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

Las Vegas Longevity Workshop

Last week, I mentioned the longevity workshop I attended in Las Vegas. This week, I’m going to illustrate how hanging out with the participants energized me, and I’m going to talk a little about the workshop itself.

First, let me tell you why it was such a positive event for me.

We had 16 attendees, plus me. Every one of them, all 16, shared a positive upbeat outlook on life.

Can you think of someone who brightens up your day by just walking into the room? Don’t you have someone in your life who you just love hanging around, someone who lifts your spirits by their mere presence? How about someone who shares your values, aspirations and plans?

OK, now roll those people into one… then multiply that person by 16. That’s who I spent the weekend with… 16 energizers.

In fact, it gets better. Half the attendees were geniuses and leaders in their respective fields. I’m totally in awe of some of them. They’re so brilliant, they totally humble me.

Now if that’s not enough, the workshop topic was something I am passionate about – life insurance!

What? Life insurance? I know, I know, you’re probably thinking I’ve gone off the deep end, or I’m some sort of closet life insurance salesman. Nothing could be further from the truth. I did in fact sell life insurance in a previous life, but that was traditional life insurance… and I hated it.

No, this workshop was about the only “pure” form of life insurance. Not the kind you can only benefit from by dying (which is actually “death insurance”), but the kind that could keep you from dying in the first place… Cryonics! More specifically, our topic was the strategy to preserve your assets if you experience clinical death, get cryonically preserved and get resuscitated. In other words, maybe you can “take it with you” after all.

If you’re not familiar with cryonics, research has shown that dying is a gradual process which starts after, not when, our hearts or brain waves stop. Our cells die gradually, over time. Cryonics is the science that halts this dying process with low-temperature technologies, stemming from the field of cryobiology.

If the cryonics rescue team reaches patients in time after legal death, they may be able to place them into suspended animation until such time as cures for what “killed” them are developed, and when age-reversal technologies are mature. At that time, they plan on fixing you and waking you up.

A long-shot? Maybe. Whacky? If you think so, consider this:

Cryonics depends largely on two technologies. One is cryobiology, a well-proven field that deals with ultra-low temperatures. In this case, that means storing human tissue at liquid nitrogen temperatures for future therapies. This has been routinely done for many years.

The other is neurobiology, again, a totally legitimate and non-controversial field.

So it follows that it is just as legitimate to store and recover the brain (where your memory resides) as it is to store and recover any other tissue. So cryonics should work.

Then we add another emerging, and soon to be maturing tool… regenerative medicine. We’re already growing replacement organs, and soon, they promise to be as good, or even better than the originals. You have read a lot about this in previous issues of this newsletter. Again, a well-accepted field.

As these technologies are fine-tuned, they may be more than enough for resuscitating patients. But there’s more.

Another technology that may be enormously helpful for even more perfect rescue from suspension is nanotechnology. There’s already more work in this field than I can ever hope to keep up with. Full-blown nanomedicine may be developed in as little as 19 years.

So you might look at cryonics as the purest form of life insurance. Insurance is something you hope you never need but are glad you have when you do need it… when it is no longer for sale.
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LATEST HEALTHY LIFE EXTENSION HEADLINES

Progress in Bypassing Mitochondrial Damage (September 05 2008) http://www.eurekalert.org/pub_releases/2008-09/cp-gtp082808.php
Allotopic expression of genes normally found in mitochondrial DNA is a core portion of the Strategies for Engineered Negligible Senescence. It is the process of inserting a copy of vital mitochondrial genes into the cell nucleus, and then figuring out how to get the proteins produced by those genes back to the mitochondria where they are needed. This could eliminate the contribution of mitochondrial DNA damage to aging. A technique for doing all this is now demonstrated in rats: "We obtained a complete and long-term restoration of mitochondrial function in human fibroblasts in which the mitochondrial genes ATP6, ND1, and ND4 were mutated. ND1 and ND4 are mutated in nearly all cases of Leber hereditary optic neuropathy (LHON). LHON is the most common mitochondrial disorder and is characterized by a loss of vision. They introduced the human ND4 gene with the mutation present in the majority of LHON patients into rat eyes. The treatment caused retinal ganglion cells (RGCs) to degenerate significantly when compared to those from control eyes and was associated with decreased visual performance. Importantly, reintroducing normal ND4 led to prevention of RGC loss and visual impairment, effectively rescuing the animals from impending blindness. These data represent the 'proof of principle' that optimized allotropic expression is effective in vivo and can be envisaged as a therapeutic approach for mtDNA-related diseases."

