Longevity Meme Newsletter, December 13th 2010
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December 13th 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.



- $500,000 Given to SENS Research
- An Interview with the Halcyon Molecular Founder
- On Global Aging and Visions for the Future
- Looking Back: Discovering a Genetic Pathway of Longevity
- Latest Headlines from Fight Aging!


Investor Peter Thiel recently held a gathering of high net worth philanthropists to encourage greater vision in their funding of research and development. What use is great wealth, after all, if you don't aim to reach for the sky and shake the foundations? One outcome of this gathering was a $500,000 donation for the SENS Foundation, to help fund the development of medical technologies that can repair the biochemical damage of aging:


"The global scientific community is increasingly recognizing the role of rejuvenation biotechnologies in addressing age-related disease. This week, Arizona-based businessman Jason Hope announced a $500,000 donation to SENS Foundation, a California-based non-profit organization that works to develop, promote and ensure widespread access to rejuvenation biotechnologies which comprehensively address age-related disease. 'I have had great interest in the SENS Foundation and Dr. Aubrey de Grey's work for some time now. I believe their work is essential to the advancement of human medicine and their approach to the overall problem of human aging and its associated diseases (Alzheimer's, Atherosclerosis, Diabetes, etc.) is the only way to go. Their work and the work of others that they support will drive the complete redefinition and reshaping of the healthcare, pharmaceutical, and biotech industries as we know them today. The advancement of rejuvenation biotechnologies is not only extremely important, but it is the future. I am honored to support the SENS Foundation in its efforts, and hope my support helps drive faster results for all of humanity,' said Jason Hope."


The founder and CEO of Halcyon Molecular is one of the new generation of biotech business leaders strongly in favor of engineered human longevity:


"Parts of SENS urgently should be funded and tested. That being said, I work on sequencing and not on SENS, because our approach to curing aging is first to turn biology into an information science - actually getting to untangling the morass of metabolism that SENS does an end run around. I believe we can get to a complete mechanistic understanding of human biology in only a few decades, which is a timeline more like Kurzweil's. On the other hand, if SENS were being vigorously pursued today, it might save millions of lives before the total understanding approach avails us. It is good to have multiple bets.

"As for Kurzweil, maybe this isn't fair, and I'd like to hear his thoughts on it, but I'm afraid his books demotivate people who would otherwise contribute to the cause, maybe by giving the impression to some that the Singularity is not only coming, but actually inevitable. Eat right, exercise, take these pills, and don't worry - those smart hardworking scientists over there will solve everything for you. In contrast, a great thing about Aubrey [de Grey] as a leader is that he harangues people to actually get off their asses and make a contribution.

"We might not survive the next twenty years. We may never cure aging. There is nothing inevitable about our success. Everyone who is talented enough to make a contribution should be trying to help, on all fronts, by any ethical means, like it's life and death - because it is."


You might find this recent open access paper of interest, as it examines presently widely held beliefs that are at odds with the reality of scientific progress towards greater human longevity - to the point of holding things back, in fact.


"[This paper] makes the case for reviving the Aristotelian conception of political science (namely, that it is the architectonic science). It also makes the case for prioritizing the imperative to tackle the inborn aging process and, most importantly, the obstacles that impede our ability to accurately perceive the importance of tackling aging."

Long time readers will know that I disagree with this author on a number of fundamental axioms regarding political organization and economics, but that doesn't stop it from being a well-constructed paper that is unambiguously in favor of engineering an end to aging. The future for a given field of scientific study tends to look rosier when people holding many different philosophies of life start supporting it, and especially when they have to fight against the mainstream of their community of thought in order to do that.


It is easy to forget just how recently many of the pivotal discoveries in the biology of aging were made. Only in the last fifteen years or so has it become generally accepted in the research community that aging is very changeable, altered by metabolic adaptation to environmental circumstances and adjusted by gene-engineered mutations in the laboratory.


"This article describes the discovery of a genetic pathway that regulates ageing. In spite of the fascinating qualities of the ageing process, such as its remarkably different pace in different species, until the last few decades ageing was not thought to be subject to any active regulation. Now we know that the rate of ageing is indeed subject to regulation, by classical signalling pathways. These pathways link the ageing rate to environmental and physiological cues, and may even underlie its diversification during evolution. At the heart of these pathways are stress and metabolic sensors such as insulin and IGF-1 hormones ... At the time, ageing was generally thought to be a hopelessly intractable, even futile, problem to study. We just wear out; that's it. Fortunately, because of my experience I had come to expect that biological phenomena that seemed to happen haphazardly might well turn out to be controlled by the genes. ... Not only was ageing thought to be merely a passive, entropic process, evolutionary biologists had argued forcefully that ageing could not be regulated. For example, they felt that mechanisms for regulating ageing would have no way to evolve, as ageing takes place after reproduction. These theories were thought provoking, but to my mind, they had the effect of discouraging searches for regulatory genes. It seemed to me, a molecular geneticist from the outside, that one should keep an open mind and just have a look. So I saw the analysis of ageing as a fantastic opportunity to explore the unknown and perhaps discover something new and important."


