|
|
| Are you new to healthy life extension? Click here to find out more about living a longer, healthier life. More >> |
|
|
|
|
|
You can help to make therapies for aging and life extension medicine a reality. Click here to participate in improving your future health and longevity!
|
|
|
|
|
Place our comments, news and links on your website, or subscribe to our RSS feed. Click here to see how easy it is.
|
|
|
|
|
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.
|
|
|
|
|
|
| As an addendum to prior discussions of the plasma membrane theory of longevity and related metabolic rate correlations: "Metabolism is a defining feature of all living organisms, with the metabolic process resulting in the production of free radicals that can cause permanent damage to DNA and other molecules. Surprisingly, birds, bats and other organisms with high metabolic rates have some of the slowest rates of senescence begging the question whether species with high metabolic rates also have evolved mechanisms to cope with damage induced by metabolism. To test whether species with the highest metabolic rates also lived the longest I determined the relationship between relative longevity (maximum lifespan), after adjusting for annual adult survival rate, body mass and sampling effort, and mass-specific field metabolic rate (FMR) in 35 species of birds. There was a strongly positive relationship between relative longevity and FMR, consistent with the hypothesis. This conclusion was robust to statistical control for effects of potentially confounding variables such as age at first reproduction, latitude and migration distance, and similarity in phenotype among species because of common phylogenetic descent. Therefore, species of birds with high metabolic rates senesce more slowly than species with low metabolic rates." |
| Researchers have demonstrated an Alzheimer's therapy that removes amyloid plaque, but that doesn't halt or reverse neurodegeneration: "The theory was that dementia could be slowed or reversed once the plaques were cleared, and experiments in animals have shown that removing these plaques improves brain function. ... long-term follow-up of Alzheimer's patients treated with [the therapy] did show, 'a reduction in the number of plaques in the brains of patients -- in some cases there was a virtually complete removal of plaques. Crucially, there was no evidence that the patients benefited by the removal of plaques and even those subjects with virtually complete removal continued to deteriorate and had severe end-stage dementia prior to their death.' ... [researchers now believe] that removing plaques - at least by this method - is unlikely to make a significant difference to the clinical outcome of patients with established Alzheimer's disease ... it strongly suggests that plaques are not sufficient on their own to account for disease progression." |
|
|
|
|
|
| For all the obvious reasons, actuaries would love to be able to predict human longevity with accuracy. But is that possible with present or near-future tools, even setting aside considerations of rapid progress in biotechnologies of rejuvenation? Researcher Leonid Gavrilov here excerpts some of a recent paper on that subject: "Who has a better chance to become a centenarian - a taller or a shorter person? Is it better to be slender or stout? We know that most centenarians are both short and slender in their body build, but these measurements made at older ages could be misleading because they might only reflect body shrinkage as a result of aging. We were also intrigued by other possible predictors of long life. Is it better to be a farmer or an actuary in order to survive to 100? Does the number of children a person has affect their chances to celebrate their 100th birthday? Is it better to have dark eyes or light eyes? All these personal characteristics could be useful for actuaries if a strong association between them and exceptional longevity were to be established." |
| The MIT Technology Review looks at continued attempts to understand the degree to which present healthy human longevity is influenced by genes: "An ambitious plan to sequence 100 genes in 1,000 healthy old people could shed light on genetic variations that insulate some people from the ailments of aging, including heart disease, cancer, and diabetes, allowing them to live a healthy life into their eighties and beyond. Rather than focusing on genetic variations that increase risk for disease, scientists plan to focus on genes that have previously been linked to health and longevity. ... advances in genetic screening technologies have allowed scientists to start searching the genome for clues to healthy aging and a lengthy life span. That work has revealed that the genomes of healthy old people are not blemish free. ... These people have genetic susceptibility markers for many serious diseases [but] they don't get any of these diseases. What is the explanation? What might account for their insulation from these diseases?" Genes are not fate - evidence to date suggests that lifestyle choices have much more weight for all but the most genetically unlucky, and those choices are reflected in epigenetic variations, not genetic variations. |
