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Longevity News

Aging is Slowly Stealing Our Lives
Save for the Future
Hub of NanoMedicine
Nanofactory Collaboration Colleague Awarded $3 Million
Artificial General Intelligence
Stay Happy and Save your Life
Las Vegas Longevity Workshop
Two Groups of Friends

Aging is Slowly Stealing Our Lives

posted on November 17, 2008

You and I are both aware that aging is slowly stealing our health, our vigor and our lives. Yet we function without a sense of urgency to do something about aging. Why? Because we’re bombarded with our personal and career responsibilities and daily distractions. And those squeaky wheels are what get our attention. This is totally normal and logical. We have to take care of our families, get our haircuts and pay attention to endless details. Who has time to really make a commitment to being proactive when it comes to something as abstract as age-reversal?

That’s the way I used to think. But taking paths of least resistance normally leads us down reactive paths. In other words, we usually let outside forces control our lives. It isn’t until we’re faced with a crisis that those forces take a backseat to focusing on something that may have been avoided in the first place. Sometimes, that crisis means life or death.

This really hit home when I just found out a close and loved associate was diagnosed with one of the deadliest forms of cancer. What’s even more tragic is he’s an active life extension researcher. That’s the worst of ironies.

I am saddened to report that Dr. Chris Heward, one of the original participants of MaxLife’s first international scientific brainstorm sessions to reverse aging, is fighting an uphill battle for his life. Chris is Director of the Kronos Science Laboratories of Phoenix, AZ. He has been diagnosed with terminal, Stage-IV Esophageal Cancer. The cancer has metastasized to several other organs, and consequently his condition has a poor prognosis (50% mortality in 90 days and about 99% in a year).

Since surgery is no longer a realistic option, Chris has proposed to undergo an experimental but very promising immunotherapy treatment in Boca Raton, FL. However, this treatment requires blood donors less than 30 years old with "A" or "O" positive or negative blood types and no prior history of cancer in their families. If you are in—or if you know anyone in this category who would be willing to donate several units of blood to retrieve the granulocyte cells, please get in touch with me as soon as possible. Not only could this experimental treatment save Chris, but it could lead to a universal cure for many types of cancer. Here’s an opportunity to contribute to a great cause that could ultimately save many lives by making a simple referral.

Thank you in advance for your attention to this critical matter.
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LATEST HEALTHY LIFE EXTENSION HEADLINES

Researchers on Aging (November 14 2008) http://www.mcclatchydc.com/226/story/55835.html
An article of quotes from various noted aging reseachers: "Aging is caused by the gradual, lifelong accumulation of a wide variety of molecular and cellular damage. The free radical theory is the most widely accepted theory of aging. But the idea that aging is caused by one thing is naive. One general theory can never fit all. Clearly, it's the combination of genes that your parents dealt you and the lifestyle choices you make and the environmental toxins one is exposed to. One need only count the number of ways a car will fail to start to appreciate that aging can be caused by a large number of problems. Like any machine, it's going to wear out. About 25 percent of how a person ages is due to inherited genes. Certain genes control a cell's ability to repair damaged DNA. If those genes are defective, they can't do their job. Not everybody will be susceptible to diseases like Parkinson's or cancer as they age. But each one of us will lose muscle mass and muscle strength. That's why this research is so important. Frailty affects all of us."

Enhanced Longevity through Telomerase (November 14 2008) http://www.sciencenews.org/view/generic/id/38552/title/Telomere_enzyme_a_likely_key_to_longevity
From Science News: "the enzyme telomerase can extend the lifespan of mice by about 24 percent. Telomerase lengthens telomeres - the 'caps' on the end of chromosomes that protect DNA from damage. Like burning fuses, telomeres normally get shorter each time that most body cells divide. While the enzyme enables cells to keep dividing, it also takes cells one step closer to growing and proliferating out of control - that is, becoming cancerous. Lab animals with extra genes for telomerase often die young from tumors. [researchers] engineered mice to have not only an extra copy of the gene for telomerase, but also extra anti-tumor genes to combat the enzyme's cancer-causing potential. In the altered mice, signs of aging such as poor coordination or degraded tissue health were delayed compared to mice that had only the extra copies of anti-tumor genes." Most interesting; you might also want to look at recent research that suggests telomerase operates by protecting mitochondria, and less damaged mitochondria means better preservation of telomeres - but, more importantly for life span, less oxidative stress.

Better Synthetic Cartilage (November 13 2008) http://www.sciencedaily.com/releases/2008/11/081113075959.htm
From ScienceDaily: "Until now, creating synthetic cartilage was complex but not impossible. The problem was that it was impossible to imitate the perfection of human cartilage due to the difficulty in orienting the collagen nanofibers [in] a particular configuration: in parallel, in a circle, or crossed. The fibers that form the cartilage that protects the knee are aligned in parallel. [Researchers have now] achieved this using the electrospinning method. Collagen nanofibers are obtained by exposing the collagen to electrical discharges. The collagen is extruded, in the form of a nanofiber thread, through a fine needle and is deposited on an electric collector consisting of two grounded plates. The student placed a nonconductive material between the two conducting plates. The nanofibers aligned on top of each other perfectly in parallel lines between the two conducting plates." Innovations in engineering the simpler forms of human tissue have been arriving more rapidly of late - more scientists are involved, the tools are improving, and the cost of research is falling. This is all groundwork for the next decade and tissue engineering of complex replacement organs.