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!



Friday, December 10, 2010
From Newsweek: "Luke Masella was born with spina bifida, a birth defect that paralyzed his bladder. By the time he was 10 years old, despite various treatments, his kidneys were failing. Toxins were building up in his blood, and he had lost 25 percent of his body weight. That's when Luke and his parents opted for a radical solution - a brand new bladder. It might sound like science fiction, but growing new organs from scratch has already become reality. In addition to bladders, scientists have engineered new skin, bone, cartilage, corneas, windpipes, arteries, and urethras. Human organs fail for a multitude of reasons; genetic deformities, injuries, and disease can all damage them. Organ transplantation is an option, of course, but it's risky, and too often there aren't enough donated organs to meet the growing need. So 25 years ago, a group of scientists embarked on an audacious quest: the creation of whole new organs. Brothers Joseph and Charles Vacanti at Harvard Medical School and Robert Langer of the Massachusetts Institute of Technology first promoted the idea of 'tissue engineering' or 'regenerative medicine.' The scientists knew that every organ has a 'scaffolding' - a structure that gives it shape - and many different types of cells with different functions. There are millions of cells, all arranged in an exact order. ... After the scaffolding came the hard part, the part that caused most scientists outside the field to predict that growing new organs would fail. Even if you could build a scaffolding and procure the cells to drape onto that scaffolding, then what? Surely no scientist could assemble millions of cells, one by one and each in the right place, as if the organ were a giant jigsaw puzzle." But of course researchers have proven that they can do this, and the field is presently progressing very rapidly.

Friday, December 10, 2010
From Mike Kope, SENS Foundation CEO: "Last night, Peter Thiel hosted 'Breakthrough Philanthropy', a dinner and presentation event showcasing eight non-profit organizations focused upon game-changing approaches to their fields. It was a wonderful opportunity for us to convey our message to a large group of entrepreneurs and philanthropists interested in the genuinely transformative. Our thanks to the Thiel Foundation, and the Seasteading Institute, for their efforts in creating that event. Here are my remarks from the presentation. ... We've gotten very good at conquering infectious diseases. None of you will suffer from polio, or smallpox, or, likely, measles or diptheria. But the truth is, we haven't extended that kind of success to the problems of aging. You will know someone suffering from cancer, from Alzheimer's, from Parkinson's disease. We haven't yet eradicated a single, major age-related disease. This is despite great advances in therapeutics, despite trillions in research underway around the globe, and despite the brightest minds working in an entire, thirty year long biotech revolution. Ten years ago, our CSO Aubrey de Grey first suggested … a slightly different revolution. His core idea was a damage repair model called SENS, and a recognition of a simple problem: when medical science focuses upon disease - when we wait for disease to develop - then what we learn is how to chase the pathology - and we haven't gotten very good at that. But if we look instead at the damage building up as a result of the normal metabolism of being alive, then we can learn to repair that damage before those deadly pathologies develop. That's it; that's all that SENS means: it's a model that steps away from the expensive and tangled 'pathology chase' and focuses instead upon identifying, addressing and removing the damage that is building up inside you; the damage that will eventually cause disease."

Thursday, December 9, 2010
The viewpoint of researchers in the mainstream of biogerontology is that they have demonstrated slowed aging in a wide range of animals, this is the best they've managed so far, and therefore the research community should be first of all working to do more or less exactly the same thing in humans: "Over the last two centuries, there has been a significant increase in average lifespan expectancy in the developed world. One unambiguous clinical implication of getting older is the risk of experiencing age-related diseases including various cancers, dementia, type-2 diabetes, cataracts and osteoporosis. Historically, the ageing process and its consequences were thought to be intractable. However, over the last two decades or so, a wealth of empirical data has been generated which demonstrates that longevity in model organisms can be extended through the manipulation of individual genes. In particular, many pathological conditions associated with the ageing process in model organisms, and importantly conserved from nematodes to humans, are attenuated in long-lived genetic mutants. For example, several long-lived genetic mouse models show attenuation in age-related cognitive decline, adiposity, cancer and glucose intolerance. Therefore, these long-lived mice enjoy a longer period without suffering the various sequelae of ageing. The greatest challenge in the biology of ageing is to now identify the mechanisms underlying increased healthy lifespan in these model organisms. Given that the elderly are making up an increasingly greater proportion of society, this focused approach in model organisms should help identify tractable interventions that can ultimately be translated to humans."

