Longevity Meme Newsletter, May 22 2006

May 22 2006

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.



- Are We Bound by a Moral Imperative?
- Science Week at Fight Aging!
- Discussion
- Latest Healthy Life Extension Headlines


What does the existence of a moral imperative to accelerate progress towards healthy life extension technologies - to alleviate as much age-related suffering and death as soon as possible - mean for you and I? What do we understand by "moral imperative?" This is the sort of thing that ethicists spend too much time on:


The material referenced by the Fight Aging! post linked above makes for interesting reading, but I think it's an exercise in common sense to cut to the chase: you don't owe anything to anyone that you haven't contracted and chosen to provide. No philosophy can create an obligation - only choice made of free will can do that. I have decided that I should act in support of healthy life extension research, for reasons both selfish and altruistic. This is my moral imperative, home-crafted and unique. I think that we demonstrate ourselves better people for helping to advance anti-aging research - but this is a choice each person must make for his or herself. Find your own moral imperative: I persuade, you decide.

If you decide "yes," I can think of few better first steps than to join The Three Hundred in support of the MPrize for anti-aging research:



By the luck of the draw, this past week has seen a number of science-heavy posts at Fight Aging! - the latest issue of Rejuvenation Research is out too. Those readers who like to keep up with medical research of relevance to developing healthy life extension technologies might want to take a look:


"The latest Rejuvenation Research is out ... More researchers are looking into ways to alleviate or prevent age-related damage to mitochondrial DNA - this is one area of basic anti-aging science in which funding from traditional disease-focused sources is plausible, given the strong (and growing) weight of evidence associating mitochondrial dysfunction with widespread and well-known age-related conditions. Other groups are making progress in methods of replacing damaging mitochondrial DNA, a different approach to the SENS proposal of moving these genes into the comparatively well-protected nucleus. Competition and variety are good signs - may the best methodologies win."


"Plasma membrane redox systems across various species form a big topic - big enough for their own conference. As you might note from the papers above, or indeed from pretty much anything I post on the topic of mitochondria, metabolism is a fearsomely complex system. Greater understanding of the biochemistry of metabolism could lead to technologies of optimization - meaning least amount of age-related damage generated per unit time - that are demonstrably better than the practice of calorie restriction. Don't hold your breath there, however; this has the look of a topic that will still be hotly debated and the subject of ever-deeper investigation in 2016 and 2026. Meanwhile, calorie restriction is as simple a matter as putting thought into eating less in the right way. More to the point, tinkering with metabolic optimization seems to be a far less effective path forward than to aim at directly and effectively repairing what we know to be the root biochemical causes of aging."


"Stem cell populations power healing processes; declining effectiveness in this task will clearly cause degeneration, as wear and tear outpaces repair. What is the cause of this decline, and how much does it contribute to frailty, suffering and death versus other classes of age-related cellular damage? Scientists are investigating, but it doesn't even seem clear at this point as to whether biochemical changes or declining numbers of cells are the real culprit - it might be both or neither, or different for differing populations. Much more work is yet to be done, but this, for me, is one of the most exciting areas of stem cell research - how much more healthy life could we gain through repairing or replacing our failing stem cells?"


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!


Founder, Longevity Meme



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/

What Is Known About Brain Aging? (May 21 2006)
What is known about brain aging and what can be done about it? Comparatively little at this point, sad to say. Obviously, neurodegenerative conditions - based on what are essentially structural or infrastructural failures in the brain and supporting organs - must be understood and prevented or cured if we are to enjoy much longer, healthier lives brought on by advancing medical technology. Real progress is being made in that arena, though not yet in the realm of preventing the known roots of age-related damage. Beyond that, however, there are the poorly understood ways in which a lifetime of thought and activity changes the structure and wiring of our brains - sometimes for the worse. At the end of the present day, as illustrated by this Washington Times piece, we are left with a proven "use it or lose it" and the knowledge that much more research is required.

People Die Too Young (May 21 2006)
Methuselah Foundation volunteer April Smith writes an obituary, making the points that should always be made: "When we talk about the possible lifespan gains from [calorie restriction (CR)], people often ask if the five or ten or even twenty years that we might gain from CR are worth the trouble. When I think about what Jaroslav Pelikan could have done with five, ten, or twenty more years, I have to answer a resounding YES! ... what books would he have written between 82 and 85? Between 85 and 90? Between 90 and 100? What lectures would he have given, what students would he have inspired? The world has lost a great thinker, teacher, and writer, and I believe he died too young. It's a classic example of how bodies begin to deteriorate at just the point when experience and education combine to form tremendous wisdom. Death steals wisdom from the world, and I don't think we should quietly accept this theft."

