New "Miracle" Anti- Aging Products

It was a fun week.

I just returned from a large annual anti-aging conference and trade show. Every year unveils new “miracle” anti-aging products. Doctors and others lectured for almost a week, and the trade show lasted three days. Thousands attended, mostly physicians.

It was an interesting mix of practitioners, serious scientists, some serious and not so serious participants and a few hundred companies and individuals promoting a huge mix of anti-aging products and services.

I especially enjoyed meeting new people in this exciting field and getting together with old friends. Saturday evening was most stimulating, because I had a chance to take part in brain-stretching discussions with very legitimate scientists, physicians and activists at a private event. We even had a chance to discuss some of the newer products and services on the market. Some credible, backed by scientific studies. Some were worthless snake oil. And there were a whole lot in between that I just couldn’t figure out. I’m not the only one either.

So out of the hundreds or thousands of anti-aging products displayed at shows like this… or especially on the Internet, how do you know what works and what doesn’t? That’s an important question, since your life may depend on it.

How’s that? Your life?

Sure. And here’s why.

As you’ve heard me say over and over, we are going to be able to reverse the damage aging does to you one of these days. And when that happens, you, if you are still alive, could be transformed from the old person you are growing into, to a twenty-something improved version of your former self. And then, you will essentially have a youthful open-ended lifespan ahead of you.

But whether or not you live long enough to see that day could be largely up to you. Don’t forget, your genes only account for 25-35% of your destiny. (And science is working on fixing that 25-35% too.) You largely control the rest.

That’s why knowing which supplements or medical treatments work, and which don’t, might save your life. The extra few or more years the effective ones could add to your lifespan could very well be the difference between your living long enough to take advantage of tomorrow’s life extending miracles… or just barely missing out.

I had a very interesting conversation with two separate gentlemen at the event which led me to a conclusion. Maximum Life Foundation may be positioned to filter most of the anti-aging claims and information that overwhelm us. If we can find out what actually works and what doesn’t, then you will have a handy source of information. It will take several months to work out the details and to determine if we have the time to do this. And if we or someone else can, you will benefit.

Meanwhile, I just finished my longevity book, Life Extension Express, "7 steps you can take now, to catch the emerging wave of medical breakthroughs… for a youthful, indefinite (yes, indefinite) lifespan."

You can get a big jump on boosting your longevity by reading it. You’ll be able to get a copy from Amazon soon, but better yet, you can have a FREE downloadable copy by going to www.MaxLife.org now.
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LATEST HEALTHY LIFE EXTENSION HEADLINES

Gene Therapy Versus Periodontitis and Arthritis (December 12 2008) http://www.eurekalert.org/pub_releases/2008-12/uom-gte121008.php
Via EurekAlert!: "Using gene therapy, [researchers] found a way to help certain cells using an inactivated virus to produce more of a naturally-produced molecule soluble TNF receptor. This factor is under-produced in patients with periodontitis. The molecule delivered by gene therapy works like a sponge to sop up excessive levels of tumor necrosis factor, a molecule known to worsen inflammatory bone destruction in patients afflicted with rheumatoid arthritis, joint deterioration and periodontitis. Targeted Genetics released human trial results that showed the same gene therapy approach [had] positive affects in human patients with rheumatoid arthritis. The company tested 127 human subjects and showed a 30 percent improvement in pain relief, and gain of function, among other enhancements using the gene treatment. The gene also delivers quite a bit of genetic bang for the buck. The periodontal tissues were spared from destruction by more than 60-80 percent with the use of gene therapy. If you deliver the gene into the target cells once, it keeps producing in the cells for a very long period of time or potentially for the life of the patient. This therapy is basically a single administration, but it could have potentially life-long treatment effects in patients who are at risk for severe disease activity."

Manipulating Heart Cells into Regeneration (December 11 2008) http://www.eurekalert.org/pub_releases/2008-12/haog-hra121108.php
Via EurekAlert!: "Up until today scientists assumed that the adult heart is unable to regenerate. Now, researchers and cardiologists [have] been able to show that this dogma no longer holds true. [They] were able to show that the body`s own heart muscle stem cells do generate new tissue and improve the pumping function of the heart considerably in an adult organism, when they suppress the activity of a gene regulator known as beta-catenin [which] plays an important role in the development of the heart in embyros. [Researchers] could now show that beta-catenin is also important for the regeneration of the adult heart. They suppressed this factor in the nucleus of the heart cells in mice. This way they activated heart precursor cells (stem cells) to turn on the regeneration of heart in adult mice. Four weeks after blocking beta-catenin, the pumping function of the heart of the animals had improved and the mice survived an infarction much better than those animals with a functioning beta-catenin gene."