Thursday, December 9, 2010
Thoughts on engineered longevity are boxed into the standard, simplistic media viewpoint at Washington Examiner - everything is politics, and politics supposedly looks like this: "The right's reaction, I predict, will be to call for a moratorium on such innovations until we can determine whether life-extension therapies are 'playing God.' The playing God argument is, well, played out. If keeping people alive longer through conventional means isn't playing God, there is nothing categorically different about introducing breakthroughs that prevent age related illnesses to begin with. I dare say, people who believe in the sanctity of life will do well to consider the benefits of life-extending technologies for humanity. After all, as I suggest above, driving people into black markets is no way to enforce morality. And driving people into the grave because of some errant idea about God's plan doesn't do justice to what God's plan might actually be (i.e. that it may include life extension therapy). The left's reaction will be no less predictable. The left will say we should have a moratorium on the technology until we can figure out how to give everyone 'access' and quell Malthusian concerns about resource depletion and overpopulation (which will be unfounded). They will lament the gap between the poor short-livers and the rich long-livers. Then they'll try to cast life extension as a 'public health' good in order to socialize it, regulate it and ration it. This would be a grave mistake - one as serious as if we'd said people have a basic right to mobile devices. Socializing mobile technology would not only have retarded its development, but it would have limited its uptake. Almost everyone has a cellphone today, even though they didn't in 1990. Markets have meant better, faster and cheaper tech for the masses over time. It will be no different for life-extension therapies if they are left primarily to market forces."

Wednesday, December 8, 2010
Better repair after major damage is a step below preventative repair beforehand, but it's an improvement over the present state of affairs: "A new technique that jump-starts the growth of nerve fibers could reverse much of the damage caused by strokes ...This therapy may be used to restore function even when it's given long after ischemic brain damage has occurred. ... Currently doctors can do little to limit stroke damage after the first day following a stroke. Most strokes are ischemic (caused by blood clots). A drug called tPA can limit damage but must be given within the first three hours for the greatest benefit -- and most patients do not receive treatment within that time frame. [Researchers] report on a treatment called anti-Nogo-A therapy. Nogo-A is a protein that inhibits the growth of nerve fibers called axons. It serves as a check on runaway nerve growth that could cause a patient to be overly sensitive to pain, or to experience involuntary movements. (The protein is called Nogo because it in effect says "No go" to axons.) In anti-Nogo therapy, an antibody disables the Nogo protein. This allows the growth of axons in the stroke-affected side of the body and the restoration of functions lost due to stroke. ... Nine weeks after their stroke, six rats received anti-Nogo therapy, four rats received a control treatment consisting of an inactive antibody and five rats received no treatment. Nine weeks later, rats that had received anti-Nogo therapy regained 78 percent of their ability to grab pellets. By comparison, rats receiving no treatment regained 47 percent of that ability."

Wednesday, December 8, 2010
An open access paper: "In animal models, single-gene mutations in genes involved in insulin/IGF and target of rapamycin signalling pathways extend lifespan to a considerable extent. The genetic, genomic and epigenetic influences on human longevity are expected to be much more complex. Strikingly however, beneficial metabolic and cellular features of long-lived families resemble those in animals for whom the lifespan is extended by applying genetic manipulation and, especially, dietary restriction. Candidate gene studies in humans support the notion that human orthologues from longevity genes identified in lower species do contribute to longevity but that the influence of the genetic variants involved is small. Here we discuss how an integration of novel study designs, labour-intensive biobanking, deep phenotyping and genomic research may provide insights into the mechanisms that drive human longevity and healthy ageing, beyond the associations usually provided by molecular and genetic epidemiology. Although prospective studies of humans from the cradle to the grave have never been performed, it is feasible to extract life histories from different cohorts jointly covering the molecular changes that occur with age from early development all the way up to the age at death. By the integration of research in different study cohorts, and with research in animal models, biological research into human longevity is thus making considerable progress."

Tuesday, December 7, 2010
It takes a peculiar kind of societal madness to support an entire industry of people devoted to telling us solemnly just how bad, terrible, and wrong it would be to use medicine to live longer. Here is an open access paper in which a bioethicist bemoans the inevitability of extended healthy life - calling it tragic: "Biogerontology is sometimes viewed as similar to other forms of biomedical research in that it seeks to understand and treat a pathological process. Yet the prospect of treating ageing is extraordinary in terms of the profound changes to the human condition that would result. Recent advances in biogerontology allow a clearer view of the ethical issues and dilemmas that confront humanity with respect to treating ageing. For example, they imply that organismal senescence is a disease process with a broad spectrum of pathological consequences in late life (causing or exascerbating cardiovascular disease, cancer, neurodegenerative disease and many others). Moreover, in laboratory animals, it is possible to decelerate ageing, extend healthy adulthood and reduce the age-incidence of a broad spectrum of ageing-related diseases. This is accompanied by an overall extension of lifespan, sometimes of a large magnitude. Discussions of the ethics of treating ageing sometimes involve hand-wringing about detrimental consequences (e.g. to society) of marked life extension which, arguably, would be a form of enhancement technology. Yet given the great improvements in health that decelerated ageing could provide, it would seem that the only possible ethical course is to pursue it energetically. Thus, decelerated ageing has an element of tragic inevitability: its benefits to health compel us to pursue it, despite the transformation of human society, and even human nature, that this could entail."

