Tuesday, January 13, 2009

Value Reflections

One of the advantages of old age is your increased ability to reflect. You can reflect on the mistakes you made and on your regrets as some people choose to do most of the time. That’s called dwelling. Or, you can briefly reflect on those negative experiences and learn from them. That’s called wisdom.

An even more positive form of reflection is value reflection. No matter whom you are or how you measure your levels of happiness and success, you definitely have created and/or experienced values during your lifetime. Value reflection is one of the most rewarding and pleasurable experiences of life. Who doesn’t like to relive happy memories? Who doesn’t take pride and pleasure in looking back on the positive contributions you made to society, your market, your family, your friends and to yourself?

We all carry within us a treasure of values to be proud of, and with each passing year, that treasure grows, whether you are aware of it or not.

With extended longevity, imagine your possibilities. Not only is technology growth exponential, but so is personal growth. And if you remain vibrant, your enthusiasm can actually intensify with age.

In past issues, I wrote about how the power of technology doubles every year, including the technology that contributes to radical life extension. That means next year will see a doubling of all that power we made since the beginning of history. And here is what that means to you:

If you take the healthy steps to live an extra year, the technology that could lead to your open ended lifespan doubles in that year. If you decide to adopt a lifestyle that adds ten more quality years to your life, life enhancing technology will increase by over 1000 times! And then if you try just a little harder and add another extra year, the power of that technology will double to 2000 times. That means your 11th extra year was just as beneficial to you as those first extra ten.

Then add another year and… well, you get the idea. Before you know it, we will have cracked the longevity code, and you will be on your way to endless youth.

And what could one of the most pleasurable things about that be? As I said, more and more years to add happiness and value and even better value reflection. Imagine what you can accomplish in two lifetimes. In three or more. Imagine how big your values treasure chest will grow as you exponentially acquire wisdom.
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LATEST HEALTHY LIFE EXTENSION HEADLINES

The Life Expectancy Puzzle of Left-Handedness (December 05 2008) http://pmid.us/19044215
Many identified differences in human longevity between groups lack conclusive explanations, such as why women have a greater life expectancy. Differences in life expectancy due to handedness are another puzzle: "Many studies report that left-handers have a shorter longevity than right-handers, and the present study may provide a possible explanation for that finding. In a Cardiac Rehabilitation Unit for the elderly with a mean age of 75.2 years the prevalence of left-handers was 16.7%. This latter value was significantly different from the 6.7% in controls of similar age. These data suggest that heart disease may be one reason for a reduced longevity among left-handers. Left-handers use the right hemisphere for movement, and unilateral activation of that hemisphere in the form of EEG desynchronization and deactivation in the form of EEG slow waves are both related to cardiac abnormalities." In the grand scheme of things these differences are unimportant: the greatest determinant of our future longevity is progress in the application of aging research.

On Immunosenescence (December 05 2008) http://pmid.us/19047800
Researchers discuss the failing, age-damaged immune system: "At present, individuals can live up to 80-120 years, a time much longer than that of our ancestors, as a consequence of the improvements in life conditions and medical care. Thus, the human immune system has to cope with a lifelong and evolutionarily unpredicted exposure to a variety of antigens, which are at the basis of profound age-related changes globally indicated as immunosenescence, a multifaceted phenomenon that increases morbidity and mortality due to infections and age-related pathologies. The major changes occurring during immunosenescence are the result of the accumulation of cellular, molecular defects and involutive phenomena (such as thymic involution) occurring concomitantly to a hyperstimulation of both innate and adaptive immunity (accumulation of expanded clones of memory and effector T cells, shrinkage of the T cell receptor repertoire, progressive activation of macrophages), and resulting in a low-grade, chronic state of inflammation defined as inflammaging. It is unknown whether inflammaging, which represents a risk factor for most age-related pathologies, is a cause or rather an effect of the aging process. Centenarians seem to be equipped with gene variants that allow them to optimize the balance between pro- and anti-inflammatory molecules, and thus to minimize the effects of the lifelong exposure to environmental insults and stressors."

