Longevity Meme Newsletter, March 08 2010

March 08 2010

The Longevity Meme 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 the Longevity Meme.



- A Flow of New Donors at the Methuselah Foundation
- Medical Tourism for Stem Cell Therapies
- On Incentives and Cryonics
- Discussion
- Latest Healthy Life Extension Headlines


Let me direct your attention to the donor lists at the Methuselah Foundation - it seems like a sign of progress that a steady flow of new donors is emerging from beyond to community that originally helped the Foundation get off the ground:


"It's worth repeating that these are entirely new donors; folk from beyond the community of early supporters who dug deep to boost the Foundation's launch and sustain its growth in the first few years of operation. This view doesn't include the more than 200 people who are members of the 300, and who make recurring donations to the Foundation that average out to around $85/month each. You'll see from the graphic above that new members of the 300 are amongst the new faces joining the Methuselah Foundation community as well.

"This, I think, is a promising sign. Broadly speaking, there are two ways to sway the world to your point of view: either convince the leaders and the crowd follows, or convince the crowd, and the leaders are carried along whether they want to be or not. Of course it's not that black and white in practice, and any organization speaks to both sides of the house. It's a bootstrapping process, with a little progress with the leaders here, a little progress with the crowd there, and a lot of feedback and communication taking place between all parties to muddy the waters. But the bottom line is that more new donors means that more people are hearing about longevity science and taking it seriously. Progress is underway."


Medical tourism exists primarily because the regulatory regime in countries like the US is harsh beyond all reasonable levels, the bureaucratic mindset spun out of control. So the application of new research, such as the growing knowledge of stem cells and regenerative processes, happens in other parts of the world:


"Five years, a decade, or longer might pass these days between the early commercial availability of new therapies overseas and their final and expensive passage through the FDA course of hurdles and obstacles. But when responsible companies are regularly offering safe (and much cheaper) therapies in India, Vietnam, and China years ahead of their availability in the US, something has to give. ... a wide range of interested parties in the US advocate against medical tourism; to hear them speak, anything less than the full FDA process of years, trials, and tens of millions of dollars will lead to anarchy, and all providers outside the US are evil snake-oil salesmen. Nothing could be further from the truth. Less regulated markets have their own for-profit watchdogs, and aggressive competition shakes out fraud and failure much more rapidly than regulators. In a regulated market, fraud and failure become a part of the landscape, supported by the regulators. Rather than small opportunists trying to put one over on a handful of people until discovered, you'll see massive entities engaged in shaping regulations over years and decades to their advantage, covering up and excusing extensive abuses with the regulator's aid, and so forth.

"Look at the shoes on your feet - they are pretty essential for most people. Absent shoes, you would struggle more than you would like. But when was the last time you had a serious issue with fraud in the shoe market? When was the last time you had any sort of issue in the shoe market? Yet it is as free as any market is likely to be these days. The average person is likely to think little about dealing with shoe shopping and a lot about dealing with minor medical issues - and that is a mark of the level of regulator-induced dysfunction in the medical industry. If you are perfectly happy with the state of the shoe marketplace, but believe that heavy regulation is required for medicine, then you should probably take a closer look at your axioms."


A conclusion was reached this week to the legal fight between cryonics provider Alcor and relatives who were holding up the cryosuspension of Mary Robbins:


"Were I involved with Alcor in any administrative role, I would certainly be thinking about what more could be done to help members avoid this sort of situation - potentially a good investment in time and effort, all things considered. The last thing you want is for every greedy fool who believes cryonics is a waste to think they can pressure or commit fraud upon their dying relative in order to get at funds earmarked for cryopreservation. But this is a situation that you can avoid with a little forethought: set up the financial arrangements such that your relatives have neither incentive nor ability to get at the money. In a post at Depressed Metabolism entitled Ten Ways to Avoid Being the Next Cryonics Legal Case, Rudi Hoffman lays out the steps with characteristic bluntness."

The bottom line is that human nature is human nature. If you think that your closest relatives will respect your beliefs and the scientific evidence for cryonics when they could stand to gain $50-100,000 by consigning to you to rot in the grave, then you are probably too trusting. Armor these financial affairs, as they are too important to leave any clear opening for other people to interfere.


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!




Here, researchers identify another piece of the molecular machineries of metabolism that help to determine life span: "a protein called Sestrin [serves] as a natural inhibitor of aging and age-related pathologies in fruit flies. ... Sestrins are highly conserved small proteins that are produced in high amounts when cells experience stress. Sestrin function, however, remained puzzling until [researchers] found that these proteins function as activators of AMP-dependent protein kinase (AMPK), and inhibitors of the Target of Rapamycin (TOR). AMPK and TOR are two protein kinases that serve as key components of a signaling pathway shown to be the central regulator of aging and metabolism. ... AMPK is activated in response to caloric restriction, a condition that slows down aging, whereas TOR is activated in response to over-nutrition, a condition that accelerates aging. Activation of AMPK inhibits TOR, and drugs that activate AMPK or inhibit TOR can delay aging in several different model organisms including mammals. But how the body keeps the activity of these two protein kinases in balance to prevent premature aging was unknown. ... In future work, [researchers plan] to examine whether the mammalian Sestrins also control aging and metabolism, and whether defects in proper Sestrin expression will provide the explanation to some of the currently unexplainable degenerative diseases associated with old age."

