Researchers are foraging for longevity-related genes that have nothing to do with the known processes of life extension through calorie restriction: "We believe that for the first time, we have a biochemical route to youth and aging that has nothing to do with diet. ... The chemical variation, known as acetylation because it adds an acetyl group to an existing molecule, is a kind of 'decoration' that goes on and off a protein - in this case, the protein Sip2 - much like an ornament can be put on and taken off a Christmas tree ... Acetylation can profoundly change protein function in order to help an organism or system adapt quickly to its environment. Until now, acetylation had not been directly implicated in the aging pathway, so this is an all-new role and potential target for prevention or treatment strategies, the researchers say. The team showed that acetylation of the protein Sip2 affected longevity defined in terms of how many times a yeast cell can divide, or 'replicative life span.' The normal replicative lifespan in natural yeast is 25. In the yeast genetically modified by researchers to restore the chemical modification, life span extended to 38, an increase of about 50 percent. The researchers were able to manipulate the yeast life span by mutating certain chemical residues to mimic the acetylated and deacetylated forms of the protein Sip2. They worked with live yeast in a dish, measuring and comparing the life spans of natural and genetically altered types. ... When we give back this protein acetylation, we rescued the life span shortening in old cells. Our next task is to prove that this phenomenon also happens in mammalian cells."

Link: http://www.hopkinsmedicine.org/news/media/releases/hopkins_scientists_turn_on_fountain_of_youth_in_yeast

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

A reminder that progress in the production of nanoscale scaffolds and surfaces is just as important as progress in biology in the stem cell field: "It's easy to give a stem cell a goal in life, apparently. Simply placing a cell in contact with a surface can provide sufficient information (a cue) to dictate how the cell will develop, and incredibly, even simple length-scale changes are enough to affect the outcome of the cell development. Far-fetched as this may sound, if you think about the nature of stem cells for a moment, it becomes less surprising that they are so responsive to their environment: how else to explain the extraordinary variety of cell types that derive from a uniform base material? As stem cells continue to be the focus of much research into the concepts of regenerative medicine and tissue engineering, a corollary challenge for materials science is the design and build for artificial substrates that can mimic biological environments and thereby control the growth and specialization of the cells. For one thing, the subtleties make it easy to grow off in the wrong direction. Growing muscle tissue will need a different set of conditions from, say, a new liver, but the differences in the environment might turn out to be very slight. A small change in the period of a pattern on the substrate might result in completely the wrong kind of tissue. A challenge of a more mechanical nature is the actual fabrication of the substrates. Most cell-growth environments have cues that act over a number of different length scales, with multiple patterns and features of various sizes interacting to produce the end result. Current micro- and nanofabrication techniques don't mimic this complexity too well, or rather, don't mimic it too well without complex multi-step procedures, expensive instrumentation, and expertise on fabrication that is not readily available to medical researchers."

Link: http://www.materialsviews.com/details/news/1400141/Shrink-Wrap_Stem_Cell_Growth.html

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

Long after the time in which anyone can easily recall who was US president in 2011, or what party was in power, or which wars of declining empire are fought, and then long after anyone even cares about that ancient history, and later, long after the whole download slope of the history of the US is but a footnote of interest to scholars of the transition from second to third millennium, and later still, long after anyone can even find out with any great reliability who was US president in 2011, the first half of the 20th century will be recalled as the dawn of the era in which aging was conquered.

Progress in science and technology is really the only thing that matters in the long term. In that area of human endeavor, the truly transformative advances stand out like beacons across millennia of time - even long after the details of that period are hard to reconstruct, archaeologists can show clearly both when and how the use and understanding of technology changed. So we see the impact of agriculture and we know when it began, for example: it looms large in our considerations of deep human history at the present time, because it utterly transformed the course of our species. Similarly for iron working, and other important advances.

The advent of ways to reverse the effects of aging, largely through biotechnologies in the early stages of development that will repair the low-level biochemical damage that causes aging, will transform the shape and course of human society no less than the great advances of prehistory and early history - but undoubtedly much faster, as we're far better at talking to one another and coordinating our efforts in these years.