Dormant Emergency Stem Cells (December 04 2008) http://www.eurekalert.org/pub_releases/2008-12/haog-dsc120408.php
An intriguing discovery from a cancer research group that I suspect has more promise for the field of regenerative medicine: "Up to now, scientists have assumed that adult stem cells have a low division rate. According to theory, they thus protect their DNA from mutations. [Researchers] have now discovered a group of stem cells in mouse bone marrow that remain in a kind of dormancy [and] divide only about five times throughout the life of a mouse. Translated to humans, this would correspond to only one cell division in 18 years. In contrast, stem cells of the larger group, the 'active' stem cells, divide continuously about once a month. However, in an emergency such as an injury of the bone marrow or if the messenger substance G-CSF is released, the dormant cell population awakes. Once awakened, it shows the highest potential for self-renewal ever to be observed in stem cells. If transplanted into irradiated mice, these cells replace the destroyed bone marrow and restore the whole [blood] system. It is possible to isolate new dormant stem cells from the transplanted animals and these cells are able to replace bone marrow again – this can be done several times in a row. The situation is different with 'active' stem cells, where bone marrow replacement can successfully be carried out only once."

Evidence Against the Cancer Stem Cell Theory (December 03 2008) http://www.eurekalert.org/pub_releases/2008-12/uom-usp112608.php
It would be good for all of us if the cancer stem cell theory turns out to be true for even a majority of cancer types - as this would mean that a side-effect of stem cell research will be a cure for cancer. Unfortunately, there are good reasons to believe that this will not be the case; nothing in human biochemistry is as simple as we'd like. From EurekAlert!: "the cancer stem-cell model [must] be reassessed because it is based largely on evidence from a laboratory test that is surprisingly flawed when applied to some cancers. I think the cancer stem-cell model will, in the end, hold up for some cancers. But other cancers, like melanoma, probably won't follow a cancer stem-cell model at all. Scientists previously estimated that only one in 1 million melanoma cells has the ability to run wild, exhibiting the kind of unchecked proliferation that leads to new tumors. These aggressive interlopers are the cancer stem cells, according to backers of the model. But after updating and improving the laboratory tests used to detect these aberrant cells, [researchers] determined that at least one-quarter of melanoma cells [have] the ability to form new tumors. The assay on which the field is based misses most of the cancer cells that can proliferate to form tumors. Our data suggest that it's not going to be possible to cure melanoma by targeting a small sub-population of cells."

Senescent Cells and Cancer (December 03 2008) http://dx.doi.org/10.1371/journal.pbio.0060301
One of the consequences of an aging immune system is that it stops removing senescent cells - certainly, senescent cells increase dramatically with age. Here is a look at why that process is likely to increase your cancer risk: "Although 'cellular senescence' can suppress tumor formation from damaged cells by blocking the cell division that underlies cancer growth, it has also been implicated in promoting cancer and other age-related diseases. To understand how this might happen, we measured proteins that senescent human cells secrete into their local environment and found many factors associated with inflammation and cancer development. Senescent cells promote the growth and aggressiveness of nearby precancerous or cancer cells. Our findings support the idea that cellular senescence can be both beneficial, in preventing damaged cells from dividing, and deleterious, by having effects on neighboring cells; this balance of effects is predicted by an evolutionary theory of aging." Senescent cells are a prime target for the same sorts of discerning therapies being developed to kill cancer cells with no side-effects.

Towards Tuning the Immune System (December 02 2008) http://www.sciencedaily.com/releases/2008/11/081130153102.htm
Researchers are making good progress towards control over immune cells, and future goals seems likely to be applicable to the restoration of some function to an age-damaged immune system. Researchers have identified "seven different receptors on T cells that can tamp down immune responses during a prolonged battle with an infectious pathogen or against developing cancer. Chronic over-stimulation of the immune system can lead to poor control of infections and cancer, so the results explain why it is that these key immune cells gradually become 'exhausted' and ineffective over time. We are starting to see a picture emerging of a really tuneable array of inhibitory receptors expressed on T cells. That suggests it may be possible to not only dramatically enhance antiviral or antitumor T cell responses, but also to fine tune which response you want to enhance in order to reverse T cell exhaustion and continue fighting an infection or disease. This presents us with a great clinical opportunity. T cells have a lot of weapons at their disposal to control viral infection and most of them are disarmed when these cells become exhausted. It may be possible to selectively rearm T cells while generally reinvigorating them."

