Nanofactory Collaboration Colleague Awarded $3 Million

Dear Future Centenarian,

Are you plagued with information overload? It gets worse every day, doesn’t it? If it weren’t for Reason at www.longevitymeme.org, I’d never have the time to sort through all the daily longevity news that you see in this letter. He does a terrific job, I distill it down and slightly edit it, and presto, you spend a few minutes every week to pick and choose whatever hits your hot button. There’s something for almost everybody in each issue, maybe even some life-saving info for you or a loved one.

Here is an excerpt from a release that I got from another source. An article like this might not catch your attention. On the surface, it looks like just another narrow-niche, hi-tech article aimed toward a limited audience. In reality though, it could hold the key to your full age-reversal plus open-ended youth in a super-human body. I’ll tell you why in a moment.
Nanofactory Collaboration Colleague Awarded $3M to Conduct First Diamond Mechanosynthesis Experiments
Professor Philip Moriarty of the Nanoscience Group the School of Physics at the University of Nottingham (U.K.) has been awarded a five-year $3M grant by the U.K. Engineering and Physical Sciences Research Council (EPSRC) to perform a series of laboratory experiments designed to investigate the possibility of diamond mechanosynthesis (DMS). DMS is a proposed method for building diamond nanostructures, atom-by-atom. Moriarty’s experiments begin in October 2008.
The Nottingham work grew out of continuing discussions on DMS between Moriarty and Robert Freitas, a Senior Research Fellow at the Institute for Molecular Manufacturing (IMM) (Palo Alto, California, U.S.).
Freitas and Ralph Merkle, also a Senior Fellow at IMM, founded the Nanofactory Collaboration in 2001 to pursue molecular manufacturing via DMS. Moriarty is interested in testing the viability of positionally-controlled atom-by-atom fabrication of diamondoid materials as described in the Freitas-Merkle minimal toolset theory paper. Moriarty’s efforts will be the first time specific predictions of DFT in the area of mechanosynthesis will be rigorously tested by experiment.
The article goes into more detail, but the implication for your longevity is this:
DMS is the first step on the way to full-blown nanomedicine. Nanomedicine may be the holy grail of indefinite lifespans. Next week, we’ll go a little deeper and take a peek into the future that nanomedicine has in store for you.
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LATEST HEALTHY LIFE EXTENSION HEADLINES

Calorie Restriction: Animals Versus People (September 25 2008) http://www.sciencedaily.com/releases/2008/09/080924151018.htm
The present scientific consensus on calorie restriction in humans is that it will do wonderful things for your health and resistance to age-related disease, but won't extend the maximum human life span to the same degree that is seen in lower animals: "In the majority of the animal models of longevity, extended lifespan involves pathways related to a growth factor called IGF-1 (insulin-like growth factor-1). In calorie-restricted animals, levels of circulating IGF-1 decline between 30 percent and 40 percent. We looked at IGF-1 in humans doing calorie restriction [and] found no difference in IGF-1 levels between people on calorie restriction and those who are not. We know there are two major influences on IGF-1 levels: calorie intake and protein intake. So we decided to look at the influence of protein. Six [human testers] agreed to lower their protein intake and after three weeks their circulating IGF-1 declined dramatically. It's much easier to restrict protein than to restrict calories. If our research is on the right track, maybe humans don't need to be so calorie restricted. Limiting protein intake to .7 or .8 grams per kilogram per day might be more effective. That's just a hypothesis. We have to confirm it in future studies."

Nitric Oxide and Aging Blood Vessels (September 24 2008) http://pmid.us/18805864
Nitric oxide is important in the operation of the endothelium - the lining of blood vessels - but diminishes with age: "The normal endothelium exerts a major vascular protecting role by secreting substances, above all nitric oxide (NO). In disease conditions (such as the presence of cardiovascular risk factors) the activation of endothelial cells can lead to the production and release of contracting factors, which counteract the beneficial effects of NO, and reactive oxygen species (ROS), which in turn cause NO breakdown. Aging has been demonstrated to be associated to a progressive impairment in endothelial function both in conduit arteries and resistance vessels, mainly because of an increased production of ROS.

Therefore, it is conceivable that endothelial dysfunction plays a major role in favoring age-related increased cardiovascular risk in the elderly. "This is an example of the way in which age-damaged cells cause problems in the normal operation of surrounding tissue: cells taken over by damaged mitochondria are exporting reactive oxygen species that breakdown NO, and senescent cells are pushing out their own cocktail of unhelpful chemical instructions as well.

Out of Context, Many Old Cells Work Just Fine (September 23 2008) http://pmid.us/18802086
It is a recurring theme in stem cell and immune system research that cells removed from the context of the aging cellular environment can do their jobs just as well as cells in a young environment: "Understanding how aging impacts the function of memory CD4 T cells is critical for designing effective vaccines. Our studies show that immunological memory generated during youth functions well into old age, whereas that generated later in life functions poorly. This is the result of declines in the function of naive CD4 T cells from aged individuals and contributes to reduced efficacy of vaccines in the elderly. To begin to identify the cause of this defect, we examined the function of memory T cells generated from bone marrow precursor cells (BMPC) from young or aged mice in young hosts. In two different models, memory cells derived from young and aged BMPC exhibit good ex vivo and in vivo function. Importantly, memory CD4 T cells generated from aged BMPC exhibit potent cognate helper function for humoral responses, which are critical for effective immunization. These results indicate that there are no apparent age-related intrinsic defects in BMPC with regards to generation of functional memory T cells." As for many aspects of aging, the problem is one of failing systems and signal controls, not failing components.

NOTE: Maybe many do work fine, but we believe most don’t, due to accumulated mutations.