So in the final analysis, how much of what we do in our day to day lives actually matters? That's a meaning of life sort of a question, so everyone gets to write their own answer into the box and it's still right, but it's intended to provoke thought. Do you care about end results, or do you care about the journey? Billions of lives in the future hang in the balance of a few dollars or a convincing argument for the development of rejuvenation biotechnology: it's early enough still that we're talking butterfly wings and hurricanes when it comes to how our efforts today will affect the next four decades of progress in ways to slow and reverse aging. I suppose, for someone like myself who isn't in it so much for the journey, it's the case that you can choose to live a life in which you made a difference, or you can choose to live a life in which it doesn't much matter whether you ever existed.

The future can be made a golden place within our lifetimes, and billions of people who are presently destinated to suffer and age to death could instead by saved through biotechnology to live full, healthy, and vigorous lives thousands of years long. That all depends on how well and rapidly the present research community works on the first generation of rejuvenation therapies, which in turn depends on acts of fundraising and persuasion carried out by otherwise ordinary folk like you and I. There's an avalanche to be started here, a few pebbles that will bring the whole slope rushing down with it, profoundly transform humanity in the process by banishing aging and the decrepitude, disease, and death it brings.

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

The Genomics X Prize has been a while in the building, and has a focus on the genetics of human longevity. It has been in the news of late: "The contest to sequence 100 complete human genomes of people who are over 100 years old in one month for $1,000 or less per genome has started its recruitment process and has pulled in new several new partners to help it develop its sampling, protocols, informatics, and other scientific needs. ... The Archon Genomics X PRIZE [is] an incentivized prize competition that will award $10 million to the first team to rapidly, accurately and economically sequence 100 whole human genomes to a level of accuracy never before achieved. The 100 human genomes to be sequenced in this competition will be donated by 100 centenarians (ages 100 or older) from all over the world, known as the Medco 100 Over 100. Sequencing the genomes of the Medco 100 Over 100 presents an unprecedented opportunity to identify those 'rare genes' that protect against diseases, while giving researchers valuable clues to health and longevity. These centenarians' genes are providing us with a window to the past that will significantly impact the future of healthcare. The result will be the world's first 'medical grade' genome, a critically-needed clinical standard that will transform genomic research into usable medical information to improve patient diagnosis and treatment. This global competition will inspire breakthrough genome sequencing innovations and technologies that will usher in a new era of personalized medicine."

Link: http://genomics.xprize.org/

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

Some people have demonstrably better mitochondrial DNA, others worse. Here, a study shows correlations between some variants and old-age frailty: "Mitochondria contribute to the dynamics of cellular metabolism, the production of reactive oxygen species, and apoptotic pathways. Consequently, mitochondrial function has been hypothesized to influence functional decline and vulnerability to disease in later life. ... mitochondrial DNA (mtDNA) variation was compared in frail and non-frail older adults. Associations of selected SNPs with a muscle strength phenotype were also explored. Participants were selected from the Cardiovascular Health Study (CHS), a population-based observational study ... Three mtDNA SNPs were statistically significantly associated with frailty across all pilot participants or in sex-stratified comparisons." Given the degree to which mitochondrial composition correlates with species life span differences, we should not be surprised to find some variations significant in human life span.

View the Article Under Discussion: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2883558/

Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

I was struck by an article on the website of the San Francisco Chronicle that reports for the first time that workers age 65 and over outnumber employed teenagers: http://tinyurl.com/27opz5h.  There are a variety of factors at work here, including unfortunately the devastating effect of the recession on the work opportunities for young people.  The impact of the economy on investment portfolios and real estate values have undoubtedly caused people over age 65 to reconsider their need to continue to work. 

There has been speculation for some time that some aging Baby Boomers would prefer to continue to work past normal retirement age.  A variety of news reports coming out of Washington over the past several weeks also indicate that deficit reduction negotiations that are likely to begin in the fall may lead to increases in the normal retirement age within the Social Security program sometime in the future.  There’s a strong likelihood that the newly identified workforce trend marks the beginning of a tendency to see employment as a key component for financing longevity regardless of whether the trend is fostered by personal preference or by retirement plan formulas.

