LONGEVITY MEME NEWSLETTER
January 31st 2011
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.
- The Mainstreaming of Uncertainty Over Life Expectancy
- Genescient on Genescient
- NOVA on Longevity Science
- Crunching the Numbers on a Longevity Study
THE MAINSTREAMING OF UNCERTAINTY OVER LIFE EXPECTANCY
So much money rests upon statistical predictions of life span that this is one of the few areas in which there is a great deal of discussion over the future of biotechnology and longevity science:
"Following on in the theme of last week's post on the spreading ideas of longevity science, I think it's fair to say that uncertainty in projected life expectancy is now a fairly mainstream concept. Vast sums of money - the massive industries of pensions, life insurance, and so forth - rest upon reasonably accurate actuarial projections of life span and mortality rate. ... Unfortunately for these industries, and for governments whose politicians have made promises of future entitlements based upon old projections of life span, the advance of biotechnology is making the future exceedingly uncertain. Uncertain in a good way, of course - more life for us. If there are people and institutions out there whose livelihoods depend upon betting against increasing longevity ... well, the sooner they find a different business to be in, the better off they'll be. ... Retirement is one of many things that will be changing. I think that the idea of uncertainty in future life span due to advancing biotechnology may be a good path for many new faces to find their way to the healthy life extension community. It is a way past the unspoken assumption that so many people have: that their lives will look the much same as those of their parents and grandparents in scope."
GENESCIENT ON GENESCIENT
One of the Genescient VPs recently wrote a great overview on the company's work in the genetics of longevity:
"It's an interesting piece. My take on Genescient remains much the same: their work is a very efficient next generation approach to what is a comparatively ineffective course of action in regards to aging. In this it epitomizes the mainstream of aging and longevity research - the development of ever more sophisticated methodologies aimed at slowing down the aging process through manipulation of metabolism. Sadly, however, any foreseeable method of slowing aging will be of little use to people who are already old ... and none of us are getting any younger as we wait on progress in research and development.
"Genescient generates a raft of genetic and other information that will be useful throughout the life science field - including aging research - regardless of the outcome of their other work. The company will also make the founders a large pot of money if there's any justice in the world, given that they are effectively a next generation Sirtris. But none of this changes the fact that, from the perspective of progress towards extending human life, all that investment would be far better spent on SENS."
NOVA ON LONGEVITY SCIENCE
A recent NOVA edition looked at some of the work taking place on longevity science and related biotechnology:
"This isn't earthshaking stuff, and should all be familiar old news to readers here, but I'm all for seeing more high quality productions that aim to introduce the public to the fundamental ideas of applied aging and longevity research ... As was pointed out to me in a private email, there is a refreshing lack of negativity in the program - it's a generally positive outlook on the science that is presented. That may be a sign of progress."
CRUNCHING THE NUMBERS ON A LONGEVITY STUDY
What do scientists look at when the conduct a study of human longevity? How do these longitudinal studies generally run? A recent open access paper and related materials provide some insight:
"Some people have better genes than others, at least when it comes to living a longer, healthier life. They are perhaps more resistant to some forms of biological damage, perhaps have better repair mechanisms, perhaps can respond more effectively at a cellular level to good diet and lifestyle choices. The reasons why natural longevity has an inherited component are largely unknown and will be a subject for research for the next few decades - indeed, I expect the first generation of meaningful rejuvenation therapies to arrive in advance of a full understanding of the natural differences in human longevity. That full understanding simply isn't necessary for researchers to make progress in repairing and reversing the known biochemical differences between an old person and a young person.
"A recent open access paper crunches some the numbers from the Long Life Family Study and presents graphs and tables that illustrate the degree to which long-lived folk have better measures of health throughout their old age when compared with the rest of us. It is an interesting read on a number of levels, not least as an introduction to how these studies work under the hood, and what the researchers are looking at."
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!
LATEST HEADLINES FROM FIGHT AGING!
PROHIBITIN AND CALORIE RESTRICTION
Friday, January 28, 2011
More sophisticated studies of the biological changes produced - quite quickly - by calorie restriction continue to yield new information: "Caloric restriction (CR) is well known to expand lifespan in a variety of species and to retard many age-related diseases. The effects of relatively mild CR on the proteome profile in relation to lifespan have not yet been reported, despite the more extensive studies of the stricter CR conditions. Thus, the present study was conducted to elucidate the protein profiles in rat livers after mild CR for a relatively short time. Young growing rats were fed CR diets (10% and 30% CR) for 1 month. ... The most remarkable protein among the differentially expressed proteins was found to be prohibitin, the abundance of which was increased by 30% CR. Prohibitin is a ubiquitously expressed protein shown to suppress cell proliferation and to be related to longevity. The increase in prohibitin was observed both in 10% and 30% CR by Western blot analysis. Furthermore, induction of AMP-activated kinase (AMPK) protein, related to the actions of prohibitin in promoting longevity, was observed. The increased prohibitin level in response to subtle CR suggests that this increase may be one of the early events leading to the expansion of lifespan in response to CR."