Reactive Carbonyl Species, ALEs, and Aging (September 04 2008) http://pmid.us/18721793
Free radicals (such as reactive oxygen species) are increasingly generated with age - this is the end of a long chain of consequences that starts with damaged mitochondrial DNA. How do those oxidizing agents actually cause widespread harm to bodily systems? This paper gives an overview of one broad set of mechanisms, wherein step one is the creation of reactive carbonyl species (RCS) by free radicals: "Most of the biological effects of RCS [are] due to their capacity to react with cellular constituents, forming advanced lipoxidation end-products (ALEs). Compared to reactive oxygen and nitrogen species, lipid-derived RCS are stable and can diffuse within or even escape from the cell and attack targets far from the site of formation. Therefore, these soluble reactive intermediates, precursors of ALEs, are not only cytotoxic per se, but they also behave as mediators and propagators of oxidative stress and cellular and tissue damage. The causal role of ALEs in aging and longevity is inferred from the findings that follow: a) its accumulation with aging in several tissues and species; b) physiological interventions (dietary restriction) that increase longevity, decrease ALEs content; c) the longer the longevity of a species, the lower is the lipoxidation-derived molecular damage; and finally d) exacerbated levels of ALEs are associated with pathological states."

Update on the Longevity Science Amex Members Project (September 04 2008) http://blog.methuselahfoundation.org/2008/09/an_update_on_your_votes_and_un.html
From the Methuselah Foundation blog: "I'm pleased to say that the pro-longevity science community rallied to vote the Amex Members Project submission "Undergrads Fighting Age Related Disease" into the top 25 projects by vote totals - and made it the most discussed project of all. Thank you! That discussion is still ongoing, by the way, and people unfamiliar with longevity research have questions about the project. Feel free to jump in and help answer them. What comes next? Well, between now and September 9th - less than a week away - the Members Project advisory panel will look at the projects, votes, and discussions, and announce the final 25. Those 25 projects will be voted on by Amex card holders to determine which 5 will be funded. So, all you generous folk who rounded up your friends and spread the word: we're going to do it all again for those with American Express cards starting on the 9th. We here at the Methuselah Foundation are looking forward to it!"

Another Regenerative Strategy for Hearing Loss (September 03 2008) http://www.eurekalert.org/pub_releases/2008-09/ctco-hrm090308.php
Following on from the gene therapy approach for age-related deafness mentioned a few days ago, here's a cell-based therapy via EurekAlert!: "hearing loss due to cochlear damage may be repaired by transplantation of human umbilical cord hematopoietic stem cells. The team used animal models in which permanent hearing loss had been induced by intense noise, chemical toxicity or both. Cochlear regeneration was only observed in animal groups that received HSC transplants. Researchers used sensitive tracing methods to determine if the transplanted cells were capable of migrating to the cochlea and evaluated whether the cells could contribute to regenerating neurons and sensory tissue in the cochlea. Our findings show dramatic repair of damage with surprisingly few human-derived cells having migrated to the cochlea. A fraction of circulating HSC fused with resident cells, generating hybrids, yet the administration of HSC appeared to be correlated with tissue regeneration and repair as the cochlea in non-transplanted mice remained seriously damaged."

