Fight Aging!

FIGHT AGING! NEWSLETTER
May 23rd 2011

The Fight Aging! Newsletter is a weekly email containing news, opinions, and happenings for people interested in aging science and engineered longevity: making use of diet, lifestyle choices, technology, and proven medical advances to live healthy, longer lives. This newsletter is published under the Creative Commons Attribution 3.0 license. In short, this means that you are encouraged to republish and rewrite it in any way you see fit, the only requirements being that you provide attribution and a link to Fight Aging!

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CONTENT

- Introducing Open Cures
- The Most Mainstream of Longevity Science
- When Did We Become Suicidal, Negligent Barbarians?
- Discussion
- Latest Headlines from Fight Aging!

INTRODUCING OPEN CURES

The Vegas Group volunteer initiative is now renamed to Open Cures. The goals and background for this effort remain the same, and are explained at the Open Cures website, and in the discussion group:

http://www.opencures.org
http://groups.google.com/group/opencures

"We live in the midst of a revolution in biotechnology, a time of rapid and amazing progress; but this revolution is less than ideal when it comes to producing results in the clinic. Thanks to legal strictures placed upon medical development by government bodies - such as the Food and Drug Administration in the US - a range of biotechnologies with the potential to extend healthy life have been demonstrated in the laboratory but remain undeveloped for human use. ... To match the hectic, revolutionary change in the science of biotechnology, which leads to important new breakthroughs announced on a near-weekly basis, we would like to see sweeping changes in the way in which science demonstrated in the laboratory becomes medicine practiced in the clinic. The present system in the US and Europe is clearly broken."

Our present efforts focus on documenting the most promising longevity-enhancing biotechnologies in order to better make them useful and attractive for overseas developers, groups that are not subject to FDA restrictions. To this end, we will be offering bounties on some of the needed documentary material:

http://www.opencures.org/bounties

"Bounties are funded by Open Cures patrons as a way of speeding up work and attracting new volunteers to the initiative. At the present time, bounties focus on documentation needs: each award is made to the writer who first posts sufficiently good material to the Open Cures discussion group. Writers should expect some back and forth, questions asked, and friendly conversation when they do so. The bounty is then awarded when the writer releases their posted work under an open license; until that time, he or she retains copyright.

"The primary purpose of awarding bounties is to discover good life science freelance writers, and who can therefore be paid a modest rate to produce further work on an ongoing, occasional basis. It is important to build lasting relationships with enthusiastic freelance writers who know the ins and outs of practical biotechnology - so when you submit good work that arrives too late to win a specific bounty, or is beaten out by another author, you are still a candidate for future writing projects."

So if you know people who may be interested in the project, please point them to the Open Cures website. If you are interested in funding one of the upcoming bounties, either contact me or join the Open Cures discussion group and introduce yourself.

THE MOST MAINSTREAM OF LONGEVITY SCIENCE

Some thoughts spurred by an article surveying the dominant themes in present day work on interventions in the aging process:

https://www.fightaging.org/archives/2011/05/a-look-at-the-most-mainstream-of-longevity-science.php

"It is all a matter of great expense to achieve very modest goals in slowing aging, and that almost as a side-effect of the main aim, which is to catalog and understand the biochemistry of metabolism. ... This sort of research accounts for the vast majority of funding in longevity science, and if that remains true then we'll live just a little bit longer than our parents. Perhaps as much as ten years longer if the metabolic engineers pull an unexpected amazing advance from their hats within the next decade.

"From where I stand, that outcome would be a disaster - a missed opportunity with a cost of more than 50 million lives lost to aging and disease each and every year. If we reach 2040, after five decades of a scientific revolution in biotechnology, computing, and the ability to manipulate the fundamental components of life, and have not yet developed true rejuvenation biotechnology, capable of repairing the biochemical damage that causes aging ... well, we failed, and then some.

"Presently, that grand failure through a focus on trivial success is exactly where the scientific and medical development community is headed. Their timelines are for drugs and metabolic manipulations that give a small number of additional years of life to emerge by 2030 - decades of tinkering, decades of trials, and we're all old by the time that any modestly useful result emerges into general use. Yet the research community, the public, and the press are all absolutely focused on slowing aging, where they think about aging at all. Far too few people realize just how damaging to our prospects this state of affairs will be in the long run.