A Recellurization Update (September 23 2008) http://www.popsci.com/node/24069
Via Popular Science: "Some people say they can grow a heart from scratch in 10 years, which is ridiculous. But Dr. Taylor's approach is more realistic because it's so simple and elegant. By using an existing heart, she's taken away all of the structural issues. Taylor's system involves flushing animal hearts of cells using a cleanser, at which point only the extracellular matrix remains and 'the hearts look almost clear'. The next step is to infuse the hearts with a mix of mature and progenitor cardiac cells, which can come from a patient's own body to ensure compatibility. Incredibly, for reasons the team still doesn't understand, the cells seem to know how to divide and proliferate into cardiac tissue inside the empty-shell hearts. This year, Taylor has continued to forge ahead toward her goal of creating transplantable, made-to-order human organs. Soon after she published her rat-heart results, she started working on making recellularized pig hearts - closer in size and shape to the human equivalent - that could pump blood and generate electrical impulses. Our hope is that someday we'll be able to take a cadaver or pig organ, decellularize it, and transplant your own cells into the matrix to make an organ that matches your body."

A Potential Downside to Exercise Mimetics (September 22 2008) http://ouroboros.wordpress.com/2008/09/22/amp-activated-kinase-the-target-of-exercise-mimetics-may-contribute-to-photoaging-and-cell-death/
From Ouroboros: "AMP-activated kinase (AMPK) agonists mimic the effects of exercise, raising the possibility of a 'workout pill' that could simulate the effects of vigorous activity. The applications to human health are, to mildly understate the case, significant; it sounds almost too good to be true, and it leaves one looking for the catch. It turns out that AMPK is activated by certain types of genotoxic stress, and contributes to UV-induced apoptosis in the skin. Activation of AMPK could exacerbate the pro-aging effects that UV light exerts on the skin. Judging from the peroxide results, this also applies to endogenously generated reactive oxygen species (ROS) - which one can't avoid by simply staying out of the sun. Before we panic and throw the exercise mimetic baby out with its carcinogenic bathwater, I'd want to see whether AMPK agonists like AICAR do in fact synergize with stresses like UV and peroxide to increase apoptotic cell death in the skin. If they do, well, I think we found that catch."

More Multipotent Stem Cells Discovered (September 22 2008) http://www.eurekalert.org/pub_releases/2008-09/chop-pri092208.phpFrom EurekAlert!: "The scientists [identified] cells known as pericytes that are multipotent, meaning they have broad developmental potential. Pericytes are found on the walls of small blood vessels such as capillaries and microvessels throughout the body and have the potential to be extracted and grown into many types of tissues. We believe pericytes represent one of the most promising sources of multipotent stem cells that scientists have been searching for in the quest to make regenerative medicine possible. These cells can be extracted easily and painlessly from convenient sources such as fat tissue, dental pulp, umbilical cord and placental tissue, then grown in culture to large numbers and, possibly, re-injected into the patient to heal a broken bone, a failing joint or an injured muscle. Researchers were able to identify pericytes in all human tissues they analyzed, including muscle, fat, pancreas, placenta and many other samples. Through purification in the lab, these pericytes could then be coaxed into becoming whatever type of tissue the scientists desired. For instance, the researchers took pericytes from the pancreas and then reinjected them into an injured muscle. The cells immediately began regenerating muscle tissue."

Artificial General Intelligence

I wish you could have been with me Wednesday evening. I was treated to a personal demonstration of a technology that could change the world in ways we can’t even imagine. One of the changes that will affect you could lock in full age reversal and open-ended youth and health ahead of even my ambitious schedule.

The technology I’m describing is Artificial General Intelligence (AGI).

AGI is a new kind of computer application. This technology will allow computers to learn, think and respond like humans. They will exhibit REAL intelligence. Such intelligent systems do not exist yet – however, the required knowledge to build them does, and it has already led to an embryonic prototype. That’s what I experienced Wednesday.

AGI makes up one part of the MaxLife plan to accelerate extreme life extension capabilities. Research aims to create this broad human-like intelligence, rather than narrowly "smart" systems that can operate only as tools for human operators in well-defined domains such as tracking inventory or landing airplanes.

Imagine machine intelligence with the ability to think and learn on its own as well as humans do. That’s in our future. For example, if it gets an education equivalent to a biotech researcher, it could do the research. The developers estimate a sophisticated working system could take less than 10 years to complete. Two years later, we could potentially have a fully-trained PhD-equivalent AGI doing research.

Imagine a PhD lab assistant which would have total recall and tirelessly work around the clock. It would be able to download all the data it needs from the Internet almost instantaneously. It could collaborate with humans and other AGI. And then, it could be quickly copied as many times as necessary.

Imagine unleashing 100,000 AGI researchers. Imagine how much faster they would develop real anti-aging therapies.

So keep posted and hang on for a long ride Methuselah.
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$1 BILLION ALREADY INVESTED IN SOMETHING YOU CAN DO FOR FREE

"Two pilot studies were undertaken to examine the effects of alternate day fasting and calorie restriction on indicators of health and longevity in humans. In this study, we used sera collected from those studies to culture human cells and assessed the effects on growth, stress resistance and gene expression. Cells cultured in serum collected at the end of the dieting period were compared to cells cultured in serum collected at baseline (before the dieting period). This resulted in increased stress resistance and an up-regulation of genes proposed to be indicators of increased longevity."

As of late 2008, I'd guesstimate that something in the order of one to two billion dollars have been invested into developing drugs that will produce some fraction of the effects of calorie restriction on mammalian biochemistry - such as increasing the expression of Sirt1. They aren't done yet, and years of trials and further development lie ahead. Most people can get these benefits today and for free, however, by simply eating a less calorie-packed diet. You should look into it: calorie restriction isn't anywhere near as hard as those who have never tried it make it out to be. You can find an introduction at the Longevity Meme website:

http://www.longevitymeme.org/topics/calorie_restriction.cfm

TRY NOT TO STAB YOURSELF REPEATEDLY

Words of wisdom:

http://www.fightaging.org/archives/001572.php

"On March 19, 2008 a Symposium on Pathophysiology of Aging and Age-Related diseases was held in Palermo, Italy. Here, the lecture of V. Nicita-Mauro on Smoking, health and ageing is summarized. Smoking represents an important ageing accelerator, both directly by triggering inflammatory responses, and indirectly by favoring the occurrence of several diseases where smoking is a recognized risk factor. Hence, non-smokers can delay the appearance of diseases and of ageing process, so attaining longevity.