NANOPARTICLES SPUR WOUND HEALING
Friday, January 28, 2011
An example of one of the ways in which the natural process of healing can be adjusted, or rescued when it fails: "investigators have developed a novel system for delivery of growth factors to chronic wounds such as pressure sores and diabetic foot ulcers. ... the team [reports] fabricating nanospheres containing keratinocyte growth factor (KGF), a protein known to play an important role in wound healing, fused with elastin-like peptides. When suspended in a fibrin gel, these nanoparticles improved the healing of deep skin wounds in diabetic mice. ... It is quite amazing how just one dose of the fusion protein was enough to induce significant tissue regeneration in two weeks. Previous reports have suggested that KGF can help heal chronic wounds. But in most studies the growth factor was applied to the surface of the wound, limiting its availability to deeper tissues and requiring repeat applications to produce any clinical benefit. Using large quantities of growth factor would make this therapy extremely expensive. Our work circumvents these limitations by more efficiently delivering KFG throughout the wound to stimulate tissue regeneration. ... The authors describe developing a fusion protein from recombinant KGF and elastin-like-peptides, which are major constituents of skin and other connective tissues. Laboratory experiments showed that the fusion protein retained the wound-healing properties of both elastin and KGF and that it rapidly and efficiently self-assembled into nanoparticles in response to a simple increase in temperature. When applied to deep skin wounds in genetically diabetic mice, the nanoparticles accelerated healing by stimulating the formation of both surface epithelial tissue and thick fibrous connective tissue."
ENHANCING MEMORY WITH INSULIN-LIKE GROWTH FACTOR
Thursday, January 27, 2011
From ScienceDaily: "A naturally occurring growth factor significantly boosted retention and prevented forgetting of a fear memory when injected into rats' memory circuitry during time-limited windows when memories become fragile and changeable. ... To our knowledge, this is the first demonstration of potent memory enhancement via a naturally occurring factor that readily passes through the blood-brain barrier - and thus may hold promise for treatment development ... The staying power of a memory depends on the synthesis of new proteins and structural changes in the connections between brain cells. These memory-strengthening changes occur within time-limited windows right after learning, when memories undergo consolidation, and also right after a memory is retrieved, a process called reconsolidation. Hints from other studies led the researchers to suspect that IGF-II plays a role in these processes within the brain's memory center, the hippocampus, where it is relatively highly concentrated. The little-known growth factor is part of the brain's machinery for tissue repair and regeneration; it is important during development and declines with age. ... learning boosted the expression of naturally occurring IGF-II in the hippocampus. So the researchers injected synthetic IGF-II directly into the hippocampus during windows of consolidation or reconsolidation, when memories are malleable. Remarkably, the rats' memory markedly improved - with the effects lasting at least a few weeks. An examination of the animals' brains revealed that IGF-II had strengthened the cellular connections and mechanisms underlying long-term memory - a process called long-term potentiation."
THE 2ND ANNUAL YOUNG CRYONICISTS GATHERING
Thursday, January 27, 2011
The cryonics community last year held an outreach event for younger members - a part of the necessary structure of cryonics as a process is a continuing community to maintain the preserved bodies and brains of those who preceded them. This year the event will be held in May: "This cryonics focus group seminar hosted by Bill Faloon and Carin Idun will be held on Thursday, May 19 and Friday, May 20, 2011, in Fort Lauderdale, Florida. Invitations were mailed to CI and Alcor members ages 13-29. The purpose of the young cryonicists' seminars is to develop a continuing social network of like-minded individuals who otherwise might not have the opportunity to meet in person. This gathering is open to young cryonicists from all cryonics organizations. Registered participants will also enjoy the opportunity to attend the Suspended Animation conference. You must be registered in advance to attend." As I noted last year, "this sort of event sounds like something worth making an institution in the community. Cryonics has a long way to go to become mainstream, but every step is a step closer. So many, many lives will be lost between now and the advent of working rejuvenation medicine - and the methodology presently exists to save those lives though cryonics. Most people are not aware of it or interested in it, however, and cryonics provision needs to be scaled up to handle the masses. Scaling is a trivial problem compared to convincing people that a viable workaround to death exists; as soon as there is desire for a product, there will be competition and development."
