Longevity Meme Newsletter, July 10 2006
LONGEVITY MEME NEWSLETTER
July 10 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
- Coming Soon: SENS Challenge Results
- The Life Extension Survey
- See the Immortality Institute Redesign
- Discussion
- Latest Healthy Life Extension Headlines
COMING SOON: SENS CHALLENGE RESULTS
By way of a reminder, the judges' opinions on the submissions for the $20,000 SENS Challenge will be announced at the Technology Review on the 11th of this month. An opinionated summary of the submissions from last month can be found in the following Fight Aging! post:
https://www.fightaging.org/archives/000872.php
Links to more commentary from around the web are here:
https://www.fightaging.org/archives/000873.php
https://www.fightaging.org/archives/000874.php
We can hope that this challenge continues to bring positive attention to the near future of healthy life extension research, thus raising awareness of the plausibility of significant results with greater funding. We are now past the time in which greatly extended healthy life spans were impossible. A range of possible medical technologies to attain this goal can now be visualized; there is no excuse for holding back. You can read more about some of these potential solutions at the SENS website:
THE LIFE EXTENSION SURVEY
Some of the enterprising volunteers at the Immortality Institute have been running an outreach, awareness and community growth program in MySpace - and more power to them for getting up and doing something to make a difference. We need more of that.
Readers here may find one of the program components to be interesting; results from the Life Extension Survey (or LESurvey) show how the average MySpace denizen - which is more or less to say the average younger American - feels about healthy life extension. Read more, along with links to forum discussions on the outreach effort, in this Fight Aging! post:
https://www.fightaging.org/archives/000899.php
Surveys are notoriously fickle, unreliable tools, but I found this interesting: for the question on length of life desired, most people answered: "Depends how things go, but I would like to have the choice to live as long as I want." A tremendous well of resources for the future of longer, healthier lives lies out there, just waiting for advocates to find the key to tapping it.
SEE THE IMMORTALITY INSTITUTE REDESIGN
Speaking of the Immortality Institute, I recommend you take a look at the recently redesigned home page:
I think it far more accurately reflects the present composition of the membership, aims of the Institute and volunteer efforts presently taking place. It serves well to highlight the healthy life extension supporters and active scientists in fields important to aging and anti-aging research who have made the Institute forums a watering hole.
I highlight a few of the better recent discussions on healthy life extension science and volunteer activities in the following post:
https://www.fightaging.org/archives/000898.php
If you feel, as I do, that the Institute serves an important purpose in the present community of healthy life extension research and activism, then please consider joining as a member:
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/
Switching On Heart Repair (July 09 2006)
http://www.eurekalert.org/pub_releases/2006-07/uops-pre070706.php
EurekAlert! notes progress in manipulating existing repair systems in the body: "we asked, 'What would be the most ideal, natural way of fixing any sort of problem like this?' If you look at nature, the best way is to simply re-grow the tissue. We know that if we take out a piece of the liver, our body has programming to grow it back to how it was ... [scientists] first identified the signals in the rat heart that currently prevent the ability to re-grow damaged heart tissue. The researchers then manipulated those signals so the heart could work to regenerate itself. ... [researchers] investigated myocardial regeneration by initiating heart cell division and replication. They did this by expressing the cell-cycle regulator, a protein called cyclin A2. It is unique in its control at two major transitions of the cell cycle and is the only cyclin that is completely silenced after birth in mice, rats and humans. This approach - using cyclin A2 expression via gene transfer - yielded improved myocardial function."
Brian Alexander on Growth Hormone (July 09 2006)
http://www.latimes.com/features/magazine/west/la-tm-shots28jul09,0,4924753.story
Brian Alexander, author of "Rapture: How Biotech Became the New Religion", takes a sensible look at the science and use of growth hormone: "Growth hormone stimulates the production of insulin growth factor 1, which, in turn, affects everything from sugar-regulating insulin to sex steroids such as testosterone and estrogen. A chart of these hormone interactions looks like a map of the London Underground drawn by MC Escher. And as with that massive subway, one train at one stop can wreak havoc with the whole system. ... The right word is 'overwhelming.' It is extremely complex. ... Researchers still know little about the influence of supplemental growth hormone on cancer cells, diabetes and other diseases ... Life extension can be achieved in lab animals, and research being conducted on mice and monkeys will probably pay off for humans someday. But so far, [studies] show that restoring growth hormone to old animals actually shortens, not lengthens, their life spans."
A Look Back At the Worms (July 08 2006)
http://pub.ucsf.edu/today/cache/feature/200607065.html
UCSF Today reports on a presentation given by Cynthia Kenyon: "Kenyon identified the gene daf-2 that codes for hormone receptors that bring insulin and IGF-1, an insulin-like growth factor, into cells. ... Lower levels of these hormones promote cell maintenance and stress resistance. If there is no receptor for the insulin to enter the cell, cells remain in this maintenance phase and age at a slower rate ... By treating worms with a chemical mutagen that damages daf-2, Kenyon found that the worm's life span increased up to six times its normal existence. ... I'm not saying that people will be able to live for 500 years. But my prediction is that these two hormones also affect aging in humans and that therapies can be developed to ward off age-related diseases and provide five to 10 additional healthy years of life." Her prediction is in much the same ballpark as the Longevity Dividend proposals - in line with what one would expect from tinkering with metabolism in the near term.