Steps towards Liver Regeneration (November 13 2008) http://www.uphs.upenn.edu/news/News_Releases/2008/11/liver-stem-cell-marker.html
Discovering a stem cell population is the first step to regenerating the tissue they support: "A novel protein marker has been found that identifies rare adult liver stem cells, whose ability to regenerate injured liver tissue has the potential for cell-replacement therapy. In the future, this marker will allow for the isolation and expansion of these stem cells, which could then be used to help patients whose livers can no longer repair their own tissue. In a healthy liver, proliferation of mature liver and bile-duct lining cells is sufficient to maintain the necessary size and function of the organ. This even works when the liver is confronted with mild and acute injury, but the situation changes when injury to the liver is chronic and severe. For chronic injury, the liver uses a back-up system that stimulates stem cells to proliferate and eventually differentiate into new liver cells. [Researchers] found that these dual-potential stem cells can be identified and potentially isolated from other liver cells."

More on Myelin Loss (November 12 2008)
http://www.eurekalert.org/pub_releases/2008-11/mnia-itw111208.php
You might recall that age-related thinning of the myelin that insulates nerves strongly correlates with declining brain function. Researchers investigating MS are making progress into the mechanisms by which this happens: the protein netrin-1 "is known to guide and direct nerve cell axons to their targets. Blocking the function of netrin-1 and one of its receptors in adult neural tissue causes the disruption of myelin. We've known for just over 10 years that netrin is essential for normal development of the nervous system, and we also knew that netrin was present in the adult brain, but we didn't know why. The new findings show that
netrin-1 and its receptor are needed to hold paranodal junctions in place, and thereby maintain the structure of myelin. The paranodal junction is a highly specialized region of contact where an oligodendrocyte cell attaches itself to the nerve cell's axon. This juncture acts as a molecular fence, which organizes and segregates the distribution of key proteins along the nerve cells axon and plays an imperative role in the proper conduction of electrical signals along the length of the nerve cell. When the function of netrin-1 and its receptor is disrupted, the organization of this adhesive junction comes apart, disrupting the function of nerve cells in the brain and spinal cord."

Brain Growth Receptors and Lifespan (November 10 2008) http://dx.doi.org/10.1371/journal.pbio.0060274
A very readable overview of recent research from PLoS Biology: "When resources are short, growing organisms face an existential choice: should you ignore the shortage and hope for better times soon, or scale back and live within your limited means? And if you do scale back, will there be any payoff later in life? For animals, these choices are played out hormonally, with environmental fluctuations leading to internal rearrangements in endocrine signal and response throughout the growing body. In mammals, two principal hormones - growth hormone (GH) and insulin-like growth factor 1 (IGF-1) - promote growth. Remarkably, inhibiting one or both of these two not only retards growth, but also extends lifespan, not just in lab animals, but possibly also in people: mutations that reduce the function of the IGF-1 receptor have recently been discovered in centenarians (who are also short). Growth occurs throughout the body, and receptors for IGF-1 are found in every organ on virtually every cell. But [researchers have now shown] that it is the IGF-1 receptors in the brain that set the pattern for growth and lifespan."

Mainstream Press on the Singularity and Longevity (November 10 2008) http://english.ohmynews.com/ArticleView/article_view.asp?menu=A11100&no=384115&rel_no=1
An interesting, if flawed, article on the singularity and engineered longevity via the Korean OhmyNews: "Amidst the rapid changes of society ranging from general advances in science and technology to politics and social policy, with respect to knowledge, there is an emergent issue that promises to radically change our lives and our reality. It is predicted that within less than 20 years, the human lifespan will be extended to perhaps 150 or more years. Scientists and futurists on the cutting edge of thought about science and society believe that the increase in lifespan is one step towards what will be known as the Singularity, at which time, life might be extended indefinitely depending upon environmental conditions. The Singularity is the term used for a technological integration unheard of; it is a theoretical future point of unprecedented technological progress, caused in part by the ability of machines to improve themselves using artificial intelligence. It was just over a hundred years ago, when the human lifespan began to double to what it is today. It is possible that most people who lived only to 35 years of age thought that to live to 72 years would be too long and that they would be too tired. Nevertheless, we have adjusted and found life to be meaningful, even in our current 'long' life of 72 years."

Save for the Future

posted on October 13, 2008

What a week!

If you are in any market, you probably got slaughtered last week. If you didn’t, I want you to handle my investments.

Although I attribute most of the sudden losses to panic selling, it’s still very sobering. We’ll see lots of ripple effects that could last for a long time. We’ll also see more controls which will lead to more erosion of your freedoms.