Metformin as Calorie Restriction Mimetic (September 02 2008)
http://pmid.us/18728386
This paper is illustrative of the thinking that leads to trying anti-diabetic drugs as calorie restriction mimetics: "Studies in mammals have led to the suggestion that hyperglycemia and hyperinsulinemia are important factors both in aging and in the development of cancer. It is possible that the life-prolonging effects of calorie restriction are due to decreasing IGF-1 levels. A search of pharmacological modulators of
insulin/IGF-1 signaling pathway (which resemble effects of life span extending mutations or calorie restriction) could be a perspective direction in regulation of longevity. Antidiabetic biguanides are most promising among them. Here we show the chronic treatment of female outbred SHR mice with metformin (100 mg/kg in drinking water) slightly modified the food consumption but decreased the body weight after the age of 20 months, slowed down the age-related switch-off of estrous function, increased mean life span by 37.8%, mean life span of last 10% survivors by 20.8%, and maximum life span by 2.8 months (+10.3%) in comparison with control mice." Full calorie restriction does better than that (30-40% maximum life span extension), but this is a strong argument for its effects on insulin metabolism to be one cause of enhanced health and longevity.

Another Human Longevity Gene Association (September 02 2008) http://www.telegraph.co.uk/earth/main.jhtml?view=DETAILS&grid=&xml=/earth/2008/09/01/sciage101.xml
The Telegraph reports on confirmation that a class of longevity genes indentified in lower animals also has an effect on human populations: "The gene linked with better health and a longer life is called FOXO3A and although similar genes have been shown to prolong life span in other species, this is the first time that FOXO has been linked directly to longevity in humans. Each gene comes in two copies and the team found the longevity effect of this letter was additive: those with one copy doubled their odds of living an average 98 years. Men who had two G copies did even better and almost tripled their odds of living nearly a century, and were markedly healthier at older ages. We screened 213 of the long-lived participants' DNA and 402 of the average-lived, focusing on five genes. These genes were selected for good reason because they involved in the insulin pathway and signaling, which studies of other animals have shown is linked with longevity." This doesn't tell us laypeople more than we already knew: that insulin metabolism is significant in health and longevity variations within a species.

On the Way to Controlling Telomerase (September 01 2008) http://www.eurekalert.org/pub_releases/2008-08/twi-lso082608.php
Researchers are making progress in figuring how to control telomerase, and through it influence telomeres, cancer, and aging. From EurekAlert!: Researchers "have deciphered the structure of the active region of telomerase, an enzyme that plays a major role in the development of nearly all human cancers. The landmark achievement opens the door to the creation of new, broadly effective cancer drugs, as well as anti-aging therapies. Researchers have attempted for more than a decade to find drugs that shut down telomerase - widely considered the No. 1 target for the development of new cancer treatments - but have been hampered in large part by a lack of knowledge of the enzyme's structure. The findings [should] help researchers in their efforts to design effective telomerase inhibitors. Telomerase is an ideal target for chemotherapy because it is active in almost all human tumors, but inactive in most normal cells. That means a drug that deactivates telomerase would likely work against all cancers, with few side effects." Long-term deactivation will cause massive issues, of course, but that's not the intent for the moment. Given new information about telomerase and mitochondria in aging, there are potentially more interesting end results than good cancer therapies.

Two Kinds of Friends

I divide my close friends into two general groups.

1. The Miscellaneous Group: This includes lifelong friends as well as recent acquaintances. I share either/or history and some values with this group. I see some frequently but most infrequently. All-in-all, group is shrinking in size. That’s because many of us have grown or are growing apart. In other words, we don’t have much in common anymore. And outside of rehashing old times (which I find more-and-more boring), hanging out together is pretty much a waste of time. The few that I do enjoy spending with share common goals and typically look forward rather than backwards.

2. Life Extensionists/Futurists: This is my favorite and larger group of the two. It’s also expanding rapidly. It’s rare to hear these members talking of the past, and they are far more stimulating. They typically live actively in the present with long-term positive views of the future. And for the most part, they do their best to insure a profound future for all of us. They may take various paths and contribute in a number of ways such as doing research, volunteering for various future-focused movements, building positive value-laced enterprises, running companies and foundations, marketing positive products and services and actively participating in events, seminars and workshops that point toward noble goals such as (my favorite) radical life extension.