THE BIG THINK SERIES ON LONGEVITY
Wednesday, January 26, 2011
SIngularity Hub likes the Big Think series on longevity: "Thinking about living forever? You've got a lot of reading to do...or maybe you can just watch a few videos. The science surrounding longevity is a hive of interweaving studies and counterstudies that can leave the average reader confused. Singularity Hub will always give you a look at the best life-extension technologies as they emerge, but what if you need the very basics? In that case, BigThink's series "Living Longer, Better - and Maybe Forever" is a fun place to start. With videos from Aubrey de Grey, Ray Kurzweil, Leonard Guarente, and many others the series gives its audience a first look at some of the technologies and possibilities for the future of human life. ... If you have to begin with one expert to introduce you to longevity, it should probably be Aubrey de Grey. The rather-famous scientist has made a career of studying how human-life could be extended well beyond the means of today. Passionate, thoughtful, and sporting an unforgettable beard, de Grey's talks about longevity are typically as insightful as they are memorable. ... Part of what makes the BigThink 'Living Longer, Better - And Maybe Forever' series a good place to start is that the videos selected are a small sample of the much longer footage collected. Aubrey de Grey, for instance, has more than a half hour of interview videos available on BigThink divided into sections for easy browsing. If any of the speakers in the series interest you, you can be almost certain that there is more video of their thoughts for you to explore."
SENS FOUNDATION FAQ POSTED
Wednesday, January 26, 2011
The SENS Foundation has posted a FAQ on their work to defeat degenerative aging: "Can anything really be done about age-related degeneration and disease? Isn't getting sicker as we get older just a fact of life? It is informative to think about similar questions which might have been asked at different points over the past century. Can we really do anything about wound infections? After the invention of antibiotics the answer was a resounding, 'Yes'. When will the next outbreak of smallpox occur? After the WHO's program of eradication the answer became, 'Never'. Cholera, and John Snow's work on its epidemiology; polio, and the Salk vaccine... the list goes on. All these advances in medicine changed the answers to questions, and showed that a 'fact of life' is often just a problem waiting for a solution. So it is with the sickness of older age. It has not yet been addressed effectively, but that does not mean that it cannot be addressed. It simply means that we have to find new ways to tackle the problem, and the most promising of these is rejuvenation biotechnology. ... Wouldn't it be easier to find ways to slow down age-related degeneration than to reverse it? First, let's be clear on what 'reversing age-related degeneration' means, in rejuvenation biotechnology. We are not trying to reverse the process which causes degeneration: that process is highly complicated and not well understood. Rather, we are working to repair the result of that process, sidestepping our ignorance of the process itself. We believe that this side of the problem of age-related degeneration can be solved more rapidly and effectively. The human body, by its nature, is a very complex system, built from finely-regulated, metabolic subsystems. Tinkering with one aspect inevitably ripples in unexpected ways through the entire system, and in ways which we can rarely predict with any great confidence. This entails a high risk of negative side-effects occurring when any one of them is modified. Reversing age-related degeneration - in the damage repair sense - avoids the complex pathways of metabolism, and has the potential to be simpler and more effective than methods which only slow it down."
PROGRESS IN PROGERIA RESEARCH
Tuesday, January 25, 2011
The accelerated aging condition progeria so far appears to be an extreme example of one type of cellular damage that usually only provides a very modest contribution to degenerative aging. Here is news of recent research: "Hutchinson-Gilford Progeria Syndrome, also known as progeria, is caused by a mutation in the gene encoding for the protein lamin A, an important component of the membrane surrounding a cell's nucleus. The mutation results in a truncated form of lamin A called progerin, which in turn causes misshapen cell nuclei and DNA damage. ... [researchers] have produced the world's first human cell model of progeria, a disease resulting in severe premature ageing in one in four to eight million children worldwide. This model has allowed them to make new discoveries concerning the mechanism by which progeria works. ... the team used a novel technique of deriving induced pluripotent stem (iPS) cells from cells of human progeria patients. This human progeria model allows the group to trace and analyse the distinctive characteristics of progeria as it progresses in human cells. ... The researchers used their iPS cells to identify two types of cells - mesenchymal stem cells (MSCs) and vascular smooth muscle cells (VSMCs) - that were particularly adversely affected by progeria. This means that a young patient with progeria would typically have fewer MSCs and VSMCs than other children. MSCs were found to be very sensitive to a low oxygen environment and their losses could delay renewal of the various tissues they gave rise to, thus exacerbating the patient's symptoms of ageing. The same effect on VSMCs could explain why their number was reduced in the patient's heart vessels. ... This new study provides further evidence for the role of lamin processing in connective tissue function, as well as insights into the normal ageing process. We hope to soon find new routes of intervention to treat this incurable disease. Such interventions may be of use in treating atherosclerosis in general, a condition afflicting many millions of individuals."