A number of research groups are looking into ways to manipulate muscle regeneration and maintenance, and an advance here could be useful as a therapy to address age-related loss in muscle mass and strength: "Researchers have long questioned why patients with Duchenne muscular dystrophy (DMD) tend to manage well through childhood and adolescence, yet succumb to their disease in early adulthood, or why elderly people who lose muscle strength following bed rest find it difficult or impossible to regain. Now, researchers [are] beginning to find answers in a specialized population of cells called satellite cells. Their findings [suggest] a potential therapeutic target for conditions where muscle deterioration threatens life or quality of life. ... Suspecting a genetic switch that might turn off satellite cell proliferation in these circumstances, the scientists looked to a gene called Ezh2, known to keep the activity of other genes in check. When they genetically inactivated Ezh2 in satellite cells of laboratory mice, the mice failed to repair muscle damage caused by traumatic injury - satellite cells could not proliferate. Ezh2 expression is known to decline during aging, and the new research in mice suggests that therapies to activate Ezh2 and promote satellite cell proliferation might eventually play a role in treating degenerative muscle diseases. ... in the elderly, tweaking the gene in satellite cells would not increase their lifespan, but could increase their quality of life by helping to prevent falls and enabling them to move and walk better and go about their daily activities."

Link: http://www.nih.gov/news/health/apr2011/niams-15.htm

A headline reporting a new Harris Poll survey stated that “Very few Americans find statements by financial institutions completely believable.”  One specific item of interest was that 51 percent of the respondents said that a statement made by someone who works for a health insurance company was believable (2 percent completely believable, 49 percent somewhat believable) while 49 percent answered not at all believable.  Banks, investment firms and government agencies that regulate financial institutions all fared poorly in the believability research. 

These results are not shocking in light of the health care debate and economic stresses that reverberate throughout the economy.  However, the survey shows the depth of the difficulty people have with companies and government agencies that are indispensible to their financial well being. 

This is a good time for intermediaries, whether they are trusted authors, financial advisors, academics and others to fill the void that is obviously missing in the public’s confidence in key industries.  Changes in health care, for example, are sure to cause people to have to rethink sometimes decades old strategies to financing coverage.  The health insurance industry will play a key role in the implementation of health reform, so designing a system in which the public has a basic level of trust is not a trivial matter.

Via EurekAlert!: "Two methods of extending life span have very different effects on memory performance and decline with age. ... While the nematode C. elegans is already well known for its utility in longevity research, previously it was not known how the memory of C. elegans compares with that of other animals, or whether longevity treatments could improve learning and memory. To answer these questions, [researchers] designed new tests of learning and memory in C. elegans, then used these tests to identify the necessary components of learning, short-term memory, and long-term memory. They found that the molecules required for learning and memory appear to be conserved from C. elegans to mammals, suggesting that the basic mechanisms underlying learning and memory are ancient. The authors also determined how each of the behaviors declines with age, and tested the effects of two known regulators of longevity - dietary restriction and reduced Insulin/IGF-1 signaling - on these declines. Surprisingly, very different effects on memory were achieved with the two longevity treatments: dietary restriction impaired memory in early adulthood but maintained memory with age, while reduced Insulin/IGF-1 signaling improved early adult memory performance but failed to preserve it with age. These results suggest not only that longevity treatments could help preserve cognitive function with age, but also that different longevity treatments might have very different effects on such declines."

View the Article Under Discussion: http://www.eurekalert.org/pub_releases/2010-05/plos-pmw051210.php

Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

A new popular science book on the manipulation of metabolism to slow aging, the author inspired by the Longevity Dividend initiative: "No scientific advances inspire more media hype than ones in gerontology, the study of aging. Even the crustiest editors have been known to turn giddy when new light is shed on the topic and take to blowing raspberries at the Reaper with headlines suggesting immortality elixirs are just around the corner. Biologists aren't so easily wowed, though, and before the mid-1990s they generally saw gerontology as a dismal bog where once-promising peers sank out of sight, or worse, re-emerged clutching beakers of snake oil. ... Studying the details of this inexorable, chaotic decay seemed a waste of time to most life scientists. ... Then in 1988 a miracle happened - the University of Colorado's Thomas Johnson reported that a gene mutation in nematodes could more than double their life spans. Five years later, Cynthia Kenyon at the University of California, San Francisco, nailed a similar worm 'gerontogene' dubbed daf-2. These flabbergasting discoveries revealed that not everything about aging is intractable chaos - worms, at least, apparently possessed gene-encoded modules poised to oppose the ravages of advancing age when activated by a single mutation. Optimists soon speculated that similar modules exist in mammals."