"This is why efforts like the SENS Foundation are so important: we need to see more groups building a platform, a body of work, and successfully making inroads into persuading the scientific community to work on repair of aging rather than just slowing it down. It won't take any longer to achieve meaningful success in repair-based research, given where things stand today, but the resulting difference to our lives and our health couldn't be greater."

WHEN DID WE BECOME SUICIDAL, NEGLIGENT BARBARIANS?

Possibly somewhere around 1940:

https://www.fightaging.org/archives/2011/05/when-did-we-become-suicidal-negligent-barbarians.php

"Our descendants will look back on us with some horror: an era of peoples who could have largely saved themselves from oblivion, but didn't. Suicidal, negligent barbarians they'll call us - and they'll be right. We have had the tools to preserve the brains of the dead for the long haul for quite some time now, and preserve them well enough that the fine structures storing the data of the mind remain intact. Death is death, but oblivion only occurs when the present detailed arrangement of matter in your brain is destroyed. For so long as that data is preserved, there is the chance that future technology and circumstances will lead to a restoration of life, such as through the use of advanced nanotechnology and charitable groups dedicated to returning the preserved to active life once more.

"Sympathy is appropriate for those with high ideals and no possibility of ever achieving them - simply born too soon. But what of those who could achieve but turn aside and shirk the task? That would be us. I'd say we and our immediate forebears became suicidal, negligent barbarians about ten years after it became possible to build an industry to preserve brains, with a cost at scale that was affordable to the masses - on a par with funerals, for example.

"For preservation methods along the lines of plastination, that point probably came and went somewhere in the 1930s or early 1940s, with the growth of the chemical industry into a true giant. The 1930s also saw the development of the first electron microscopes, and life scientists of the time arguably possessed enough knowledge of the cell to make educated guesses about which forms of chemical or low-temperature preservation would retain the data of the mind.

"Here we stand, three generations removed, a thousand distinct human cultures in which there is little to show that we desire anything other than oblivion or self-delusion when it comes to our lives. Judging by actions rather than words, people who greatly desire both lasting life and health are a minority indeed. And with each passing year, another fifty million lives vanish into the maw to be destroyed utterly."

DISCUSSION

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!

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LATEST HEADLINES FROM FIGHT AGING!

ON CRYONICS AND DEFINITIONS OF DEATH
Friday, May 20, 2011
https://www.fightaging.org/archives/2011/05/on-cryonics-and-definitions-of-death.php
From Depressed Metabolism: "It has been said that if you want to persuade someone, you need to find common ground. But one of the defining characteristics of cryonics is that proponents and opponents cannot even seem to agree on the criteria that should be employed in discussing cryonics. The cryonics skeptic will argue that the idea of cryonics is dead on arrival because cryonics patients are dead. The response of the cryonics advocate is that death is not a state but a process and there is good reason to believe that a person who is considered dead today may not be considered dead by a future physician. In essence, the cryonics advocate is arguing that his skeptical opponent would agree with him if he would just embrace his conception of death ... Cryonicists have named their favorite conception of death 'information-theoretic death.' In a nutshell, a person is said to be dead in the information-theoretic sense of the word if no future technologies are capable of inferring the original state of the brain that encodes the person's memories and identity. There are a lot of good things to be said about substituting this more rigorous criterion of death for our current definitions of death. However, in this brief paper I will argue that our best response does not necessarily need to depend on skeptics embracing such alternative definitions of death and that we may be able to argue that opponents of cryonics should support legal protection for cryonics patients or risk contradicting conventional definitions of death."