CR Mimetics Are Not CR (December 10 2008) http://pmid.us/19056839
By way of a reminder that there's still a world of difference between calorie restriction (CR) and a CR mimetic drug that reproduces some of the same observed biochemical changes: "resveratrol may produce calorie restriction-like effects on metabolic and longevity endpoints in mice. In this study, we sought to determine whether resveratrol treatment elicited other hallmark changes associated with calorie restriction, namely bradycardia and decreased body temperature. We found that during short-term treatment, wild-type mice on a calorie-restricted diet experienced significant decreases in both heart rate and body temperature after only 1 day whereas those receiving resveratrol exhibited no such change after 1 [week]. We also used [obese] mice to study the effects of long-term treatment because previous studies had indicated the therapeutic value of resveratrol against the linked morbidities of obesity and diabetes. After 12 [weeks], resveratrol treatment had produced no changes in either heart rate or body temperature. Strikingly, and in contrast to previous findings, we found that resveratrol-treated mice had significantly reduced endurance in a treadmill test. We conclude that the bradycardia and hypothermia associated with calorie restriction occur through mechanisms unaffected by the actions of resveratrol."

Another Approach to Restoring Hair Cells (December 10 2008) http://www.google.com/hostednews/ukpress/article/ALeqM5hI6vwfg3SuetvGrNdvVr1wKBUq6Q
Researchers are exploring a range of options to restore the hair cells of the ear that are lost with age, leading to deafness: "Damage to hair cells in the inner ear due to ageing and overstimulation is a major cause of deafness, affecting 10% of the worldwide population. The cell loss is irreversible because the cells have a limited capacity to regenerate. However, a new study suggests that the ependymal layer of the lateral ventricle of the brain contains stem cells which share characteristics with inner ear hair cells and which have the potential to reproduce. According to the scientists, these cells could potentially be transplanted from a person's brain into their ear, where they would undergo a functional switch to enable them to replace the damaged ones. The authors concluded that transplanted cells could alter their functions to work as inner ear hair cells and thus restore hearing. They suggested their findings on the flexible function of certain cells could also be extended to offer treatment for other problems affecting the nervous system."

Hourglass VI (December 09 2008)
http://ouroboros.wordpress.com/2008/12/09/hourglass-vi-a-carnival-of-biogerontology/
The sixth edition of the Hourglass blog carnival on aging and longevity science is up at Ouroboros. One of the linked posts is a series of thoughts on the way in which we humans cut ourselves short by discounting the
future: "The best example of human’s irrational dealing with the future is what is called hyperbolic discounting (also called: temporal discounting, or future discounting). Hyperbolic discounting is the human preference for small immediate reward over larger future payoffs. The further the time in the future of the reward the greater the discounting. Humans are generally bad at delaying rewards and hence we too easily take the immediate smaller reward rather than delaying our immediate gratification for a greater reward in the future. I propose here that unless humans soon become better at thinking about the future - and not discounting it so much - we might not be able to make the changes we need for a better world and society. The same could be said about longevity research - if we can not imagine ourselves living longer and healthier lives - and not imagine it as only happening to a 'stranger' we [are] unlikely as a society to invest in this imagined future."

Newsweek on Mainstream Longevity Science (December 08 2008) http://www.newsweek.com/id/172561/output/print
Newsweek has a general interest article up online on the topic of mainstream longevity science: projects aimed at the hard target of metabolic manipulation to slow aging. "Since the days of Ponce de Leon, if not before, people have been seeking the elusive Fountain of Youth. Until recently, such pursuits were the realm of quacks and charlatans. And there are still plenty of snake-oil salesmen out there on the Internet and in so-called anti-aging clinics, hawking everything from longevity-bestowing Ecuadoran waters (which are probably harmless) to growth hormones (which could be downright dangerous for adults). But serious scientists are now bringing respectability to the field, unraveling the secrets of aging on a cellular level and looking for ways to slow it down. And while the science is still young (so to speak), legitimate longevity-boosting treatments could be available in 10 to 15 years - although the gains would be [modest]. Some critics of the scientific quest for longevity say it's God's will that we should die when our time comes. But in the past century, a clean water supply, antibiotics, vaccines and improved medical care have boosted life expectancy at birth by roughly 50 percent in the United States - from 48 for men and 51 for women in 1900 to 75 for men and 80 for women today. No one seems to object to that."

A Viral Cause for Alzheimer's? (December 08 2008) http://www.sciencedaily.com/releases/2008/12/081207134109.htmThis release via EurekAlert! is very compelling - but how does it fit in with the good evidence that Alzheimer's is a form of diabetes? "The virus behind cold sores is a major cause of the insoluble protein plaques found in the brains of Alzheimer's disease [AD] sufferers. [researchers] investigated the role of herpes simplex virus type 1 (HSV1) in AD. Most people are infected with this virus, which then remains life-long in the peripheral nervous system. HSV1 DNA is located very specifically in amyloid plaques: 90% of plaques in Alzheimer's disease sufferers' brains contain HSV1 DNA, and most of the viral DNA is located within amyloid plaques. The team had previously shown that HSV1 infection of nerve-type cells induces deposition of the main component, beta amyloid, of amyloid plaques. Together, these findings strongly implicate HSV1 as a major factor in the formation of amyloid deposits and plaques, abnormalities thought by many in the field to be major contributors to Alzheimer's disease."

A Valuable Lesson

As promised, I’m going to pass on a valuable lesson from Dr. Pete Hilgartner.

What is your first reaction to a crisis? Let’s say you get diagnosed with a serious illness. First your heart skips a beat and then thunders like a jackhammer. Maybe you break out in a cold sweat. Then when reality sets in, do you retreat? Do you roll up in a fetal position, pull the covers over your head and hope your problems disappear? Do you tend to sleep more, head for the liquor cabinet or pray harder than you had in years?