Aging, Immunodeficiency, Inflammation (May 20 2006)
Via the open-access journal Immunity & Aging, a look at how the aging immune system harms us by doing both too little and too much (a full PDF is available): "Aging is associated with a paradox of immunodeficiency and inflammation (an evidence of hyperactive immune system). Apoptosis is associated with cellular depletion and suppression of inflammatory response. In this brief review, we will present evidence for the role of increased apoptosis in immunodeficiency and paradoxical increased inflammation associated with human aging. In particular, a role of apoptotic antibodies in failure to generate anti-inflammatory responses in dendritic cells will be discussed."

Reprogramming T Cells (May 20 2006)
This Medical News Today piece on reprogramming the activity of T cells in our immune system is focused on HIV and hepatitis as applications, but this misses the most obvious use for those of us interested in healthy life extension. We know that - as a result of past chronic infections "using up" capacity - the ability of T cells to react to new threats declines with age. The declining immune system plays a large part in age-related frailty, suffering and eventual death. If scientists have a way to reprogram this part of the immune system, then new therapies could rejuvenate its effectiveness. From the article: "The concept that T cell deletion and inactivation is neither an inevitable nor permanent consequence of persistent viral infection - that it is reversible - and that its reversal leads to control of viral infection, should have important implications for the future design of therapeutic approaches to resurrect T cell responses."

On Sepsis and VEGF (May 19 2006)
An overview of recent research into sepsis and its role in age-related mortality, via Senior Journal: "Vascular endothelial growth factor, or VEGF, was initially identified as a potent stimulator of endothelial permeability, causing 'leakiness' in the endothelial cells that line the body's blood vessels. ... [VEGF] thus serves as a key mechanism behind the onset and perpetuation of [sepsis]. ... [researchers] treated animals with protein inhibitors of VEGF or neutralizing antibodies against VEGF receptors, and demonstrated significant protection against morbidity (as measured by cardiac dysfunction, inflammation, coagulation and permeability) and mortality." Sepsis is an end-stage failure due to age-related damage; we must invest more in ways to ensure that no-one accumulates that level of cellular damage in the first place. Plugging holes in the failing dam is not a viable path forward to healthy life extension.

Mapping DNA Repair (May 19 2006)
Like all things, your DNA accumulates damage over time; complex, highly efficient biochemical systems are in place to repair that damage, but some still leaks through. This accumulation is one root cause of aging, and so the more we know about DNA repair, the better. Here, The Scientist notes that researchers have "used a systems biology approach to create a map of transcriptional networks that are activated when yeast DNA is damaged. We now know an order of magnitude more pathway connections than were known before, as far as how information is transmitted through the cell in response to damage ... Looking at cellular processes from a wide-angle view -- rather than the one-gene, one-protein approach of classical biology -- permits the construction of 'a complete wiring diagram' of transcriptional interactions, [which] will help scientists control cellular response to DNA damage."

Still the Knee-Jerk Opposition (May 18 2006)
(From the Palm Beach Post). While advocates are generating wider support for healthy life extension research, all too many people still knee-jerk in opposition to the idea: "Humans instinctively strive for longer life. Doctors and scientists who make medical breakthroughs are heroes. ... But what happens when science messes with one of nature's fundamentals: that the older generation will die off to make way for the younger generation? ... life as designed by modern medicine is bound to come into serious conflict with life as designed by nature. If future generations are going to have a right to life, those who already have life will have to recognize an obligation to die." Aging is just as much one of "nature's fundamentals" as anthrax, living in caves, and dying, parasite- and disease-ridden, in your 20s. I look forward to seeing a follow-up article to advocate these wonderful, natural concepts.

Looking to the Future (May 18 2006)
Worthwhile thoughts from Gregory Stock can be found in this press release: "Evolving science and technology, including genomics and nanomedicine, will radically alter healthcare in a way that will 'transcend biological limits that other generations have only dreamed of,' ... The next frontier is not space, it's our own selves. We are reworking our biology. This will change the way we have children, change the way we manage our emotional states and will even alter our life spans. ... These developments are not only going to reshape medicine and healthcare, they are going to alter the fabric of humanity. ... We have entered a new millennium and long before the next one arrives, future human beings will look back and see it not as a horrible moment in time when we trashed this environment, but will see it as a glorious moment that laid the very foundation for our future."