Tuesday, December 7, 2010
Investor Peter Thiel has put millions into rejuvenation biotechnology research, you might recall. Here he's calling for others to show the same foresight: "Silicon Valley billionaire Peter Thiel worries that people aren't thinking big enough about the future. So he's convening an unusual philanthropic summit tonight at which he will introduce other wealthy tech figures to nonprofit groups exploring such futuristic - some might say 'far out' - ideas as artificial intelligence, the use of 'rejuvenation biotechnologies' to extend human life, and the creation of free-floating communities on the high seas. 'We're living in a world where people are incredibly biased toward the incremental,' said Thiel, explaining that he wants to challenge his peers to pursue more 'radical breakthroughs' in their philanthropy by supporting nonprofit exploration of technological innovations that carry at least the promise of major advances for the human condition. 'Obviously there are a lot of questions about the impact of these things,' he added. 'If you have radical life extension, that could obviously lead to repercussions for society. But I think that's a problem we want to have.' The list of expected attendees is closely guarded, but aides said it includes such figures as venture capitalist Pierluigi Zappacosta, a co-founder of Logitech, and Infoseek founder Steve Kirsch. ... Other presentations will be made by representatives from Humanity Plus, which promotes the idea that high-tech prosthetics and other scientific advancements can enhance human physical capabilities; the Foresight Institute, which focuses on the potential for medical and manufacturing advances through nanotechnology, or building things at the atomic level; and the SENS Foundation, which sponsors research into prolonging life by reversing the damage caused by normal aging."

Monday, December 6, 2010
On a number of fronts, researchers are within reach of making cavities in teeth a thing of the past: scientists "have deciphered the structure and functional mechanism of the glucansucrase enzyme that is responsible for dental plaque sticking to teeth. This knowledge will stimulate the identification of substances that inhibit the enzyme. Just add that substance to toothpaste, or even sweets, and caries will be a thing of the past. ... The main cause of tooth decay, the bacterium Streptococcus mutans, also uses this enzyme. Once attached to tooth enamel, these bacteria ferment sugars releasing acids that dissolve the calcium in teeth. This is how caries develop. ... [Researchers expect] that specific inhibitors for the glucansucrase enzyme may help to prevent attachment of the bacteria to the tooth enamel. Information about the structure and functional mechanism of the enzyme is crucial for developing such inhibitors. Thus far, such research has not been successful ... The various inhibitors studied not only blocked the glucansucrase, but also the digestive enzyme amylase in our saliva, which is needed to degrade starch." It's just a matter of time and funding before a suitable inhibitor is found.

Monday, December 6, 2010
Opponents of engineered longevity often put forward a false choice between quality of life and length of life. But medicine of the future will give us both: "one of the ten most-read articles on the BBC news website at the moment is a piece by Joan Bakewell suggesting that greater longevity may not be desirable. It's a superficially thoughtful commentary, but in truth it just runs through a series of standard knee-jerk reactions, most of which don't stand up to much scrutiny. Firstly, there is the implicit assumption that any extra years of life are bound to be of extremely low quality, due to physical and mental frailty. But one thing that actually unites almost all scientists in this area - from the mainstream ones like S Jay Olshansky who seek to slow the aging process by a few years, to the 'heretics' like [Aubrey] de Grey who seek to conquer it entirely - is that they don't think an increased lifespan would be beneficial unless 'healthspan' is boosted to an equivalent (or more likely greater) degree. There's always the danger of unintended consequences, of course, but there's no reason to fear the stated goal of the research. ... Finally, there's the general sense in Bakewell's article that 'a fuller life is better than a longer one'. This is a superficially attractive philosophy, but once again, it looks somewhat different if you just tweak the implicit parameters a little. What if the 'fuller life' lasted a mere twenty years, and the 'longer life' lasted eighty? Would anyone seriously suggest that the fullness of the twenty years entirely makes up for the tragedy of the lost sixty years? Some might, but it would be a far tougher case to make, simply because of our perceptions of what a 'natural' lifespan is. And yet the span we fetishise as being optimal is just a random quirk of the stage of evolution we happen to be at - some species live much shorter lives than we do, other species much longer."


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