Longevity Meme Newsletter, July 26 2010

July 26 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.



- TransVision and Singularity Summit Conferences
- An Interview With David Stipp
- Following Up on Cryonics in the Media
- Discussion
- Latest Healthy Life Extension Headlines


A couple more conferences of interest to supporters of longevity science are coming up later this year:


"TransVision 2010 is a global transhumanist conference and community convention, organized by several transhumanist activists, groups and organizations, under the executive leadership of the Italian Transhumanist Association (AIT) and with the collaboration of an Advisory Board. The event will take place on October 22, 23 and 24, 2010 in Milan, Italy with many options for remote online access."

Transhumanism, as I may have remarked on previous occasions, is simply common sense applied to technology and life in an age of change. But there are enough fools in the world for common sense to need its advocates. The conference has a good list of speakers set up already - the usual suspects, plus some of the Eurozone folk who don't often make it to the US conferences. If you're in the area this October, you should make an effort to attend.


"I should also note that the Singularity Summit 2010 will be held next month in San Francisco. ... The development of Strong artificial intelligence, the neuroscience that may contribute to that goal, and its ultimate consequences form the main focus of the presentations - topics of only indirect interest to engineered longevity, I feel. Faster and more capably machines and faster and more capable minds will make advances in technology arrive more rapidly, but they aren't direct contributions to progress in longevity science. However, you'll also find Gregory Stock, who has written on the topic of radical life extension, and Ellen Heber-Katz, who has produced very interesting work on enhanced regeneration in mammals, speaking at the event. So there's a little of something for everyone."


David Stipp is the author of a recently released book on longevity science. In the Fight Aging! post linked below, you'll find referenced an interview that presents a more nuanced version of Stipp's viewpoints than has appeared in articles to date:


"The main barrier, as with all anti-aging research, is that there's no funding. We've got ever more promising basic research and yet I don't know of anybody funding clinical work on agents that will possibly slow aging. ... There's no economic incentive. A single drug in clinical development generally costs around a billion dollars, from the very beginning to the end. A pharmaceutical company can only afford to spend that kind of money on trials of something it knows it can sell as a prescription drug, with a pretty high profit. The issue here is that you can't sell something as a prescription drug unless the Federal Drug Administration recognizes that there's an indication for it. And the FDA does not consider aging a disease, so it wouldn't give regulatory approval to a prescription drug used to treat aging."


A recent New York Times article on cryonics spurred a great deal of online discussion. A selection of links and quotes can be found at the following Fight Aging! post for those interested in browsing:


"While there are more than the usual number of people talking about cryonics of late, we shouldn't forget that the staff and volunteers of cryonics organizations continue to do their work in the background, just as they did before this latest burst of publicity. ... Doing beats talking about doing. In a better world, we would all tend to pay more attention to the people who are getting things done rather than filling out column inches."


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!




The latest Methuselah Foundation newsletter is out: "2010: Where We Are Now: Methuselah Foundation took on a big challenge: extending healthy human life. From SENS to My Bridge 4 Life, we've supported and incentivized major initiatives and research to fulfill our mission. In 2010 we are focusing our attention on tissue and whole organ engineering. Read this newsletter and follow the links to our site to learn more about what we are doing now so you live longer and healthier. ... This year we are focusing our efforts on tissue engineering and organ replacement. We are looking ahead 10 years and projecting that, with our help, everyone who needs an organ will get an organ. ... Prizes have proven to be the most powerful tool for inspiring radical scientific breakthroughs. That's why we offer prizes, including the recently announced NewOrgan Prize. The end result will allow many people to live longer and - if history is an indicator - the many innovations that come as a result of this work are unimaginable today. To build a replacement organ, from a patients own cells, and have it fully function, scientists must first develop and preserve all the tissues that build that organ - including muscle, nerves, arteries and veins. ... Leaders in the science of organ engineering have joined the NewOrgan Advisory Board. ... The members of our Scientific Advisory Board are frontrunners in the research and development of new organ technology. "

