Longevity Meme Newsletter, May 29 2006
LONGEVITY MEME NEWSLETTER
May 29 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.
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CONTENTS
- SENS Science Outside SENS
- Bemoaning the Bemoaning
- Calorie Restriction Reduces Inflammation
- Discussion
- Latest Healthy Life Extension Headlines
SENS SCIENCE OUTSIDE SENS
The Strategies for Engineered Negligible Senescence (SENS) strongly imply a direction for both medical research and implementation of therapies in order to halt and reverse the root causes of age-related degeneration. It is prevention writ large, in other words - and prevention is almost always the most cost-effective strategy for any system, be it a body, engine or business:
Unfortunately, modern medicine, research infrastructure and the culture of medical science are almost entirely focused on repairing end-stage problems - specific age-related diseases - that have long passed the point of prevention. That is where the large-scale research funding is; that is where the venture capital for commercialization is; that is the approach dictated by government regulation. It's a sad state of affairs to be in; we have a good starting point to fix the foundations of the dam, but it's an uphill battle to convince anyone to do anything but wait until the cracks appear and then start patching.
Still, as the patchers make progress in understanding the essential nature of their cracks, their best methodologies start to overlap with the methodologies of prevention. This is where we are today in medical research - a modicum of SENS science is happening as an incidental part of research aimed at treating specific age-related conditions. A recent example of the type can be found in this Fight Aging! post:
https://www.fightaging.org/archives/000856.php
It demonstrates what can be done with precision chemistry these days. Researchers have acquired a nice lump sum to commercialize a method of gumming up the harmful production of lipofuscin, one of the many different types of extracellular chemical junk that contribute to aspects of age-related degeneration. In this case, it accumulates in the retina and causes blindness - unless you introduce small molecules designed to interfere in that process. Clever stuff.
Biomedical gerontologist Aubrey de Grey's presently favored methodology for dealing with accumulated chemical junk in and around our cells is called LysoSENS. Since we know all this junk is eventually broken down after our deaths, it makes sense to find the bacteria doing the job and copy their enzymes. Donations to the Methuselah Foundation presently fund the earliest stages of LysoSENS research; you can find out more at the following locations:
https://www.fightaging.org/archives/000676.php
http://www.mprize.org/index.php?pagename=researchdonors
Variety in approaches is a very good thing; in all things scientific, the more the merrier, and the more rapidly that cures will be developed.
BEMOANING THE BEMOANING
Just what is it about people who vocally reject the concept of living a longer, healthier life that leads to more attention being sent their way? Why is this more fascinating for the media than the growing number of people willing to stand up and be counted in support of better, longer, healthier lives? You'll note a bumper crop of anti-life-extension pieces in the headlines from the past week; we've been treated to a parade of folk trying to convince us that we should put aside research and suffer and die on time.
Bah, humbug to all that!
Their choice is their choice; I respect that and only wish to have my choice - to fight to advance healthy life extension science and the choice to live a longer, healthier live - respected in return. Read the articles, and then read this longer pontification on why we hear so much from those who reject efforts to enable longer lives and prevent age-related suffering:
https://www.fightaging.org/archives/000861.php
CALORIE RESTRICTION REDUCES INFLAMMATION
This should catch your eye: further confirmation that the practice of calorie restriction (CR) reduces chronic inflammation in humans, just as in other mammals:
https://www.fightaging.org/archives/000860.php
Inflammation is a real bugbear when it comes to detrimental effects on your long-term health, level of cellular damage and susceptibility to age-related diseases. You owe it to yourself to at least be aware of the present scientific consensus on this topic:
https://www.fightaging.org/archives/000806.php
There you go - yet another reason to look into CR and discuss its implementation in your life with your physician. It's really not hard; find out more here:
https://www.fightaging.org/archives/2002/11/calorie-restriction-explained/
DISCUSSION
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!
