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We help you stay up to date with the most interesting news in medicine, politics and the healthy life extension community. You can help us by contacting us when you see interesting items online. You can search past news postings through Google by using the form to the right.
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| If only the future of longevity science was as widely supported, understood and acclaimed as the future of regenerative medicine and tissue engineering. The Times Online notes that "within decades stem-cell technology will make it possible to grow replacements for virtually any part of the human body ... the emerging field of regenerative medicine would enable a patient's own cells to be used to build hearts, livers and kidneys, complete with their own blood supply, to replace diseased organs. The advance could make many transplants unnecessary and allow the regeneration of brain tissue and limb parts. ... We know the human genes that can do this do exist, because human foetuses can do it. If a finger is lost before three months' gestation in the womb, it will grow back. The genes are there; we just need to know how to reactivate them. When we started on this work in the 1960s, we knew all these things would become possible . . . it will not be far off. The biggest stumbling block has been money, but now there is huge investment in the field and things are moving rapidly." |
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| A great deal of tomorrow's better, more effective medicine will rest on targeting nanosystems that can deliver therapies to specific cell populations in the body. Much of this development is taking place in the cancer research community, but you can be sure there are a thousand and one other uses: "Using nanoworms, doctors should eventually be able to target and reveal the location of developing tumors that are too small to detect by conventional methods. Carrying payloads targeted to specific features on tumors, these microscopic vehicles could also one day provide the means to more effectively deliver toxic anti-cancer drugs to these tumors in high concentrations without negatively impacting other parts of the body. ... Most nanoparticles are recognized by the body's protective mechanisms, which capture and remove them from the bloodstream within a few minutes. The reason these worms work so well is due to a combination of their shape and to a polymer coating on their surfaces that allows the nanoworms to evade these natural elimination processes. As a result, our nanoworms can circulate in the body of a mouse for many hours. ... We are now using nanoworms to construct the next generation of smart tumor-targeting nanodevices." |
| The Buck Institute for Age Research is one of the recipients of research funds awarded by the California Institute for Regenerative Medicine (CIRM): CIRM "has awarded $20.5 million to the Buck Institute for Age Research to build a 'CIRM Center of Excellence' on its Novato campus. ... The Buck Institute's proposed research program for the Center of Excellence is guided by the promise that human embryonic stem cells may provide a model system to study and understand the process of human aging and age-related disease. ... The specific aims are to use human embryonic stem cells or their differentiated progeny to study how cells self-renew and to examine processes involved in the biology of aging including DNA repair, genome integrity and programmed cell death. The long-term goal of the program is to unravel the mysteries of aging and age-related human diseases by understanding the fundamental biological process of aging in appropriate human cell models." Which is an excellent summary of the slow boat, look-but-don't-intervene approach, and shows why those researchers invested in this approach - rather than the much more direct repair of damage approach and the goal of curing aging as soon as possible - believe, incorrectly, that any successful intervention in aging is a long way away. |
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| Researchers talk about the basis for animal longevity at the Post-Gazette: "What is it about tortoise biology that makes them so long-lived? The same thing can be asked of some even more intriguing creatures in the Methuselah Club, including the rough-eye rockfish (up to 205 years), the bowhead whale (211 years) and the ocean quahog clam (225 years). ... In the bowhead whales, researchers have been able to chart the slow change in the orientation of amino acids in their eyelids, he said, while the rockfish and quahog lay down age-related rings, the rockfish in an ear bone and the quahog on its shell. ... Dr. de Magalhaes said he did a survey two years ago of hundreds of species of mammals, and 'what we showed is there is really no correlation between metabolic rate and life span in mammals.' ... 'I'm a little bit skeptical about the idea that telomeres contribute that much to aging,' said Dr. de Magalhaes, given the fact that mice, which live about four years, have longer telomeres than humans. ... scientists have been able to create mice with short telomeres and with long telomeres, and 'the mice with long telomeres don't have a significant difference in life span.' Unfortunately, the article doesn't delve into mitochondrial biochemistry, which looks like it might be much of the root of differences in life span, in mammals at least. |