All too often, I get bogged down in the sea of minutia and the distractions of business and life that tends to bury us if we’re not constantly on guard. One of the challenges in my life is to evaporate that sea to a puddle. I’m gradually succeeding, but I’m not there yet. So when I have the chance to shut everything else out and spend time with Group #2, it breathes new life into me. I enjoyed that pleasure the past two weekends.

Two weeks ago, I and a couple of M.D.s got to address a group of life extensionists.

Pure rapture.

Just associating with like-minded people energizes me beyond description. It also validates and reinforces my resolve to conquer aging in our lifetimes.

This past Saturday, I took part in a life extension workshop in Las Vegas. The personal and business challenges that sometimes consume me did not enter my mind the entire weekend. How could they? Almost every minute was spent with some very close friends and with some not as close, but still enormously treasured acquaintances. Every single one of them shares most of my deepest goals and aspirations.

Most people take a two week or longer vacation to recharge. For me, it only takes a day in the company of members of Group #2. If you consider yourself a member of this group, you’re invited to a get-together at my home in Huntington Beach, CA, tentatively scheduled for Sat, Nov 22nd. If so, email me for directions and a final date and time.

Next week I’ll tell you a little about last weekend’s workshop.
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LATEST HEALTHY LIFE EXTENSION HEADLINES

Thinking About Replacing the Brain (August 29 2008) http://www.memebox.com/futureblogger/show/827-our-future-brain-damage-resistant-with-unique-new-abilities
Some thoughts on the decades following the biotechnology revolution from FutureBlogger: Once nanotechnology is as far advanced as biotechnology is today, what sorts of capabilities start to look plausible? "By the mid-2030s, we could be replacing brain cells with damage-resistant nanomaterials that process thoughts much faster than today's biological brains. The new brain would include our same consciousness, memories and personality that existed before the conversion, but it would run much faster and would increase our memory a thousand-fold. A daily pill would supply nanomaterials and instructions for nanobots to format new neurons and position them next to existing biological brain cells to be replaced. These changes would be unnoticeable to us, but within six months, we would be enjoying our new brain. Should a person with the new damage-resistant brain die in an accident, their body could be a total loss, but the brain would survive. Biological brains die within minutes after the heart stops; our new brain will simply turn itself off and wait for a new power supply. All memories and consciousness would remain intact after a fatal accident. Rescue workers would remove the brain from the deceased body and reinstall it into a newly-cloned body." A lot of work remains to be accomplished before the golden future becomes a reality - first things first.

Vote For Amex Funding For Longevity Science (August 28 2008) http://www.membersproject.com/project/view/BVVE2C
The Methuselah Foundation volunteers are looking for more signatures in the next five days to help put the "Undergrads Fighting Age Related Disease" project high in the top 25 Amex Members Projects - and thus eligible for some of the $2.5 million in funding offered by American Express. There are five days left to put your name to this project in support: 1200 signatures have been gathered in the past two weeks, putting longevity science solidly in the running. At least that many more votes are needed before voting closes - which is where you and your friends come in. Visit the Methuselah Foundation blog or the project Facebook group to find out how to sign up - or just click through to this project and follow the directions. You don't have to be an American Express member, but you do have to be a US resident. One last thing: it's important to note that of all the projects submitted to date, Undergrads Fighting Age Related Disease has by far the most comments. This counts heavily in the final selection, so jump into the project comments section and tell the world why you support longevity science and the defeat of age-related disease.