HUMANITY+ UK 2010 CONFERENCE (March 05 2010)
Biogerontologist Aubrey de Grey is amongst the speakers scheduled for a transhumanist community conference to be held in London in April. "How will accelerating technological change affect human mental and physical capabilities as well as the environment in which we live? Humanity+ UK2010, a one-day conference in London on 24 April 2010, gathers together some of the leading thinkers to discuss these and many other topics. ... Over the last year, the regular Saturday meetings of the UK Transhumanist Association have attracted larger and larger crowds eager to listen to and debate with speakers seeking to answer these vital questions. ... Inspired by the increasing popularity of these regular meetings, this one-day conference [gathers] together some of the leading thinkers in nanotechnology, biotechnology, cognitive science and their real-world implications. ... With 9 speaker sessions and two panel discussions confronting the big issues of tech change, this is your opportunity to engage in some of the big debates that will shape our future." I see that David Pearce will be speaking also: "In 1995, he wrote an online manifesto, The Hedonistic Imperative, advocating the use of biotechnology to abolish suffering throughout the living world." The Hedonistic Imperative - the urge to engineer paradise through technology - is an important contribution to transhumanist thinking, especially for those of us interested in engineering away the horrific, worldwide suffering caused by degenerative aging.

Something to think about from EurekAlert!: "IGF-I is a protein hormone similar in structure to insulin and is regulated in the body by growth hormone (GH). Levels of GH and IGF-I decline progressively with age in both men and women and this drop is thought to be related to deteriorating health conditions found with advanced age. In an attempt to combat aging some people use GH as its actions elevate IGF-1. This study however showed that older men who had higher levels of IGF-I were more likely to die from a cancer-related cause in the following 18 years than men with lower levels. ... This is the first population-based study to show an association of higher IGF-I levels with increased risk of a cancer-related death in older men. Although the design of this study does not explicitly show that the higher IGF-I levels caused the cancer death, it does encourage more study as well as a reexamination of the use of IGF-I enhancing therapies as an anti-aging strategy. ... researchers used data on 633 men aged 50 and older from the Rancho Bernardo Study, a population-based study of healthy aging. ... In this study, the increased risk of cancer death for older men with high levels of IGF-I was not explained by differences in age, body size, lifestyle or cancer history." You might compare this with other findings on IGF-1 levels in long-lived humans.

From the IEET Blog: "When I was in undergrad, a professor asked our whole class a strange question. ... 'Lets say that I have in my hand, right now, a pill. This pill, if you take it, will make you ageless. [If] you would take this pill, raise your hand.' ... His point was not that people want to age and die but that we naturally distrust such offers. It simply sounds too good to be true. ... Our brains are trained, over time, to understand what a reasonably possible benefit can exist for a given price. A free pill that has no side-effects and no Twilight Zone caveats (you have to be alive, can't die so are tortured, etc) seems more impossible than the idea of anti-aging itself. The problem is that this protective aspect of our mind can become over excited, so we stop believing certain solutions are ever possible. To cure, or even significantly reduce the damages caused by aging, are such an epic benefit that it seems our minds will actively manufacture problems, because the benefit must have some sort of epic cost associated. So we tell ourselves curing aging will cause too many problems and that aging has a lot of natural beauty to it and creates a lot of meaning and that all of that is good."

It is good that more new theories on the mechanisms of Alzheimer's disease are emerging, such as this, via EurekAlert! One thing you don't want to see in an advancing field of science is a monoculture of ideas. "For years we thought that A-beta was just metabolic garbage produced as a byproduct of other processes within the brain, but these data suggest it is a normal component of the brain's innate immune system. It looks like factors that trigger hyperactivity of the innate immune system - not only infection but also traumatic brain injury and stroke, which are already known to increase the risk for Alzheimer's - could cause excessive deposition of A-beta. ... The researchers suggest that chronic activation of the innate immune system in response to either a persistent or transient infection of the central nervous system might lead to excess production and accumulation of A-beta. Known Alzheimer's risk factors ā€“ such as stroke, head injury and exposure to certain anesthetics ā€“ could also trigger the innate immune system and increase A-beta production, leading to an excessive and dangerous inflammatory response within the brain. ... Now we need to figure out what is triggering the innate immune system, particularly as we age, and what genes control A-beta's role in the innate response. If we can identify which pathogens are more likely to trigger A-beta plaque aggregation, we might develop ways to prevent or control that response, for example by immunization."