Reason
Founder, Longevity Meme
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LATEST HEALTHY LIFE EXTENSION HEADLINES
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/
Repairing Humans via Brain Prosthesis (May 28 2006)
http://abclocal.go.com/wjrt/story?section=healthfirst&id=4184600
From ABC12, an unexpectedly transhumanist look at the near future of medical research: "Over the years, we've heard miraculous stories about people getting artificial arms, legs, even hearts. Some doctors say they can create artificial [brain parts] that may help millions of people with diseases like Alzheimer's, Parkinson's, and epilepsy. ... neuroscientist Theodore Berger has developed the first artificial brain part - a hippocampus to help people with Alzheimer's form new memories. ... There's no reason why we can't think in terms of artificial brain parts in the same way we can think in terms of artificial eyes and artificial ears ... Information would come into the brain the same way, but would be re-routed to a computer chip, bypassing the damaged area of the hippocampus. ... What we're hoping to do is replace at least enough of that function, so there's a significant improvement in the quality of life."
Inducing a Regenerative Environment (May 28 2006)
http://www.newswiretoday.com/news/5678/
(Via Newswire Today!). One possibly viable alternative to stem cell based regenerative medicine is to alter the local biochemical environment to stimulate healing that would not normally take place: "The main finding of our study is that you can deliver growth factors to the environment around injected cells using nanofibers ... Most past studies inject proteins directly into tissues like the heart. Many proteins delivered this way don't stay in the tissue very long. Our new technology allows the growth factor to be delivered for many weeks in a highly controlled way ... We think this is just the beginning of how we can design the local environment around cells to encourage them to do things that can help the injured tissue. We just delivered one factor, but there's no reason you can't deliver many factors that are needed."
Free Radical Theory of Greying (May 27 2006)
http://www.fasebj.org/cgi/content/abstract/fj.05-4039fjev1
Some interesting ideas are coming out of further investigations of the biochemistry of greying hair: "Intriguingly, the continuous melanin synthesis in the growing (anagen) hair follicle generates high oxidative stress. We therefore hypothesize that hair bulb melanocytes are especially susceptible to free radical-induced aging. ... We found evidence of melanocyte apoptosis and increased oxidative stress in the pigmentary unit of graying hair follicles. The 'common' deletion, a marker mitochondrial DNA-deletion for accumulating oxidative stress damage, occurred most prominently in graying hair follicles. ... We conclude that oxidative stress is high in hair follicle melanocytes and leads to their selective premature aging and apoptosis. The graying hair follicle, therefore, offers a unique model system to study oxidative stress and aging and to test antiaging therapeutics in their ability to slow down or even stop this process."
Another Blow For Programmed Aging (May 27 2006)
http://www.medicalnewstoday.com/medicalnews.php?newsid=43893
How much do genetic programs contribute to degenerative aging? If they contribute greatly, then fighting aging would be a matter of understanding and changing these programs - but the job is much harder if degeneration predominantly results from the accumulation of random damage. Here, Medical News Today reports on another nail in the coffin of programmed aging theories: "One long-standing observation concerning the physiological decline that accompanies aging is its variability - some people age better than others. However, there has thus far been little or no evidence supporting the existence of similar [variability] at the level of gene expression. ... Using a wide range of expression data from both humans and rats, the researchers showed that levels of gene expression become more variable with age. Furthermore, they found that the tendency toward increased variation is not restricted to a specific set of genes, implying that increased [variability] is the outcome of random processes such as genetic mutation."
Funding For MRL Mouse Research (May 26 2006)
http://unews.utah.edu/p/?r=050306-6
Research into regenerating MRL mice is attracting more attention and more funding these days; a better understanding of the biochemistry involved in mammalian regeneration of organs may just lead to impressive therapies for injury and some forms of age-related damage in humans. "Although most mammals cannot restore tissue efficiently [the] MRL mouse can regenerate a portion of the ear as well as its heart tissue following injury. ... researchers aim to prove that mammals can form the required progenitor cells for regeneration just as a salamander does. By studying salamanders and MRL mice, the researchers hope to identify the specific types of cells, molecular signals, genes and cellular scaffolding required for regenerative cell growth. In essence, they seek as comprehensive an understanding as possible of the mechanisms and processes - to obtain the blueprint for regenerative growth."