"Forms of slow self-destruction are many and varied amongst us humans: Smoking, not practicing calorie restriction, failing to keep up a good relationship with a physician, piling on the visceral fat, failing to exercise, and so forth. The vast majority of people are quite comfortable engaging in habits that cause great harm to the old person they will one day be - cutting off years or even decades of health. This is all a good example of time preference at work: we are hardwired to deeply discount the value of the future, even when it's our own future. What we don't value, we squander - you can see that maxim in action everywhere."
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LATEST HEALTHY LIFE EXTENSION HEADLINES

Lurking Behind the TOR Gene (September 19 2008) http://www.eurekalert.org/pub_releases/2008-09/uouh-lca091808.php
Researchers have known for a few years that the TOR gene is important in calorie restriction and other related ways of extending healthy life. Recent research follows the chain of biochemical cause and effect beyond TOR: "In C. elegans, the tiny roundworm that our lab studies, as well as some other animals, a loss of TOR has been shown to slow aging. Our work with C. elegans reveals that TOR depends on a second gene called pha4/FoxA to control the aging process. When there's lots of food, TOR gets active, which decreases the action of pha4/FoxA down the line, and that in turn shortens the lifespan of C. elegans. When there's little food, there'slittle TOR and more pha4/FoxA, and that results in a longer lifespan. Many organisms have a TOR gene and a gene similar to pha4/FoxA, such as single-cell yeasts, roundworms, and mammals including humans. In mammals, FoxA controls cell metabolism and there is a lot of it in breast and prostate cancers. The findings of this research establish that animals use both genes to sense the amount of food that is available and control the length of lifespan. Further research will be required to establish whether a similar relationship between these factors can control metabolism, longevity or disease in humans."

Early Experiments in Cryonics (September 18 2008) http://www.depressedmetabolism.com/2008/09/15/early-total-body-washout-experiments-in-cryonics/
Depressed Metabolism takes another look at the early days of cryonics: "The question of whether cryonics 'works' or not is too general and hides the point that progressive breakthroughs can make the concept more plausible. During its existence as a research program, cryonics researchers have shown great interest in recovering animals from ultra-profound hypothermic temperatures (lower than 5 degrees Celsius). The ability to routinely lower the temperature of mammals to temperatures close to zero degrees Celsius and recover them without adverse effects to the brain does make the initial stages of cryonics reversible. Less known than those record setting experiments are earlier explorations in cryonics into whole body asanguineous hypothermia. The following document by cryonics researcher and Alcor patient Jerry Leaf documents a Trans Time experiment during the early days of total body washout experiments in cryonics. This account was published in the November/December 1977 issue of Long Life Magazine."

Struggling to Break Out of the Old Paradigm (September 17 2008) http://www.redorbit.com/news/health/1558015/listening_to_resveratrol/
From RedOrbit, an example of someone caught halfway between paradigms: learning about the potential of longevity science, but having trouble envisaging the changes it will herald for institutions of insurance, development, and regulation. "Currently our drug development and approval systems aim at disease-specific treatments. Indeed, the Food and Drug Administration approves medications only for specific indications, and 'mortality,' a universal condition, would seem unlikely to qualify under the current system. Further, if senescence begins in one's 30s but the outcome (that is, death) can be measured only in one's 70s or 80s, how will researchers be able to perform timely clinical trials in humans? Health insurance is based on the principle of risk pooling. Because nobody can be certain that they will remain healthy, the disease-free are willing to share the cost burden with the sick. But if resveratrol-like drugs are recommended for everybody over 30 at risk for mortality (a universal condition), there would be no risk pooling." When you catch yourself asking"how will this ever fit?" then the answer is usually "it won't fit, and will never fit in the present structure, because things will change in the future so as to accommodate it."

Learning from AIDS (September 17 2008) http://www.sciencedaily.com/releases/2008/09/080916143900.htm
There are similarities between the progression of AIDS and what happens (more slowly) to our immune systems with aging. Forced overactivation and exhaustion of resources are the focus here. AIDS researchers are making steps towards understanding mechanisms that would allow the immune system to be tuned down for specific threats, to prevent it grinding itself into oblivion. "During both HIV infection in humans and SIV infection in macaques, the host immune system becomes highly activated, experiences increased destruction and decreased production of key immune effector cellsand progressively fails as a result. In contrast, natural hosts for SIV infection, like sooty mangabeys, do not exhibit aberrant immune activation and do not develop AIDS despite high levels of ongoing SIV replication. Sooty mangabeys, dendritic cells produce much less interferon alpha - an alarm signal to the rest of the immune system - in response to SIV. As a result, the dendritic cells are not activated during the initial or chronic stages of SIV infection, and mangabeys fail to mount a significant immune response to the virus." It seems reasonable to expect this knowledge to be applicable to the long-term response to CMV in humans, an important contributor to age-related immune system failure.

A Better Lifestyle Means More Telomerase? (September 16 2008) http://www.sfgate.com/cgi-bin/article.cgi?f=/c/a/2008/09/16/MNEL12UBJ5.DTL
The San Francisco Chronicle reports on an intriguing, if small, study: researchers "studied the levels of an enzyme called telomerase in the prostate tissue of the 30 cancer patients who had volunteered to follow a low-fat diet, exercise moderately and reduce their stress. After only three months, 24 patients showed a highly significant increase in their telomerase levels - an indication that the cell-protecting telomeres in their cells were being restored. The long telomere proteins protect the ends of chromosomes in the body, but they shorten naturally and ultimately die unless the telomerase enzyme acts to repair them and increase their length. Even with only 30 patients [the] association between their extremely healthy habits and the increased amount of telomerase proved highly [statistically] significant." Telomerase is apparently also involved in reducing age-related damage to mitochondria, which in turn slows the rate at which failing mitochondria cause telomeres to shorten.