How about when you life’s savings gets wiped out overnight due to mismanagement, theft, the economy or just by hard luck?

Or what do you do when the economy slows down, and your customers’ orders slow to a trickle, or you get laid off?

What about when all the real estate equity you built over the years vanishes overnight?

Time to retreat, right? Batten down the hatches. Cut expenses. Downsize. Deprive yourself until things get better. That’s what most people do, and that’s one reason the press tells you our economy sucks.

What if there was a better way to handle crises? Well there is. In fact there are two. The first is offered up by Dr. Pete. The second by yours truly.

Dr. Pete is a fascinating guy and a successful student of life. He was very sickly as a child, way sicker than most people could tolerate. But his illnesses motivated him to set lofty goals. He decided to win an Olympic gold metal, to become an officer in the Marine Corps and to become a physician. He was well on his way to a shot at the gold when his aching back tripped him up. So he joined the Marines and later became a successful physician.

The Marines taught him one of life’s great lessons. They taught him how to survive an ambush.

Capt. Pete survived six ambushes in fact. He realized he survived them the same way he survived his childhood injuries and the same way he’s surviving today’s economic climate. When you’re ambushed, the Marines teach you to head for an escape route. But what is there is none? What do you do when the enemy closes off all escape? Then you make yourself as small a target as possible, right? Wrong!

If you want to escape, to survive, you do the counter-intuitive. You do the unexpected. You expand… and attack. But don’t just sort of expand. Expand with decisiveness, purpose, order and with a plan. Play offense instead of defense. Overcome your fear and take the fight to the enemy. Dr. Pete and most of the company he commanded live today because of that one critical lesson.

Have you noticed that when people are filled with fear, they tend to withdraw? They stop communicating. If they do communicate, it’s usually to complain about how bad things are. When you’re down, be a beacon of optimism. Take charge of your situation. Every cell in your body will react and rally you to your recovery.

Can you force yourself to expand, when every fiber of your existence wants to do what everyone else is doing; succumbing and contracting to fear? Yes, you can!

I have another way to not only survive, but to prosper as well. It’s your surest path to sound health and longevity. In a word, it’s “prevention”. Expand now, and avoid your ambushes. Head off disease and illness by taking precautionary measures now and forever.

It’s a well-known fact that people will go to the ends of the earth searching for cures but will ignore preventative measures. Terminal diseases and what is happening now are concretes. The threat of disease and the future are abstracts. So we live for the moment while internal time bombs tick away. Sooner or later, one catches up with you. And more often than not, it’s too late. If you catch it early enough and/or expand and attack, you have a chance to beat it back. But not all of Capt. Pete’s soldiers got out alive.

Will tomorrow’s technologies obsolete death from aging and other diseases? I’m certain of it. Will we all live to see the day? Unfortunately, no. And most of those who miss the extreme longevity boat will miss it because of inattention to prevention. Some will make it because they will expand when their crisis catches up with them. But with so much at stake, why roll the dice? Play to win, not to not lose. Expand right now, before it’s too late.

Now getting back to reacting to a health crisis. I’m afraid I have some terrible news for you. You have a terminal disease that no one has ever survived. You were born with it, and you too will die from it – unless you improve your odds by expanding and by preventing. It’s called aging. Instead of complaining about it, or even joking about it, for the first time in history, you can actually do something about it. One contribution many of us can make is supporting the research that will conquer the effects of aging while you are still alive. The other is simply taking a proactive approach to your health to keep yourself alive until emerging medical miracles will give you a new lease on life.
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LATEST HEALTHY LIFE EXTENSION HEADLINES

The Most Important Research (November 07 2008) http://www.exchangemagazine.com/morningpost/2008/week45/Friday/1107018.htm
From the Exchange Morning Post, a statist, public funding viewpoint on longevity science: "Learning how to turn back time - or at least how to slow the aging process - may be more important for improving our overall health than the discovery of a cure for cancer. There are real, tangible benefits, for society as well as individuals, to slowing down the aging process. 'By extending the life span, people would remain in the workforce longer, personal income and savings would increase, age entitlement programs would face less pressure from shifting demographics, and national economies would flourish'. Almost half of the current population over 75 years old is limited in their activity by chronic conditions, with costs to society set to rise dramatically. Given the current predicament we face, we can't ignore the call to tackle aging more aggressively. To those who ask: 'Can we really afford to invest more in such research?' we can reply: 'Can we really afford not to tackle aging?' The greatest obstacle will be convincing the general public that slowing the aging process is both feasible and deserving of a larger share of the funds available for scientific research."