|
|
|
|
|
| The MIT Technology Review looks at a promising strategy in tissue engineering: "Tissue engineers are ambitious. If they had their way, a dialysis patient could receive a new kidney made in the lab from his own cells, instead of waiting for a donor organ that his immune system might reject. Likewise, a diabetic could, with grafts of lab-made pancreatic tissue, be given the ability to make insulin again. But tissue engineering has stalled in part because bioengineers haven't been able to replicate the structural complexity of human tissues. Now researchers have taken an important first step toward building complex tissues from the bottom up by creating what they call living Legos. These building blocks, biofriendly gels of various shapes studded with cells, can self-assemble into complex structures resembling those found in tissues. ... This will be an effective way to put the cells where we want them to be. You can probably generate a tissue with a higher complexity [using] the new method than is possible with a scaffold that has to be seeded with cells." Compare and contrast with the use of whole-organ cell matrix templates, another recent development aimed at solving the same problem. |
| Chronic stress correlates with shorter telomeres, as well as with worse health. Via EurekAlert! researchers are proposing a mechanism by which telomere length is reduced by stress, leading to a worse immune response: "Short telomeres are linked to a range of human diseases, including HIV, osteoporosis, heart disease and aging. ... an enzyme [called telomerase] keeps immune cells young by preserving their telomere length and ability to continue dividing. ... the stress hormone cortisol suppresses immune cells' ability to activate their telomerase. This may explain why the cells of persons under chronic stress have shorter telomeres. ... When the body is under stress, it boosts production of cortisol to support a 'fight or flight' response. If the hormone remains elevated in the bloodstream for long periods of time, though, it wears down the immune system. We are testing therapeutic ways of enhancing telomerase levels to help the immune system ward off cortisol's effect. If we're successful, one day a pill may exist to strengthen the immune system's ability to weather chronic emotional stress." |
|
|
|
|
|
| Here's another Future Current transcript of biomedical gerontologist Aubrey de Grey at Aging 2008: "Aging is bad for you. It is a degenerative condition, and thus a theoretical target of regenerative medicine. What I have come here today to tell you, and what my scientific colleagues will be telling you over the next hour or so, is that it is no longer simply a theoretical target of regenerative medicine. It is on its way to becoming a practical one. Why is that? Really it comes down to this definition of aging that I have written down. This is something that gerontologists and people who study the biology of aging have known for a very long time, but it has not always been stated quite so explicitly. Aging is very definitely a side effect of being alive in the first place. You accumulate various types of damage, just in the same way that a simple man-made machine like a car will accumulate damage as a side effect of its normal operation. Again, just like man-made machines, the human body can tolerate that damage with more or less no loss of function or performance for a very long time. The damage only starts to really matter when it reaches a threshold of abundance that is prejudicial to the optimal performance of metabolism." |
| A Future Current transcript of one of Aubrey de Grey's presentations at Aging 2008: "Some people say, 'I don't want to live to a thousand.' I don't want to live to a thousand, necessarily. I don't even know if I want to live to a hundred. But I do know I want to make that choice when I am 99, rather than having it gradually removed from me by declining health. This is what it comes down to. The extension of lifespan by the defeat of aging is not the point - at least it is not the main point for me, and I do not think it is the main point for most people who are engaged in this crusade. The purpose is to alleviate the suffering that goes with getting decrepit, frail and dependent. Of course, this includes not just those who are suffering that, but the suffering of their loved ones. The extension of average lifespan is essentially a side benefit. It is something that will happen because the way that we are going to do this, using regenerative medicine, will also mean that you have only the same probability you did when you were a young adult of dying peacefully in your sleep without any of these diseases. In other words, a very low probability indeed. You will indeed on average live a great deal longer, and I don't think you’ll complain if you do. However, that is not the purpose. The purpose is to alleviate suffering." |