LiveScience on the MPrize (May 26 2006)
http://www.livescience.com/humanbiology/060526_aging_contests.html
LiveScience redeems itself somewhat for the past few days of anti-life-extension nonsense with a straightforward piece on the MPrize for anti-aging research and the SENS Challenge: "Anyone debating the scientific feasibility of extending the human life span will find that it's only a matter of time before the name "Aubrey de Grey" comes up. The controversial Cambridge University researcher has been making news in recent years by claiming that humans could soon enjoy thousand-year lifetimes and by helping to establish two contests: one to spur anti-aging research and another to debunk his own audacious claims. In 2003, de Grey helped establish [with entrepreneur Dave Gobel] the Methuselah Foundation and create the M-Prize, a $1.5 million award available to any scientist who can slow or reverse the effects of aging in mice. Private donations made since 2003 have bumped the prize value up to nearly $3.5 million."
Progress Towards Cavity Vaccines (May 25 2006)
http://www.forsyth.org/news_disp.asp?content_id=100535
Lumping the mechanisms of tooth decay under "damage that accumulates with age" is pushing the definition a little, but it's an interesting thought experiment. Other systems in the body rack up damage as they run - some will be comparatively easy to suppress, low-hanging fruit for modern medicine. "Researchers at The Forsyth Institute have made significant advances in research to develop a vaccine against cavities. [A research team] discovered key molecules that can stimulate a human immune response and has successfully conducted immunization trials in animal models. ... Forsyth's strategy is aimed at stimulating the production of antibodies that inhibit the enzyme that allows bacteria to accumulate on teeth. The researchers believe that the best way to protect against caries over the long term is to vaccinate children at about the age of one, after teeth have begun to emerge, but before [bacteria] have begun to colonize the tooth surfaces."
Oxidative Stress, Neurodegeneration (May 25 2006)
http://www.medicalnewstoday.com/medicalnews.php?newsid=43994
(From Medical News Today). Scientists are increasing their understanding of the biochemical mechanisms by which oxidative stress causes neurodegeneration: researchers "have discovered a mechanistic link between cellular stress caused by free radicals and accumulation of misfolded proteins that lead to nerve cell injury and death in neurodegenerative disorders such as Alzheimer's and Parkinson's Disease. That link is Protein Disulphide Isomerase (PDI) ... The accumulation of misfolded proteins is a common pathogenic mechanism in many diseases, including neurodegenerative disorders. In normal circumstances, PDI levels increase in response to accumulation of misfolded proteins due to cellular stress. ... molecules related to the free radical NO, which is present in elevated levels in neurodegenerative diseases, [alters PDI's structure to block] its normal neuroprotective function, which ultimately leads to nerve cell injury and even death."
A Switch For Muscle Atrophy (May 24 2006)
http://newswire.ascribe.org/cgi-bin/behold.pl?ascribeid=20060524.111825
Via AScribe, news of a possible new approach to preventing age-related muscle atrophy: "muscle weakness caused by atrophy during aging can lead to serious falls and bone loss. Exercise is the most beneficial strategy to treat atrophy. However, many individuals are too ill to adequately participate in exercise programs. We've found a chemical 'switch' in the body that allows us to turn atrophy on, and, from that, we also have learned how to turn atrophy off ... The Merg1a protein is a channel that normally passes a small electrical current across the cell. The researchers implanted a gene into the skeletal muscle that resulted in a mutant form of this protein that combines with the normal protein and stops the current. The researchers found that the mutant protein would inhibit atrophy." Nice work; other groups are also looking into ways to halt or reverse age-related muscle loss, or sarcopenia.