An Overview of Cryonics (November 07 2008) http://kn.theiet.org/magazine/issues/0819/science-without-deadline.cfm
A good article on cryonics from Engineering and Technology: "The field of cryonics, which made its debut in the 1960s, continues to push the envelope and search for a solution to death. The process consists of preserving legally dead humans or pets at very low temperature (below -130C) in the hope that future science can restore them to life, youth, and health. The advancement of medicine and science is so much faster than it used to be. Science fiction is becoming science fact on a daily basis. All of a sudden, cryonics doesn't look quite so far-fetched. Most cryonicists believe reanimations will occur within 50 to 100 years for those currently being cryopreserved. Within that time frame, virtually all current diseases should be curable and elderly people can probably be rejuvenated to a youthful condition. With full disclosures and signed consent, [cryonics] is highly ethical. When you think about the grand scheme of things, cryonics is a lot more conservative than burial or conventional cremation. Tissue preserved at the temperature of liquid nitrogen does not deteriorate, even after centuries of storage. Therefore, if current medical technology can’t keep us alive, we can instead choose to be preserved in liquid nitrogen, with the expectation that future medical technology should be able to reverse any cryopreservation injury and restore good health.

Cells as Vectors for Targeted Therapies (November 06 2008) http://www.eurekalert.org/pub_releases/2008-11/miot-mct110508.php
The possibilities of bioengineering are endless, and one of the most energetic branches of the research community is involved in developing methods of precisely targeting therapies: "MIT engineers have outfitted cells with tiny 'backpacks' that could allow them to deliver chemotherapy agents, diagnose tumors or become building blocks for tissue engineering. The polymer backpacks allow researchers to use cells to ferry tiny cargoes and manipulate their movements using magnetic fields. Since each patch covers only a small portion of the cell surface, it does not interfere with the cell's normal functions or prevent it from interacting with the external environment. Researchers worked with B and T cells, two types of immune cells that can home to various tissues in the body, including tumors, infection sites, and lymphoid tissues - a trait that could be exploited to achieve targeted drug or vaccine delivery. The researchers found that T cells with backpacks were able to perform their normal functions, including migrating across a surface, just as they would without anything attached. By loading the backpacks with magnetic nanoparticles, the researchers can control the cells' movement with a magnetic field."

Towards a Rejuvenated Thymus (November 06 2008) http://www.uga.edu/news/artman/publish/081106_Manley_Research.shtml
One approach to the issue of declining naive T-cells with age - and consequence failure of the immune system - is to boost production by manipulating the thymus: "a key gene may be crucial to maintaining the production of the thymus and its disease-fighting T-cells after an animal's birth. The discovery could help scientists find out how to turn the thymus back on so it could produce T-cells long after it normally shuts down most of its function, which, for humans, occurs by early adulthood. If the finding leads to further ways to manipulate the gene, the result could be a new avenue for the body to fight disease more effectively as the body ages. Such things as infectious diseases, inflammation and heart problems are all related to immune response. You don't have to think far to see how understanding the effect of this gene could affect the quality of life for older people and others as well. If [physicians] were able selectively to turn T-cell production back on, then many diseases that currently afflict older people could become manageable if not, in cases, entirely absent."

Boosting the Aging Immune System (November 05 2008) http://pmid.us/18981163
Many research groups are working on ways to boost the effectiveness of an exhausted immune system - due to either chronic viral infection or aging - without necessarily aiming to address the root causes: "In contrast to most normal somatic cells, which show little or no telomerase activity, immune cells up-regulate telomerase in concert with activation. Nevertheless, during aging and chronic HIV-1 infection, there are high proportions of dysfunctional [immune cells] with short telomeres. Exposure of CD8(+) T lymphocytes from HIV-infected human donors to a small molecule telomerase activator (TAT2) modestly retards telomere shortening, increases proliferative potential, and, importantly, enhances cytokine/chemokine production and antiviral activity. The enhanced antiviral effects were abrogated in the presence of a potent and specific telomerase inhibitor, suggesting that TAT2 acts primarily through telomerase activation. Our study is the first to use a pharmacological telomerase-based approach to enhance immune function."

Incremental Improvements in Scaffolding (November 03 2008) http://www.technologyreview.com/printer_friendly_article.aspx?id=21625&channel=biomedicine&section=
From the MIT Technology Review: "Engineering heart tissue presents particularly tough problems for researchers, since the heart is an active organ. Scaffolds designed for other kinds of tissues did not have the right mechanical properties for heart tissue. Heart tissue must be flexible enough to change shape as the heart contracts, but also strong enough to withstand the intense forces generated by these contractions. The researchers designed the scaffold to encourage cells to align themselves in the same direction to better mimic this property of natural heart muscle tissue. Using a laser cutting technique, they created a pattern of oblong holes in the polymer; the result is a flexible, honeycomb-like structure that is stiffer in one direction than another. Just as rowers line up in one direction to propel a boat forward, 'all the heart muscle cells in a given region have to be lined up and contracting in the same direction' in order for the heart to beat efficiently. The honeycomb-like scaffold [represents] a 'substantial jump' toward that goal. If we had a biodegradable biomaterial, which had beating heart cells, we might be able to return function to [damaged parts] of the heart."

A General Interest Calorie Restriction Article (November 03 2008) http://afp.google.com/article/ALeqM5i8eh2v_zPiht03CZWKvVulsaPYqAAs the science advances, these articles get more positive. Recall the ridicule heaped upon the practice of calorie restriction even just a few years ago. "Some people are doing it strictly to enhance longevity. Others do it to avoid age-related disease, or because they already have diabetes, high cholesterol or clogged arteries and want to clean up their bodies by using diet. In rich countries, 90 percent of the population probably eats, on average, about 50 percent too much. Even if they were to reduce their calorie intake by half, they would still only be at baseline. A wealth of scientific evidence has confirmed that maintaining that balance helps prevent type-2 diabetes, cardiovascular disease and cancer. But experiments with both animals and humans have also shown that pushing one's calorie intake 10 to 20 percent below that baseline threshold -- without lowering nutrients -- may provide additional health advantages. Will this add 10 years to your life? Nobody knows. But one thing is sure -- calorie restriction will help you reach your maximum lifespan potential, which is different for all of us depending on our genetic profile."