COMMENTARY ON MEASURING TELOMERES
Friday, May 20, 2011
https://www.fightaging.org/archives/2011/05/commentary-on-measuring-telomeres.php
With the advent of commercial telomere length measurement services, there's been a lot of unscientific hype in the media of late about tests that will show how long you're going to live. Some more sensible commentary here from FuturePundit: "the test can not precisely predict your year of death. Too many factors (accidents, suicide, and murder aside) influence your date of death. Take cancer for example. There's a lot of randomness involved in determining when we'll get cancer. The accumulation of damage in cells can make them turn cancerous. But just when the right set of genetic mutations or other cancer-promoting damage will occur in some cell in one's body is as hard to predict as when someone will win a lottery. Many things have to line up just right all in the same cell to make it cancerous. Every day is basically another throw of the dice. Will a bunch of mutations all line up to send a cell of yours into dangerous mad replication and growth? Better longevity tests seem useful for retirement planning. Should you save enough money to support yourself to age 95? Or expect to die by your late 60s? A telomere test could help you decide difficult questions about your savings rate and career choices. Do you need to work past age 70 to save enough money to avoid going broke in your 80s and avoid poverty in your 90s? A better sense of the odds would help. Of course, before we hit our biological shelf life expiration date some of us just might live long enough to still be around when rejuvenation therapies become available. Injections of youthful stem cells with long telomeres could replace older tired cells with short telomeres. This would be great for the immune system, for example, because a youthful immune system will do a better job of fighting cancer. Also, youthful cells for the cardiovascular system could cut the risk of heart disease, stroke, and other killers." The high level point being that unless you are old already the future of your life span has less to do with your telomeres and more do to with progress in medical science.

ALCOR VIDEO LIBRARY UPDATED
Thursday, May 19, 2011
https://www.fightaging.org/archives/2011/05/alcor-video-library-updated.php
From Alcor News: "The Alcor Video Library has recently added new material. It now includes a short Video Tour of Alcor Facility and five complete presentations from the 2006 Alcor Conference. The video quality has also been significantly upgraded. ... The Limitless Future (28-minutes). Alcor documentary video (2005). Discover how leading-edge science at the Alcor Life Extension Foundation is getting closer to making the dream of a vastly extended lifespan come true and how our notion of "death" is shifting. Includes interviews with world-renowned scientists including Dr. Aubrey de Grey, [explaining] how life can be cryopreserved on the verge of death and then revitalized, giving us a second chance at a long and productive life, and Dr. Ralph Merkle, Distinguished Professor of Computing at Georgia Tech, exploring how molecular-sized machines will be able to repair damage to your body from aging or the devastating effects of cancer and other illnesses, including frostbite." You might also take a look at some of the other videos linked in the post, such as a presentation on the economics of longevity: "In this talk, Dr. Friedman shares his insights into the many potential consequences of an extended lifespan. He asks provocative questions about the future of the family unit, a typical career path, and the economic outlook for society as a whole."

MORE HEART PATCHING
Thursday, May 19, 2011
https://www.fightaging.org/archives/2011/05/more-heart-patching.php
Patching a damaged heart is on the agenda again, with nanoscale-featured scaffold material this time: "When you suffer a heart attack, a part of your heart dies. Nerve cells in the heart's wall and a special class of cells that spontaneously expand and contract - keeping the heart beating in perfect synchronicity - are lost forever. [At present] surgeons can't repair the affected area [but the] best approach would be to figure out how to resuscitate [it] ... scientists turned to nanotechnology. In a lab, they built a scaffold-looking structure consisting of carbon nanofibers and a government-approved polymer. Tests showed the synthetic nanopatch regenerated natural heart tissue cells ­- called cardiomyocytes - as well as neurons. In short, the tests showed that a dead region of the heart can be brought back to life. ... the engineers employed carbon nanofibers, helical-shaped tubes with diameters between 60 and 200 nanometers. The carbon nanofibers work well because they are excellent conductors of electrons, performing the kind of electrical connections the heart relies upon for keeping a steady beat. ... In tests with the 200-nanometer-diameter carbon nanofibers seeded with cardiomyocytes, five times as many heart-tissue cells colonized the surface after four hours than with a control sample consisting of the polymer only. ... The scaffold works because it is elastic and durable, and can thus expand and contract much like heart tissue. ... It's because of these properties and the carbon nanofibers that cardiomyocytes and neurons congregate on the scaffold and spawn new cells, in effect regenerating the area."