|
|
|
|
|
| I've seen a lot of nonsensical, willfully obtuse objections to living a longer, healthier life through technology in the past five years. I think this Wall Street Journal piece tops them all, however. "As for recurrent rejuvenation [it] it fares poorly in a comparison with reincarnation, its closest analogue. According to a basic Hindu understanding, reincarnation involves a succession of new bodies - human, perhaps, but also animal or insect - for the same soul, one that has not yet improved sufficiently to break out of the cycle of life and death and enter the realm of enlightenment. Recurrent rejuvenation, though [keeps] the same body in a continuous loop from youth to age and back again, while the mind is free to accumulate and store all its successive experiences. So a question: Wouldn't [you] be a bit of a wreck after the preserved pain (physical and psychological) of having lived so many years and gone through the aging process 10 or 20 times? A soul in the Hindu reincarnation cycle might not have attained Nirvana, but at least the bad karma carried over from one life can be expunged in the next." Some people are just never going to get it - which is fine, a choice on their part. It's somewhat saddening to see so many slow and painful suicides in the making, however, when compared to the alternative of enhanced healthy longevity that researchers are working towards. |
| The Daily Bruin talks to some of the folk who were at Aging 2008: "Defeating the effects of time by finding a cure for aging has become the focus of multiple areas of research, bringing the possibilities of achieving immortality from fantasy into the realm of science. The new possibilities offered by regenerative medicine illustrate how advancements in therapy on the molecular and cellular level may be able to extend the healthy human life span within the next 20 years ... Finding a cure for aging is no longer a theoretical target or a fantasy, but on the way to becoming a practical target. Aging is the most universal degenerative condition and is now becoming the target of regenerative medicine ... The body is a really complicated machine, but it's still a machine, so its healthy lifespan can be extended indefinitely by sufficiently comprehensive repair and maintenance, just like simple man-made machines. ... Aging is a complex phenomenon that affects many different systems ... understanding it and fixing the damage as it comes can potentially cure the harmful effects of aging and as a result, elongate the healthy human lifespan." |
|
|
|
|
|
| Long-lived naked mole-rats are little goldmines of information on how metabolism and membrane composition relates to species longevity. From Ouroboros, a new twist: "Stress resistance at the cellular level is correlated with longevity at the organismal level, to such an extent that one can screen for longevity mutants by first identifying stress-resistant animals. ... It would therefore come as a surprise if a long-lived organism turned out to be unusually sensitive to stress - and in particular, sensitive to particular stresses. In one fell swoop, this would falsify both the general, well-accepted correlative pattern (stress resistance = longevity) and the somewhat more fanciful model of a central [stress resistance mechanism related to longevity]. ... Short version: naked mole rats are more resistant than mice and rats some stressors, but not all of them. Heat and starvation, two of the classic and longest-known types of stress known to correlate with longevity, work in the expected direction, with the mole rat more resistant. Beyond that, curiously, it’s hard to find patterns." If you have to bet on biology, always bet that it's going to turn out to be more complex than presently thought. |
| From TechNewsWorld: "More than 200 scientists and longevity activists gathered at UCLA recently to discuss advancements in repairing humans. New technology is making it possible to imagine a world with ever greater life spans, but old world issues pervaded the discussions. ... 'We should mount a war on aging where it is not a disease, it is THE disease,' said Gregory Stock, Ph.D., director of the UCLA Program on Medicine, Technology and Society. To do this, Stock proposed an 'aggressive publicly funded program.' While no one challenged this idea on the panel, during the two days of the conference, it was clear that some questioned the efficacy of such a plan. Indeed, in a less formal setting, [Bruce] Ames lamented the fact that under the mostly government-run system of science grants, the 'true visionaries are not getting funding.' This is not surprising, given that government agencies are by nature political, making decisions with an eye toward public opinion, not necessarily the best and brightest ideas. Agencies like the U.S. National Institutes of Health and particularly the Food and Drug Administration typically become risk averse over time, as it's easier to deny approval for an idea or product that no one ever finds out about than it is to take a chance on a revolutionary idea and have it flop." |