A Jobe Kind of Year

Dear Future Centenarian,

It’s been a Jobe kind of year so far. Let me count the ways:

We launched a market trading technology that took 12 years to develop that was designed to raise hundreds of millions of dollars for life extension research. Good news, right? Wrong! We launched it on the exact day the markets fell apart. A bunch of money vanished, and critical life extending projects are on hold..
I hired a contractor to build a real estate project. He promised a 10 month delivery date. Here it is, over three years later, and still not quite done. Meanwhile, the bottom fell out of the market this year, and poof, a couple of million plus – up in smoke.
The same contractor got into a dispute with a sub contractor, who put a lien on the property since the contractor won’t pay. Legal fees and headaches all last week. He cost me hundreds of hours wasted on a project that was supposed to be turnkey.
Father Time stole another year from me.
A borrower defaulted on a big loan.
Verizon inadvertently disconnected my Internet service 17 days ago… and it took 15 of those days to get me back online. When I checked to see why, they inactivated my account instead of reconnecting it. Almost four hours spent on phone calls with about a dozen different representatives. Sound familiar?
There is a situation as bad as #2 that I don’t even want to talk about.
There’s another as bad as #7.
A funder for a key longevity technology was not able to perform on his commitment. Meanwhile, the markets hit the skids, and now it will be 10 times harder to get funding. I believe thousands of lives may ultimately terminate as a result, and a small fortune is jeopardized.
My electric bed took on a mind of its own. From time-to-time, without any warning, the head and foot rise in unison, trapping me in a wedge. The last time it happened, the head inclined just fast enough to barely keep me from reaching the remote. The more I stretched, the farther out-of-reach it got. I had to get rescued. A little joke on Dave.
The final straw. My Vita-Mix (my most important health drink tool) gave out yesterday J.

You might be wondering why I’m sharing my tales of woe with you. Sure, I know, you have your own challenges to cope with. Once again, all this has something to do with your health and longevity.

I’m one of those guys you might hate running into when you are troubled. Instead of getting sympathy, you’ll get an irritating dose of sunshine and a pep talk, just when you wanted someone to share your misery with. Well, I should say, I’m usually that optimistic guy. I have to admit that numbers 1-11 above started consuming my thoughts. And that’s bad. It’s bad because it’s extremely unhealthy, life-shortening and counterproductive… and because I know better.

Do you know your thoughts affect every single cell in your body? Positive, loving grateful thoughts keep you healthy and make you live longer. Negative thoughts destroy you from the inside out. What happens to you usually doesn’t matter one bit. How you react means everything. A new friend reminded me of this in a very interesting way. His name is Dr. Pete Hilgartner, and I’m going to share his words of wisdom with you next week.

I don’t care what your situation is. You have plenty to be grateful for. I know I do. I have lots of positive things and people in my life. I’ve been fortunate enough to have attracted better friends, partners and relationships than most could ever hope for. I also lucked out in the health department. And get this. Just yesterday, a close friend and associate told me a benefactor pledged enough funding to finish developing a technology which may allow you and me to actually live as long as we want someday.

Then there are the little things I tend to take for granted. I started yesterday with a nutritious, delicious breakfast and ended it with a fabulous dinner. I live in one of the best climates in the world. I have a warm comfortable bed, even though it attacks me once in a while. My shoes fit. I have shoes. I have feet! And I have a couple of pages of more things to be grateful for. Just writing this makes me feel a lot better, because when you think a grateful, happy or loving thought, there’s no room in your mind for anything else. So happiness is simply deciding what you want to dwell on. And happiness equates to healthfulness. Sure, you have to face your problems, health and otherwise. But when you do, think of solutions rather than dwelling on the negatives.
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LATEST HEALTHY LIFE EXTENSION HEADLINES

Unregulated Prices Fall, While Quality Improves (October 31 2008) http://www.lef.org/magazine/mag2008/sep2008_Would-You-Tolerate-This-Abuse_01.htm
A piece from the LEF Magazine that makes the points about modern medical research that most people don't think about: "the public today tolerates federal and state laws that enable pharmaceutical companies to conduct business as a virtual monopoly. The result is that Americans pay outlandish prices for mediocre drugs that are often laden with side effects. Unlike regulated prescription drugs, the cost of dietary supplements has plummeted over the past three decades. In a free market environment, technological breakthroughs that occurred in telecommunications will also happen in medicine. More frightening is the suffocating effect that regulation has on the discovery of life-saving therapies. Just imagine if advancement in clinical medicine progressed at the same rapid rate as telecommunications. If it did, we would probably have cures for most killer diseases today!" Heavily regulated markets are bloated, slow markets, in which the incentives are so set as to discourage progress. Present regulation is a very real threat to the future of your health and longevity.