SUPERCOOLING APPLIED TO CRYOPRESERVATION
Tuesday, January 25, 2011
Of possible long-term relevance to cryonics: "A technology used to freeze sushi is solving a dilemma for organ storage. By borrowing tech used to preserve high-end food delicacies, a Hiroshima University research group proved it possible to safely freeze whole teeth and their delicate attaching tissues. As long as the freezer stays cold, the folks at Hiroshima U. think your teeth could be stored for 40 years, no problem. But the sushi-storage system isn't a one trick pony: internal organs could be next thanks to the magic of supercooling. In typical cryo-storage, fast freezing of organs requires poisonous levels of anti-freeze, and let's face it, no one wants a poisoned kidney transplanted into their body. But slower freezing causes cell popping ice crystals to form. So, what do you do to prevent ice crystals during slow freezing? Use magnets. ABI is the Japanese company producing the freezer system. ABI's 'Cells Alive System' (CAS) vibrates water with magnetic fields, preventing freezing, even at supercool temperatures of -10 degrees Celsius (According to the Patent.) When the field is turned off, the water in the food instantly freezes. No time for ice growth. ... A very tricky part of tooth preservation is keeping tooth ligaments alive, or even some of the ligament cells. Implanting ligaments is important. We have ligaments attached to teeth because the force of chewing could grind our chompers out of our jaws. When the research team tried slow freezing a whole fresh tooth without the CAS magnetic fields, the ligaments didn't survive and were severely damaged. However, a CAS magnetically vibrated tooth's ligaments survived. CAS frozen ligament cells grew as well as those from a fresh tooth, and showed only minor damage."
THOUGHTS ON THE NON-ISSUE OF OVERPOPULATION
Monday, January 24, 2011
A post from the author of the Finnish language book Evolving Humanity: "The replenishment rate required to keep a population stable is about 2.1 children per woman. The average fertility rate in a lot of industrialized countries is well below this - for instance, 1.58 in Canada, 1.42 in Germany, 1.32 in Italy, 1.20 in Japan and 1.04 in Hong Kong. The EU average is 1.51. Yes, in a lot of poor countries the figures are considerably higher - Niger tops the chart with 7.68 children per woman - but even then the overall world population growth is projected to start declining around 2050 or so. To give a sense of proportion: suppose that tomorrow, we developed literal immortality and made it instantly available for everyone, so that the death rate would drop to zero in a day, with no adjustment to the birth rate. Even if this completely unrealistic scenario were to take place, the overall US population growth would still only be about half of what it was during the height of the 1950s baby boom! Even in such a completely, utterly unrealistic scenario, it would still take around 53 years for the US population to double - assuming no compensating drop in birth rates in that whole time. We've adapted to increasing lifespans before. Between 1950 and 1990, the percentage of population over 65 almost doubled in Sweden, going from 10.3 to 18.1. (In the United Kingdom it went up from 10.7 to 15.2, in the US from 8.1 to 12.6, and in the more-developed countries overall it went from 7.6 to 12.1.) The beauty of economics is that like all resource consumption, having children is a self-regulating mechanism: if a growing population really does exert a heavy strain on resources, then it will become more expensive to have children, and people will have less of them. ... I see no reason to presume that radical life extension and indefinite youths would pose us any problems that we couldn't handle, at least not on the overpopulation front." You might also look at the demographic models mentioned in the Fight Aging! archives.
THE POTENTIAL TO BLOCK METASTASIS
Monday, January 24, 2011
Blocking metastasis would be a big step towards the defeat of cancer, and a number of different approaches show promise. Here, researchers "have discovered a rogue gene which - if blocked by the right drugs - could stop cancer in its tracks. ... the discovery is a breakthrough in our understanding of how cancer spreads. It is hoped the research will lead to new drugs that halt the critical late stage of the disease when cancer cells spread to other parts of the body. The culprit gene - known as WWP2 - is an enzymic bonding agent found inside cancer cells. It attacks and breaks down a natural inhibitor in the body which normally prevents cancer cells spreading. .... by blocking WWP2, levels of the natural inhibitor are boosted and the cancer cells remain dormant. If a drug was developed that deactivated WWP2, conventional therapies and surgery could be used on primary tumours, with no risk of the disease taking hold elsewhere. ... the discovery could lead to the development of a new generation of drugs within the next decade that could be used to stop the aggressive spread of most forms of the disease, including breast, brain, colon and skin cancer. ... The late-stages of cancer involve a process known as metastasis - a critical phase in the progression of the disease that cannot currently be treated or prevented. The challenge now is to identify a potent drug that will get inside cancer cells and destroy the activity of the rogue gene. This is a difficult but not impossible task, made easier by the deeper understanding of the biological processes revealed in this study."