View the Article Under Discussion: http://www.the-scientist.com/news/display/57510/

Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

This release via ScienceDaily summarizes the goals of present day calorie restriction research: "Organisms from yeast to rodents to humans all benefit from cutting calories. In less complex organisms, restricting calories can double or even triple lifespan. It's not yet clear just how much longer calorie restriction might help humans live, but those who practice the strict diet hope to survive past 100 years old. ... calorie restriction influences the same handful of molecular pathways related to aging in all the animals that have been studied. Aware of the profound influence of calorie restriction on animals, some people have cut their calorie intake by 25 percent or more in hopes of lengthening lifespan. [Researcher Luigi Fontana] is less interested in calorie restriction for longer life than in its ability to promote good health throughout life. ... Right now, the average lifespan in Western countries is about 80, but there are too many people who are only healthy until about age 50. We want to use the discoveries about calorie restriction and other related genetic or pharmacological interventions to close that 30-year gap between lifespan and 'healthspan.' However, by extending healthy lifespan, average lifespan also could increase up to 100 years of age."

View the Article Under Discussion: http://www.sciencedaily.com/releases/2010/04/100415141123.htm

Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

A detailed examination of recent progress from the SENS Foundation: "Recent years have seen both substantial progress, and significant frustration, in the preferred regenerative engineering approach to the treatment and prevention of Alzheimer's disease (AD), and the eventual regeneration of genuinely youthful cognitive function: immunotherapeutic clearance of beta-amyloid (AmyloSENS). ... results appear to many to commend an earlier window of opportunity for intervention, before concomitant [damage] and neuronal losses have made the removal of beta-amyloid alone insufficient for cognitive rescue. Early intervention might also maximize the therapeutic window for vaccination, preventing the burden of beta-amyloid neuropathology from ever reaching levels so high as to interact with other forms of aging damage in already frail and immunosenescent people." Present work on immune therapies for clearing unwanted biochemical junk from the body looks promising - there is every sign that today's advances will broaden into a general technology platform for this purpose. Researchers will be able to develop therapies that can be applied incrementally throughout life to remove the age-related gunk like beta-amyloid before it rises to dangerous levels.

View the Article Under Discussion: http://www.sens.org/node/757

Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

Earlier this year, I noted a paper by Frank Lichtenberg that correlates life expectancy with the pace of introduction of new drugs - both of which are metrics that can be measured fairly well, and are fairly well recorded over the past few decades. So we see the expected result: one fairly general measure of the pace of progress in medicine is linked to longevity, most likely indicating that more rapid development of new medicine leads to longer lives, even when that medical progress is largely old-style drug discovery and commercial development. Here, I'll point out a few other papers along the same lines by the same author, one recent and the others from past years:

Pharmaceutical Innovation and Longevity Growth in 30 Developing and High-income Countries, 2000-2009

We examine the impact of pharmaceutical innovation, as measured by the vintage of prescription drugs used, on longevity, using longitudinal, country-level data on 30 developing and high-income countries during the period 2000-2009. We control for fixed country and year effects, real per capita income, the unemployment rate, mean years of schooling, the urbanization rate, real per capita health expenditure (public and private), the DPT immunization rate, HIV prevalence and tuberculosis incidence.

Life expectancy at all ages and survival rates above age 25 increased faster in countries with larger increases in drug vintage. The increase in drug vintage was the only variable that was significantly related to all of these measures of longevity growth. ... Pharmaceutical innovation is estimated to have accounted for almost three-fourths of the 1.74-year increase in life expectancy at birth in the 30 countries in our sample between 2000 and 2009, and for about one third of the 9.1-year difference in life expectancy at birth in 2009 between the top 5 countries (ranked by drug vintage in 2009) and the bottom 5 countries (ranked by the same criterion).

What to take away from this: even under the outright terrible systems of regulation that presently exist in most countries with advanced medical research communities, regulation that greatly slows progress and increases costs, the great utility of biotech research and development still filters through to this degree. Imagine how much better off we'd all be if there were no massive government agencies devoted to slowing down and blocking progress in medicine!