From ShrinkWrapped: "If a physical change affects half of all people as they age, this would seem to suggest that it is a normal variant of human aging, which to the best of our knowledge is an accumulation of metabolic and genetic errors that accrue as we get older until some sub-unit(s) of the processes reach a threshold at which continued functioning of the body is impossible. Our current regulatory apparatus remains trapped in a 20th century mindset which fails to recognize how various diseases are nothing more than unfortunate variants of the aging process that all of us will one day fall prey to. For example, in Alzheimer's 'Disease' errors of metabolism (malformed proteins) in neurons in the brain lead to an accumulation of defective protein parts which eventually disrupt the functioning of the neuron, ultimately killing it. When this process has gone on long enough to have damaged and destroyed some as yet unknown fraction of the brain, the person becomes neurologically symptomatic. This 'Disease' is not communicable, nor is it caused by an exogenous agent. The damage to the brain occurs as the result of biological failure that all of us will have to face in one form or another. ... The FDA does not recognize aging as a treatable condition and only approves treatment for 'Disease.' ... Because the FDA only evaluates treatments for Diseases, and its definition of disease versus aging is completely arbitrary (why is Type II Diabetes a disease while Sarcopenia, the loss of muscle mass and function that accompanies aging, is not?) we are forced to develop treatments that primarily address symptoms rather than either repairing damage or rejuvenating systems."

KurzweilAI looks at the recent scientific publication promoted by the LifeStar Institute: "Unfortunately, most biogerontologists see aging-intervention strategies as a considerable deviance from mainstream thinking, which is based on the notion that aging is a certainty and that pursuit of any kind of 'fountain of youth' or life-extension therapies will only end in failure. But de Grey is not swayed by the skeptics. He says perspectives are changing ... Five of the other authors [of the paper] are among the absolute top tier of biogerontologists, whose views are universally respected in the field. Their voice here will make a huge impact on thinking about the issue, both within the field and beyond. The surprising conclusion from the past two decades of research on biological aging is that aging is plastic. Within a species, maximum life span is not fixed, but can be increased by dietary manipulation (particularly calorie restriction) or genetic manipulation. ... But a new world of indefinite lifespans has also raised questions about potential population impacts. ... 'Contrary to what is widely assumed, however, the net effect should be relatively minor,' the authors respond, reasoning that new human births have a greater effect on population than adding a fraction of life span to existing humans. ... A policy of aging as usual will lead to enormous humanitarian, social, and financial costs. Efforts to avert that scenario are unequivocally merited, even if those efforts are costly and their success and full consequences uncertain. To realize any chance of success, the drive to tackle biological aging head-on must begin now."

The Methuselah Foundation provides profiles of the most recent Mprize competitors: "Holly Brown Borg’s acquaintance with Ames dwarf mice led her to aging research. While she was in a postdoctoral position she began working with these small but long-lived mice to do studies on immunology. At that time she was working with Andrzej Bartke, he holds the Mprize for Longevity for a mouse that lived almost 5 years, double the normal lifespan. After heading to North Dakota, where she became an Assistant Professor in Pharmacology, Physiology and Therapeutics, Holly continued to follow the progress of the mice. Their long life intrigued her. What was it that caused them to live so much longer than other mice? The human nutrition center on campus suggested that Holly turn her attention to methionine metabolism. This essential amino acid is critical for protein synthesis and growth, and is also integral to metabolism. To go a bit deeper, glutathione, an important antioxidant, is generated by the methionine (MET) pathway. Glutathione is made up of three amino acids, the key one in these studies is cysteine. The essential amino acids, MET and cysteine, can be easily modified in the diet. The Ames mice have highly active methionine metabolism but when they are given growth hormone, this activity goes down. This was the proof Holly needed that methionine metabolism is regulated by growth hormone."

From CBC News: "Scientists in Toronto are trying to crack the secrets of regeneration to trigger the human body to grow tissues and organs damaged by disease. In his lab at Mount Sinai Hospital, Dr. Ian Rogers is working on a replacement pancreas that would be grown in a lab and then placed in those with Type 1 diabetes to restore their insulin production. ... At this stage, Rogers's team is building a pancreas out of a surgical sponge, a three-dimensional structure seeded with insulin-producing islet cells. The pancreas would be grown in the lab and then placed under the skin of those with Type 1 diabetes to restore their insulin production. But making a pancreas is complicated, Rogers said. The most advanced research at his lab is simpler: regenerating blood vessels so people with Type 2 - or adult onset - diabetes who have damaged fingers and toes can avoid amputation. In theory, any condition where cells are damaged - from insulin-producing cells in diabetes to brain cells in Alzheimer's and Parkinson's disease, to retina cells in blindness, to damaged areas in the heart - could one day be repaired. ... If we can find a way to replace these cells back in to where it's missing, we can envision a cure for these diseases which are currently devastating."