Over at the Immortality Institute forums, researcher John Schloendorn (who worked on LysoSENS and is now one of the driving forces behind Livly) remarks: "I have a bazillion surplus Ending Aging books sitting at my house in Mountain View, CA. If anyone has a creative use for them, I can give them out for the cost of shipping or free if you pick them up." Ending Aging is a great book, and there are some good ideas in that discussion thread as to what to do with Schloendorn's surplus copies, such as handing them out at conferences, or donating them to libraries. If you have a good idea as to what to do with the copies, or would like one yourself, jump on in and have your say.

The irreverent Viceland interviews Aubrey de Grey: "Typically, today, the therapies [of regeneration] involve things like injecting stem cells into the spinal cord or the heart in the vicinity of a trauma, to stimulate rebuilding of the damaged tissue, or else wholesale surgical replacement of an organ such as the heart or bladder with one created in the laboratory by tissue engineering. But as we progress, it will broaden to include 'molecular-level' regeneration, such as injecting enzymes (or the genes encoding them, depending on the target tissue) that can break down unwanted molecular byproducts of metabolism that are accumulating in cells as 'garbage' and that eventually impair cell function. In the case of injecting genes, we're talking about the standard techniques being developed for somatic gene therapy for inherited diseases: packaging the new DNA in a virus that worms its way into cells and integrates into the chromosome. (In many cases it will be doable much more safely, however, by performing this manipulation on stem cells outside the body, which can be verified for the correct genetic alteration before being injected.) The type of damage we repair need not be restricted to sudden, trauma-derived damage either - the gradually progressive damage that comprises aging is just as legitimate a target for regenerative medicine."

From the New York Times: "What, Iā€™d like to know, will persuade the majority of Americans who remain sedentary to get off their duffs and give their bodies the workout they deserve? My hope is that every new testimonial to the value of exercise will win a few more converts until everyone is doing it. ... Physical inactivity is one of the strongest predictors of unsuccessful aging for older adults and is perhaps the root cause of many unnecessary and premature admissions to long-term care. ... [It has long been] well established that higher quantities of physical activity have beneficial effects on numerous age-related conditions such as osteoarthritis, falls and hip fracture, cardiovascular disease, respiratory diseases, cancer, diabetes mellitus, osteoporosis, low fitness and obesity, and decreased functional capacity. ... exercise [produces] a significantly reduced risk of cognitive impairment after two years for participants with moderate or high physical activity [when older] than 55. ... Sedentary skeptics are fond of saying that of course exercise is associated with good health as one ages; the people who exercise are healthy to begin with. But studies in which some participants are randomly assigned to a physical activity program and others to a placebo (like simply being advised to exercise) call their bluff. Even less exacting observational studies, like the Nurses' Health Study, take into account the well-being of participants at enrollment."

Cancers depend on continually lengthening telomeres to overcome limits on cell proliferation. If that process can be blocked, it would stop cancer in its tracks. This is the basis of the SENS approach to cancer, WILT, but there are other initiatives aimed at a similar goal: "It starts with the enzyme telomerase, which affects the caps, or telomeres, at the end of a chromosome. Telomeres shorten over time. But telomerase prevents this from happening, making the cell immortal. If cancer is triggered in the cell, the presence of telomerase leads to the growth of the cancer. Telomerase is kept in control by the protein TRF1, which keeps the telomeres operating correctly. But another protein, Fbx4, can bind to TRF1 and degrade it, causing the telomeres to lengthen. Now, researchers have discovered, a third protein, TIN2, can step in and override Fbx4 by binding to TRF1 first and preventing Fbx4 from attaching to it. This finding paves the way for developing a drug that acts like TIN2, keeping everything in check ... In 90 percent of cancers, no matter what caused the cancer to form, it needs telomerase activity to maintain the cell. Without telomerase, the cell will die. Our work is key to understanding a detailed mechanism for how these molecules interact and how to design a drug to block Fbx4."

The NetAge Project website contains a lot of interesting information, even if the user interface leaves something to be desired: "Hundreds of genes and miRNAs have been identified as being involved in the determination of longevity, aging patterns and in the development of age-related diseases (ARDs). The interplay between these genes as well as the role of miRNAs in the context of protein-protein interaction (PPI) networks has as yet been poorly addressed. This work was undertaken in order to integrate the data accumulated in the field, from a network-based perspective. The results are organized in the NetAge database-an online database and network analysis tools for biogerontological research. ... The NetAge database contains gene sets and miRNA-regulated PPI networks for longevity, ARDs and aging-associated processes, and also common signatures (overlapping networks). The database is available through the NetAge website, which provides the necessary bioinformatics tools for searching and browsing the networks, as well as showing network info and statistics. By making these resources available online, we hope to provide the scientific community with a new, network-oriented platform for biogerontological research, and encourage greater participation in the systems biology of aging."



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