| The Methuselah Foundation has reached $7 million pledged to Strategies for Engineered Negligible Senescence research, aimed at the repair and reversal of molecular and cellular damage that causes aging. "Congratulations are due to all the Methuselah Foundation volunteers and generous donors who have made our ongoing SENS research programs a reality. Thank you all! You can find out more about the SENS research funded and organized by the Methuselah Foundation at our website, and in the most recent progress report ... The Foundation currently sponsors research in two of the seven strands of the SENS program: preventing the harm caused by mitochondrial mutations (MitoSENS) and degrading damaging, long-lived cellular debris (LysoSENS). ... A selection of [further] projects within the SENS plan are ready to be launched as Foundation-sponsored research programs. [As] for MitoSENS and LysoSENS, these projects will start small (likely with only a single researcher), with the aim of delivering high leverage in terms of the credibility of the approach." |
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| This is interesting news from the Australian, considering past work on rebooting the human immune system to repair otherwise irreversible damage: "Dr Freedman, who specialises in treating [multiple sclerosis (MS)], wanted to study how the disease unfolds. He set up an experiment in which doctors destroyed the bone marrow and thus the immune systems of MS patients. Then stem cells known as hematopoeitic stem cells, blood-forming cells taken from the bone marrow, were transplanted back into the patients. ... We weren't looking for improvement. The actual study was to reboot the immune system. ... Once MS is diagnosed [you've] already missed the boat. We figured we would reboot the immune system and watch the disease evolve [but] have yet to get the disease to restart ... Not a single patient, and it's almost seven years, has ever had a relapse ... We are trying to find out what is happening and what could possibly be the source of repair." This is still a comparatively unsafe procedure, but with enough incentive, resources will be allocated to make it safer and better. This is good, because benefits to health and longevity are likely to result from a safe way of rebooting an age-damaged immune system. |
| Regenerative medicine moves forward, organ by organ: "The trachea and other respiratory tubes, like most tubes in the body, have an intricate, three-layer architecture. The inner layer, or epithelium, interacts with whatever is flowing through the tube; in the case of the trachea, air. The middle layer is composed of muscle that constricts or relaxes the tube, and the outer layer consists of connective tissue that supports microvessels and small nerves. ... researchers found that it is not necessary to recapture the ordered layering to heal injuries. Instead, they concentrated on restoring cellular health. When cells are intact and have regained their biological function, they need only reside near the injured tissue to enhance overall repair. [Scientists] achieved this repair state by delivering a mixture of new healthy cells derived from the epithelial lining and the nourishing blood vessels. The combination of epithelial and endothelial cells take over the biochemical role lost with cell damage. The healthy cells release growth factors and other molecules necessary for healing tissue, and can modulate their delivery in response to physiological feedback control signals." |
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| Over at Nature, an interview with the new chief science officer of the California Insitute for Regenerative Medicine: "I really think that we're getting awfully close to working with patients now. We will never institutionally neglect basic science, but the shift to translational work is definitely now a priority ... The unknown is that we have no control over the cells once they're transplanted or transfused. I feel very strongly that the animal models of disease do not reflect the heterogeneity of the environments into which we will be putting the cells in diseased humans. Pharmacologically induced Parkinson's disease is not the same as the natural human disease, for example. ... The immunogenicity issue of the transferred cells is far from solved. People are also concerned about tumorigenesis, and there's been a lot of in vitro progress in addressing that. ... I think people underestimate how expensive this research is. Yes, it's a lot of money, but it's certainly not unlimited. We have to figure out a way to be involved in clinical trials, and how best to use our resources in clinical trials. ... We've got to make concrete decisions, at least as far as phase I trials, in the next couple of months." |
| The purpose of cryonics is to preserve the body and brain with as little small-scale damage as possible for revival via plausible future technologies, most likely medical nanomachinery. To save lives, in other words. Depressed Metabolism has previously argued that it's something of an accident of history that the cryonics industry uses cold-based preservation rather than a form of warm chemical preservation, and here elaborates on future molecular nanotechnologies that may achieve warm biostasis: "To see how one approach would work, imagine that the blood stream carries simple molecular devices to tissues, where they enter the cells. There they block the molecular machinery of metabolism - in the brain and elsewhere - and tie structures together with stabilizing cross-links. Other molecular devices then move in, displacing water and packing themselves solidly around the molecules of the cell. These steps stop metabolism and preserve cell structures." |
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| It looks plausible that some portion of the health and longevity benefits of calorie restriction stem from a reduction in the intake of dietary advanced glycation end products (AGEs). AGEs are created in the body as a metabolic side-effect, but also found in your food: "Increased oxidative stress (OS) underlies many chronic diseases prevalent in aging. Data in humans confirm the hypothesis that [AGEs] and other oxidants derived from the diet may be major contributors to increased OS in normal adults as well as those with diabetes mellitus or kidney failure. Mice fed a diet with a lowered (approximately 50%) content of AGEs or a typical calorie-restricted (CR) diet, accumulated a smaller amount of AGEs [and] did not have increased oxidant stress or cardiac or kidney fibrosis with aging. However, the findings in mice fed a CR diet with an increased content of AGEs resembled those in mice fed a nonrestricted diet that had the usual higher content of AGEs. Thus, there was an inverse correlation between the dietary AGE content, [oxidative stress], organ damage, and life span." |