Meanwhile, I’m working on keeping you alive for a long time, so if the markets are stressing you out, relax and review my previous commentaries on stress.

But this market made one more thing crystal clear to me. You may need money, if you want to dodge the grim reaper. Lots of it. If you didn’t lose money last week, it might be because you don’t have any to lose. And yes, that could be bad if you want to live for an extremely long time.

Let’s face it… the first people who are going to get effective life-extending treatment are those who will be able to afford it. If you’re old and broke when the longevity boat arrives, you might miss it. Sure, prices will come down, and pretty rapidly too. But many of us are on the bubble as it is, and not being near the front of the line could just cost you your life. So what are you going to do about it?

All your life, you have been told to save for the future, and you’re most certainly familiar with the magic of compound interest. As we age, we may regret not starting to save years ago. Now, many people who didn’t save figure it’s too late to amass any kind of fortune, so they live day-to-day, paycheck-to-paycheck. But what if you knew beyond a shadow of a doubt, you would be biologically transformed into a 25-year old, twenty or thirty years from now, if you had $500,000 in the bank at that time. Do you realize that if you socked away about $30,000 in a segregated investment account that compounded at around 10% growth per year, you would have your $500,000 in less than thirty years? (10% is roughly the historical annual growth of the stock market.)

In other words, $30,000 could be the difference between your being part of the last generation to die from aging or part of the first to live endlessly. What if you don’t have $30,000? That’s easy. Save $3,000 now and $3,000 every year in the same type of account, and presto! You’ll have your magical $500,000 in less than thirty years.

I have no idea what full rejuvenation will cost when it’s available, so plan for more, not less. Wouldn’t it be nice to be young again with a pile of money in the bank?
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LONGEVITY AND THE COMPOSITION OF MITOCHONDRIA

Comparisons of mitochondrial biochemistry between species of differing innate longevity is one several branches of research to demonstrate the importance of our mitochondria to aging:

http://www.fightaging.org/archives/001584.php

"Mitochondria, the power plants of your cells, generate damaging reactive oxygen species (ROS) in the course of their operation: ROS will race off to damage the first thing they can find by reacting with it, such as a cell membrane. Mitochondria themselves have membranes, and are first in line to be damaged by the ROS they generate. Eventually damage accumulates and cascades to change the surrounding cellular environment very much for the worse. This process is an important root cause of degenerative aging."

This process is why those species more resistant to the damaging effects of reactive oxygen species live longer than their peers. "Resistance" here means that the membranes of mitochondria and other cellular components are built of tougher stuff: proteins less likely to be succumb to ROS attack. Even in primates, mitochondrial composition differences are significant between species and highly correlated with longevity. This all reinforces just how central our mitochondria are to aging, and how vital it is to speed research into repairing damaged mitochondria in humans:

http://www.fightaging.org/archives/001395.php
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LATEST HEALTHY LIFE EXTENSION HEADLINES

Update on Viruses Versus Cancer (October 10 2008) http://www.sciencedaily.com/releases/2008/10/081008151320.htm
A number of groups are presently working on ways to use viruses to precisely target and kill cancer cells. Here's an update on one of them from ScienceDaily: "The Senecavirus [is] harmless to normal human cells, but could infect certain solid tumors, such as small cell lung cancer, the most common form of lung cancer. Scientists at Neotropix say that, in laboratory and animal studies, the virus demonstrates cancer-killing specificity that is 10,000 times higher than that seen in traditional chemotherapeutics, with no overt toxicity. The company has developed the 'oncolytic' virus as an anti-cancer agent and is already conducting early phase clinical trials in patients with lung cancer. Researchers went on to identify several areas on the viral protein coat that they think might hook onto receptors on cancer cells in the process of infecting them. It will be critically important to find out what region of its structure the virus is using to bind to tumor cells, and what those cancer cell receptors are. Then we can, hopefully, improve Senecavirus enough to become a potent agent that can be used with many different cancers."

Cuervo On Autophagy (October 10 2008) http://websites.afar.org/site/PageServer?pagename=IA_spotlight_main
A piece from earlier this year at InfoAging: "Aging is characterized primarily by the decline of function in various cellular and molecular systems in the body. These changes are influenced by three factors:
genetics, metabolism, and the environment. The focus in Dr. Cuervo's lab is the metabolic changes and resulting damage from these changes that are experienced with age, specifically damage to proteins. Every person experiences this damage to some degree, regardless of their age, but when it comes to repairing or removing the damage, the difference between young and old is clear. In younger people, the damaged or misfolded proteins can be repaired by what are known as chaperone proteins. Yet, like an old car, proteins that have undergone too much repair are not worth maintaining and so they are transported by the chaperone to the lysosome as 'trash' where they bind to a receptor and undergo autophagy (literally, self-eating) inside the organelle. Dr. Cuervo's research focuses on this pathway and how a major decline in its functionality is seen in older organisms." The piece goes on to describe how researchers restored this functionality to youthful levels in aged mice.

