targeted antioxidants can increase life span in mice, and mitochondrial damage is important in aging - this research is consistent with all of that, and may lead to another way to extend life via protection of mitochondria.

Wednesday, August 31, 2011
Researcher João Pedro de Magalhães and colleagues are working on a new online resource: "We have developed a new web portal to integrate molecular, physiological ,and pathological age-related data that may be of interest. ... The Digital Ageing Atlas is a portal of changes covering different biological levels. There are currently portals for both humans and mice. The idea is to integrate molecular, physiological and pathological age-related data and create an interactive portal that serves as the first centralised collection of ageing changes and pathologies. ... It allows users to search and retrieve age-related changes at different levels, allowing a better understanding of the interplay between such changes and obtain new insights. We also think this will be an important new resource for modelling and for the systems biology of ageing and hope you will find it useful. Although so far we focused mostly on human aging, a preliminary mouse version of the portal is on-line already."

Tuesday, August 30, 2011
Given the current state of research, I'd say that optimizing exercise for its effects on longevity is as much a fool's game as optimizing diet - if you want to take it on as a hobby, then by all means, but don't expect to beat the scientific community in terms of finding a better way, or to know how well you're doing. Obtaining significant benefits to life expectancy is easy: just exercise as recommended by physicians, the standard 30 minutes of aerobic exercise a day. The tricky question is whether there is a reliable way of gaining more expected years of life than are provided by that 80/20 position. But the research keeps rolling in, so perhaps one day there will be sufficient weight of evidence to say in confidence that one way of exercising is significantly better than another: "A study conducted among cyclists in Copenhagen, Denmark showed that it is the relative intensity and not the duration of cycling which is of most importance in relation to all-cause mortality and even more pronounced for coronary heart disease mortality. The [study] concluded that men with fast intensity cycling survived 5.3 years longer, and men with average intensity 2.9 years longer than men with slow cycling intensity. For women the figures were 3.9 and 2.2 years longer, respectively ...The groups were adjusted for differences in age and conventional risk factor levels. Current recommendations prescribe that every adult should accumulate 30 minutes or more of moderate physical activity in leisure time, preferably every day of the week. The optimal intensity, duration and frequency still have to be established. ... this study suggests that a greater part of the daily physical activity in leisure time should be vigorous, based on the individuals own perception of intensity."

Tuesday, August 30, 2011
Via EurekAlert!: "It is a well-established fact that as we grow older, our bones become more brittle and prone to fracturing. It is also well established that loss of mass is a major reason for older bones fracturing more readily than younger bones, hence medical treatments have focused on slowing down this loss. However, new research [shows] that at microscopic dimensions, the age-related loss of bone quality can be every bit as important as the loss of quantity in the susceptibility of bone to fracturing. Using a combination of x-ray and electron based analytical techniques as well as macroscopic fracture testing, the researchers showed that the advancement of age ushers in a degradation of the mechanical properties of human cortical bone over a range of different size scales. As a result, the bone's ability to resist fracture becomes increasingly compromised. This age-related loss of bone quality is independent of age-related bone mass loss. ... Mechanical properties of stiffness, strength and toughness arise from both the characteristic structure at the nanoscale, and at multiple length scales through the hierarchical architecture of the bone. These length scales extend from the molecular level to the osteonal structures at near-millimeter levels. An osteon is the basic structural unit of compact bone, comprised of a central canal surrounded by concentric rings of lamellae plates, through which bone remodels. ... Mechanisms that strengthen and toughen bone can be identified at most of these structural length scales and can be usefully classified, as in many materials, in terms of intrinsic toughening mechanisms at small length scales, promoting non-brittle behavior, and extrinsic toughening mechanisms at larger length scales acting to limit the growth of cracks. These features are present in healthy, young human bone and are responsible for its unique mechanical properties. However, with biological aging, the ability of these mechanisms to resist fracture deteriorates leading to a reduction in bone strength and fracture toughness."

Monday, August 29, 2011
Small blood vessels are a great challenge in tissue engineering: both creating them in the first place in order to supply blood to constructed tissue, and then linking them into the body's existing blood supply when tissue is transplanted. The smaller the blood vessels, the harder this all becomes - so better ways of linking blood vessels together are necessary. "Reconnecting severed blood vessels is mostly done the same way today - with sutures - as it was 100 years ago ... Now, a team of researchers [has] developed a sutureless method that appears to be a faster, safer and easier alternative. In animal studies, a team [used] a poloxamer gel and bioadhesive rather than a needle and thread to join together blood vessels ... The big drawback of sutures is that they are difficult to use on blood vessels less than 1 millimeter wide. ... Sutures are troublesome in other ways, too. They can lead to complications, such as intimal hyperplasia, in which cells respond to the trauma of the needle and thread by proliferating on the inside wall of the blood vessel, causing it to narrow at that point. This increases the risk of a blood clot getting stuck and obstructing blood flow. In addition, sutures may trigger an immune response, leading to inflamed tissue that also increases the risk of a blockage. The new method could sidestep these problems. ... [Researchers used a] thermoreversible poloxamer called Poloxamer 407. It is constructed of polymer blocks whose properties can be reversed by heating. [They modified] the poloxamer so that it would become solid and elastic when heated above body temperature but dissolve harmlessly into the bloodstream when cooled. The poloxamer then was used to distend both openings of a severed blood vessel, allowing researchers to glue them together precisely. The researchers used a simple halogen lamp to heat the gel. In tests on animals, the technique was found to be five times faster than the traditional hand-sewn method, according to the study. It also resulted in considerably less inflammation and scarring after two years. The method even worked on extremely slim blood vessels - those only 0.2 mm wide - which would have been too tiny and delicate for sutures."

Monday, August 29, 2011
From the SENS Foundation: "The fifth biannual Strategies for Engineered Negligible Senescence biomedical conference is just days away. Getting ready for the trip has cast my mind back not only to previous meetings of this exciting interdisciplinary series, and also to the recent 40th meeting of the American Aging Association (AGE). Along with its international sister organization, the International Association for Biomedical Gerontology (IABG), AGE was the first, and remains the premier, professional scientific organization focused specifically on biomedical research in aging. That is, much of biogerontology research is dedicated to pursuing an ever-more-granular understanding the metabolic processes that contribute to, or fail as a result of, the degenerative aging process. But the scientists at AGE (and IABG) focus their work not on understanding age-related decay, but on its biomedical amelioration. ... While the rest of the conference included a wide diversity of biogerontology research, there was still a noticeably higher content of experimental interventions in the aging process and aspects of age-related degeneration than in previous years. ... Organized by Dr. de Grey, the preconference 'Late-onset intervention against aging: Tools, approaches, impact' brought the focus squarely back on AGE's interventive raison d'être -- and shed its most intense light on progress toward interventions that could meaningfully bend the degenerative aging curve when administered to persons who are already in the last decades of a current life expectancy. It is these people - individuals past the age of ~60 - for whom the medial need for intervention is most pressing, and whose generational demographic trajectory under 'aging as usual' poses the most dire social challenges. Therefore, therapies that will slow, arrest, or reverse age-related ill-health and frailty stand to provide the most good - to each aging person, and to societies as a whole."



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