Mitochondrial Function and Aging (September 16 2008) http://www.boston.com/news/health/articles/2008/09/15/power_outage/?page=fullThose of you familiar with the mitochondrial free radical theory of aging -damage to mitochondrial DNA leads to loss of function and a spreading chainof biochemical dysfunctions - will notice a subtle disconnect between this research and the popular science view of mitochondrial function and aging, as outlined in this Boston Globe article. The popular view is very much concerned with contribution to particular diseases, and in finding drugs that improve mitochondrial function as a way of slowing that contribution -without necessarily understanding why those drugs work. We know enough to do much better than that - repairing mitochondrial damage completely, for example, and thus totally removing its contribution to aging. But until thepublic at large realizes this, funding will continue to move towards the established old-school drug discovery programs. These programs focus on treating specific diseases of aging by patching over or slowing down root causes - as opposed than aiming to repair them fully

Aging, the New Frontier

Dear Future Centenarian,
We are finally moving from an era where nothing could be done to defeat aging into an era where advancing technology will give us the tools to overcome it. All the old attitudes are no longer relevant.
We’re so used to people dying from age related causes that we accept it as a normal part of life. And we become desensitized to this death. But let’s look at it from a different angle and see if you think about it differently.
Robert Freitas, a brilliant scientist and perhaps the world’s utmost authority on Nanomedicine, offers some interesting ways to view aging. He points out the following:
100,000 lives are lost every single day from aging related causes. They’re scattered all over the world, so we hardly notice. But what if 400 jetliners fell out of the sky in a single day? We would be astonished, outraged and sickened. Yet effectively, that’s equivalent to 400 jetliner crashes.
If 400 planes crashed every day, wouldn’t the world marshal all its powers to insure aircraft safety, especially if we had no choice but to fly?
What if we could avoid… or at least postpone most aging related deaths?
Then why isn’t treating aging a #1 priority?
After all, if you or a loved one had a major medical condition such as cancer, heart disease or suffered a stroke, wouldn’t you ask for the very best medical care?
If we had a treatment that could reverse Alzheimer’s, Parkinson’s, osteoporosis, arteriosclerosis or diabetes… who in their right mind would turn it down?
Now it is aging, the new frontier. Since it kills everyone who survives or dodges diseases, might not aging be considered a disease as well? MaxLife looks at it as a curable disease, in fact the mother of most diseases. And we’re determined to do something about it.
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LATEST HEALTHY LIFE EXTENSION HEADLINES

The Dreaded Reactive Oxygen Species (July 25 2008) http://www.eurekalert.org/pub_releases/2008-07/uorm-ruk072108.php
It's good to see more research groups looking into targeting antioxidants to the mitochondria. From EurekAlert!: "Researchers have taken a first snapshot of how a class of highly reactive molecules inflicts cellular damage as part of aging, heart disease, stroke, cancer, diabetes, kidney disease and Alzheimer's disease to name a few. Researchers have discovered a tool that can monitor related damage and determine the degree to which antioxidant drugs effectively combat disease. Our study provides a better glimpse of why a cell under assault by disease makes 10 times as many reactive oxygen species [ROS] as the same cell when healthy. We have discovered a chemical tool for investigating how diseases cause damage, mitochondrion by mitochondrion. Efforts to develop antioxidant drugs (e.g. vitamin E) to treat diseases of increased oxidative stress have met with limited success to date because they tried to eliminate ROS, rather than maintain the right amount, Sheu said. He established the Mitochondrial Research & Innovation Group (MRIG) [in] 2002 with the goal of designing therapies to deliver precise amounts of antioxidants to the mitochondria of diseased cells only. MRIG teams are, for example, screening through compounds to confirm that oxidative stress can be reversed by mitochondria-specific drugs."

On Hormesis and Longevity (July 24 2008) http://pmid.us/18648625
A nice overview of hormesis: "Aging is characterized by a stochastic accumulation of molecular damage, progressive failure of maintenance and repair, and consequent onset of age-related diseases. Applying hormesis in aging research and therapy is based on the principle of stimulation of maintenance and repair pathways by repeated exposure to mild stress. In a series of experimental studies we have shown that repetitive mild heat stress has anti-aging hormetic effects on growth and various other cellular and biochemical characteristics of human skin fibroblasts undergoing aging in vitro. These effects include the maintenance of stress protein profiles, reduction in the accumulation of oxidatively and glycoxidatively damaged proteins, stimulation of the proteasomal activities for the degradation of abnormal proteins, improved cellular resistance to ethanol, hydrogenperoxide and ultraviolet-B rays, and enhanced levels of various antioxidant enzymes. Anti-aging hormetic effects of mild heat shock appear to be facilitated by reducing protein damage and protein aggregation by activating internal antioxidant, repair and degradation processes."

Yeast and Aging Research (July 22 2008) http://ouroboros.wordpress.com/2008/07/21/biogerontology-rising-recent-progress-in-yeast-aging-research/
Ouroboros looks at the humble yeast in context: "Our understanding of aging in animals owes a great debt to a large body of careful work in a single-celled organism, the brewer's yeast Saccharomyces cerevisiae. Indeed, as I've argued before, yeast is one of the two organisms with the strongest credible claim to have started modern biogerontology. An unusually large crop of yeast aging papers have appeared over the last few months, and I thought it would be appropriate to spend a few paragraphs describing them - in honor of this humble organism that rises our bread, ferments our beer, and has done so much to open our eyes to the fundamental mechanisms of aging. Yeast mutants in worm longevity genes are significantly more likely to be long-lived than randomly chosen mutants - suggesting [that] genes that modulate aging have been conserved not only in sequence, but also in function, over a billion years of evolution. Given this functional conservation, it is reasonable to use yeast to help answer questions about aging in general, so long as these questions as cell-biological in scope."