| Ouroboros on just how many stem cells we have: "It is widely accepted that stem cells are involved in tissue regeneration. It is also widely accepted that (in most organs) stem cells are vanishingly rare. So: if there doesn't happen to be a stem cell adjacent to a site of damage, how can stem cells be involved in the process of tissue repair? There might be more stem cells than we think, because we've been missing them for some reason. This possibility is strongly supported by the recent findings of Zuba-Surma et al., who have discovered a population of tiny pluripotent cells (termed, appropriately, very small embryonic-like, or VSELs) scattered throughout the body. ... Note that both VSEL number and potency diminish with age, consistent with the decrease in proliferative and regenerative capacity that we see in older animals. ... Required skepticism: VSELs are both brand new and (so far as I can tell) idiosyncratic to a single group's work. Before we get too worked up about this, I'd like to see the work reproduced by other labs and in other systems. Hopefully that sort of confirmation is already underway." The easier stem cells become to source, the faster research and development will proceed. |
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| In a similar fashion to the way in which antioxidants change from dubious to demonstrably beneficial for lifespan when targeted to mitochondria, it is proposed that chelation targeted to the cell's lysosomes can slow the accumulation of lipofuscin in your cells. You might recall that lipofuscin buildup with age contributes to age-related degeneration by eventually destroying the ability of cells to function. "Since the sensitivity of lysosomes to oxidative stress can be manipulated by altering the intralysosomal level of redox-active iron, it follows that lipofuscin formation might also be influenced. It is suggested that pulse doses of iron chelators that easily penetrate membranes could be used to diminish lipofuscinogenesis." But don't run out to buy chelation products - ingesting that stuff won't send it anywhere near your lysosomes, just as swallowing antioxidant products won't affect your mitochondria. More engineering is needed, and in this case a technology demonstration to confirm the proposal. |
| Stress speeds some modes of age-related decline, probably via the mechanisms of chronic inflammation: "Responses to stress anticipate adaptation to an unacceptable disparity between real or imagined personal experience and expectation, including adaptive stress, anxiety, and depression. However, if stress persists, it may lead to chronic diseases, ranging from inflammation and cancer to degenerative diseases. For some time, only remarkable stress was acknowledged to induce immune and vascular alterations, such as infection or hypertension. Now it is known that moderate stress independent of conventional risk factors can induce a potent alteration of health conditions and consequently shorten life quality and lifespan. ... Stressful life conditions turn out to induce a diffuse (systemic) pro-inflammatory status. Subclinical chronic inflammation is an important pathogenic factor in the development of metabolic syndrome, a cluster of common pathologies, including cardiovascular disease." As for other lifestyles that induce chronic inflammation, you can wait (and suffer) while researchers build drugs that block the mechanisms at fault, or you work to change your circumstances to cause less damage over the long run. |
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| Life expectancy is increasing, and the rate of increase is accelerating. People live longer than they expect to live. If you lay the foundations of your future - savings, investment, work - with an eye to your grandparent's lifespan and strategies, then you're not planning well. "As greater longevity is increasingly becoming a fact of life, people are leaving themselves vulnerable to financial hardship at a time when they are most in need ... Nearly half the population of the UK said they were only expecting to live to the same age as their parents' generation ... Interestingly, whilst people do not realise the possibility of themselves living longer than their parents, they do recognise that their children will live longer lives than they will. However, 18-24 year olds grossly underestimate this, with only 25% of them thinking that their children will live longer, whilst 44% 55 year olds thought this. ... People acknowledge increased longevity for younger generations but do not realise that this is a very real issue for them today." Plan for an interesting future - and recognize that you have more than enough time to save and invest all you will need, even in the best scenarios of radical life extension. |
| The Understanding Aging conference will be held in Los Angeles in late June, and the early registration and abstract submission deadlines are only two weeks away. By mail from conference organizer Aubrey de Grey: "The program has over two dozen confirmed speakers, all of them world leaders in their field. As for previous conferences I have [co-] organised, the emphasis of this meeting is on 'applied biogerontology' -- the design and implementation of biomedical interventions that may, jointly, constitute a comprehensive panel of rejuvenation therapies, sufficient to restore middle-aged or older laboratory animals (and, in due course, humans) to a youthful degree of physiological robustness. ... registration for the conference includes preferential admission to the free public preconference 'Aging: the disease, the cure, the implications.'" You'll recognize many of the names on the conference agenda - an assembly of leaders in their fields and people of influence. |
