Longevity Meme Newsletter, September 17 2007

September 17 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.



- Reports From SENS3
- More Recent Aging and Longevity Research
- Discussion
- Latest Healthy Life Extension Headlines


Michael Rae, co-author of Ending Aging, has written a couple of long reports on some of the research presented at the recent Strategies for Engineered Negligible Senescence conference (SENS3). You'll find them at the Methuselah Foundation blog:


"Unlike most other parts of the cell, mitochondria house many of the genes encoding their essential proteins within themselves. These genes are vulnerable to the constant assault of free radicals produced by the mitochondria as a side-effect of their role as cellular power plants. When mitochondrial DNA is damaged, it cannot make the proteins needed to carry on the essential business of generating energy for the cell; the ensuing metabolic damage is the driver of age-related rise in oxidative stress. This oxidative stress fuels free radical damage and interferes with essential signaling pathways in cells far from the original site of the damage.

"PhD candidate Mark Hamalainen of Cambridge University presented the initial success in his Methuselah Foundation-funded work on allotopic expression, showing evidence that his allotopically-expressed genes could encode the relevant proteins and that these were taken up into the mitochondria. In this case, the genes encode healthy and defective versions of the protein that is miscoded in Neuropathy, Ataxia and Retinitis Pigmentosa (NARP), a hereditary mitochondrial disease characterized by blindness and weak and uncoordinated muscles. Well done! It is good to see Foundation-funded research make such solid progress; many thanks go to the generous donors who have made this possible."


"In 2003, Dr. Zheng Cui and his colleagues at the Comprehensive Cancer Center of Wake Forest University reported the discovery of mice with immune cells that rendered them invulnerable to cancer ... Last year, Dr. Cui electrified the world when he showed that the new strain's cancer-fighting abilities were caused by a particular subset of their immune cells -- members of a class of white blood cell known as neutrophil granulocytes. These cells are from the innate immune system, meaning that they don't have to 'learn' to identify a narrowly-defined enemy, but are constantly on the lookout for broadly-defined 'foreign' cells.

"At SENS3, Dr. Cui presented the next logical step in his research: work demonstrating the existence of, and characterizing, high-potency cancer-killing granulocytes in humans."


The most recent Nature Collection takes aging research as its topic. It is free to access, and the full papers are available to read online:


"Cannily sponsored by Sirtris, you'll note - raising a nine-figure stack of venture capital for the main order of business allows many associated perks along the way. Also worth noting: "free" means you can request a free print copy in addition to reading the papers online. The biochemistry of calorie restriction, stem cells and cancer as it relates to aging forms the order of the day - a good first-order approximation of the weight of research in mainstream gerontology at present. Go and take a look."

In addition, the latest issue of Rejuvenation Research is now out:


"It's weighty, bulked out by papers from the Edmonton Aging Symposium held in March. The results presented by LysoSENS researchers funded by the Methuselah Foundation are worth pointing out again. Medical bioremediation has a great future ahead of it - it's clearly one of those ideas, so obvious in hindsight, whose time has come. You should expect to see companies founded on applications of this technology base a decade from now, just as they are founded today on the application of calorie restriction science."

I recommend revisiting the Edmonton Aging Symposium website to look at their video archive; it's a great resource:



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/

SENS3 Posts From Attila Chordash (September 14 2007)
Molecular biologist Attila Chordash continues to turn out posts on his favored presentations at the recent SENS3 conference on rejuvenation and longevity science. The view of researcher Michael Rose's approach to engineering longevity is interesting: "The script is: breed mice with delayed reproduction over multiple generations (let evolution by natural selection give us the answer of how to build a long-lived animal), and then reverse engineer this answer to develop anti-aging therapies for genetically unaltered humans. The experimental basis of this proposal: Rose's own ancient experiments with fruit flies [showed] that there is a plateau in mortality rates after many generations of breeded Drosophilas with delayed reproduction time which leads to the cessation of the aging process." This is an extension of the search for longevity genes; let evolutionary pressure do some of the legwork first, in terms of identifying the biochemistry that is most important. Still, fundamentally this is a reengineering approach, not a repair approach - and therefore most likely much harder.