New York Times on Sirtris (July 22 2008) http://www.nytimes.com/2008/07/22/health/research/22long.html?pagewanted=all
The New York Times looks at Sirtris Pharmaceuticals: "The hope is that activating sirtuins in people would, like a calorically restricted diet in mice, avert degenerative diseases of aging like diabetes, heart disease, cancer and Alzheimer's. There is no Food and Drug Administration category for longevity drugs, so if the company is to submit a drug for approval, it needs to be for a specific disease. Nonetheless, longevity is what has motivated the researchers and what makes the drugs potentially so appealing. Dr. Christoph Westphal, the chief executive of Sirtris, said of the potential of the drugs, 'I think that if we are right, this could extend life span by 5 or 10 percent.' He added that his goal was to develop drugs against specific diseases, with the extension of life being 'almost a side effect of our medicine.'" There you have the most serious problem facing longevity science today: that its direct application is not permitted by the FDA. Until this changes no serious investment will be made in the US to bring longevity science to the clinic. This is a tragedy of so great a scale as to beggar belief.

Thoughts on Mortality and Its Evasion (July 21 2008) http://tacit.livejournal.com/250032.html
An interesting LiveJournal post: "A person immune to the ravages of old age would still not be immune to death; accident, violence, and other misadventure is perfectly capable of ending even a 25-year-old's life. It simply means that person no longer has a cap on the maximum time he can live, if he so chooses. And that's really what it's all about. Choice. If you go into the doctor's office, and he tells you that you have a bacterial infection, which will slowly grow progressively worse until it kills you painfully, then offers you an antibiotic pill that will completely eradicate the infection, I bet you'll take it. Even if you don't fancy the thought of living forever. There's an important point in that.

Even folks who don't much want to live forever still probably don't want to die today. Or tomorrow. Someday, perhaps, if that 'someday' is held in the abstract; some future time when things no longer seem interesting. But not today. And that's the point. A solution for aging puts the power to choose in your hands. Old age forces your hand; you don't get the choice to see your grandkids graduate from school, or to celebrate your fiftieth anniversary. The choice is made for you. And I don't see how that benefits anyone."

Growing Blood Vessels (July 21 2008) http://news.bbc.co.uk/2/hi/health/7514317.stm
Researchers continue to work at the blood vessel problem in tissue engineering. From the BBC: "Scientists have used human cells to grow new blood vessels in a mouse for the first time. The ability to develop swiftly a new network of tiny blood vessels - known as capillaries - would be a prize for scientists. There are dozens of potential applications in medicine, particularly in the treatment of conditions which involve damage to a tissue's blood supply, such as that to the heart muscle following a heart attack. However, the complex structure of these vessels has slowed progress. What's really significant about our study is that we are using human cells that can be obtained from blood or bone marrow rather than removing and using fully developed blood vessels. It could certainly assist in the connection of other engineered organs to the body's blood supply. Although this approach is not yet suitable for clinical use, it is interesting that they have demonstrated you have all the elements you need to create a functional network of capillaries from a small amount of blood."
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DISCLAIMER: News summaries are reported by third parties, and there is no guarantee of accuracy. This newsletter is not meant to substitute for your personal due diligence and is not to be taken as medical advice. For originating report, please see www.longevitymeme.org/newsletter/.
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Biological Evolution

Dear Future Centenarian,
We’ve come a long way in our lifetimes. In fact, we have accomplished as much then as we did in all of recorded history. At least technologically. As a race, we really didn’t seem to have learned many lessons. Oh sure, maybe our justice systems are a little more fair (and maybe not), we may have developed a little more tolerance and compassion, and maybe we’re not quite as barbaric. All in all though, we react to intrusions about the same as prehistoric man.
We still settle disputes and differences about the same way. We either initiate or answer with violence for the most part. But instead of clubbing each other senseless and confining our rage, jealousies, pettiness and intolerances to an area roughly equivalent to our immediate reach and to one enemy or victim at a time, we now have these wonders of science at our disposal, capable of inflicting widespread death and destruction.
Then, we had clubs and primitive minds. Now we have nukes, biological and chemical weapons, potentially devastating nanotechnology capabilities… and primitive minds.
While we have evolved in some ways at light speed, our ability to solve social problems and disputes and our tendency to hate hasn’t changed since caveman days. Look, we’re on the cusp of breaking through to indefinite lifespans and solutions for health problems, poverty and pollution. But what good does it do us when emotionally unstable individuals have abilities to wipe out millions with no more effort or forethought than swinging a club?
Fortunately, the human race is extremely resilient and resourceful. We often respond to challenges in creative and unexpected ways. A relatively new foundation recognizes this challenge and is taking it on as part of its agenda. See more information at www.InnerSpaceFoundation.org.
They recognize that biological evolution is a somewhat haphazard and non-optimizing process that has produced many undesirable artifacts. Among a large number and wide variety of such artifacts, two stand out as the underlying causes of the most pervasive and extreme human suffering: mental and lifespan limitations. Mental inabilities, including the failure to resolve conflicts non-violently, are universal. They must ultimately serve to explain our ongoing failures to end human warfare, crime, poverty, and famine, and to completely cure diseases, disabilities, aging and death. Therefore, these inabilities are fundamentally even more harmful to humanity than the categories of biomedical dysfunction we currently labor to cure.
This belief forms the core of the Bioprogressive philosophy. The overall goal of the InnerSpace Foundation (IF) is to accelerate developing biomedical technologies for transcending these limitations. IF is taking specific steps toward enhancing memory, learning and cognition. These near-term goals should ultimately help us to eliminate or transcend other unwanted artifacts of Darwinian evolution.
IF, among others, have longer-term goals aimed at preserving memories. So hang on. We have some interesting times ahead.
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CANCER AND IMMUNE SYSTEM PROFICIENCY

Are some immune systems much better than others at destroying cancer in its earliest stages? It seems that this is the case. Can we copy that proficiency and use it as a therapy? The prospects look promising:

http://www.fightaging.org/archives/001525.php

"First, we had cancer-resistant mice and asked, 'What can we learn from it?' The reason it's resistant is because it has very different white cells. So then that immediately prompted the concept of therapy, because you can easily transfer white cells. You can extract them as a therapeutic agent and give them to another mouse. It's a therapy. It's much better than to find the gene. If you find the gene, then you have to understand the mechanism, and you have to find a way to put the gene into the cell, into all the cells you want to, and that would not work very easily. The technology as we speak right now is not really mature for that area. You might have to wait another 10, 20 years before that technology catches up with the concept. However, what we found is a cell as a therapeutic agent, so why not go ahead and see how it works. It worked really well in mice, so the next question, very obviously, is can we find a similar cancer resistance for humans as a donor for a therapeutic agent. And the answer is yes, we did find quite a few of them ".