TOWARDS TREATMENTS FOR AGE-RELATED MUSCLE LOSS
Wednesday, May 18, 2011
https://www.fightaging.org/archives/2011/05/towards-treatments-for-age-related-muscle-loss.php
Stem cell therapies are one theoretical path towards therapies for sarcopenia, the loss of muscle mass and strength with age. Here, researchers have discovered "the mechanism that causes stem cells in the embryo to differentiate into specialised cells that form the skeletal muscles of animals' bodies. ... The field has the potential to revolutionise medicine by delivering therapies to regenerate tissue damaged by disease or injury. Differentiation happens soon after fertilisation, when embryonic cells are dividing rapidly and migrating as the animal's body takes shape. ... The scientists investigated the effect of a known signalling pathway called NOTCH on muscle differentiation. They found that differentiation of stem cells to muscle was initiated when NOTCH signalling proteins touched some of the cells. These proteins were carried by passing cells migrating from a different tissue - the neural crest - the progenitor tissue of sensory nerve cells. Muscle formation in the target stem cells occurred only when the NOTCH pathway was triggered briefly by the migrating neural crest cells. ... This kiss-and-run activation of a pathway is a completely novel mechanism of stem cell specification which explains why only some stem cells adopt a muscle cell fate. ... the team would now focus on unravelling the mechanisms of embryonic muscle cell differentiation at the molecular level as a necessary step to regulating regeneration of the muscles in human patients."

SENS FOUNDATION SEEKS ACADEMIC COORDINATOR
Wednesday, May 18, 2011
https://www.fightaging.org/archives/2011/05/sens-foundation-seeks-academic-coordinator.php
From the SENS Foundation: "SENS Foundation is a 501c3 non-profit which works to develop, promote and ensure widespread access to rejuvenation biotechnologies which comprehensively address the disabilities and diseases of aging. The Foundation combines significant direct research efforts with education, affiliation and outreach programs. The SENS Foundation Academic Initiative (AI) is the nexus of its educational activities, which includes student mentoring, small but growing grants and scholarship programs, and coursework development. SENS Foundation is seeking a staff member to be Academic Coordinator. The Academic Coordinator will oversee the Academic Initiative and be responsible for designing, implementing and expanding projects and programs that support the aims of SENS Foundation. Additional responsibilities will include managing AI volunteer staff and students; maintaining active communication with SENS Foundation management, the Foundation Research Center, and AI volunteers; and establishing and maintaining reporting measures to document AI operations. The AC will report to the CEO, and work closely with the CSO, Vice President, and Director of Research Operations. Major projects already in development include the creation of online undergraduate courses in longevity science, development of a comprehensive training program, continuance and expansion of the scholarship and mentoring program, and implementation of a comprehensive marketing strategy to expand and promote the Academic Initiative."

STEM CELLS REVERSE PARKINSON'S IN RATS
Tuesday, May 17, 2011
https://www.fightaging.org/archives/2011/05/stem-cells-reverse-parkinsons-in-rats.php
Promising news: "A team of researchers [has] now compared the ability of cells derived from different types of human stem cell to reverse disease in a rat model of Parkinson disease and identified a stem cell population that they believe could be clinically relevant. ... Parkinson disease results from the progressive loss of a specific subpopulation of nerve cells. Current treatments provide only relief from the symptoms of the disease and cannot reverse the nerve cell loss. Stem cells are considered by many to be promising candidate sources of cells to reverse nerve cell loss in individuals with Parkinson disease through their ability to regenerate and repair diseased tissues. ... There are two types of stem cell considered in this context: embryonic stem (ES) cells, which are derived from early embryos; and induced pluripotent stem (iPS) cells, which are derived by reprogramming cells of the body such that they have the ability to generate any cell type. In turn, cells of the body can be reprogrammed to become iPS cells in one of two ways: the reprogramming proteins can be transferred directly into the cells (protein-based iPS cells) or viruses can be used to deliver to the cells the genetic information necessary for producing the reprogramming proteins (virus-based iPS cell). [Researchers] found several problems with cells derived from virus-based human iPS cells that precluded their use in the Parkinson disease model but found that nerve cells derived from protein-based human iPS cells reversed disease when transplanted into the brain of rats modeling Parkinson disease. They therefore conclude that protein-based human iPS cells could be used in the treatment of individuals with Parkinson disease."