A Good Example of a Cell Signaling Application (October 09 2008) http://www.xconomy.com/boston/2008/10/09/provasculon-a-biogen-backed-startup-testing-regenerative-medicine-on-hearts/
An important field resulting from stem cell research is the discovery and application of biochemical signals to direct existing stem cells in the body - they can be made to repair damage where they would ordinarily remain inactive. Only where stem cells themselves are damaged would new cells be needed: in most situations, greater control over the cells you have is good enough. Via Xconomy: "Provasculon is tackling one of the bigger ideas in regenerative medicine - how to stimulate growth of new blood vessels after they've been damaged by a heart attack. Iin rat studies that a novel protein was able to stimulate a certain type of stem cells (better known to scientists as endothelial progenitor cells) to migrate to damaged heart tissue, promote growth of new blood vessels, and ultimately help the heart pump better after a heart attack. The trick here is that Provasculon is trying to make a genetically engineered form of the key protein, SDF-1, that is able to avoid certain enzymes in the body that would like to chop the protein up and render it useless."

All Problems Are a Matter of Atoms (October 08 2008) http://www.acceleratingfuture.com/michael/blog/2008/10/physical-basis-for-problems/
The ultimate goal of medicine is to be able to reliably and precisely manipulate any the molecules in our bodies: all disease, all aging, is a matter of the wrong molecules being in the wrong place at the wrong time. From Accelerating Future: "It's important to realize the obvious: that every human problem, every malady, every concern, every evil, is at root simply a suboptimal arrangement of atoms and molecules. If this sounds quasi-spiritual, it's because it is - for millennia, pre-scientific humans have attributed all ills to various agents - the gods, magicians, and other humans. This is because these ills demand an explanation, and we didn't have a plausible one, so we made it up. Now, at least in the abstract, we have a concrete, very likely correct answer: suboptimal atomic arrangements. This realization is neither trivial nor too broad to be useless. If your problems are caused by the gods (that some people sadly still believe in...), then to solve them, you either need to give up, on engage in rituals [that] have an empirical impact of precisely zero." There is a simple criteria by which to judge whether new technologies will enable better medicine: do they give us the ability to more precisely and easily move atoms around? Modern biotechnology and the molecular manufacturing that will follow are both good examples.

Pondering Aging Stem Cells in the Gut (October 08 2008) http://www.sciencenews.org/view/generic/id/37382/title/Old_age_causes_problems_for_gut_cells
From Science News: "Old age can hit animals in the gut. That's where elderly fruit flies experience a signaling imbalance that disrupts renewal of the gut wall, new research shows. The discovery could help scientists understand why the body's organs malfunction in old age, and why intestinal cancer is so common among older people. Normally, 'adult' stem cells in the intestinal wall churn out a steady stream of new cells to replenish the lining [but] in older animals, this balance seems to be breaking down. The imbalance appears to be triggered by stress - not psychological stress, but the chemical stresses put on cells by free radicals or by chronic inflammation, both of which get worse as an animal ages. Cells in the gut lining respond to this stress by activating a protective gene [which] is part of a signaling pathway that spurs intestinal stem cells to grow and divide. In response, another signaling pathway - called the Delta/Notch pathway - ramps up to try to keep that growth in check. But too much Delta/Notch can also derail the natural conversion of these stem cells into mature gut cells, causing an abnormal accumulation of halfway converted cells. [This] malfunctioning of adult stem cells in old age [is] very similar to what happens in certain human stem cell populations."

Attacking Macrophages in Fat (October 07 2008) http://www.eurekalert.org/pub_releases/2008-10/cp-ki093008.php

You might recall that the reason excess fat tissue is so damaging seems to be due to roaming macrophages that release inflammatory biochemicals. Via EurekAlert!, a demonstration that reinforces this point: "Over the past decade, it has become quite clear that obesity gives rise to a state of chronic, low-grade inflammation that contributes to insulin resistance and type 2 diabetes [researchers] recently found that a specific subset of macrophages invades obese fat and muscle tissue. Although little was known about them, those macrophages are defined by a CD11c marker expressed on their surfaces. They also produce high levels of proinflammatory chemicals that are linked to the development of obesity-associated insulin resistance. We used a genetic 'trick' that allowed us to rapidly kill these macrophages. The treatment killed these cells within hours, and insulin resistance simply reversed itself. It argues strongly that macrophages are causative for the inflammation that leads to diabetes [in those who are obese]. The most interesting thing is that this reversal occurs very rapidly. Twenty-four hours later the animals' insulin response had completely normalized. They were still obese, but no longer insulin resistant."

Hub of NanoMedicine

posted on October 6, 2008

To continue last week’s discussion of nanomedicine, here’s why you’d be interested in living long enough to see it get fully developed:

Nanotechnology refers to the control of matter on a scale normally between 1-100 nanometers. One nanometer is a billionth of a meter or 80,000 times smaller than a human hair.

We work with the world’s recognized authorities on medical applications and implications of molecular nanotechnology, or Nanomedicine. They have launched a program aimed at developing a provable nanomedical life extension technology. This may be the ultimate technology which can cure aging and reverse its effects.