Most People Won't Determine the Difference (September 14 2007)
A post from the Digital Rules blog reminds us interest in healthy life extension is more widespread than we sometimes think. "The last day of the Forbes Global CEO Forum featured a rousing panel on life extension, which I moderated. How many years can you add to the span of your life if you do everything right ... diet, exercise, accident and disease prevention, etc? Five years? Ten? Twenty? More? What new drugs, diagnostics and cures now in development have the potential to add even more years to our lives - healthy years?" Sadly, it is also a reminder that most people will not exert the effort required to determine the difference between (a) nonsense and hype, (b) marginally useful good health practices, (c) forward looking longevity science that will in fact extend life significantly. Never mind distinguishing between probably ineffective and probably effective forward-looking longevity science. This is how the desire for longevity - expressed in the willingness to pay for progress and personal gain - is subverted into the waste and lies of the "anti-aging" marketplace. We must continue to raise the level of education regarding healthy life extension - by doing so, we help to steer resources to the research with the best chance of extending our healthy life span.

Understanding Retinal Regeneration (September 13 2007)
Researchers continue to decipher the biomechanisms of retinal regeneration that take place throughout life, but fade in old age to cause blindness: "Rod cells make up the majority of photoreceptors in the human eye ... Rod cells contain tiny organelles called the 'outer segment,' which contain about 1,000 flattened discs containing rhodopsin - a visual pigment that absorbs light. Each day, our eyes shed the top 10 percent of these discs, but until now, no one really knew how the retina generated new discs. We believe we have solved that riddle ... There are currently more than 100 retinal eye diseases in human populations, and problems with rhodopsin trafficking or outer segment development are thought to play a role in many of these potentially blinding conditions. In fact, we got interested in this type of research because we knew that breakdowns in rhodopsin trafficking were crucial to a common eye disease, retinitis pigmentosa." Identifying mechanisms is very empowering in this age of biotechnology - it can lead quickly to targeted, effective therapies.

Eat Less, Live Longer (September 13 2007)
KQED's QUEST recently aired a piece on the science of calorie restriction, discussing the past few years of research with scientists working at the Buck Institute for Age Research: "Have we found the fountain of youth? Scientists are discovering ways to make animals live dramatically longer through calorie restriction. While the technique has attracted a small, but devout following, skepticism abounds. ... Alzheimer's, Parkinson's, cancer, stroke, and arthritis have one thing in common: age. By focusing on the connection between aging and disease, scientists at the Buck Institute for Age Research are striving to develop diagnostic tests and treatments that will prevent or delay these conditions." Calorie restriction is not the fountain of youth for us - but it is a helpful way to raise our chances of living to benefit from the real rejuvenation medicine of future years. No fountain of youth exists today, but it is within our power to band together, research, and find out how to build medical technology to repair aging and make the old youthful once more.

Cancer Stem Cells Drive Metastasis (September 12 2007)
From The Scientist: "This is a confirmation of what a lot of people have been talking about, the hypothesis that cancer stem cells are the source of metastasis ... Although the study focused on pancreatic cancer, he noted, it could apply to many other tumors as well ... Recent research has suggested that some tumors, including breast, colon, brain, prostate, and most recently, pancreas, arise from a small subset of stem-like cells called cancer stem cells, which often are marked by the cell surface antigen CD133. These cells induce tumor formation and are often resistant to conventional therapies. Researchers assumed that some segment of these cells also drove metastasis, but this had remained unproven. ... [this] begins to put a definition on the cells responsible for metastasis." Cancer without metastasis would be much less threatening an age-related disease. If we're lucky enough to find that metastasis relies on a small, distinct population of cells, then we can expect significant progress over the next decade.

Why Deathism? (September 12 2007)
Thoughts from the Frontier Channel: "During the Singularity Summit 2007, one of the most unexpected moments came during a panel session on day one. Peter Voss and Dr. Stephen Omohundro sat down to answer questions from the audience after their own individual presentations. Voss had suggested during his talk that [artificial intelligence] could benefit health and longevity research. An audience member asked, with apparent anger and passion, why anyone would want to extend healthy lifespan and attempt to prevent death. Voss seemed surprised by the question, and asked the audience if anyone really wanted to die. A significant minority raised their hands, cried out, and applauded. A philosophical chasm was then suddenly laid bare, thought it appeared that neither side could wrap their heads around the alternative view. After Voss defended radical life extension, a larger portion of the crowd applauded. Why would anyone defend death, especially with applause?" Casual deathists are everywhere; I bear them no ill will, so long as they're not trying to cut my life short as well.