Inflammation and Muscle Strength (July 08 2006)
http://dx.doi.org/10.1016/j.amjmed.2005.10.049
A result from the Longitudinal Aging Study Amsterdam gives yet another reason to try to avoid chronic inflammation: "The findings of this prospective, population-based study suggest that higher levels of IL-6 and CRP increase the risk of muscle strength loss, whereas higher levels of ACT [alpha1-antichymotrypsin] decrease the risk of muscle strength loss in older men and women." ACT "limits tissue injuries during inflammations, since it is an effective inhibitor of proteolytic enzymes that are released by inflammatory cells." Correlation is not causation - but it's not hard to think up possible ways in which greater age-related cellular damage due to inflammation could lead to loss of muscle strength.
Looking at Geron's Research (July 07 2006)
http://www.genengnews.com/news/bnitem.aspx?name=3153413
Via Genetic Engineering News, a long release that provides some insight into aims and progress in human embryonic stem cell (hESC) research at Geron. It covers four areas: "(1) GRNOPC1, Oligodendroglial Progenitor Cells for acute spinal cord injury, (2) GRNIC1, Islet Clusters for diabetes, (3) GRNCM1, Cardiomyocytes for myocardial infarction and (4) osteoprogenitor cells for bone fractures and osteoporosis. ... Our most advanced product, GRNOPC1 for acute spinal cord injury, is in multiple IND-enabling studies. Its in vivo mechanism of action includes myelination and trophic support of damaged spinal cord neurons, resulting in significant locomotor recovery of spinal cord injured rodents. As our work progresses with other hESC-derived cell types such as cardiomyocytes, islets, hepatocytes and osteoprogenitor cells, we are hopeful that these cell types will also demonstrate significant, long-term regenerative capacity in animal models, setting the stage for clinical trials in patients."
Calorie Restriction and Muscles (July 07 2006)
http://www.canada.com/topics/news/national/story.html?id=1eacdcc4-0ed7-4c55-9f13-a04746fdcce5
Canada.com notes the results of a study to published this month: "researchers found that elderly rats on a calorie-restricted diet had the muscle mass and function of much younger rats. ... It's the equivalent of an 80-year-old rat with the muscles of a 20-year-old rat ... From a young age, the rats ate about 40 per cent fewer calories than normal, although their diet was rich in nutrition. ... elderly rodents on [calorie restriction] experienced only a 20 per cent drop in muscle mass and no loss of muscle function. By contrast, rats eating a normal diet lost 50 per cent of their muscle mass and 50 per cent of their muscle function at old age. ... We know (calorie restriction) extends life span. What we've shown is it also maintains muscle function. ... The study suggests restricted-calorie diets preserve the function of mitochondria which provide the body's cells with energy as the animals grow old. The diets appear to help the aging rats rebuild and replace muscle."
Another Positive Cryonics Article (July 06 2006)
http://www.eastvalleytribune.com/index.php?sty=68980
A nice piece on Alcor and cryonics can be found at the East Valley Tribune: "Because of the increase in clientele, Alcor, a nonprofit organization, has recently had to expand the 'patient bay' that now holds 28 [vitrified] bodies and 46 heads. The patients range from a 21-year-old woman who died of a mysterious illness to a 99-year-old man who died of old age. They will remain in longterm storage until the thawing process is perfected and cures are found for old age, cancer and other diseases, Jones said. While the odds of reanimation are questionable, Jones said amazing medical advancements such as cloning and stem cell research are making the possibility of cryonics not so far-fetched. ... Science fiction is becoming science fact on a daily basis. Why is it such a stretch for this to be along that path?"
On Alzheimer's Progression (July 06 2006)
http://www.sciencedaily.com/releases/2006/07/060706083004.htm
ScienceDaily reports on a possible biochemical mechanism for the early progression of Alzheimer's disease (AD): "People with AD exhibit elevated levels of beta-amyloid peptides that cause plaque buildup in the brain (the main characteristic of AD). In the earliest stages of Alzheimer's, beta-amyloid peptides are on the rise, especially in the two connected brain regions critical for memory functions - the hippocampus and entorhinal cortex. ... one reason for that early increase of beta-amyloid peptides: an enzyme that breaks down beta-amyloid peptides, also referred to as an insulin-degrading enzyme (IDE), is not active in the brain in the cases at high-risk for developing AD. ... researchers suggest that boosting IDE activity pharmacologically may reverse beta-amyloid peptide accumulation." This may tie in with recent research suggesting Alzheimer's to be a form of diabetes.