Another Advance In Reprogramming Cells (August 28 2008) http://www.sciencedaily.com/releases/2008/08/080828082819.htm
As ScienceDaily notes, researchers "report having achieved what has long been a dream and ultimate goal of developmental biologists - directly turning one type of fully formed adult cell into another type of adult cell. The team is able to turn mouse exocrine cells, which make up about 95 percent of the pancreas, into precious and rare insulin-producing beta cells. Unlike the process involved in creating induced pluripotent stem cells (iPS) [this] direct reprogramming technique does not require turning adult cells into stem cells and then figuring out how to induce them to differentiate into a desired cell type. We're intrigued by the possibility that this approach, which has worked for pancreatic insulin-producing cells, could be more widely applied to many kind of cells, especially those that are lost in disease or following injury. And at the same time, we are exploring the possibility of using this general approach in a clinical context to make new beta cells for patients."

An Interview With Doug Melton (August 27 2008) http://www.technologyreview.com/printer_friendly_article.aspx?id=21307
The Technology Review interviews researcher Doug Melton: "If a patient has Parkinson's disease, their dopamine-producing cells are gone. We don't understand anything about what makes those cells go away - the field is kind of stuck because you can't watch the progression of the disease. Stem cells can make neurons in a dish. Imagine you have iPS cells from a healthy person and from a Parkinson's patient. If you make dopamine neurons from both sets of cells in separate dishes, you can look at what went wrong with the diseased stem cell. The same approach will work with different degenerative diseases, such as diabetes or ALS. I think it will change the way degenerative diseases are studied - we'll reduce the whole process of disease to a petri dish. Within a few years, researchers the world over should have access to disease-specific cells that can be turned into cell types defective in a particular disease. Science clearly works best when you have a lot of bright, motivated people working on these problems. The institute has sent thousands of human embryonic stem-cell lines to hundreds of labs all over the world. We like to think that has been helpful in encouraging basic research on embryonic stem cells."

Microglia Versus Alzheimer's (August 26 2008) http://www.sciencedaily.com/releases/2008/08/080825194705.htm
Researchers are attempting to convince the body's defenses to attack the amyloid plaques of Alzheimer's disease (AD): "by stimulating a brain cell called a microglia the cells will partially engulf the senile plaques ... [this is] the first time that this phenomenon, believed to take place in living brain, has been duplicated in the laboratory. The plaques themselves are not sufficient microglial activators. But when the microglia were treated with inflammatory stimulants, they attacked the plaques. In AD patients, microglia are not coping with the plaque build-up. Therefore plaques accumulate faster than the microglia can digest them. If we can enhance microglial digestion of these plaques, we will have a fighting chance to eliminate AD. The next step is to find a therapeutic drug that will stimulate the microglia to devour the plaques." Time will tell whether new methods of

The Bad Trends (August 25 2008) http://www.futurepundit.com/archives/005479.html
There are plenty of good trends in medicine research and development. The trend in bioinformatics and computational power, for example. Unfortunately, some of the bad trends are blocking movement of research into the clinic. Via FuturePundit: "Why do terminally ill patients have to wait so long to get access to the only treatments that hold any promise of saving their lives? And why is it not their right to decide? The FDA approved just 16 new drugs last year, and is on pace to approve only 18 this year. That's down from a high of 53 in 1996 and 39 in 1997. This trend does not bode well for the development of rejuvenation therapies. The FDA will hold off approval of an anti-cancer drug for people who have a fatal disease. Never mind that people who have a fatal disease are going to die anyway. The FDA won't let people take a risk when they have little to lose. That makes no sense to me. Rejuvenation therapies are going to treat that fatal disease called aging. Absent those therapies we are all going to die from complications of aging. Faced with rising risks of death combined with increasing pain and disablement people should be given wider latitude to try new and unproven therapies." The FDA should turn down completely; it is a roadblock to progress, and the cause of great and ongoing suffering.

Two Groups of Friends

I divide my close friends into two general groups.

1. The Miscellaneous Group: This includes lifelong friends as well as recent acquaintances. I share either/or history and some values with this group. I see some frequently but most infrequently. All-in-all, group is shrinking in size. That’s because many of us have grown or are growing apart. In other words, we don’t have much in common anymore. And outside of rehashing old times (which I find more-and-more boring), hanging out together is pretty much a waste of time. The few that I do enjoy spending with share common goals and typically look forward rather than backwards.