Incremental Improvements in Stem Cell Therapy (October 31 2008) http://www.eurekalert.org/pub_releases/2008-10/hms-scp102908.php
Researchers continue to find ways to alter stem cells to produce better therapies: "Adult stem cells resemble couch potatoes if they hang out and divide in a dish for too long. They get fat and lose key surface proteins, which interferes with their movement and reduces their therapeutic potential. Now, via a simple chemical procedure, researchers have found a way to get these cells off the couch and over to their therapeutic target. To do this, they simply added a molecule called SLeX to the surface of the cells. The procedure took just 45 minutes and restored an important biological function. Delivery remains one of the biggest hurdles to stem cell therapy. The blood stream offers a natural delivery vehicle, but stem cells don't move through blood vessels normally after being expanded in culture. Our procedure promises to overcome this obstacle. Karp cautions that his lab's discovery must be validated in animals, before doctors can apply it in the clinic. He's collaborating with another lab to test the homing ability of the SLeX-dotted cells in mice."

A Little More on IGF-1 and Growth Hormone (October 30 2008) http://dx.doi.org/10.1371/journal.pbio.0060254
Following up on a recent Fight Aging! post, more on the role of IGF-1 in longevity: "Using a mouse model relevant for humans, we showed that lifespan can be significantly extended by reducing the signaling selectively of a protein called IGF-I in the central nervous system. This caused growth retardation, smaller adult size, and metabolic alterations, and led to delayed mortality and longer mean lifespan. Thus, early changes in neuroendocrine development can durably modify the life trajectory in mammals. The underlying mechanism appears to be an adaptive plasticity of somatotropic functions allowing individuals to decelerate growth and preserve resources, and thereby improve fitness in challenging environments. Continuously low IGF-I and low growth hormone levels favor extended lifespan and postpone age-related mortality. Our results further challenge the view that administration of GH can prevent, or even counteract human aging. This knowledge is important since growth hormone is often prescribed to elderly people in an attempt to compensate the unwanted effects of aging."

Ouroboros on Mitochondrial Uncouplers (October 30 2008) http://ouroboros.wordpress.com/2008/10/30/mitochondrial-uncouplers-mimic-the-effects-of-calorie-restriction/
From Ouroboros: researchers "suggest that mitochondrial uncoupling is an effective mimic of [calorie restriction (CR)]. In mitochondria, the electron transport chain uses electrons from glucose and lipids to pump protons across a membrane. This proton gradient can be used to make energy in the form of ATP through oxidative phosphorylation. The process is kind of like generating hydropower. Uncouplers work by putting a leak in the dam, which lets water through without going to the generator. They 'uncouple' the electron transport chain from oxidative phosphorylation, thus reducing the efficiency of energy production. Although animals have uncoupling proteins (these proteins are important for thermogenesis, especially during hibernation), so far there are no known agonists. The researchers instead used low doses of the mitochondria uncoupler DNP.
The DNP treated mice ate the same amount of food as control mice but had lower body mass [and] showed many phenotypes observed in calorie restricted mice. Like CR mice, DNP treated mice had higher rates of respiration with lower production of ROS. Most importantly, DNP treated mice showed an extended lifespan. This study suggests that mitochondrial uncouplers are an effective mimic of calorie restriction and might be a realistic therapeutic intervention for delaying aging and extending lifespan."

Lipids and Alzheimer's (October 28 2008) http://www.medicalnewstoday.com/articles/126012.php
The brain is complex organ, and Alzheimer's is a complex disease: a wide range of strategies produce results that look promising while not addressing the root cause. Indeed, distinguishing symptoms from root causes in Alzheimer's is still an ongoing concern. Here is a potential strategy I have not seen mentioned before: "scientists working with laboratory mice have discovered that complete or partial removal of an enzyme that regulates fatty acid levels lessened the memory and learning deficits of Alzheimer's. The most striking change we discovered in the Alzheimer mice was an increase in arachidonic acid and related metabolites in the hippocampus, a memory center that is affected early and severely by Alzheimer's disease. An enzyme called group IVA phospholipase A2 (or PLA2) released arachidonic acid [in] the brain. Removal or even partial reduction of PLA2 prevented memory and learning deficits and other behavioral abnormalities in the Alzheimer mice." It is worth noting that PLA2 is upstream in biochemical signaling processes that lead to inflammation - I suspect this has more to do with inflammation than fatty acids per se.

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

Financial Support for Aging Research

Financial Support for Aging Research

Last week, we talked about the potential (optimistic) cost to reverse aging within the next couple of decades.
Historically financial support for aging research and efforts to extend the healthy lifespan has been spotty. Venture capital firms typically aim for profitable exits from their investments within two to four years. The research and product development we support typically takes longer to mature. Governments aren’t providing much funding. Pharmaceutical and biotech companies’ support of basic aging research is hindered due to the fact that there are no generally accepted biomarkers for human aging that would allow the FDA to approve a drug designed to slow the aging process. These companies are forced to develop drugs for specific diseases. And the FDA doesn’t recognize aging as a disease.
For example, 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.”

