Reverse Aging by 2029

Life Expectancy

noreply@blogger.com (Biscuit) — Mon, 24 Nov 2008 17:19:00 +0000

Can your expectations determine how long you will live?

I believe lots of us actually die because of our expectations. We're conditioned to believe the average lifespan is around eighty years, so we wind down and die right on schedule. We usually get what we expect, not what we want. What if you expected to live to 100? Wouldn't you naturally gravitate toward the habits that will make that happen? Wouldn't your thoughts and emotions be more positive? How about longer? Loads of research tells us we should stay healthy for up to 100 years. But why don't we? Could it start with your attitude? Don't cop out by blaming it on your genes or on luck. Really, 65–75% of it is the choices you make. Your genes account for less that 35%.

This is backed up by hard science. Studies have shown that people who just think they are aging faster actually do age faster!

If you always think the glass is half full, you're on the right track. Mayo Clinic research shows that people with positive outlooks typically live 19% longer than people who see the glass as half empty. Although it's questionable if this can be attributed to optimists being more likely to seek medical help when they're ill, or if their immune systems strengthen as a result of their sunny outlook. The end result is though, they live longer. Optimists are also less likely to suffer depression and helplessness than their pessimistic counterparts.

To support the hypothesis that their immune systems are actually strengthened, Dr. Bruce Lipton’s experiments, and that of other leading-edge scientists, have examined in great detail the processes by which your cells receive information. The implications of this research radically change our understanding of life. It shows that genes and DNA do not control your biology. Instead, DNA is controlled by signals from outside your cells, including the energetic messages emanating from your positive and negative thoughts.

He clearly describes the connection between your core thoughts, beliefs and attitudes and how your cells function as a result. Happy thoughts put your cells’ functions in balance. Hateful, angry and resentful thoughts do the exact opposite. They suppress your immune system, alter your hormones, upset your digestive system, and diminish your brain function and respiration.

Dr. Lipton’s profoundly hopeful synthesis of the latest and best research in cell biology and quantum physics is being hailed as a major breakthrough showing your body can be changed as you retrain your thinking. His book, The Biology of Belief is a groundbreaking work in the field of New Biology.

In addition, an often repeated study showed that when a person’s living cells from different organs are put in separate dishes, cells from one organ would respond when cells from a different organ in a different dish were stimulated. If the cells were from two different people, they would not get the reaction. This means the trillions of cells in your body are always in direct communication with one another, even if they are not in direct contact by chemical or neurological pathways.

Stub a toe, and all your cells react. Poison your body with cigarette smoke or toxic food, and you stimulate every cell. Subject yourself to uncontrolled stress, and you stress tens of trillions of cells. Now can you see why stress management and attitude are so critical to your health and longevity?

Now that you know your thoughts affect every single cell in your body, what are you going to do about it? Since you now realize positive, loving and grateful thoughts keep you healthy and make you live longer, while negative thoughts destroy you from the inside out, you have a big anti-aging advantage. What happens to you usually doesn’t matter one bit. How you react means everything.

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LATEST HEALTHY LIFE EXTENSION HEADLINES

Cryonics as Emergency Medicine (November 21 2008) http://www.depressedmetabolism.com/2008/11/19/cryonics-sets-example-for-emergency-medicine/
From Depressed Metabolism: "One of the most neglected aspects of cryonics is that its procedures, and the research to support them, can have important practical applications in mainstream fields such as organ preservation and emergency medicine. Contrary to popular opinion, cryonics does not just involve an optimistic extrapolation of existing science but can set the standard for these disciplines. As a matter of fact, that is exactly what cryonics, and cryonics associated research, has been doing over the last 25 years. It is encouraging to observe that some of the procedures that are routine in cryonics stabilization protocol are starting to catch on in mainstream emergency medicine practice as well. For example, contemporary cryonics stabilization protocol has been strongly shaped by the idea that the best strategy to limit brain injury after cardiac arrest is to combine a number of different interventions: cardiopulmonary support, induction of hypothermia, and administration of circulation-supporting and neuroprotective medications. It is therefore very encouraging to learn that the Wake County EMS group in North Carolina has achieved impressive results in treating out-of-hospital cardiac arrest victims using a protocol that closely follows elements of current cryonics stabilization protocol."

Building New Pancreatic Cells (November 21 2008) http://www.sciencedaily.com/releases/2008/11/081120130539.htm
Regenerative medicine advances, step by step: "researchers have developed an unlimited number of pure insulin-producing cells from mouse embryonic stem cells (ESCs). These pure insulin-producing cells, which according to electron microscopy studies, have the same sub-cellular structures as the insulin-producing cells naturally found in the pancreas, were highly effective in treating diabetes in the mouse model. The transplants of pure insulin-producing cells reduced the blood glucose levels of diabetic mice with high blood glucose levels. None of the diabetic mice involved in the transplant experiments developed teratoma, which are a type of tumor often associated with ESCs and which could complicate their use in human therapeutic treatment. Furthermore, the pure insulin-producing cells managed to retain their insulin-production and glucose-sensing capacity over time. Besides providing a tool to facilitate basic research in test tubes and animals, these insulin-producing cells may be also used to replace the isolated native pancreatic cells that are hard to obtain in a large amount, for pharmacological tests."