From a broad assessment of cutting edge cancer research, it seems that we are well on the way to turning cancer into a controllable chronic illness. You'll have outbreaks, they'll be caught early, and the medicine of the 2020s will eliminate them. The question is whether this is good enough: is a comprehensive suite of low-risk, safe cancer cures enough to remove cancer as a threat while our lives are extended by other medical technologies?
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LATEST HEALTHY LIFE EXTENSION HEADLINES

The Broadening Search for Longevity Genes (July 17 2008)
http://www.technologyreview.com/printer_friendly_article.aspx?id=21092
The MIT Technology Review looks at continued attempts to understand the degree to which present healthy human longevity is influenced by genes: "An ambitious plan to sequence 100 genes in 1,000 healthy old people could shed light on genetic variations that insulate some people from the ailments of aging, including heart disease, cancer, and diabetes, allowing them to live a healthy life into their eighties and beyond. Rather than focusing on genetic variations that increase risk for disease, scientists plan to focus on genes that have previously been linked to health and longevity. Advances in genetic screening technologies have allowed scientists to start searching the genome for clues to healthy aging and a lengthy life span. That work has revealed that the genomes of healthy old people are not blemish free. These people have genetic susceptibility markers for many serious diseases [but] they don't get any of these diseases. What is the explanation? What might account for their insulation from these diseases?" Genes are not fate - evidence to date suggests that lifestyle choices have much more weight for all but the most genetically unlucky, and those choices are reflected in epigenetic variations, not genetic variations.

Self-Assembly in Tissue Engineering (July 16 2008) http://www.technologyreview.com/printer_friendly_article.aspx?id=21080
The MIT Technology Review looks at a promising strategy in tissue engineering: "Tissue engineers are ambitious. If they had their way, a dialysis patient could receive a new kidney made in the lab from his own cells, instead of waiting for a donor organ that his immune system might reject. Likewise, a diabetic could, with grafts of lab-made pancreatic tissue, be given the ability to make insulin again. But tissue engineering has stalled in part because bioengineers haven't been able to replicate the structural complexity of human tissues. Now researchers have taken an important first step toward building complex tissues from the bottom up by creating what they call living Legos. These building blocks, biofriendly gels of various shapes studded with cells, can self-assemble into complex structures resembling those found in tissues. This will be an effective way to put the cells where we want them to be. You can probably generate a tissue with a higher complexity [using] the new method than is possible with a scaffold that has to be seeded with cells." Compare and contrast with the use of whole-organ cell matrix templates, another recent development aimed at solving the same problem.

Stress, Cortisol, and Shortened Telomeres (July 16 2008) http://www.eurekalert.org/pub_releases/2008-07/uoc--usi071508.php
Chronic stress correlates with shorter telomeres, as well as with worse health. Via EurekAlert! researchers are proposing a mechanism by which telomere length is reduced by stress, leading to a worse immune response: "Short telomeres are linked to a range of human diseases, including HIV, osteoporosis, heart disease and aging. An enzyme [called telomerase] keeps immune cells young by preserving their telomere length and ability to continue dividing. The stress hormone cortisol suppresses immune cells' ability to activate their telomerase. This may explain why the cells of persons under chronic stress have shorter telomeres. When the body is under stress, it boosts production of cortisol to support a 'fight or flight' response. If the hormone remains elevated in the bloodstream for long periods of time, though, it wears down the immune system. We are testing therapeutic ways of enhancing telomerase levels to help the immune system ward off cortisol's effect. If we're successful, one day a pill may exist to strengthen the immune system's ability to weather chronic emotional stress."

Why Fight Aging? (July 15 2008)
http://www.acceleratingfuture.com/people-blog/?p=2307
A Future Current transcript of one of Aubrey de Grey's presentations at Aging 2008: "Some people say, 'I don't want to live to a thousand.' I don't want to live to a thousand, necessarily. I don't even know if I want to live to a hundred. But I do know I want to make that choice when I am 99, rather than having it gradually removed from me by declining health. This is what it comes down to. The extension of lifespan by the defeat of aging is not the point - at least it is not the main point for me, and I do not think it is the main point for most people who are engaged in this crusade. The purpose is to alleviate the suffering that goes with getting decrepit, frail and dependent. Of course, this includes not just those who are suffering that, but the suffering of their loved ones. The extension of average lifespan is essentially a side benefit. It is something that will happen because the way that we are going to do this, using regenerative medicine, will also mean that you have only the same probability you did when you were a young adult of dying peacefully in your sleep without any of these diseases. In other words, a very low probability indeed. You will indeed on average live a great deal longer, and I don't think you’ll complain if you do. However, that is not the purpose. The purpose is to alleviate suffering."

On the Way to Longevity (July 14 2008)
http://www.dailybruin.ucla.edu/news/2008/jul/14/within-20-years-you-wont-have-grow-old/
The Daily Bruin talks to some of the folk who were at Aging 2008: "Defeating the effects of time by finding a cure for aging has become the focus of multiple areas of research, bringing the possibilities of achieving immortality from fantasy into the realm of science. The new possibilities offered by regenerative medicine illustrate how advancements in therapy on the molecular and cellular level may be able to extend the healthy human life span within the next 20 years. Finding a cure for aging is no longer a theoretical target or a fantasy, but on the way to becoming a practical target. Aging is the most universal degenerative condition and is now becoming the target of regenerative medicine. The body is a really complicated machine, but it's still a machine, so its healthy lifespan can be extended indefinitely by sufficiently comprehensive repair and maintenance, just like simple man-made machines. Aging is a complex phenomenon that affects many different systems. Understanding it and fixing the damage as it comes can potentially cure the harmful effects of aging and as a result, elongate the healthy human lifespan."
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DISCLAIMER: News summaries are reported by third parties, and there is no guarantee of accuracy. This newsletter is not meant to substitute for your personal due diligence and is not to be taken as medical advice. For originating report, please see www.longevitymeme.org/newsletter/.