Dr. Christoph Westphal, the chief executive of Sirtris, said of the potential of the resveratrol based drugs they are developing, “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 is no FDA category for longevity drugs, so if the company is to submit a drug for approval, it needs to be for a specific disease. However, longevity is what has motivated the researchers and what makes the drugs potentially so appealing.

There you have the most serious problem facing longevity science today. The FDA does not allow its direct application. Until this changes, no serious investment will be made in the US to bring longevity science to the clinic. This is a tragedy of astronomical proportions and is beyond belief.
Congress did supplement scarce aging research dollars by establishing the National Institute on Aging in 1974, but that money has primarily gone to disease specific research, such as Alzheimer's disease, or towards the behavioral aspects of aging.
Next week, we’ll look at the possibilities of significant private money finally joining the hunt.
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VOTE FOR "UNDERGRADS AGAINST AGE RELATED DISEASE"

I don't know if you're familiar with the American Express Members Project: It is an open vote to determine how that company will set up a philanthropic program. One of the suggested projects was put forward by a Methuselah Foundation volunteer, and we're looking for enough votes to move it into the next round of consideration:

"You can help by voting: it's free and won't take more than a few minutes. We just need you to go to the Members Projects website and nominate the "Undergrads Against Age Related Disease" project. You don't need to be an Amex card holder, but you do need to be a US resident."

You'll find the project description at the following link:

http://www.membersproject.com/project/view/BVVE2C

"A program that utilizes college undergraduates to perform research in a variety of scientific venues surrounding fighting age related diseases such as Alzheimer's, Parkinson's, Heart Disease, [Cancer, and] overall extension of healthy human life. Hiring researchers is exceedingly expensive. By outsourcing projects to undergraduate students, laboratory use and labor costs are negligible, and the students receive college credit for their work"
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LATEST HEALTHY LIFE EXTENSION HEADLINES

Towards Tissue Engineered Corneas (August 15 2008) http://www.hindustantimes.com/storypage/storypage.aspx?id=34901c8e-1148-44b8-ae83-395922ea0f64
From the Hindustan Times: "Half a dozen eye hospitals in India are collaborating with a research centre in Chennai to create the inner layer of the cornea, the vital window of the human eye. Nichi-In Centre for Regenerative Medicine (NCRM) hopes to make corneal endothelium (inside cell layer) available on a commercial scale. About 100,000 people are in need of eye transplant every year, yet only about 10,000 are able to get donated eyes. The wait for a donor can be endless for the other 90,000. Imagine what a boon it will be if an eye stem cell bank could provide these lab generated endothelial layer of the cornea. The eye has three main parts. The first is the cornea, which is a transparent film like structure that transmits light into the eye. The other two are the lens and retina. During eye transplant, only the cornea is taken from the donor, not the whole eye. Nichi-In is now growing the animal and human corneal inner layer cells on a nano-scaffolding. The research centre is hoping to begin phase I clinical trials on humans in six months."

Ouroboros on Open Science (August 15 2008) http://ouroboros.wordpress.com/2008/08/14/opening-science-how-unconferences-changed-my-life/
Open science, analogous to open source software development, is the way of the future. It greatly increases diversity and speed of work by lowering the cost of information, and thereby allowing many more people to participate in research. In a world in which information transmission is easy, it makes no sense to lock up scientific data. Publish early, publish often should be the mantra. From Ouroboros: "The world implied by these concepts is one of radical sharing, in which credit still goes where credit is due but by dramatically different mechanisms. Open science isn’t so much 'pay it forward' (though there is a bit of that) as an effort to create a (scientific) world in which no one is paying at all, a world in which there's no incentive to withhold or protect ownership of data. The science fiction writer Iain M. Banks once wrote that 'money implies poverty' - indeed, many of the current models of data ownership and publication, and their accompanying 'currencies' of proprietorship, prestige and closed-access publication, imply a world in which data is scarce and must be hoarded. But data is not scarce anymore."

Cryonics Versus Rejuvenation Medicine (August 14 2008) http://www.depressedmetabolism.com/2008/08/13/thomas-donaldson-on-cryonics-and-anti-aging/
Via Depressed Metabolism, arguments for a present focus on the development of cryonics over the development of rejuvenation medicine: "In his article 'Why Cryonics Will Probably Help You More Than Antiaging' (2004), cryonics activist Thomas Donaldson contrasts cryonics with antiaging as a means to life extension and argues that a major advantage of cryonics is that cryobiology research can move at a much faster pace than anti-aging research, especially as it pertains to humans. Not only that, but its progress almost totally lacks the problems of proving that an advance has happened. The state of a brain, or even a section of brain, after vitrification and rewarming to normal temperature, shows directly whether or not the method used improved on previous methods. Cryonic suspension is able at least to preserve our brains in a reversible form, allowing restoration of vital functions and looks likely to come much sooner [than rejuvenation medicine]." Which is all true - but problems left to other people to solve have a way of remaining unsolved. We should work on both cryonics and rejuvenation medicine, not leave the latter for future generations.