The older papers provide some more numbers to further flesh out the picture sketched by Lichtenberg and his colleagues. Medical progress is good - we should have more of it:

Pharmaceutical innovation and the longevity of Australians: a first look (2008)

We examine the impact of pharmaceutical innovation on the longevity of Australians during the period 1995-2003. Due to the government's Pharmaceutical Benefits Scheme, Australia has much better data on drug utilization than most other countries. We find that mean age at death increased more for diseases with larger increases in mean drug vintage. The estimates indicate that increasing the mean vintage of drugs by 5 years would increase mean age at death by almost 11 months. The estimates also indicate that using newer drugs reduced the number of years of potential life lost before the ages of 65 and 70 (but not before age 75). During the period 1995-2003, mean age at death increased by about 2.0 years, from 74.4 to 76.4. The estimates imply that, in the absence of any increase in drug vintage, mean age at death would have increased by only 0.7 years. The increase in drug vintage accounts for about 65% of the total increase in mean age at death.

Pharmaceutical Innovation, Mortality Reduction, and Economic Growth (1998)

We perform an econometric investigation of the contribution of pharmaceutical innovation to mortality reduction and growth in lifetime per capita income. In both of the periods studied (1970-80 and 1980-91), there is a highly significant positive relationship across diseases between the increase in mean age at death (which is closely related to life expectancy) and rates of introduction of new, priority (as defined by the FDA) drugs. The estimates imply that in the absence of pharmaceutical innovation, there would have been no increase and perhaps even a small decrease in mean age at death, and that new drugs have increased life expectancy, and lifetime income, by about 0.75-1.0% per annum.

The connection between wealth and longevity is strong. For a deeper historical perspective, you might look back at these posts:

• Longevity Tends to Change Economic Behavior for the Better
• Wealth and Longevity

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

From LiveScience: "Blind salamanders once thought to be baby dragons can live at least as long as most people, scientists now find. Adults of this species live nearly 69 years on average, with a predicted maximum age of more than 100 years, three times longer than related species Surprisingly, the long-lived amphibian doesn't seem to have an especially low metabolism nor unusual levels of protective antioxidant molecules to explain why it lives so long. As such, this salamander could help uncover mechanisms that could help keep us young. The olm or proteus (Proteus anguinus) lives in the limestone caves of southern Europe. ... Zoologists have been intrigued by the olm for centuries because of its longevity, as it often lives more than 70 years in zoos. The salamander's longevity is especially unusual given its tiny size. ... So why might the olm have such an outstanding life span? It might live a long time by not living very much at all. ... Although the olm does not have a remarkably low metabolic rate, it is extremely inactive during its life." Examining animals that are long-lived in comparison to similar species may give more of an insight in the biology of aging. Studies of naked mole-rats are proving fruitful, for example.

View the Article Under Discussion: http://www.livescience.com/animals/methuselah-salamanders-human-longevity-100719.html

Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

A New York Times bestselling author of five books and easily recognized as a trailblazer in functional and integrative medicine, youd think Dr. Frank Lipmans philosophy on health aging will be quite the journal entry, sprawling into different facets that all explore a branch, all intertwining like a spiders web in order to achieve prime aging.

To our surprise, its not. In fact, it couldnt be simpler.

"Basically, eat less, laugh more, deal with your stress, take sleep seriously. What else would be important?" Dr. Lipman said in a recent podcast.

However, while he definitely has the formula down when it comes to aging gracefully, Dr. Lipman recently said that hes fascinated with our current pursuits to prolong our health, and not just our lives.

As such, he commented on it, saying that we should be aware of increasing our health span, not our life span.

So, how do you do it? Here are his tips, according to a recent post on mindbodygreen.

Physical adversity is the way to go

According to Dr. Lipman, a little bit of stress is actually good for you, which should come in the form of physical adversity such as fasting and high-intensity exercise. The idea is that your body is stressed a little bit to stimulate longevity genes, which then teaches your body to handle bigger stressors better. But dont starve yourself because the idea is that a little goes a long way.

Move intentionally

This isnt just about exercising more, although thats always a good idea. Per Dr. Lipman, this is about exercising intentionally and intelligently. The key, according to him, is to push your body in an intentional way that would test it but not enough to cause injury. Its harder to recover as you get older, and so its important to change the way you do your routines to better suit your body.

Dont take life too seriously

The last piece of advice, per Dr. Lipman, is to simply not take life too seriously and have some fun. These days, everyone is too caught up with numbers and metrics that its easy to forget how to enjoy things while were at it. Eat less and laugh more. Your life would be all the more better.