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David A. Kekich
Maximum Life Foundation
714-641-0700/Fax 714-464-4135
www.MaxLife.org

"Where Biotech, Infotech and Nanotech
Meet to Reverse Aging by 2029"

A Real Boost for Aging Research

Friday, June 27th I attended Aging 2008 - Aging: the Disease, the Cure, the Implications at UCLA. It was sponsored by Dr. Aubrey de Grey and the Methuselah Foundation. About 700 people attended a stimulating three hour session featuring an All-Star lineup of aging researchers, advocates and personalities.

Most of the attendees spent the next couple of hours networking at an outdoor dinner. In my opinion, some of the more important and interesting people in the world were there, including some movers and shakers who are launching exciting companies and research projects – projects that could have a big impact on your health and longevity.

Here is a list of the speakers:
Dr. Bruce Ames, Professor of Biochemistry and Molecular Biology at UC Berkeley
G. Steven Burrill, Chairman of Pharmasset and Chairman of Campaign for Medical Research
Dr. Aubrey de Grey, Chairman and CSO of Methuselah Foundation and author of Ending Aging
Dr. William Haseltine, Chairman of Haseltine Global Health
Daniel Perry, Executive Director of Alliance for Aging Research
Bernard Siegel, Executive Director of Genetics Policy Institute
Dr. Gregory Stock, Director of Program on Medicine, Technology & Society at UCLA School of Medicine
Dr. Michael West, CEO of BioTime and Adjunct Professor of Bioengineering at UC Berkeley
I also got a Methuselah Foundation T-shirt, one of the coolest T-shirts I ever saw.

Aging 2008 was the opening session for the technically focused Understanding Aging conference which took place Saturday and Sunday. Thirty four scientists presented over the weekend. I believe this was the most extensive scientific longevity conference ever held in the US. Hopefully, the Methuselah Foundation will offer videos.

Open-forum events like this enable scientists to bounce ideas of one another, to cross pollinate ideas and to open up various research programs to debate and scrutiny. As a result, it fast tracks longevity research. Congratulations to Aubrey de Grey and all the Methuselah Foundation volunteers who made it happen.

Then last week, I attended a presentation to an investment banker to fund two very progressive adult stem cell companies. He made a verbal commitment, and funding might take place as early as this month. Once these companies are launched, human therapies could be accelerated. That could translate to the first round of therapies becoming available by next year. Anti-aging science is ratcheted up one more notch.
All-in-all that was a very productive week for life extension. Let’s look forward to many more.

Is Curing Aging Just a Scientific Challenge? The Answer Below May Surprise You.

Dear Future Centenarian,

I wish you could have been with me last week. Please let me explain…

I attended a week-long conference for two reasons. First, my assistant went on his honeymoon then, and it was convenient for me to hole up and rest in a hotel for 5 days. Second, it gave me a good chance to spend some time with some friends who I hadn’t seen for a while. Oh and there was a third reason too… I figured I couldn’t help but pick up a nugget or two of valuable information.

Well, here’s what happened:

I didn’t get much rest. The conference started at 9 am each day and ran until almost 8 pm. And it was so captivating that I didn’t want to miss a word.
I hardly got to spend any time with my friends (See #1).
I picked up my nugget or two in the first 10 minutes. Five days and a whole tablet full of notes later, I looked back on the most insightful and valuable conference I ever attended.

Without going into detail, it was advertised as a business building and development conference. The organizer, Eben Pagan, walked nearly 200 attendees through the trials and tribulations he endured in building his business (and his incredible life) and how to shortcut them. Eben disclosed, step-by-step, how he built a business that triples every year. It already earns well over $2 million a month – and is still exploding. But there was more. Much more.

Why do I mention this in a life extension newsletter? Because solving the aging puzzle and delivering extreme life extension to you is as much a business and marketing challenge as a scientific one. Last week’s education is fast tracking that challenge for me. It could do the same for you, your project or your business.

If you’d like details, go to http://getaltitude.com.

Network Your Way to Immortality

Dear Future Centenarian,

Saturday evening, I enjoyed life extension and stem cell technology conversation and dinner at an incredible couple’s home. Their guests were incredible as well. Not only were they bright, well informed and enthusiastic about extreme life extension, but they were a mix of savvy and successful scientists and business people. The latter will have as much to do with your longevity as the former. Maybe more. You’ll see what I mean when you read the attached PowerPoint.

Since 2000, Maximum Life Foundation designed a scientific and financial roadmap to reverse the human aging process. The attachment illustrates an aggressive approach to solving aging in your lifetime. You’ll notice what a surprisingly small investment we think it will take. But we can back up our scientific and financial assumptions. Now it’s time to implement the plan.

AGE Breakers

Dear Future Centenarian,

Advanced glycation endproducts (AGEs) are a range of metabolic byproducts that gum up the works in your biochemistry, such as by sticking vital chemical compounds together so that they can't perform their role. The more AGEs in your system, the worse the damage they cause, directly contributing to age-related degeneration and disease:

A number of groups are at the stage of animal or early human trials with designed or discovered compounds, many focused on diabetes due to the increased level of AGEs associated with that condition, and the fact that regulatory agencies do not recognize aging as a disease - and thus will not approve a therapy designed to repair a cause of aging. For example, the AGE-breaker compound C36 has been evaluated on diabetic rats:

"Unfortunately, past evidence suggests that excitement over work in rodents should be muted at best - the history of ALT-711 or alagebrium demonstrates that different types of AGEs are important in shorter-lived mammals versus humans. So far, promising work in mice and rats has translated poorly into human therapies - in most cases, through trying to address the wrong AGEs."