They constructed a preliminary R&D roadmap and have already achieved some of their objectives. They have even established six currently active collaborations.

The technology should have commercially useful early applications. If successful, the company will eventually own a must-have product – indefinite life extension and aging reversal. In a nutshell, nanomedicine could eventually build or repair almost every cell in your body, from the bottom up, atom by atom. When we get to the 2020s, we will ultimately have perfected the machines of nanotechnology, nanobots, which are blood cell-sized devices that can go inside your body and brain to perform therapeutic functions, as well as to advance the capabilities of our bodies and brains.

If that sounds too futuristic, I'll point out that we already have blood cell-size devices that are nano-engineered, working to perform therapeutic functions in animals. For example, one scientist cured type I diabetes in rats with this type of nanoengineered device. And some of these are now approaching human trials. The 2020s will be the "golden era" of nanotechnology.

If you want to see who is at the hub of nanomedicine, visit these two websites:

http://www.MolecularAssembler.com/Nanofactory

http://www.MolecularAssembler.com/Nanofactory/Media/PressReleaseAug08.htm

Nanomedicine promises to give us complete control of matter and a very efficient way to cure aging damage, injuries and diseases. So keep fit and lean in the meantime. You don’t want to miss this boat.

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SLOW AND STEADY WINS THE RACE

Some food for thought on the way in which you approach the health basics - exercise, diet, supplementation, and relationships with physicians:

http://www.fightaging.org/archives/001582.php

"Following up on growing evidence that higher levels of conscientiousness are associated with greater health protection, the authors conducted a meta-analysis of the association between conscientiousness-related traits and longevity. Higher levels of conscientiousness were significantly and positively related to longevity. Associations were strongest for the achievement (persistent, industrious) and order (organized,
disciplined) facets of conscientiousness. Results strongly support the importance of conscientiousness-related traits to health across the life span."

The persistent application of good habits and good choices pays well. The basics are not rocket science, but they do make a significant difference over the years.
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LATEST HEALTHY LIFE EXTENSION HEADLINES

More on Comparative Longevity (October 03 2008) http://www.bucknell.edu/x45446.xml
Researchers continue to try to learn from differences in longevity and metabolism between species: "Haussmann studied cacti and turtles before zeroing in on a small, marine bird that contradicts traditional assumptions about aging. Leach's storm-petrels should die young but live a long life and break the conventional rules. First of all, they're small, and there tends to be a relationship between body size and life span. Elephants live longer than humans. Humans live longer than mice. So this bird shouldn't live long, but it does. His studies of storm-petrels have shown that certain characteristics of DNA - specifically lengths of the protective telomeres at the tips of DNA - are associated with species that live longer lives and possibly with how susceptible they are to cancer-causing tumors. [Bird species] with shorter life spans, such as zebra finches, lost their protective telomere caps quickly over time. Species such as the common tern, which lives to be about 30 years old, had less shortening over time." The petrels apparently produce more antioxidants as well - which may tie into the evidence suggesting that mitochondrial damage is the cause of shortened telomeres. Antioxidants slow the rate of that damage. The question remains as to where telomere length sits in the spectrum of cause and effect.

The Novel Paradigm of Longevity Science (October 01 2008) http://www.acceleratingfuture.com/people-blog/?p=2366
Over at Future Current, one of the presentations from Aging 2008: "What can each of us do to advance a new paradigm for health promotion and disease prevention in the 21st century that makes as its central tenet the slowing of aging? Recently, the board of directors of [the Alliance for Aging Research] committed to an aggressive effort to speak out for longevity science, which I think is a more elegant way of saying biogerontology, in order to hasten the social benefits extending healthy aging, a goal that we have referred to as 'pursuing the longevity dividend.' Now, the members of my board are not naive. They know very well that longevity science continues to be a tough sell. Let's face it, call it by any name, the quest for significantly extended lifespan has an image problem. Most established scientific leaders have been brought up to believe that aging is not only unchangeable, but not even very interesting. Now let's move to lay people. Most of them think there is not anything you can do about aging. They believe that even if you could, it would be a social and an economic catastrophe. Too many sick, old people sitting around, not pulling their weight. Even if people believed there could be some scientific breakthrough that would make it possible to extend the healthy years of life, many will set themselves up in opposition because it sounds unnatural or upsetting to social norms or religious beliefs. What will it take to overcome negative assumptions among the public?"