|
|
|
|
|
| Anne C. ponders long-term maintenance of the brain: "One of the most fascinating things about the brain is how it must simultaneously change constantly over time (in response to new information and other inputs) and maintain the aspects of its structure that permit it to keep functioning as a person wants it to as he or she ages. This is true for the body as a whole, of course, but particularly interesting to consider in the case of the brain, as (unlike other organs and parts, which can be transplanted or replaced by prostheses) the brain is unique to each individual in such a way that you wouldn't ever be able to replace it with another and expect to get 'the same person' as a result. ... It is this uniqueness and irreplaceability of brains that makes them of special concern in thinking about healthcare across the lifespan. ... I [think] it more than reasonable to surmise that the conditions presently grouped together as 'the dementias' will likely someday: (a) subsume the phenomenon of milder memory loss and progressive cognitive difficulty currently considered 'normal aging', and (b) become amenable to preventative, maintenance, and rejuvenation treatments." |
| A research group is proposing that buildup of advanced glycation end-products (AGEs) causes DNA damage in addition to known other issues: "The scientists studied semen samples from men with diabetes who were receiving insulin therapy. ... when we looked for DNA damage, we saw a very different picture. Sperm RNA was significantly altered, and many of the changes we observed are in RNA transcripts involved in DNA repair. ... Diabetics have a significant decrease in their ability to repair sperm DNA, and once this is damaged it cannot be restored ... We found a class of compounds known as advanced glycation end products (AGEs) in the male reproductive tract. These [accumulate] during normal ageing. They are dependent on life style - diet, smoking etc - and in many diabetic complications are centrally implicated in DNA damage. ... The scientists intend to follow up their work by trying to determine how AGEs cause and contribute to DNA damage. They believe that they may have uncovered a new role for AGEs, and that their influence goes far beyond diabetes and its complications." I think that this is proposed on a fairly weak correlation, but we'll see where it goes. |
|
|
|
|
|
| Via EurekAlert!, advocacy from those who believe that engineering metabolism to slow the accumulation of age-related damage is the only way ahead: "The traditional medical approach of attacking individual diseases -- cancer, diabetes, heart disease, Alzheimer's disease and Parkinson's disease -- will soon become less effective if we do not determine how all of these diseases either interact or share common mechanisms with aging ... all living things, including humans, possess biochemical mechanisms that influence how quickly we age and, through dietary intervention or genetic alteration, it is possible to extend lifespan to postpone aging-related processes and diseases. ... We believe that the potential benefits of slowing aging processes have been underrecognized by most of the scientific community. We call on the health-research decision-makers to allocate substantial resources to support and develop practical interventions that slow aging in people." Meanwhile, initiatives to raise funding to develop the means to repair - rather than just slow - the damage of aging continue. I believe those initiatives to be the superior path forward, as they seem likely to be less complex, less costly, and more effective. |
| How far we've come in the past five years, from the days in which the mainstream media poured scorn on the practice of calorie restriction. If there is a lesson here, it is to observe the way in which the Calorie Restriction Society engaged and encouraged the research community: progress in science is a necessary accompanyment to progress in advocacy for a cause. From MSNBC: "While the quest for the proverbial Fountain of Youth is endless and typically fruitless, one method known to extend the human lifespan by up to five years has quietly become accepted among leading researchers. The formula is simple: Eat less. It could add years to your life, several experts now say. And done in moderation, it could at least help you live a more healthy life. The only question is: Will the average person do it? ... Here's a rough rule of thumb that many experts generally agree on now: Eat 15 percent less starting at age 25 and you might add 4.5 years to your life ... Eating fewer calories also reduces age-related chronic diseases such as cancers, heart disease, and stroke in rodents. That's important because it suggests ways to not just make us live longer, but to allow us to age more gracefully, healthwise." |