Life is Everything. Death is Nothing

Dear Future Centenarian,

To seek to provide the choice of healthy longevity for all who want it is an aspect of the better side of human nature:

http://www.fightaging.org/archives/001254.php

"Helping to make life longer and better, one action at a time, is a core human ideal. There are no special cases, no magical transition point at which it's fine and dandy to write people off or justify their deaths.

Healthy life extension flows quite naturally from the same mindset that helps neighbors and appreciates modern medicine. We all recognize that which is unpleasant in commonplace life, and it's only natural to work to remove that unpleasantness. Seeking equality of opportunity by helping people to overcome the limitations of their own personal human condition is a worthy goal today, and will be just as much so in a future of far greater opportunity. The foundation of opportunity is life - is being alive, and possessed of the vigor to take advantage of that fact. Without that, there is nothing. So I think we really have to start there, with aging, a great injustice blindly inflicted upon humanity by chance, physics and evolution.

To not seek the cure for aging would be just as strange as to fail to seek a cure for cancer or Alzheimer's - it would be inhuman and unnatural for the species that helps its neighbors and appreciates the good things in life."

What is Your Life Worth… Really?

Dear Future Centenarian,

If you knew technologies over the next few decades could deliver to you a chance for an open-ended youthful lifespan, how much would you donate to the research?

Say you want to live a much longer, healthier life. Would you help to achieve that goal by donating 90% of your net worth in support of research? If so, when? When you are terminally ill when it would probably be too late? Years or decades down the road? How about now? If not, how much?

There are no right answers in consideration of personal economic choices, but these are question you might ask yourself. Wealth at any level is worthless to the dead, and being alive and healthy allows you to generate more wealth. Logically we should all be willing to devote most of our net worth to longevity research at the most effective time. If we can buy time with money - and we can begin to now in earnest, for the first time in history, by supporting the research that will lead to the first healthy life extension medicine - then we should all be in that market.

MaxLife believes the tiniest fraction of most wealthy individuals’ net worth or annual income could reverse aging in less than 30 years. It also believes most of the money could be invested… not donated… in for-profit enterprises. More on this topic in a week or two.

Who Doesn’t Want to Live Longer?

Dear Future Centenarian,

Casual deathists are everywhere. I'm sure you all know someone who responds to the concept of healthy life extension with "I can't see why anyone would want to live past 100." This is what they have been taught throughout their lives, implicit in the way their peers and parents plan, act and talk. Perhaps "learned deathism" is a better term. A longevity revolution is right around the corner, yet we structure our lives in the same way our grandparents did:

There's nothing wrong with choosing not to strive for more healthy life, but I believe it's our responsibility to at least point out the lazy assumptions and false information that forms the basis of most casual deathism. Kevin Perrott, organizer of the Edmonton Aging Symposium, recently did a sterling job of this in a letter to the Globe and Mail, reproduced in this Fight Aging! post:

http://www.fightaging.org/archives/001332.php

For Reversing Aging, SENS Makes Sense

Dear Future Centenarian,

Where has summer gone? For that matter, where have the past few years gone? Days, weeks, months and years fly by too quickly now. What did you do this past year to help insure your longevity? You most likely belong to the last generation to die “on time”, or you will be part of the first generation to escape death for aging. It’s partly your choice.

A few days ago, I started reading Aubrey de Grey’s new book, Ending Aging: The Rejuvenation Breakthroughs That Could Reverse Human Aging in Our Lifetime. If you want an education on what causes aging damage and how to fix it, I suggest you get a copy. It is fascinating, and it could help you help yourself to extreme life extension.

Go to http://www.amazon.com/Ending-Aging-Rejuvenation-Breakthroughs-Lifetime/dp/0312367066.

With Friends Like This…

Dear Future Centenarian,

Admittedly, I’m a wild eyed optimist, especially regarding the prospects of indefinite youthful lifespans for you and me. But since I KNOW I’m an optimist, I try to take special efforts to see and understand pessimists’ points of view. Ten I try to balance the input and come to my own conclusions. In other words, I try to be objective about what our chances really are. I sent you my timeline and budgetary estimates several issues ago and stand by them.

So here’s an opinion from one who may be the most pessimistic of all well known gerontologists, followed by Reason’s commentary:

http://www.fightaging.org/archives/001354.php

"'We're all going to croak,' says Richard Sprott, the Ellison Medical Foundation's director, who expects that humans may eventually live as much as 30 years longer, but only in the distant future."

Read the full post; I find it incredible that anyone with Sprott's background can stand in the midst of the present outright revolution, of wild, foaming progress in bioscience, and say that things just aren't going to change all that much. It's an outlandish position - and an outlandish position held by someone who directs a fair amount of funding for aging research:

http://www.fightaging.org/archives/001331.php

It's a sad state of affairs we're in, wherein so much of the research establishment has declared defeat and stasis before even setting goals for aging science. How is it that we have an establishment community disbursing so much in the way of funds to exactly the people who are not going to make significant progress - those who say that progress is impossible or far distant in advance of any initiative?

The advance of science and technology is change itself, is the growth of opportunity and choice, and is the opening of new doors in the halls of the human condition. The hidebound and defeatist are not really contributing - if you want things done, if you want bold new progress, fund the people willing to set goals and shake trees.


NOTE: Sprott’s stance makes we want to toss my cookies. Everyone is entitled to an opinion. In his case though, I believe it will cost lives. Lots of lives. I say that not only because he may control more of the scarce “life extension” funding than almost all the administrators and researchers in the free market combined… but also because he is influential. With 100,000 people dying every day from aging, the last thing we need is anyone standing in the way of those who refuse to “go silently into the night”.

If someone were drowning and a lifeguard stood in the way of a would-be rescuer, what would you call the lifeguard? Multiply that by millions.