Engineering Stem Cells More Effectively (September 11 2007)
Watch the progress of infrastructure technologies and techniques - it is solid improvement in the foundation that enables stunning advances at the top floor of applied biotechnology. Take this for example, published at Cell Stem Cell: "Reprogramming of somatic cells to the pluripotent stem cell state may allow the development of in vitro models of disease and could provide a mechanism for the generation of patient-specific cells of therapeutic interest. Reprogramming of mouse fibroblasts into induced pluripotent stem cells, or iPS cells, has been achieved with overexpression of oct4, sox2, klf4, and c-myc and drug selection for the reactivation of a marker of pluripotency ... Here we show that n-myc can substitute for c-myc and that drug selection is dispensable for reprogramming of fibroblasts to pluripotent stem cells. ... Our findings greatly simplify the method for induction of pluripotency and bring it one step closer to clinical applications." Generating pluripotent cells at will cheaply, quickly and reliably is a vital pillar for the ongoing development of regenerative medicine. The easier it becomes, the faster the field will move.

Another Demonstrated Cancer-Killing Virus (September 11 2007)
A number of research groups have demonstrated the use of engineered viruses for the targeted destruction of cancer cells. Here is another, aimed at cancer stem cells this time, via EurekAlert!: "We have shown first in lab experiments and then in stem cell-derived human brain cancer in mice, that we have a tool that can target and eliminate the cells that drive brain tumors ... The virus was tested against the most aggressive brain tumor - glioblastoma multiforme, which originates in the glial cells that surround and support neurons. ... Research has shown that these cancer stem cells are the origin of the tumor, that they resist the chemotherapy and radiation that we give to our patients, and that they drive the renewed growth of the tumor after surgery. So we decided to test Delta-24-RGD against glioma stem cells and tumors grown from them ... Fueyo and colleagues developed Delta-24-RGD to prey on a molecular weakness in tumors and altered the virus so it could not replicate in normal tissue. They showed [in] 2003 that the virus eliminated brain tumors in 60 percent of mice who received injections directly into their tumors. The virus spreads in a wave through the tumors until there are no cancer cells left, then it dies."

WSJ Review of Ending Aging (September 10 2007)
The Wall Street Journal reviews Ending Aging: The Rejuvenation Breakthroughs That Could Reverse Human Aging in Our Lifetime. (If the direct link is blocked by the WSJ subscription wall, you can find a PDF version of the review in the Immortality Institute book discussion): "de Grey opens by explaining his mission: extending the human life span for hundreds of years. If there is a War on Drugs and a War on Terror, then why not a War on Aging, since these days aging kills just about everyone? This idea, he says, draws irrational objections from otherwise smart people. Many believe that aging is not a disease but an inescapable aspect of life, programmed into our bodies. Readers who make it through the book's geeky midsection will come away with a workable understanding of [de Grey's] provocative view: Old age may be only the consequence of lax biological housecleaning. ... He thinks more like an engineer than a scientist: Never mind how the body works, can we fix it to keep it running longer? In the book's final section, he decries the misplaced priorities that have hindered this kind of anti-aging research: Scientists can get millions of dollars to seek cures for Alzheimer's disease that afflicts the elderly, but hardly anyone gets paid to figure out how to keep people from growing old in the first place. Part of the problem is a complacent adherence to the status quo, [de Grey] says, but he also thinks that scientists are afraid to encourage a revolutionary initiative such as rejuvenative biotech research."

Talking With Caleb Finch (September 10 2007)
The Daily Herald interviews gerontologist Caleb Finch: "In the last 200 years, one year of extra lifespan has been added for about every four years of historical time. Life expectancy has doubled since the industrial revolution, from about 40 years to near 80 years. ... Longer lifespans have been a worldwide phenomenon associated with improvements in hygiene and medical care and reductions in infectious disease. Some have explained this through the reduction of infant mortality. But we're also living longer because we're staying healthier -- kids have fewer infectious diseases to fight with. This reduction of inflammation and infection, along with the improvement of nutrition, has contributed to longevity by slowing many of the diseases of aging. ... It's by no means certain that the life span increases of the last 200 years will continue at the same rate or be available to all people. My own hunch is that life span could increase considerably more, but it may depend on finances and access to top-level medical resources." The conservative public positions of mainstream gerontology are slowly being drawn closer to a more sensible outlook - that we can do a great deal to extend human life span in the next few decades, and we should get working on that right away.



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