Longevity Meme Newsletter, November 12 2007

November 12 2007

The Longevity Meme Newsletter is a weekly e-mail containing news, opinions and happenings for people interested in healthy life extension: making use of diet, lifestyle choices, technology and proven medical advances to live healthy, longer lives.



- From the 3rd Conference on Healthy Aging and Longevity
- Regulation and Dismal Progress in Applied Medical Science
- Discussion
- Latest Healthy Life Extension Headlines


The third International Conference on Healthy Ageing and Longevity was held last year; a range of the material presented was published in the latest issue of the Annals of the New York Academy of Sciences. Some is run of the mill, some very interesting, such as the examination of cytomegalovirus and immune system aging quoted below:


"It has recently emerged that the common herpesvirus, cytomegalovirus (CMV), which establishes persistent, life-long infection, usually asymptomatically, may well be the driving force behind [changes that are] are less marked in 'successfully aged' centenarians, but most marked in people whom longitudinal studies have shown to be at higher risk of death. [These findings] support the hypothesis that persistent herpesviruses, especially CMV, act as chronic antigenic stressors and play a major causative role in immunosenescence and associated mortality."

You'll find a lot more on that topic back in the Fight Aging! archives:


It is promising that the research programs and some early trials are already underway towards eliminating CMV from the body and either destroying specific overspecialized immune cells or entirely "rebooting" the immune system into an undamaged state.



Andy Grove (of Intel fame) has been stating some of the obvious in recent days:


"During the time Andrew S. Grovespent at Intel, the computer chip company he co-founded, the number of transistors on a chip went from about 1,000 to almost 10 billion. Over that same period, the standard treatment for Parkinson's disease went from L-dopa to . . . L-dopa.

"Grove is unleashing a scathing critique of the nation's biomedical establishment. In a speech at the annual meeting of the Society for Neuroscience, he challenges big pharma companies, many of which haven't had an important new compound approved in ages, and academic researchers who are content with getting NIH grants and publishing research papers with little regard to whether their work leads to something that can alleviate disease, to change their ways."

This is a theme I agree with completely. I like to hold up quantum computing as a good example: a fiercely complex area of endeavor, but one in which companies had raised funds and started in on development within two years of the first conceptual science holding up to scrutiny. Quantum computing resources will be sold on the market within the next year or two. Does anyone in the room imagine for a second that this rapid, roiling progress would be the case if there was an FDA of Computing, ready with "thou shalt not?" Biotechnology is no tougher a field of engineering than quantum computing; there are no excuses for the present vast gap between applied medicine and the rapid advance of medical research. There is, however, the obvious set of reasons for the present state of affairs:

"One subtle way in which increased regulation and other government intervention dampens progress - quite apart from raising costs, reducing competitive development, and making it harder for now technologies to be introduced - is by encouraging the formation of research communities with no accountability for progress, and no need to define and strike out for goals."

"We humans are all backsliding apes at core; the only thing that keeps us honest and working hard is competition in the process of earning a living by building new and better things. Finding a niche where you don't have to stretch, work hard at ambitious goals, and make real progress - that's comfort for many."

We should all care deeply about the future of medical progress across decades to come, because the payoff for success is life itself - many more healthy years.


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!




To view commentary on the latest news headlines complete with links and references, please visit the daily news section of the Longevity Meme: http://www.longevitymeme.org/news/

On Intermittant Calorie Restriction (November 09 2007)
Here is more research supporting the benefits to be obtained from starting the practice of calorie restriction at any time in life. You'll benefit more if you practice longer, but there are always benefits to be gained by starting now: "Recent studies on the effects of dietary restriction (DR) in rodents and primates have shown that even late-onset short-term regimens can bring about comparable beneficial changes seen in animals subjected to life-long DR. We examined the effect of 3 months of DR on the expression of antioxidant enzymes and antioxidants, [and more] in 18-month-old middle-aged rats. The present study shows that DR initiated in late adulthood confers beneficial effects, such as attenuation of oxidative stress [and more]." The closer scientists look at the biology of calorie restriction, the more they find in the way of specific biochemical benefits, and a slowing of age-related decline in specific cellular processes. It's well worth your time to find out more about calorie restriction for humans if you haven't yet done so.