The Centers for Disease Control and Prevention (CDC) estimates that every 19 minutes an older adult dies from a fall in any part of the country. Pixabay

Original post:
Expert Reveals 3 Best Healthy Aging Tips - Medical Daily

A commentary on testing rapamycin as a therapy for age-related macular degeneration (AMD): "Although neovascular AMD only accounts for less than 15% of the overall age-related macular degeneration, it is responsible for over 80 percent of the severe vision loss cases. ... It was reported in 2004 that rapamycin (trade name sirolimus) treatment significantly reduced the extent of neovascularization [induced] in adult mice ... In an advance online publication this year [Kolosova et al] presented exciting results that rapamycin could actually prevent AMD-like retinopathy in an aging rat model that more closely resembles human AMD pathology. They investigated the effect of rapamycin on spontaneous retinopathy in senescence- accelerated OXYS rats. OXYS rats were treated orally with either 0.1 or 0.5 mg/kg rapamycin, which was given together with food. Rapamycin was found in a dose-dependent manner to reduce the incidence and severity of retinopathy, and attenuated AMD disease progression. Some histological abnormalities associated with retinopathy were notably reduced ... significantly, rapamycin prevented destruction of ganglionar neurons in the retina. Rapamycin did not exert any adverse effects on the retina in control disease-free Wistar rats, suggesting that it is safe."

Link: http://impactaging.com/papers/v4/n6/full/100469.html

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

In a number of countries one plausible path to advocacy for a cause is the establishment of a single issue political party - see, for example, the original Green Party or Pirate Party as successful examples of the type in Europe. The Russian longevity science community is beginning to take this approach: "On July 19, we made the first step towards the creation of the Longevity Party. The initiative group of 10 people gathered together in Moscow to establish the first political party aimed at extending human lifespan using technological advances. ... Among these 10 people were Mikhail Batin, Alexey Turchin, Leonid Kaganov and Elena Milova. This is the very first step in the long and hard process of legally registering a political party. I believe this is one of the most important things that happened in the past few years in fighting aging. Nowhere in the world ever before have people expressed their desire to live longer in the form of a political movement. ... The main goal of the Longevity Party is to increase human lifespan so that people could live for as long as they would like to and remain young and healthy. We would like to achieve this goal by promoting scientific research and technological advances in regenerative medicine, genetics of aging and longevity, neuroscience, computer modeling of biological processes and other areas of life extension. ... The next big thing we need to do is to finalize the Program of the Party. Then we have to have at least 2 people in 42 regions of Russia as representatives of the Party and have the founding meeting after which the Party can be registered and eventually appear in the voting ballots. Our goal is to influence the authorities to support life extension technologies and increase funding for research aimed at improving people's health and extending longevity."

Link: http://ieet.org/index.php/IEET/more/konovalenko201207261

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

A fellow that you met today will, forty years from now, have an entirely artificial immune system. It is an early model, a prosthetic replacement that is a mix of synthetic cells and less organic medical nanomachines, and requires frequent work and an open data channel to keep in line. Obtaining it wasn't a choice - it is a new treatment for a small class of acquired autoimmune conditions that somehow manage to persist through complete removal and replacement of immune cell populations. It works; he doesn't get sick, at all. Ever.

Nonetheless, you shook this man's hand today. That future lies in waiting.

Earlier you passed by a kid who will outlive you, your plans, your memory, your immediate descendants, and the first phase of terraforming to take place on Mars. The young have it good these days: a solid eighty years of probable-worst-case life expectancy at birth that will take them well into the first age of radical life extension - and that even if the next twenty years take us through a miserable economic depression coupled with a spread of repressive regulatory regimes that effectively stifle life science research and its application. Many of the youngest children of today will live for centuries, and many of those will go on to live for thousands of years.

You walked right by that kid. In fairness, he doesn't know either, of course.

Then there's that new face at the office, fresh out of college: by the 2070s she'll be a shell of the person she was. A happy shell, however, the original exterior polished up by gene, cell, and enzyme therapies to minimize the changes of aging in skin and musculature, but all of the interior organs below the neck new from labs in Thailand and Vietnam over the years, grown from her own genetic material. That took money, even though it's second string organ biotechnology by that time - but the sharp average worker you can save enough to afford that sort of thing over a lifetime. It's not as though she'll be retiring any time soon, and better low on funds than living like a 80-year old from a century past.

That probably didn't cross your mind today when the two of you happened to be in the same meeting.