Life is the Road to Utopia, If You Can Stay on It (September 30 2008) http://jetpress.org/v19/bostrom.htm
From JET, a Nick Bostrom fiction in the spirit of the Fable of the Dragon Tyrant: "Your body is a deathtrap. This vital machine and mortal vehicle, unless it jams first or crashes, is sure to rust anon. You are lucky to get seven decades of mobility; eight if you be fortune's darling. That is not sufficient to get started in a serious way, much less to complete the journey. Maturity of the soul takes longer. Why, even a tree-life takes longer. Death is not one but a multitude of assassins. Do you not see them? They are coming at you from every angle. Take aim at the causes of early death - infection, violence, malnutrition, heart attack, cancer. Turn your biggest gun on aging, and fire. You must seize the biochemical processes in your body in order to vanquish, by and by, illness and senescence. In time, you will discover ways to move your mind to more durable media. Then continue to improve the system, so that the risk of death and disease continues to decline. Any death prior to the heat death of the universe is premature if your life is good. One day you or your children should have a secure home. Research, build, redouble your effort!" The road to Utopia is to continue to live well - which, as Bostrom notes, will require great labor devoted to new medical technologies of engineered longevity.

Axolotl Biochemistry as a Goal to Aim for (September 29 2008) http://pmid.us/18814845
It is plausible that mechanisms of unlimited tissue regeneration will be learned from lesser species and then ported to humans: "Urodele amphibians such as the axolotl are the champions of tissue regeneration amongst vertebrates. These animals have mastered the ability to repair and replace most of their tissues following damage or amputation even well into adulthood. In fact it seems that the ability of these organisms to regenerate perfectly is not affected by their age. In addition to being able to regenerate, these animals display a remarkable resistance to cancer. They therefore represent a unique model organism to study regeneration and cancer resistance in vertebrates. The need for this research is even more pressing at the dawn of the 21st century as we are faced with an ever aging world population which has to deal with an increase in organ failure and cancer incidence. Studying tissue regeneration in salamanders could yield significant knowledge to help regenerative medicine achieve the desired goal of allowing humans to repair and regenerate some of their own tissues as they age."

Mechanisms of Osteoarthritis (September 29 2008) http://www.eurekalert.org/pub_releases/2008-09/uorm-nsp092508.php

Researchers continue to learn more about the underlying biochemistry of common age-related conditions: "Until relatively recently, osteoarthritis was believed to be due solely to wear and tear, and an inevitable part of aging. Recent studies have revealed, however, that specific biochemical changes contribute to the disease, changes that might be reversed by precision-designed drugs. Our study provides the first solid proof that some of those changes are related to pain processing, and suggests the mechanisms behind the effect. The study revealed that pain signals originating in arthritic joints, and the biochemical processing of those signals as they reach the spinal cord, worsen and expand arthritis. In addition, researchers found that nerve pathways carrying pain signals transfer inflammation from arthritic joints to the spine and back again, causing disease at both ends. We believe this to be a vitally important process contributing to orthopaedic and neurological diseases in which inflammation is a factor."

Artificial General Intelligence

posted on September 22, 2008

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 assistantwhich 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=full

Those 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.

Hub of NanoMedicine

posted on October 6, 2008

To continue last week’s discussion of nanomedicine, here’s why you’d be interested in living long enough to see it get fully developed:

Nanotechnology refers to the control of matter on a scale normally between 1-100 nanometers. One nanometer is a billionth of a meter or 80,000 times smaller than a human hair.

They constructed a preliminary R&D roadmap and have already achieved some of their objectives. They have even established six currently active collaborations.

If you want to see who is at the hub of nanomedicine, visit these two websites:

http://www.MolecularAssembler.com/Nanofactory

http://www.MolecularAssembler.com/Nanofactory/Media/PressReleaseAug08.htm

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SLOW AND STEADY WINS THE RACE

Some food for thought on the way in which you approach the health basics - exercise, diet, supplementation, and relationships with physicians:

http://www.fightaging.org/archives/001582.php

The persistent application of good habits and good choices pays well. The basics are not rocket science, but they do make a significant difference over the years.
______________________________

LATEST HEALTHY LIFE EXTENSION HEADLINES

Mechanisms of Osteoarthritis (September 29 2008) http://www.eurekalert.org/pub_releases/2008-09/uorm-nsp092508.php

Artificial General Intelligence

posted on September 22, 2008

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

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.
_________________________________________________
$1 BILLION ALREADY INVESTED IN SOMETHING YOU CAN DO FOR FREE

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

TRY NOT TO STAB YOURSELF REPEATEDLY

Words of wisdom:

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

LATEST HEALTHY LIFE EXTENSION HEADLINES

Mitochondrial Function and Aging (September 16 2008) http://www.boston.com/news/health/articles/2008/09/15/power_outage/?page=full

Nanofactory Collaboration Colleague Awarded $3 Million

posted on September 29, 2008

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.php

From 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

posted on September 22, 2008

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

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.
_________________________________________________
$1 BILLION ALREADY INVESTED IN SOMETHING YOU CAN DO FOR FREE

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

TRY NOT TO STAB YOURSELF REPEATEDLY

Words of wisdom:

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

LATEST HEALTHY LIFE EXTENSION HEADLINES

Mitochondrial Function and Aging (September 16 2008) http://www.boston.com/news/health/articles/2008/09/15/power_outage/?page=full

Stay Happy and Save your Life

posted on September 17, 2008

I know a life extensionist who is facing more challenges now than most people face in a lifetime. Yet he remains upbeat and optimistic. I know a person who is not interested in extreme life extension who is crushed by a disruptive, but temporary challenge, which has sunk him into a deep state of depression.