Towards Accurate Biomarkers of Aging (November 20 2008) http://www.eurekalert.org/pub_releases/2008-11/bifa-but111208.php
From EurekAlert!: researchers "have identified for the first time biomarkers of aging which are highly predictive of both chronological and physiological age. Biomarkers are biochemical features that can be used to measure the progress of disease or the effects of treatment. The research involves nematode worms, microarrays which measure changes in gene expression, and complex computer algorithms. This is the first step toward identifying similar biomarkers in humans which would provide a means of scientifically validating anti-aging therapies. This is the first evidence that physiological age can be predicted non-subjectively. This is a first step; our results were not perfect, but we were able to predict the ages of the animals 70% of the time, which is far better than anything that has been done before. Research into the biology of aging in humans has been hampered by the lack of irrefutable biomarkers that correlate with the aging process. I am confident that at some point there will be a non-subjective method of determining how old someone is with a high level of confidence."

Inflammation and Alzheimer's (November 19 2008) http://pmid.us/19014446
A prodrome is an early set of non-specific symptoms that herald a particular disease. Here, researchers point to chronic inflammation as a prodrome of Alzheimer's (AD): "Recently, the term 'inflammaging' was coined [to] characterize a widely accepted paradigm that ageing is accompanied by a low-grade chronic up-regulation of certain pro-inflammatory responses. Inflammaging differs significantly the from [traditional] acute inflammation in that it is characterized by a relative decline in adaptive immunity. While the over-active innate immunity characteristic of inflammaging may remain subclinical in many elderly individuals, a portion of individuals (postulated to have a "high responder inflammatory genotype") may shift from a state of "normal" or "subclinical" inflammaging to one or more of a number of age-associated diseases. Although conditions of enhanced innate immune response with overproduction of pro-inflammatory proteins are associated with both healthy aging and AD, it is suggested that those who age 'well' demonstrate anti-inflammaging mechanisms and biomarkers that likely counteract the adverse immunity of inflammaging. Thus, opposing the features of inflammaging may prevent or treat the symptoms of AD."

Regeneration via Embryonic Stem Cells (November 19 2008) http://www.reuters.com/articlePrint?articleId=USTRE4AI02220081119
From Reuters: "Stem cells from tiny embryos can be used to restore lost hearing and vision in animals, researchers said Tuesday in what they believe is a first step toward helping people. One team repaired hearing in guinea pigs using human bone marrow stem cells, while another grew functioning eyes in tadpoles using frog cells. They grew the stem cells into neuron-like cells in lab dishes and then transplanted them into the inner ears of the guinea pigs. Three months later, the animals appeared to have some hearing. The goal was to regrow the tiny hair cells that are essential for mammals to hear, although she is not sure yet how the stem cells made this happen. They would eventually like to try something similar in humans." These are early stage proof-of-concept demonstrations. It is an illustration of progress that they do not stand out as exceptional amidst advances in the many other lines of regenerative research presently taking place.

More on the Biochemical Value of Exercise (November 18 2008) http://www.eurekalert.org/pub_releases/2008-11/aps-eib111708.php
Exercise is good for you: "A new study confirms that exercise can reverse the age-related decline in the production of neural stem cells in the hippocampus of the mouse brain, and suggests that this happens because exercise restores a brain chemical which promotes the production and maturation of new stem cells. One hypothesis the researchers investigated is that the age-related decline in neurogenesis is tied to a rise in corticosterone in middle age. Elevation of corticosterone has been associated with a drop in the production of new stem cells in the hippocampus. The second hypothesis is that nerve growth factors -- which encourage new neural cell growth but which decrease with age -- account for the drop in neurogenesis. Production of neural stem cells improved by approximately 200% compared to the middle-aged mice that did not exercise. In addition, the survival of new nerve cells increased by 170% and growth by 190% compared to the sedentary middle-aged mice. ... Based on these results, it appears that nerve growth factor has more to do with these findings than the corticosterone."
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Aging is Slowly Stealing Our Lives

noreply@blogger.com (Biscuit) — Mon, 17 Nov 2008 17:33:00 +0000

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."

A Valuable Lesson

noreply@blogger.com (Biscuit) — Mon, 10 Nov 2008 23:06:00 +0000

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

noreply@blogger.com (Biscuit) — Thu, 06 Nov 2008 00:39:00 +0000

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.

Save for the Future

noreply@blogger.com (Biscuit) — Mon, 13 Oct 2008 16:03:00 +0000

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?
_________________________________

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.phpYou 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

noreply@blogger.com (Biscuit) — Mon, 06 Oct 2008 15:29:00 +0000

Dear Future Centenarian,

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.
______________________________________________

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.
______________________________

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."

Nanofactory Collaboration Colleague Awarded $3 Million

noreply@blogger.com (Biscuit) — Mon, 06 Oct 2008 15:27:00 +0000

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.
______________________________
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

noreply@blogger.com (Biscuit) — Mon, 29 Sep 2008 15:14:00 +0000

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

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

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

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

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

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

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

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

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

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

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

TRY NOT TO STAB YOURSELF REPEATEDLY

Words of wisdom:

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

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

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

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

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

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

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

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

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

Las Vegas Longevity Workshop

noreply@blogger.com (Biscuit) — Thu, 11 Sep 2008 15:57:00 +0000

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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