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| Correlations are pointers - they indicate where future research and development may best be directed. Here, researchers demonstrate a strong correlation between mammalian life span and various mitochondrial characteristics: "In animal cells, mitochondria are semiautonomous organelles [with] their own code and genome (mtDNA). The semiautonomy and restricted resources could result in occasional 'conflicts of interests' with other cellular components, in which mitochondria have greater chances to be 'the weakest link,' thus limiting longevity. ... (1) to what extent the mammalian maximum life span (MLS) is associated with mtDNA base composition? (2) Does mtDNA base composition correlate with another important mitochondria-associated variable - resting metabolic rate (RMR) - and whether they complement each other in determination of MLS? ... Analysis of 140 mammalian species revealed significant correlations ... To the authors' knowledge, it is the highest coefficient of MLS determination that has ever been reported for a comparable sample size. Taking into account substantial errors in estimation of MLS and RMR, it could mean that [this explains] most of the MLS biological variation. [This leads us to] mitochondria as a primary object for longevity-promoting interventions." |
| This paper proposes that the next step for recent advances in engineering pluripotent stem cells is to create these cells directly, inside the body: "Stem cells are the major factor ensuring mammalian regeneration. Cell replacement therapy is an attempt to follow this natural process. Another strategy suggests a controlled de-differentiation of somatic cells to a stem-like state with subsequent re-differentiation. Indeed, the cultured mammalian somatic cells may be reprogrammed to a pluripotent state by the induction of a specific set of genes. The next logical step toward the goal of organism rejuvenation is to test the possibility of inducing the pluripotent state in somatic cells in vivo. Such an approach has the potential to improve upon and overcome several obstacles facing today's cell replacement therapy." This is an interesting line of thinking; why not simply create new stem cells right where they are needed? |
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| If you've been following along, you'll recall that many of the most interesting biotechnology demonstrations in recent years work because they target very specific parts of the cell. For example, targeting antioxidants to the mitochondria extends life in mice where straightforward application of antioxidants does not. Here, the Telegraph reports on a related approach for an Alzheimer's therapy: hitting a part of the disease mechanism that's already been tried, but this time localizing the action of the drug to a specific structure within the cell. "The drug targets the membrane of brain cells, focusing on compartments in the membrane, called 'rafts', that play a central role in many cellular processes. Although this drug is not the first to target the enzyme, called beta secretase, it is the first to do so in the right place, in the 'intracellular membrane compartment' where the enzyme triggers the protein deposit build-ups. The team has devised a way to anchor the drug to the membrane to stop the harmful deposits." |
| ShrinkWrapped expands on the terrible cost imposed upon progress by the FDA: "The development of our cumbersome and onerous regulatory environment that will slow the availability of drugs to those who would benefit from it is a sad story of missed opportunities and risk aversion ... the FDA was established and set up a framework for approving drugs only after they were shown to be safe and effective. The terrible problem for medicine is that there is no such thing as a drug that can be proven to be completely safe. ... On every level it makes sense for us to develop anti-aging treatments. Losing the abilities of those who are most skilled and experienced on a regular basis is wasteful of human resources. Yet our current regulatory environment not only precludes developing drugs that could slow aging, but makes studies to show their safety and effectiveness impossible to perform. ... as in any bureaucracy, the FDA is not going to be able to modify its mandate without a tremendous push from those most likely to be effected by their conservatism." |
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| Dry wit from Ouroboros on the very long-lived PEPCK-Cmus mice: "It's become reflexive to ask whether a long-lived mutant is living longer because it's calorie-restricted for some reason, incidental to the main phenotype conferred by the mutation, but this is not the case here: In order to preserve their enviable bods, PEPCK-Cmus mice eat 60% more than controls - so they're not extending their lifespan by dieting. If anything, they're anti-dieting: their increased metabolic efficiency means they’re harvesting more calories per gram of carb or fat than normal animals. No word yet on what happens if you do try to calorie-restrict them; I can imagine it going either way but am holding out hope for tiny explosions. ... The PEPCK-Cmus seem to have it all: great bodies, long lives, extended reproductive and sexual lifespans, and no need to limit their appetites. The down side? Apparently, they are complete assholes: the mutants are aggressive and hyperactive, traits heretofore unheard-of among muscular, fit humans (and, indeed, in the field of biogerontology)." |
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