The point here is this: the next half century is shaping up to be a transformation to match the last, but this time in biotechnology and medicine as well as in computing. These little snapshot nascent futures are no different than my 1960s analog describing to you the future of a then-20-something-and-now-70-something individual: surrounded by monitors; in touch with distant corners of the world at the click of a button; the world's encyclopedias and research institutions available at a moment's notice; living drenched in a wealth of knowledge, and connected to half the world's population in near-instant communication; possessing such massive reserves of computation power that enormous multi-machine simulations run for little more than entertainment value; connected to this web of knowledge and communication by radio, microwave, and pocket-devices that can be used near anywhere; amidst a sea of surging culture, charged by a hundred million voices all talking at once.

This is an age of change, and much lies ahead of us. The potential for what sounds like science fiction - radical life extension, artificial organs and bodily systems, the defeat of disease and aging - lies nascent and dormant, awaiting those who will carve it from the passage of time, who will do the work to make these dreams a reality.

This is the time for it.

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

There's a fair amount of evidence implicating cytomegalovirus (CMV) in immune system decline, rhe theory here being that the immune system devotes ever more of its fixed resources to dealing with the largely harmless variants of this virus that it cannot clear. Here researchers argue against that view: "Aging is accompanied by the development of low grade systemic inflammation, termed 'inflammaging', characterised by raised serum C-reactive protein (CRP) and pro-inflammatory cytokines. Importantly, inflammaging is implicated in the pathogenesis of several of the major age-related diseases including cardiovascular disease, type 2 diabetes and dementia and is associated with increased mortality. The incidence of infection with the persistent herpes virus cytomegalovirus (CMV) also increases with age. Cross-sectional studies have proposed CMV infection as a significant driver of inflammaging, but a definitive case for CMV as a causative agent in inflammaging has not yet been made. We studied longitudinally 249 subjects (153 men, 96 women) who participated in the Hertfordshire Ageing Study at baseline (1993/5, mean age 67·5 years) and at 10 year follow up. At both times [subjects] provided blood samples for analysis of inflammatory status and CMV seropositivity. In the cohort as a whole, serum CRP and pro-inflammatory cytokines [were] increased between baseline and follow up ... These changes to cytokine status over time occurred equally in the 60% of subjects who were seropositive for CMV at baseline and follow up, the 8% who were CMV negative at baseline but who became CMV positive by the 10 year follow up, and also in the 32% who were CMV seronegative throughout. We conclude that CMV infection is not a primary causative factor in the age-related increase in systemic inflammation."

Link: http://www.ncbi.nlm.nih.gov/pubmed/22708923

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

You might recall the species of clam that can live for at least four centuries. Similarly, you might also recall the membrane pacemaker hypothesis that explains differences in longevity between species in terms of the resistance of cell membranes - and especially mitochondrial membranes - to damage. Here, the two topics are linked: "The deleterious reactive carbonyls released upon oxidation of polyunsaturated fatty acids in biological membranes are believed to foster cellular aging. Comparative studies in mammals and birds have shown that the susceptibility to peroxidation of membrane lipids (peroxidation index, PI) is negatively correlated to longevity. Long-living marine molluscs are increasingly studied as longevity models, and the presence of different types of lipids in the membranes of these organisms raises questions on the existence of a PI-longevity relationship. We address this question by comparing the longest-living metazoan species, the mud clam Arctica islandica (maximum reported longevity = 507 y) to four other sympatric bivalve molluscs greatly differing in longevity (28, 37, 92, and 106 y). We contrasted the acyl and alkenyl chain composition of phospholipids from the mitochondrial membranes of these species. The analysis was reproduced in parallel for a mix of other cell membranes to investigate if a different PI-longevity relationship would be found. The mitochondrial membrane PI was found to have an exponential decrease with increasing longevity among species and is significantly lower for A. islandica. The PI of other cell membranes showed a linear decrease with increasing longevity among species and was also significantly lower for A. islandica. These results clearly demonstrate that the PI also decreases with increasing longevity in marine bivalves and that it decreases faster in the mitochondrial membrane than in other membranes in general. Furthermore, the particularly low PI values for A. islandica can partly explain this species' extreme longevity." This emphasizes the importance of mitochondrial damage in aging and longevity, and thus the importance of research into mitochondrial repair biotechnologies for humans.

Link: http://www.ncbi.nlm.nih.gov/pubmed/22708840

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