The Point of "Ending Aging" (November 09 2007)
The intent of Ending Aging is to achieve results like this, over and over again, expanding ever outward through the population of potential supporters of longevity research over the years ahead: "It's not light [but] I think it's a very important work. In fact, if I had friends who were in medical research, or undergrads interested in biology, I'd be buying them copies right now. This interview is a good introduction to de Grey and his quest to end aging. In short, he thinks we can stop aging, reverse at least some of it, and have healthy, vigorous lives for centuries. The book gets into the how. De Grey (and his assistant, Michael Rae) do a damn good job of explaining the intricacies of the metabolic problems behind aging. His proposal is to find ways to fix the damage done over time without bothering [to] explore all of its sources or the precise ways they can lead to death. ... He's taking an engineering approach, just wanting results without explanations of everything else in the tangle. ... Getting there is going to be tough. Right now the research is still at the level of animal experiments and there's not much funding. The Methuselah Mouse Prize is being offered for researchers who increase the lifespan of mice, funded by private donations. De Grey hopes a breakthrough in rejuvenating mice will create popular support for government funding of aging research. I'd settle for eliminating the government restrictions which prevent some of the research that could be done now. And I'm thinking about how much money I'm going to put into the Mouse Prize myself." Welcome aboard.

The Longevity Dividend in the Annals of the NYAS (November 08 2007)
The principle architects of the Longevity Dividend initiative make their case in the latest Annals of the New York Academy of Sciences: "The aging of humanity is about to experience a radical change as the demographic transformation to an older world is approaching its final stage. In recent decades, scientists have learned enough about the biological aging processes that many believe it will become possible to slow aging in humans. We contend that the social, economic, and health benefits that would result from such advances may be thought of as 'longevity dividends,' and that they should be aggressively pursued as the new approach to health promotion and disease prevention in the 21st century. The time has arrived for governments and national and international healthcare organizations to make research into healthy aging a major research priority." For my part, I don't think the record of government-funded aging research to date merits much more of its continuation - but the Longevity Dividend position still represents a major conceptual leap forward for the conservative mainstream of aging research.

The Value of Research Prizes (November 08 2007)
An op-ed at the New Scientist leaps halfway from the present doleful mainstream paradigm of medical research. Halfway because it imagines a world bettered by the absence of government-enforced intellectual property, but not without government at the hub of research, sadly. "We are conditioned to think that research into new medicines will come to a halt unless pharmaceutical companies continue to be allowed exclusive rights to sell the drugs they develop. But there is another way to stimulate research that would greatly enhance access to drugs, encourage companies to develop medicines that are more medically useful - and save money too. Rather than rewarding success with legal monopolies, governments could use large cash prizes. There has recently been a surge of prizes for particular research challenges, ranging from space travel and clean energy to video rental searches and yields from silver mining. Medical examples include the Prize4Life, which aims to advance research on amyotrophic lateral sclerosis; the Archon X prize for low-cost gene-sequencing techniques; the M prize to promote longevity research; and the Grainger Challenge to protect the world's poor from contaminated well water. Prizes are a potentially powerful tool whenever there is a sustainable way to finance them." The best way to turn any powerful tool into a rusty old mess is to let the government take charge.

On Telomeres (November 07 2007)
A conservative view on the state of knowledge of telomeres and related biochemistry can be found in this paper: "Telomeres, the termini of linear chromosomes, consist of large but variable numbers of DNA oligomer repeats embedded in a nucleoprotein complex. In humans, telomere length (TL) is largely genetically determined but also featured by an age dependent attrition. TL has therefore been put forward as a marker for biological aging and was also reported to be associated with aging diseases such as cardiovascular disease. However it remains unclear whether the biomarker value in a particular disease depends on shorter TL at birth or rather if it's a mere reflection of an accelerated telomere attrition during lifetime, or else, if it is a combination of both. While the importance of telomere attrition is supported by cross-sectional evidence associating shorter telomeres with oxidative stress and inflammation, longitudinal studies are required to accurately assess telomere attrition and its presumed link with accelerated aging." A number of research groups and companies are working on safe ways to change telomere length, with the aim of impacting age-related disease or aging itself.

Exercise and Progenitor Cell Activity (November 07 2007)
Another reason why exercise is good for healthy longevity is noted at EurekAlert!: "Exercise increased the growth of new muscle cells and blood vessels in the weakened muscles of people with heart failure ... researchers investigated whether exercise training could activate progenitor cells, a pool of immature cells in skeletal muscle that can divide into various mature cells as needed for muscle repair. Compared with healthy people, those with heart failure have about a 50 percent reduction in the number of progenitor cells in their muscles ... With exercise, the number of progenitor cells became almost normal, the cells started to divide again, and they began to differentiate into myocytes (muscle cells). And that's exactly what patients with heart failure need - replacement of muscle cells." The same mechanisms are at work in the rest of us as well. While we await the advent of medical technologies capable of reversing age-related degeneration, it makes sense to take good care of our long term health and longevity. Why reduce your chances of living into the age of rejuvenation medicine when there is so much you can do to move the odds?