2. Life Extensionists/Futurists: This is my favorite and larger group of the two. It’s also expanding rapidly. It’s rare to hear these members talking of the past, and they are far more stimulating. They typically live actively in the present with long-term positive views of the future. And for the most part, they do their best to insure a profound future for all of us. They may take various paths and contribute in a number of ways such as doing research, volunteering for various future-focused movements, building positive value-laced enterprises, running companies and foundations, marketing positive products and services and actively participating in events, seminars and workshops that point toward noble goals such as (my favorite) radical life extension.

All too often, I get bogged down in the sea of minutia and the distractions of business and life that tends to bury us if we’re not constantly on guard. One of the challenges in my life is to evaporate that sea to a puddle. I’m gradually succeeding, but I’m not there yet. So when I have the chance to shut everything else out and spend time with Group #2, it breathes new life into me. I enjoyed that pleasure the past two weekends.

Two weeks ago, I and a couple of M.D.s got to address a group of life extensionists.

Pure rapture.

Just associating with like-minded people energizes me beyond description. It also validates and reinforces my resolve to conquer aging in our lifetimes.

This past Saturday, I took part in a life extension workshop in Las Vegas. The personal and business challenges that sometimes consume me did not enter my mind the entire weekend. How could they? Almost every minute was spent with some very close friends and with some not as close, but still enormously treasured acquaintances. Every single one of them shares most of my deepest goals and aspirations.

Most people take a two week or longer vacation to recharge. For me, it only takes a day in the company of members of Group #2. If you consider yourself a member of this group, you’re invited to a get-together at my home in Huntington Beach, CA, tentatively scheduled for Sat, Nov 22nd. If so, email me for directions and a final date and time.

Next week I’ll tell you a little about last weekend’s workshop.
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LATEST HEALTHY LIFE EXTENSION HEADLINES

Thinking About Replacing the Brain (August 29 2008) http://www.memebox.com/futureblogger/show/827-our-future-brain-damage-resistant-with-unique-new-abilities
Some thoughts on the decades following the biotechnology revolution from FutureBlogger: Once nanotechnology is as far advanced as biotechnology is today, what sorts of capabilities start to look plausible? "By the mid-2030s, we could be replacing brain cells with damage-resistant nanomaterials that process thoughts much faster than today's biological brains. The new brain would include our same consciousness, memories and personality that existed before the conversion, but it would run much faster and would increase our memory a thousand-fold. A daily pill would supply nanomaterials and instructions for nanobots to format new neurons and position them next to existing biological brain cells to be replaced. These changes would be unnoticeable to us, but within six months, we would be enjoying our new brain. Should a person with the new damage-resistant brain die in an accident, their body could be a total loss, but the brain would survive. Biological brains die within minutes after the heart stops; our new brain will simply turn itself off and wait for a new power supply. All memories and consciousness would remain intact after a fatal accident. Rescue workers would remove the brain from the deceased body and reinstall it into a newly-cloned body." A lot of work remains to be accomplished before the golden future becomes a reality - first things first.

Vote For Amex Funding For Longevity Science (August 28 2008) http://www.membersproject.com/project/view/BVVE2C
The Methuselah Foundation volunteers are looking for more signatures in the next five days to help put the "Undergrads Fighting Age Related Disease" project high in the top 25 Amex Members Projects - and thus eligible for some of the $2.5 million in funding offered by American Express. There are five days left to put your name to this project in support: 1200 signatures have been gathered in the past two weeks, putting longevity science solidly in the running. At least that many more votes are needed before voting closes - which is where you and your friends come in. Visit the Methuselah Foundation blog or the project Facebook group to find out how to sign up - or just click through to this project and follow the directions. You don't have to be an American Express member, but you do have to be a US resident. One last thing: it's important to note that of all the projects submitted to date, Undergrads Fighting Age Related Disease has by far the most comments. This counts heavily in the final selection, so jump into the project comments section and tell the world why you support longevity science and the defeat of age-related disease.