More on Exercise and the Aging Brain (December 01 2008) http://www.eurekalert.org/pub_releases/2008-12/rson-ehp112508.phpIt's well worth remembering that regular exercise brings benefits that no present medical technology can match-and at a fraction of the cost of medicines that do far less. EurekAlert! notes that researchers compared "brain scans of older adults who exercise to brain scans of those who do not. The researchers recruited 12 healthy adults, age 60 to 76. Six of the adults had participated in aerobic exercise for three or more hours per week over the last 10 years, and six exercised less than one hour per week. All of the volunteers underwent MRI to determine cerebral blood flow and MR angiography to depict blood vessels in the brain. Researchers were able to make 3-D models of the blood vessels and examine them for shape and size. They then compared the blood vessel characteristics and how they related to blood flow in both the active and inactive groups. The results showed that the inactive group exhibited fewer small blood vessels in the brain, along with more unpredictable blood flow through the brain. The active adults had more small blood vessels and improved cerebral blood flow. These findings further point out the importance of regular exercise to healthy aging."

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Monday, November 24, 2008

Life Expectancy

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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Monday, October 6, 2008

Hub of NanoMedicine

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.
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SLOW AND STEADY WINS THE RACE

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

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

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

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

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

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

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

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

Mechanisms of Osteoarthritis (September 29 2008) http://www.eurekalert.org/pub_releases/2008-09/uorm-nsp092508.php
Researchers continue to learn more about the underlying biochemistry of common age-related conditions: "Until relatively recently, osteoarthritis was believed to be due solely to wear and tear, and an inevitable part of aging. Recent studies have revealed, however, that specific biochemical changes contribute to the disease, changes that might be reversed by precision-designed drugs. Our study provides the first solid proof that some of those changes are related to pain processing, and suggests the mechanisms behind the effect. The study revealed that pain signals originating in arthritic joints, and the biochemical processing of those signals as they reach the spinal cord, worsen and expand arthritis. In addition, researchers found that nerve pathways carrying pain signals transfer inflammation from arthritic joints to the spine and back again, causing disease at both ends. We believe this to be a vitally important process contributing to orthopaedic and neurological diseases in which inflammation is a factor."

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Monday, September 29, 2008

Artificial General Intelligence

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

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

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

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

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

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

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

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

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

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

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

TRY NOT TO STAB YOURSELF REPEATEDLY

Words of wisdom:

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

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

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

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

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

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

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

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

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

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Friday, June 20, 2008

Network Your Way to Immortality

Dear Future Centenarian,

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

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

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Thursday, June 19, 2008

The Inevitability of Open-Ended Lifespans

Dear Future Centenarian,

Here’s an excellent commentary from Reason at LongevityMeme.org:

“The choice of living a healthy, youthful life of centuries and more is inevitable. That much is obvious, written in the present breadth of human civilization, knowledge of what is possible under the laws of physics, and pace of progress in biotechnology. The burning question in this case is whether or not it will happen soon enough to benefit you reading this today:

Replacement biological organs are a decade away, and commercial efforts to develop sophisticated repairs to age-damaged cells and vital biomechanisms will be rife in the 2020s. Computational power will be so great and so cheap that tens of thousands and then millions of research programs will be accomplished in simulation for a tiny fraction of their cost today; the priesthood of bioscience will dissolve and progress will be as diverse, energetic and imaginative as it is for open source software at present. Redesigning human biochemistry and greatly augmenting our biology with nanomachinery will be hot areas for venture funding.

I see development of the baseline technologies required for greatly extending the healthy human life span as a given for the next few decades. The biotechnology revolution is roaring ahead, and there's no halting the relentless advance of computational power. But just because we can doesn't mean we will - there is still the need to take that baseline technology and turn it to a desired use.

Given that there is no massive, serious life extension research and development community in existence today - and here, I'm thinking of a community to match the cancer research establishment in breadth and support - the future we'd like to see is still in doubt. If we want the awe-inspiring biotechnologies of the 2020s promptly put to use in repairing the damage of aging, right out of the starting gate, then we'd better get working on that now.”

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