Doleful Idiocy (May 24 2006)
http://www.livescience.com/humanbiology/060524_immortality_psychology.html
The last of the set of anti-life-extension articles at LiveScience is now up; more handwaving and psychobabble to try and justify suffering and death that could be prevented in the decades ahead. What to make of an "ethicist" who is so sure that you would be bored as a healthy, active, limber 100-year-old, he would see you die in pain from any number of presently incurable age-related conditions rather than support healthy life extension research? "I don't believe that if you give most people longer lives, even in better health, they are going to find new opportunities and new initiatives. They will want to come and play more golf maybe, but they aren't going to contribute lots of brand new ideas, at least the ones I know." I think I join many, many people in saying "speak for yourself" and "you don't know what you're talking about."
More RNAi Versus Cancer (May 23 2006)
http://www.eurekalert.org/pub_releases/2006-05/uotm-ris052306.php
Age-related cancer must be efficiently and effectively stopped in its tracks as a part of the first decades of the healthy life extension revolution; no sense in fixing all the other age-related damage if that just means ever more cancer and little more life. RNA interference (RNAi) seems like the next tool for the job based on present research: "scientists were the first to use what are known as 'small interfering RNAs' to block the spread of human colorectal cancer cells implanted in laboratory mice. Small interfering RNAs (siRNAs), first described in 2001, are tiny bits of genetic material that can prevent the translation of genes into proteins - including specific proteins involved in biochemical reactions that promote cancer and other diseases. ... Over the last couple of years people have talked a lot about cell-culture studies of siRNAs, but only a handful of labs have pushed it to animal models, which we need to do before going on to clinical trials."
Stumping for Death and Suffering (May 23 2006)
http://www.livescience.com/humanbiology/060523_immortality_moral.html
Part two of the LiveScience presentation on radical life extension isn't any better in tone than part one. This seems to be turning into a tour of all the hoary old arguments for doing nothing to stop the present toll: 100,000 deaths due to aging every day. Every day. Think about that. The words of sense in this article come from interviewees, such as John Harris or Richard Miller: "When you save a life, you are simply postponing death to another point. Thus, we are committed to extending life indefinitely if we can, for the same reasons that we are committed to life-saving. ... If you’re really interested in increasing healthy lifespan, aging research is more likely to get you there in a quick and cost-efficient way than trying to conquer one disease at a time."
More DNA Repair Research (May 22 2006)
http://www.sciencedaily.com/releases/2006/05/060519235555.htm
As a follow-on to DNA repair research from last week - a good example of the power of modern bioinformatics - ScienceDaily reports on work from another team: "For the first time anywhere, [scientists] have succeeded in observing and describing how damaged DNA is naturally identified. ... Proteins triggered by the bacteria that are similar to the protein that has been revealed in our laboratory are found in all species, including humans, and therefore one can conclude that the way in which the bacterial protein scans the DNA for lesions is similar among many forms of life. This understanding of the molecular basis of the DNA repair is a basic step in furthering our ability to understand those illnesses stemming from DNA damage, for example cancerous growths." Accumulated damage to DNA is one root cause of age-related degeneration - so the more we know about DNA repair, the better.
Trying So Hard To Find Fault (May 22 2006)
http://www.livescience.com/humanbiology/060522_immortality_social.html
Part one of a series on radical life extension at LiveScience tries hard to find fault with the idea of less suffering, less frailty and more healthy years. Makes you wonder what planet these people live on: "While scientists go back and forth on the feasibility of slowing, halting or even reversing the aging process, ethicists and policymakers have quietly been engaged in a separate debate about whether it is wise to actually do so. ... If scientists could create a pill that let you live twice as long while remaining free of infirmities, would you take it? If one considers only the personal benefits that longer life would bring, the answer might seem like a no-brainer: People could spend more quality time with loved ones; watch future generations grow up; learn new languages; master new musical instruments; try different careers or travel the world. But what about society as a whole? Would it be better off if life spans were doubled?" Be very wary of those who invoke that mythical entity "society" - they are trying to steal something from you.
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