Ageism As Economic Fear (November 06 2007)
Anne C. makes a case for ageism, in the sense of opposition to healthy life extension medicine, as irrational economic aversion. I'd call it common deathism, and it comes in varying shades of knowing or unknowing callousness. "It makes plenty of sense that a lot of what manifests as 'ageism' is actually a kind of economic phobia -- non-wealthy older people are considered (like disabled people, regardless of whether or not they would classify themselves as 'disabled') to be 'bad investments' with regard to employment, medical care, other forms of support, etc. This, combined with the independence myth can lead to particularly pernicious conditions for many. ... it's becoming more and more clear to me that, for instance, biogerontology is not likely to get much further unless great strides are made socially to affirm the value of older people and not push them to the corners, marginalize, or warehouse them by default." There are many explanations for this sort of thing; I favor fear of age-related degeneration as a contributing factor. Out of sight is out of mind, and no-one wants to think about what they believe to be inevitable suffering. But this behavior is now hindering progress that could plausibly lead to the repair of aging and radical life extension in our lifetime, if we all but put our shoulder to the wheel.

Working Towards Printed Organs (November 06 2007)
Scientists continue to make steady progress towards the use of rapid prototyping technologies in tissue engineering. A little insight into progress from ScienceDaily: "For the past four years, [researchers have] been working to refine the process of 'printing' tissue structures of complex shape with the aim of eventually building human organs. In the latest study, a research team [determined] that the process of building such structures by printing does not harm the properties of the composing cells and the process mimics the naturally occurring biological assembly of living tissues. ... As the tissue structure begins to form, the cells go through a natural process called 'sorting,' which is nature's way of determining where specific cells need to be. For example, an artery has three specific types of cells - endothelial cells, smooth muscle cells and fibroblast cells, each type needing to be in a specific location in the artery. As thousands and thousands of cells are added to the bio-paper under controlled conditions, the cells migrate automatically to their specific locations to make the structure form correctly."

Granzyme B, Atherosclerosis, Longevity (November 05 2007)
From the newswires: researchers uncovered "new knowledge of granzyme B, an enzyme that plays an important role in the immune system. ... levels of granzyme B were significantly elevated in patients with atherosclerosis. ... this enzyme's expression was blocked, atherosclerosis could be reduced by over 70 per cent [in mouse models]. Atherosclerosis is the underlying cause of most heart attacks, strokes, aneurysms and complications arising from diabetes. It is the world's leading cause of death in those over 60. ... granzyme B may play a role in hair loss and aging. During experiments in which the expression of this enzyme was blocked in mice they did not appear to age, developed much denser fur and had a significantly longer lifespan. Granzyme B is released by many immune cells to target and destroy virus-infected cells. Until recently, it was thought that immune cells delivered granzyme B directly into cells targeted for destruction. ... in certain conditions it is also released by immune cells into the space around healthy cells and in the plasma. When this occurs, it destroys key structural proteins that surround the healthy cells, [like] termites eating away at the infrastructure of a home. This can lead, for example, to a loss of the structural integrity and elasticity of blood vessels and ultimately, atherosclerosis."

Aging Immune Systems and Macular Degeneration (November 05 2007)
From EurekAlert!: "age is key in determining whether damaging blood vessels will form beneath the retina and contribute to vision loss. The scientists discovered that specific immune cells called macrophages play a role in the disease process in older mice by failing to block the development of abnormal, leaky blood vessels behind the retina. But in younger mice, macrophages typically prevent abnormal blood vessel formation. The scientists believe better understanding of how macrophages work may provide potential targets for therapies to slow or even reverse vision loss. There are two basic types of macrophages - known as M1 and M2 - and in the older mice, there was a preponderance of cells with the M2 signature. These M2 cells promoted abnormal blood vessel growth in the eyes of older mice. In younger mice, most macrophages had the M1 signature, and those cells inhibited the development of defective blood vessels ... it appears the population of macrophages drifts from the M1 type to M2 cells because of an increase in the levels of an immune system molecule called interleukin-10 (IL-10) in the eye as the mice get older."



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