Looking at the Buck Institute (July 05 2006)
http://www.marketwatch.com/News/Story/Story.aspx?guid=%7B5B206A70-D4C4-4ABB-A98A-255F64745A6B%7D
MarketWatch profiles the Buck Institute for Age Research: "Not long ago, inducing the worlds of basic biology of aging, diseases of aging and biotechnology to share ideas was far from the norm, said Gordon Lithgow, an associate professor of molecular mechanisms of aging. ... Fifteen years ago this wasn't on the agenda. No serious biologist would consider pursuing research on aging. ... Aging is perhaps the biggest risk factor for disease in developed countries. We don't know what aging is; we don't know why it causes disease and don't yet know how to intervene. ... No one really understands why we age....but there are a lot of theories." Biomedical gerontologist Aubrey de Grey would argue that scientists may lack a complete characterization of aging, but know more than enough to get on and do something about the root causes of age-related degeneration. Engineering a solution doesn't require complete knowledge - complete knowledge only makes it easier.
Repopulate the Immune System (July 05 2006)
http://www.hon.ch/News/HSN/533590.html
From HON News, signs of further progress in generating new T-cells for people with damaged immune systems: "T-cells are one the of the body's main defenses against disease. In this study, researchers demonstrated that it is possible to convert embryonic stem cells into blood-forming stem cells that, in turn, can turn into the helper T-cells. ... The human embryonic stem cells were incubated on mouse bone marrow support cells, which converted the embryonic stem cells into blood-forming cells. These blood-forming cells were then injected into a human thymus gland that had been implanted in a mouse. The thymus gland converted the blood-forming cells into T-cells." It's unclear as to whether this sort of strategy would help the aging immune system - there may be plenty of T-cells, but their programming has become unhelpful.
Engineered Cartilage Progress (July 04 2006)
http://www.eurekalert.org/pub_releases/2006-07/uob-bti070306.php
Good news from EurekAlert! on the topic of tissue engineered cartilage with possible application to repair age-damaged joints: "engineered cartilage tissue can grow and mature when implanted into patients with a knee injury. The novel tissue engineering approach can lead to cartilage regeneration even in knees affected by osteoarthritis. The tissue engineering method used in this study involved isolating cells from healthy cartilage removed during surgery from 23 patients with an average age of 36 years. After growing the cells in culture for 14 days, the researchers seeded them onto [scaffolds] and then implanted them into the injured knees of the study patients. Cartilage regeneration was seen in ten of 23 patients, including in some patients with pre-existing early osteoarthritis of the knee secondary to traumatic injury. Maturation of the implanted, tissue-engineered cartilage was evident as early as 11 months after implantation."
Towards Enhanced Heart Regeneration (July 04 2006)
http://www.sciencedaily.com/releases/2006/07/060703211008.htm
ScienceDaily notes a growing understanding of how to signal and control stem cell healing processes: "The molecule c-kit is the 'switch' that needs to be turned on by the 'SOS signals' sent by the damaged heart. By binding to another molecule called the stem cell factor - much like a lock and key - the 'turned on' c-kit activates the bone marrow cells to migrate to the heart to help stimulate new blood vessel growth. ... mice with defective c-kit bone marrow cells, could not mobilize these cells to race towards the injured site and regenerate the injured heart. ... The study may explain why some patients have mild heart attacks and others develop progressive and potentially fatal congestive heart failure. ... We know that the number of c-kit positive cells decreases with age and that elderly patients don't recover from heart attacks as well as younger patients. The key for the older patients would be to find new ways to restore this particular subset of cells in their bone marrow."
RegeneRx and Thymosin Beta 4 (July 03 2006)
http://www.regenerx.com/
RegeneRx is working on the development of synthetic Thymosin Beta 4 (TB4) therapies to enhance and direct healing: "it consists of 43-amino acid residues and is found in high concentration in blood platelets, wound fluid, white blood cells, and in most other tissues of the body. TB4 is neither a growth factor nor a cytokine. Rather, TB4 is the major actin-regulating molecule in most mammalian cells and plays an important role in the regeneration, remodeling, and healing of injured or damaged tissues. ... TB4 is multi-faceted and involved in a wide variety of biological activities including: regulation of actin, [regrowth of skin], angiogenesis, apoptosis, and anti-inflammation. ... The fact that TB4 influences so many important biological processes may be one reason why the molecule is so highly conserved and remains essentially unchanged throughout evolution."
More Knowledge Means Better Drugs (July 03 2006)
http://www.eurekalert.org/pub_releases/2006-07/uons-at070306.php
(Via EurekAlert). Drugs will come to be ever more precisely designed and efficient molecules, intended to control - or reprogram - our biochemistry in very specific ways: "c-Jun is an important disease-causing gene. It stands out because we don't see much of it in normal tissue but it is highly expressed in diseased blood vessels, eyes, lungs, joints, and in the gut - in any number of areas involving inflammation and aggressive vascular growth. ... Our experimental drug, Dz13, is like a secret agent that finds its target, c-Jun, within the cell and destroys it. It is a specific, pre-programmed 'molecular assassin'. ... [this] has the potential to treat a diverse range of health problems, from inflammation and cancer through to eye and heart disease." The best drug development is still a hybrid between the old screen-and-test methods and the designs of the future - a great deal of uncertainty about the success of such a drug remains, due to our lack of knowledge of our own biochemistry.
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