Removing the Worst Aspect of Chronic Infection (August 13 2008) http://www.eurekalert.org/pub_releases/2008-08/eu-twb_1080808.php
An important aspect of immune system aging is the lack of naive T cells resulting from long periods of chronic infection by viruses like cytomegalovirus. What if we could reconfigure the immune system to behave more rationally when presented with recurring threats, and thus not exhaust its resources? That might be a possibility: "preventing white blood cells' circulation by trapping them in the lymph nodes can help mice get rid of a chronic viral infection. Laboratory mice can fight off infection by the Armstrong strain of lymphocytic choriomeningitis virus (LCMV), but are vulnerable to chronic infection by a variant called clone 13. Infecting mice with the Armstrong strain sequesters white blood cells in the lymph nodes, while clone 13 does so less stringently. Our hypothesis was that if we could artificially induce conditions like those produced by the Armstrong strain, it would help the immune system clear an infection by clone 13. An experimental drug called FTY720 [prevents] white blood cells from leaving lymph nodes. Even if mice have a stable chronic LCMV clone 13 infection, treatment with FTY720 can still improve their immune response against LCMV enough to have them rid it from their systems. FTY720 appears to prevent 'exhaustion' in the group of white blood cells called CD8+ T cells."

Hourglass II: A Carnival of Biogerontology (August 13 2008) http://ouroboros.wordpress.com/2008/08/12/hourglass-ii-a-carnival-of-biogerontology/
From Ouroboros: "Welcome to the second installation of Hourglass, a blog carnival devoted to the biology of aging. The entries are representatives of the excellent (and growing) community of bloggers who are writing about biogerontology, lifespan extension technologies, and aging in general. Anne C. shares a parable about taking care of her friend Nigel the Fish and what that led her to realize about longevity: specifically, that environment is critical, and that the combination of extrinsic factors that one might collectively term 'nurture' can make all the difference between a short unhappy life and a long fulfilled one. Old and damaged cells enter a permanent growth arrest known as senescence, which is both good (because they can’t initiate tumors) and bad (because persistent senescent cells behave in a ridiculously antisocial manner, secreting growth factors and proteases that both encourage nearby tumors to metastasize and degrade tissue function). At his new site Anti-Ageing Research, Dominick Burton discusses ways in which specifically targeted cancer therapies might be adapted to attack senescent cells instead."

Building Better Tendons (August 12 2008) http://technology.newscientist.com/article/dn14512-labgrown-tendons-gradually-fade-to-bone.html
Laboratory tissue engineering continues to improve in sophistication, as noted by the New Scientist: "only now have researchers managed to make different tissues blend into one another, as they do naturally in the body. Such gradients are necessary for some structures and organs to function properly. In the body, gradients like this strengthen the ends of tendons that attach to bones. Currently, lab-grown tendons put into the body often fail at the attachment end because they lack this property. The new technique should lead to more lifelike artificially-grown tendons, and better treatments for injuries like ruptured Achilles tendons.
The technique could also be applicable to other tissues, such as blood vessels. At the heart of the new technique is a gene that triggers the fibroblast cells that make up tendons to start forming bone. The team used viruses carrying that gene to transform a tendon made from normal fibroblasts into one with a gradient of bony properties. So far, the researchers have shown that tendons made this way are stable when implanted under the skin of rats. The next step is to graft a tendon to connect bone and muscle in a rat and see if it really does perform better."

Demonstrating the Value of Exercise (August 12 2008) http://www.medicalnewstoday.com/articles/117929.php
Via Medical News Today, another reminder of the value of exercise: "US scientists comparing middle aged and older regular runners with healthy equivalents for more than 20 years found that vigorous regular exercise was linked to longer life and less disability in old age. Fries and his team had 538 members of a nationwide running club and 423 healthy controls from northern California fill in questionnaires every year for as long as they could, from 1984 to 2005. The mean disability score was higher for the controls than the runners at all stages of the study and went up with age in both groups, but on average, for runners the onset of disability started later. Runners' initial disability was 16 years later than nonrunners. Runners had a significantly lower risk of having a disability score of 0.5. 19 years into the study, 15 per cent of the runners and 34 per cent of the controls had died, and after adjusting for possible confounders, runners showed a greater chance of living longer. The differences in disability and longevity between the runner group and the control group continued to diverge at the end of the study, as the participants approached their 80th birthday."

Full Paper on Visceral Fat and Longevity (August 11 2008) http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2504027
You may recall a solid demonstration that visceral fat tissue negatively affects longevity from earlier this year. The full paper is now open access and available at PubMed Central: "Visceral fat (VF) accretion occurs in obesity and with aging, and a reduction in VF is a common phenotypic change in calorie-restricted [CR] mammals. VF has been shown to be the single most important determinant of metabolic syndrome, and its removal in rats results in improved insulin action and delays the onset of diabetes. Given the hazards associated with abdominal obesity, it seems plausible that the beneficial effects of CR on longevity may be due at least in part to an attenuation of VF. Our data clearly demonstrate that in mammals, VF removal and CR are associated with an increase in mean and maximum lifespan. The mean and maximum lifespan of CR rats was greater than that seen in VF-removed animals, suggesting that the life-prolonging benefit of CR is mediated in part by pathways other than those modulated by an attenuation of VF. By comparing median lifespans, we estimate that the contribution of CR to longevity in this model was 47 weeks, whereas VF removal was 9.5 weeks, as compared to [ad libitum]-fed rats, suggesting that VF reduction offered approximately 20% of the effect of CR on longevity."

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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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.