More Telomere Shortening In Men (May 17 2006)
Via FuturePundit, news of a study on telomere differences by gender: "This new study [shows] significantly shorter telomeres and higher erosion rates in men than in women, which likely causes a shorter life expectancy of male cells and tissues. Human telomeres form the terminal structures of human chromosomes and play a pivotal role in the maintenance of genomic integrity and function. During aging, telomeres gradually shorten, eventually leading to cellular senescence." The telomere theory of aging is on the way out, however, and there is some uncertainty as to just what short telomeres mean for health and longevity for any given individual. Like so many things in human biochemistry, it's a very complex question asked about a very complex system.

Aging and Amyloidosis (May 17 2006)
An interesting piece on amyloidosis from the e-journal of the Age Management Medicine Group: "The diseases with which amyloid has been most commonly associated, type 2 diabetes and Alzheimer's disease, are notable for their contribution to decreased quality of life, and mortality, in the elderly. But even among supercentenarians - those living to 110 or more - amyloidosis has emerged as a prime suspect for eventual cause of death. ... What, then, is the connection between amyloidosis and aging? To some extent, this depends upon who you ask - as does the question of whether amyloid buildup can be prevented or reversed. This illustrates the large amount of research being conducted in this area, and constantly emerging knowledge that results."

Mitochondria and Parkinson's Again (May 16 2006)
(From EurekAlert). A number of research groups have published recently on the relationship between age-related mitochondrial DNA damage and Parkinson's disease. Here is another: research "shows that oxygen free radicals are damaging proteins in mitochondria, the tiny cellular 'batteries' of brain cells. This damage may be one main cause of Parkinson's Disease (PD), the chronic movement disorder that affects at least one million Americans. [Scientists] believe the damage is taking place in a large protein structure called complex I, the first stop in the electron transport chain, which produces an electrical charge inside mitochondria. Mitochondria then use this electrical charge to make energy. ... complex I assembly in Parkinson's had 50 percent more damage from oxygen, [showed] evidence of not being properly assembled and had reduced electron flow." A good thing that methods of replacing damaged mitochondrial DNA are within sight.

Novel Gene Therapy Delivery Method (May 16 2006)
The New Scientist reports on a novel method of targeting gene therapy to a particular location. In this case the aim is to treat diabetes: "The team injected microscopic spherical shells into rodents, and using a directed ultrasonic pulse they caused the bubbles to break and release their genetic contents in the target organ. ... cells producing important proteins - such as insulin - lie inside remote structures in the pancreas organ, which itself sits beneath the stomach. It is difficult for foreign particles – such as gene-therapy viruses – to get there from the blood. Without a more sophisticated and targeted approach, cells throughout the body might pick up the gene and begin producing insulin. Since only pancreatic cells are fine-tuned to release insulin in response to food, other cells would over-produce the protein with no regard to food intake."

Reading the Immortalist (May 16 2006)
The Immortalist is a cryonics-focused community magazine; the latest issue is now online: "Why is so much attention given to the subject of 'immortality' by cryonicists? Why all the philosophical ruminations about the meaning of death and the meaning of living forever? Why all the provisions for money after reanimation in contrast to the sparse attention paid to the real problems of being cryopreserved under good conditions, or ensuring that cryopreservation will be maintained? I think that the chances of failing to be cryopreserved are over a trillion times greater than the chances of living a trillion years. I think that the chances of cryonics not working at all are over a trillion times greater than the chances of living a trillion years. And the chances of being cryopreserved under terrible circumstances (dementia, autopsy, bad ischemic damage) are over a trillion times greater than the chances of living a trillion years."

State of Alzheimer's Research (May 15 2006)
From SFGate.com, a look at the present state of research into Alzheimer's disease: "I think there is really hope that something will work in the next two to five years. It will not completely prevent the disease or reverse it, but it will have an effect on the disease process ... I think with Alzheimer's, we're now at where we were with cancer in the '70s. We have a sense of the problem, we know where we'd like to be in 20 years, but we don't know how we're going to get there. ... What we're seeing now is an explosion in understanding Alzheimer's that is underpinned by the last 30 years or so of very, very fundamental, basic science ... a lot of the major [pharmaceutical] companies [see] that clearly there's a market out there now. They are getting involved, and the venture capitalists are looking for good opportunities."



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