About 90% of the members of the life extension community who I know would fit more in the first profile. They seem to function well in the face of adversity, bounce back from setbacks and are overall, healthier than average.

I find that the majority of people with no interest in extreme life extension tend to react more negatively to challenges, and also tend to be less healthy.

Then I came across an article by Paul J. Rosch, M.D. It illustrated how optimistic people live longer. Here are some excerpts:

Numerous studies support the belief that people with an upbeat and positive perspective tend to be healthier and enjoy longer lives than those who are gloomy and cynical about the future. Always expecting the worst was linked to a 25 percent higher risk of dying before age 65 in a very long-term California study. In another report on senior citizens, researchers rated 1,000 Dutch men and women aged 65-85 with respect to their degree of optimism, health and longevity. Over the next 10 years, participants classified as being very optimistic had 55 percent fewer deaths from all causes and 23 percent less heart-related deaths than highly pessimistic controls.

So Stay Happy and Save Your Life

The article cites study-after-study proving optimism extends your life. For example, Harvard researchers found cardioprotective effects when they followed 1,306 men who had been rated for optimism and pessimism in 1986. During the next 10 years, men reporting high levels of optimism had almost half the risk of suffering any coronary complications compared to peers classified as being very pessimistic.

Optimists and happy people may also be less likely to suffer a stroke according to a University of Texas study of 2,478 senior citizens. Researchers confirmed that increasing depression ratings were associated with a significantly higher incidence of stroke.

Similar rewards were reported in a study of 600 people over age 50 in a small Ohio town in 1975. Researchers found that optimists who viewed aging as a positive experience lived about 7.5 years longer than participants with a much darker perspective. One might argue that people in poorer health would be more apt to have negative responses and also be more likely to die over the next 23 years.

However, even when health, socioeconomic status, overall morale, loneliness, race, sex, and other possible confounding factors were taken into account, a positive view of aging was still highly correlated with significantly increased longevity. Indeed, this advantage was far greater than that afforded by lowering blood pressure or reducing cholesterol, each of which was found to lengthen life about four years.

In a Mayo Clinic study, optimists:

Had fewer limitations due to physical health.
Had less pain.
Felt more energetic most of the time.
Felt more peaceful and happy most of the time.
Had fewer problems with work or other daily activities as a result of their emotional state.

If you’d like to see the whole article, go to:

http://articles.mercola.com/sites/articles/archive/2005/09/03/why-do-happy-people-and-optimists-live-longer.aspx

Over and over, I see evidence of how attitude contributes to health and longevity. If you look for the correlation, you’ll find it too. But more importantly, look within.
_________________________________________
TELOMERE LENGTH: HEALTH OR AGING?

Telomeres are protective caps on your chromosomes that shorten with both aging and ill health. What is cause and what is effect?

http://www.fightaging.org/archives/001566.php

"There are hints that shortened telomeres might be caused by damage to mitochondria, which is in turn a known root cause of many aspects of degenerative aging. In a recently published study, researchers found that telomere length in the oldest humans is still strongly correlated with health - suggesting that perhaps aging is not the primary correlation.

"This makes more sense if you think of aging as less of a process and more of an accumulation of biochemical damage. Telomere length seems to be a marker for your personal level of damage, possibly by virtue of its connections to one or more of the primary modes of damage. Many questions remain, however, as to where exactly it fits in the grand scheme of cause and effect."

_____________________________

LATEST HEALTHY LIFE EXTENSION HEADLINES

Moscow News on Kriorus (September 12 2008) http://www.mnweekly.ru/national/20080828/55343651.html
The Moscow News looks at cryonics provider Kriorus, a Russian group that aims to become the Alcor of their country: "established in 2005 with the help of the Russian Transhumanist Movement, the devotees of which believe in the process of humans becoming 'posthumans' - beings capable of waiving aging and death, and forever forgetting of such problems as disabilities and disease. Such a goal is at present obviously unattainable, but one will find that not just transhumanists or immortalists are striving to complete the research on cryonics - the issue of death and prolonging of life is close to all, and the work on cryonics has been in progress for decades.

The technology of freezing the body available today is considered to be sufficiently developed, and more or less safe; most of the problems associated with freezing living matter - such as ice crystals appearing in cells and thus causing damage - have been solved. However, it is currently impossible to successfully thaw the body or brain without causing some degree of irreparable damage - and even if it were possible, all you'd have would be a corpse. To make the lifeless body come to life, far more advanced know-how is required. Cryonicists hope not only to reanimate the body [using technologies yet to be developed], but to remove the initial cause of death or any other problems present at the time of death."