|
|
|
|
|
| An interesting paper: "In higher organisms dependent on the regenerative ability of tissue stem cells to maintain tissue integrity throughout adulthood, the failure of stem cells to replace worn out, dead, or damaged cells is seen as one mechanism that limits lifespan. In these organisms, tumor suppressors such as p53 are central participants in the control of longevity because they regulate stem cell proliferation. Several recent reports have identified p53 as a longevity gene in organisms such as Caenorhabditis elegans and Drosophila melanogaster, which lack proliferative stem cells in all but the germline and have relatively short lifespans. This has forced us to reevaluate the role of p53 in the control of lifespan. We discuss how p53 might regulate longevity in both long- and short-lived species by controlling the activity of insulin-like molecules that operate in proliferating and non-proliferating compartments of adult somatic tissues. We also discuss the hierarchical structure of lifespan regulation where loss of p53 has lifespan extending effects. Finally, we suggest a molecular mechanism by which p53 might facilitate the response to severe nutrient deprivation that allows metabolically active cells to survive periods of starvation. Paradoxically, loss of p53 function in these cells would compromise lifespan." |
| The inaugural Hourglass carnival of aging and longevity science is hosted at Ouroboros: "Welcome to the first installation of Hourglass, a blog carnival devoted to the biology of aging. This first issue corresponds with the second blogiversary of Ouroboros, but mostly I consider it a celebration of the excellent (and growing) community of bloggers who are writing about biogerontology, lifespan extension technologies, and aging in general ... BrainHealthHacks writes about recent evidence that smarter people live longer. This is true whether your metric of intelligence is education (which could be problematic, as education levels are often correlated with lifelong affluence and access to medical care) or whether you're looking at individual genetic variations correlated with both longevity and intelligence. It's a giant post that quotes several articles from the primary literature as well as studies by international organizations." You'll find an interesting view of ongoing calorie restriction studies too. |
|
|
|
|
|
| FuturePundit comments on the latest resveratrol research: "Surprisingly, resveratrol extends life of those on the calorie restriction diet. I say 'surprisingly' because calorie restriction is already causing most of the changes that resveratrol causes. But note that mice on the middle range calorie diet did not live longer as a result of resveratrol treatment. ... Maybe on the [every other day feeding] mice the resveratrol worked by mimicking the effects of calorie restriction on the feeding days? ... My reaction to this study is mild disappointment. Resveratrol did not work nearly as well as calorie restriction in extending life. You still need to starve yourself to assure a longer life." It's convenient verbal shorthand, but the practice of calorie restriction is not "starving yourself." It's important to be correct in these matters - calorie restriction is elimination of calories above those needed to be healthy, while still obtaining an optimal level of micronutrients. Many slim, healthy people are already practicing a form of mild calorie restriction when measured against commonly recommended dietary intake. Still, my fervent hope is that calorie restriction will become irrelevant and outstripped by the first medical interventions to extend healthy life, hopefully within the next 20 years. My money is on technologies of mitochondrial replacement and repair. |
| From the Methuselah Foundation: "Are you an undergraduate interested in the Strategies for Engineered Negligible Senescence and other avenues of longevity science? Have you considered volunteering with the Methuselah Foundation to help advances towards the repair of aging? Then you should visit the MFURI website to learn more about the Methuselah Foundation Undergraduate Research Initiative. ... the initiative provides students with the knowledge and logistical support to develop their own projects to further the agendas of the Methuselah Foundation, a non-profit organization which supports research and advocacy for radically extending healthy human life. As a means for promoting student interest, thousands of dollars in scholarship funds, grants, and man hours are provided annually. These support mechanisms, coupled with the logistical support of numerous dedicated, professional volunteer coordinators, provide unprecedented opportunity for student development and success in most any academic discipline. In addition to becoming eligible for scholarships and general support, MFURI students are also given the choice to perform projects and initiatives for university credit virtually anywhere within the United States." |
|
|
|