Another Advance In Reprogramming Cells (August 28 2008) http://www.sciencedaily.com/releases/2008/08/080828082819.htm
As ScienceDaily notes, researchers "report having achieved what has long been a dream and ultimate goal of developmental biologists - directly turning one type of fully formed adult cell into another type of adult cell. The team is able to turn mouse exocrine cells, which make up about 95 percent of the pancreas, into precious and rare insulin-producing beta cells. Unlike the process involved in creating induced pluripotent stem cells (iPS) [this] direct reprogramming technique does not require turning adult cells into stem cells and then figuring out how to induce them to differentiate into a desired cell type. We're intrigued by the possibility that this approach, which has worked for pancreatic insulin-producing cells, could be more widely applied to many kind of cells, especially those that are lost in disease or following injury. And at the same time, we are exploring the possibility of using this general approach in a clinical context to make new beta cells for patients."

An Interview With Doug Melton (August 27 2008) http://www.technologyreview.com/printer_friendly_article.aspx?id=21307
The Technology Review interviews researcher Doug Melton: "If a patient has Parkinson's disease, their dopamine-producing cells are gone. We don't understand anything about what makes those cells go away - the field is kind of stuck because you can't watch the progression of the disease. Stem cells can make neurons in a dish. Imagine you have iPS cells from a healthy person and from a Parkinson's patient. If you make dopamine neurons from both sets of cells in separate dishes, you can look at what went wrong with the diseased stem cell. The same approach will work with different degenerative diseases, such as diabetes or ALS. I think it will change the way degenerative diseases are studied - we'll reduce the whole process of disease to a petri dish. Within a few years, researchers the world over should have access to disease-specific cells that can be turned into cell types defective in a particular disease. Science clearly works best when you have a lot of bright, motivated people working on these problems. The institute has sent thousands of human embryonic stem-cell lines to hundreds of labs all over the world. We like to think that has been helpful in encouraging basic research on embryonic stem cells."

Microglia Versus Alzheimer's (August 26 2008) http://www.sciencedaily.com/releases/2008/08/080825194705.htm
Researchers are attempting to convince the body's defenses to attack the amyloid plaques of Alzheimer's disease (AD): "by stimulating a brain cell called a microglia the cells will partially engulf the senile plaques ... [this is] the first time that this phenomenon, believed to take place in living brain, has been duplicated in the laboratory. The plaques themselves are not sufficient microglial activators. But when the microglia were treated with inflammatory stimulants, they attacked the plaques. In AD patients, microglia are not coping with the plaque build-up. Therefore plaques accumulate faster than the microglia can digest them. If we can enhance microglial digestion of these plaques, we will have a fighting chance to eliminate AD. The next step is to find a therapeutic drug that will stimulate the microglia to devour the plaques." Time will tell whether new methods of

The Bad Trends (August 25 2008) http://www.futurepundit.com/archives/005479.html
There are plenty of good trends in medicine research and development. The trend in bioinformatics and computational power, for example. Unfortunately, some of the bad trends are blocking movement of research into the clinic. Via FuturePundit: "Why do terminally ill patients have to wait so long to get access to the only treatments that hold any promise of saving their lives? And why is it not their right to decide? The FDA approved just 16 new drugs last year, and is on pace to approve only 18 this year. That's down from a high of 53 in 1996 and 39 in 1997. This trend does not bode well for the development of rejuvenation therapies. The FDA will hold off approval of an anti-cancer drug for people who have a fatal disease. Never mind that people who have a fatal disease are going to die anyway. The FDA won't let people take a risk when they have little to lose. That makes no sense to me. Rejuvenation therapies are going to treat that fatal disease called aging. Absent those therapies we are all going to die from complications of aging. Faced with rising risks of death combined with increasing pain and disablement people should be given wider latitude to try new and unproven therapies." The FDA should turn down completely; it is a roadblock to progress, and the cause of great and ongoing suffering.
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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/.