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

A recent paper points to mitochondrially induced hormesis as a root cause of increased longevity with reduced calorie intake - which meshes well with the role of autophagy in this process. It confirms the importance of mitochondria in longevity, and once again shows that a little ongoing damage is actually a good thing: "Calorie restriction (CR) is the only proven regimen which confers lifespan extension benefits across the various phyla right from unicellular organisms like yeast to primates. In a bid to elucidate the mechanism of calorie-restriction-mediated life span extension, the role of mitochondria in the process was investigated. In this study, we found that the mitochondrial content in CR cells remains unaltered as compared to cells grown on nonrestricted media. However, mitochondria isolated from CR cells showed increased respiration and elevated reactive oxygen species levels without augmenting adenosine triphosphate (ATP) generation. The antioxidant defense system was amplified in CR mitochondria, and in CR cells a cross protection to hydrogen-peroxide-induced stress was also observed. Moreover, we also documented that a functional electron transport chain was vital for the life span extension benefits of calorie restriction. Altogether, our results indicate that calorie restriction elicits mitohormetic effect, which ultimately leads to longevity benefit."

Via PhysOrg.com: "A technique that combines nanotechnology with adult stem cells appears to destroy atherosclerotic plaque and rejuvenate the arteries ... nanoparticles (microscopic particles with at least one dimension less than 80 nm) were infused into the heart of pigs along with adult stem cells. After the nanoparticles were heated by laser light, they burned away arterial plaque. However, nanoparticles were less effective at eliminating plaque if not combined with adult stem cells. ... Unlike angioplasty, a common treatment for atherosclerosis, this new technique seems to actually demolish the plaque. ... The researchers found that plaque volume shrunk considerably in the nanoparticle groups immediately after the procedure (an average of 28.9 percent across the three groups) and six months later plaque volume had declined 56.8 percent on average. ... both groups that received stem cells showed signs of new blood vessel growth (neovascularization) and restoration of artery function."

Better maintenance means a longer life, as illustrated by the importance of autophagy in calorie restriction (CR). Researchers are now branching out beyond CR to find other ways of influencing metabolism to better maintain cells: "The conserved insulin-signaling pathway has drawn a significant amount of attention over the past few years as a major lifespan determining signaling network. In many systems, impairing this pathway impedes the ability of caloric restriction (CR) to enhance lifespan, suggesting that nutrient sensing is key to CR. ... the Titorenko laboratory [tested] the hypothesis that networks exist within cells that are not inducible, but act constitutively to extend the lifespan of cells regardless of nutrient availability ... [the study] presents an original screen designed to isolate molecules that further lengthen the life span of yeast under calorie restriction rather than imitating this effect. ... Among the chemical compounds identified, the authors focus on one group representing 6 bile acids compounds, the most efficient of them being lithocholic acid (LCA). Bile acids are mildly toxic oxidized derivatives of cholesterol that play important roles in lipid uptake by the intestine."

A long post from MSNBC's Cosmic Log: "The quest for immortality goes back to Adam and Eve, but now some smart people are getting serious about actually bringing it within their grasp. And they're getting more attention as well. Let's take Aubrey de Grey, for example: The British gerontologist has been beating the drum for anti-aging therapies for years. He plays a prominent role in a recently published book on the immortality quest titled 'Long for this World,' a new documentary called 'To Age or Not to Age' and a just-published commentary on the science of aging. In this week's issue of Science Translational Medicine, de Grey and nine other co-authors urge the United States and other nations to set up a Project Apollo-scale initiative to avert the coming 'global aging crisis.' The experts' prescription includes a campaign to raise the general public's awareness about lifestyle changes that can lead to longer and healthier lives; a lab-based effort to develop anti-aging medicines; and a push for new techniques to repair, restore or replace the cellular and molecular damage done by age. ... There is this misunderstanding that aging is something that just happens to you, like the weather, and cannot be influenced. The big surprise of the last decades is that, in many different animals, we can increase healthy life span in various ways."



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