MORE RETINAL REGENERATION
Tuesday, May 17, 2011
https://www.fightaging.org/archives/2011/05/more-retinal-regeneration.php
From EurekAlert!: researchers "are the first to regenerate large areas of damaged retinas and improve visual function using IPS cells (induced pluripotent stem cells) derived from skin. ... While other researchers have been successful in converting skin cells into induced pluripotent stem cells (iPSCs) and subsequently into retinal neurons, we believe that this is the first time that this degree of retinal reconstruction and restoration of visual function has been detected ... Today, diseases such as retinitis pigmentosa (RP) and age-related macular degeneration (AMD) are the leading causes of incurable blindness in the western world. In these diseases, retinal cells, also known as photoreceptors, begin to die and with them the eye's ability to capture light and transmit this information to the brain. Once destroyed, retinal cells, like other cells of the central nervous system have limited capacity for endogenous regeneration. ... Stem cell regeneration of this precious tissue is our best hope for treating and someday curing these disorders. ... [Researchers] harvested skin cells from the tails of red fluorescent mice. They used red mice, because the red tissue would be easy to track when transplanted in the eyes of non-fluorescent diseased mice. ... the group generated red fluorescent IPSCs, and, with additional chemical coaxing, precursors of retinal cells. ... Within 33 days the cells were ready to be transplanted and were introduced into the eyes of a mouse model of retina degenerative disease. ... Within four to six weeks, the researchers observed that the transplanted 'red' cells had taken up residence in the appropriate retinal area (photoreceptor layer) of the eye and had begun to integrate and assemble into healthily looking retinal tissue."

N-GLYCAN PROFILES AND INHERITED LONGEVITY
Monday, May 16, 2011
https://www.fightaging.org/archives/2011/05/n-glycan-profiles-and-inherited-longevity.php
Some people can live moderately longer than others due to differences in their genes that enhance the ability of a good lifestyle to extend life, or blunt the tendency for a bad lifestyle to shorten life. In this age of biotechnology it is only a matter of time before all the biochemical differences between naturally longer-lived and shorter-lived human lineages are uncovered: "The development of medical interventions for the preservation of disease-free longevity would be facilitated by markers that predict healthy aging. Altered protein N-glycosylation patterns have been found with increasing age and several disease states. Here we investigate whether glycans derived from the total glycoprotein pool in plasma mark familial longevity and distinguish healthy from unhealthy aging. Total plasma N-glycan profiles of 2396 middle aged participants in the Leiden Longevity Study (LLS) were obtained ... After normalization and batch correction, several regression strategies were applied to evaluate associations between glycan patterns, familial longevity, and healthy aging. Two N-glycan features (LC-7 and LC-8) were identified to be more abundant in plasma of the offspring of long-lived individuals as compared to controls. ... Furthermore, a decrease in levels of LC-8 was associated with the occurrence of myocardial infarction, indicating that plasma glycosylation patterns do not only mark familial longevity but may also reflect healthy aging. In conclusion, we describe two glycan features, of which increased levels mark familial longevity and decreased levels of one of these features mark the presence of cardiovascular disease."

ANOTHER PAPER ON BRANCHED-CHAIN AMINO ACIDS
Monday, May 16, 2011
https://www.fightaging.org/archives/2011/05/another-paper-on-branched-chain-amino-acids.php
Researchers continue to investigate the effects of branched-chain amino acids (BCAA) on life span in laboratory animals: "Identification of strategies mimicking key [calorie restriction (CR)] mechanisms - increased mitochondrial respiration and reduced production of oxygen radicals - is a hot topic in gerontology. Dietary supplementation with essential and/or branched chain amino acids (BCAAs) exerts a variety of beneficial effects in experimental animals and humans and has been recently demonstrated to support cardiac and skeletal muscle mitochondrial biogenesis, prevent oxidative damage, and enhance physical endurance in middle-aged mice, resulting in prolonged survival. ... A body of recent evidence suggest that amino acids, and in particular BCAAs, behave as evolutionary conserved modulators of lifespan of different organisms ... [Like exercise, BCAA supplementation] does not affect maximum lifespan, but increases the median lifespan, an indicator that specific diseases have been prevented. ... A broad range of questions await answers. The first point to be clarified is the role that specific amino acid signatures can play, directly or indirectly, in the CR effects on healthspan. ... there is need to investigate which amino acid (or specific amino acid combination) is required for the beneficial effects seen in mammals. Not last in importance, large, randomized clinical trials are necessary to assess the safety and efficacy of BCAA/amino acid supplementation for the prevention and treatment of the disabling consequences of energy depletion in the elderly."

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