Small Steps towards Medical Nanorobots (September 12 2008) http://www.sciencedaily.com/releases/2008/09/080911185104.htm
As engineered nanoparticles increase in complexity, they will at some point be sophisticated enough to be considered true medical nanorobots. That's still in the future, but you can see that the process is underway:
"Scientists have developed nanometer-sized 'cargo ships' that can sail throughout the body via the bloodstream without immediate detection from the body’s immune radar system and ferry their cargo of anti-cancer drugs and markers into tumors that might otherwise go untreated or undetected. The idea involves encapsulating imaging agents and drugs into a protective 'mother ship' that evades the natural processes that normally would remove these payloads if they were unprotected. These mother ships are only 50 nanometers in diameter, or 1,000 times smaller than the diameter of a human hair, and are equipped with an array of molecules on their surfaces that enable them to find and penetrate tumor cells in the body. We are now constructing the next generation of smart tumor-targeting nanodevices. We hope that these devices will improve the diagnostic imaging of cancer and allow pinpoint targeting of treatments into cancerous tumors."

Targeting Cancer Stem Cells (September 11 2008) http://www.ouhsc.edu/article-display.asp?idnum=1302
Given that researchers are making strong progress in both understanding the biochemistry of stem cells and in targeted cell-killing therapies, I don't expect the cancer stem cell hypothesis to remain a hypothesis for more than another few years. "After years of working toward this goal, scientists [have] found a way to isolate cancer stem cells in tumors so they can target the cells and kill them, keeping cancer from returning. A research team led [discovered] that a particular protein only appears in stem cells. Until now, researchers knew of proteins that appeared in both regular cancer cells and stem cells, but none that just identified a stem cell. The group has already begun work to use the protein as a target for a new compound that once developed would kill the stem cells and kill the cancer. By targeting the stem cells, scientists and physicians also would be able to stop the cancer from returning. Researchers expect to have initial testing completed to begin the first phase of clinical trials within 5 years. The compound, if successful in human trials, is expected to be available to the public within 10 years."

Using Signals Instead of Cells (September 10 2008) http://www.eurekalert.org/pub_releases/2008-09/afst-hes090908.php
Some first generation stem cell therapies seem to work because of the chemical signals emitted by implanted cells. An obvious next step is to only use the signals and skip the cells entirely. EurekAlert! notes a step along that path: "This method, developed in laboratory research with pigs, is the first non-cell based therapeutic application of human embryonic stem cells (hESCs). It entails using secretions from stem cells. In their studies with pigs, the researchers found that the administration of secretion from stem cells minimized heart injury by enhancing reperfusion therapy (angioplasty and cardiac bypass surgery) and reducing tissue death by another 60%. Heart function was also markedly improved. Using secretion instead of cells allows us to circumvent many highly intractable problems such as tumour formation, immune compatibility, cell viability, delivery, costs and timeliness." Researchers are still working to understand the signals that drive regeneration, but I imagine that a few years from now we will see tests of artificially produced signal chemicals to stimulate stem cells already present in the body.

Another Glenn Foundation Laboratory (September 09 2008) http://web.mit.edu/newsoffice/2008/aging-center-0909.html
The Glenn Foundation is funding a new laboratory at MIT, building upon the Harvard laboratory funded a couple of years ago. "The mission of the Glenn Foundation, founded in 1965 by Paul F. Glenn, is to extend the healthy productive years of life through research on the mechanisms of biological aging. The [Foundation] has pledged $5 million over five years to establish a new laboratory in MIT's Department of Biology to study aging. The new Glenn Laboratory for the Science of Aging will be directed by MIT Professor Leonard Guarente, a pioneer in the biology of aging. This generous gift from the Glenn Foundation will enable us to expand and intensify the study of critical regulators of aging, such as sirtuins. This work may lead to interventions to extend the healthy, productive period of our lives and forestall frailty and diseases." Laboratories founded with the explicit mission of addressing aging are an important part of the cultural sea change taking place in the aging research community.

An Update on Catalase in the Mitochondria (September 08 2008) http://pmid.us/18772469
You might recall the demonstration of extended healthy longevity in mice by localizing the antioxidant catalase to the mitochondria - a strategy replicated by other researchers to some success. Here is an update on that work: "We describe the effects of mitochondrially targeted catalase (MCAT) expression on end-of-life pathology in mice using detailed semiquantitative histopathological evaluation. We previously reported that the median and maximum life spans of MCAT mice were extended relative to those of wild-type littermates. We now report that MCAT expression is associated with reduced malignant [tumor] burden, reduced cardiac lesions, and a trend toward reduced systemic inflammation ... Combined disease burden and comorbidity are also reduced, and MCAT expression is not associated with any detrimental clinical effects. The results suggest that oxidative damage is involved in aging of [mice] via modulation of a subset of age-associated lesions. Antioxidant interventions targeting mitochondria may therefore be a viable strategy for prevention or postponement of some age-associated diseases."

Artificial General Intelligence

posted on September 22, 2008

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

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.
_________________________________________________
$1 BILLION ALREADY INVESTED IN SOMETHING YOU CAN DO FOR FREE

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

TRY NOT TO STAB YOURSELF REPEATEDLY

Words of wisdom:

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

LATEST HEALTHY LIFE EXTENSION HEADLINES