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The Central Florida Life Extension Meetup Group Alcor American Cryonics Society Cryonics Institute Immortality Institute IEET SENS (Aubrey de Grey) Ralph Merkle Nanomedicine Robert Freitas Jr. Singularity Institute
Humanists Resources
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"Do you want to be in the control group or the experimental group?" - attributed to R. Merkle
"I don't want to achieve immortality through my work... I want to achieve it through not dying."
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Life Extension Podcasts from NY Public Radio contributed by member on 2008-03-16 |
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| There are some interesting podcasts on immortalism/life extension at New York Public Radio, posted here http://www.wnyc.org/shows/radiolab/episodes/2007/06/15 Also on memory: http://www.wnyc.org/shows/radiolab/episodes/2007/06/08 and the neurological basis of identity: http://www.wnyc.org/shows/radiolab/episodes/2007/06/24 |
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The Biology of Human Longevity contributed by member on 2008-02-25 |
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| This is a cool review from the CR list... --------------- The Biology of Human Longevity: Inflammation, Nutrition, and Aging in the Evolution of Life-spans by Caleb E. Finch Academic (Elsevier), Amsterdam, 2007. 640 pp. $69.95, ?39.99, Euro58.95. ISBN 9780123736574. -------------------------------------- Metabolically speaking, we're all on fire. Current thinking in the biology of aging suggests that the normal processes cells use to burn fuel, providing energy for life, indirectly lead to much of the disease and disability that characterize aging in humans and other animals. Chemically unstable by-products of cellular oxidation--especially free oxygen radicals--can initiate the deterioration of cell membranes and macromolecules (1, 2). As small "hits" causing cellular injury accumulate, the results can range from uncorrected mutations and cancers to forms of tissue damage leading to vascular pathology and Alzheimer's disease. With heart disease, stroke, and diabetes now among the leading causes of aging-related death in the United States (3), and rising fast as baby boomers join the ranks of the elderly, these diseases are a primary target for biomedical research. In The Biology of Human Longevity, Caleb Finch spotlights the relationships among cellular processes that are considered important causes of aging-related disease. This formidable book successfully integrates the "freeradical damage" hypothesis with a new more general theory of aging having direct implications for preventing specific pathological syndromes that increase with chronological age. Finch (a professor of gerontology at the University of Southern California) weaves complex strands of evidence from medical history, molecular biology, and biochemistry (as well as evolution and anthropology) into a layered tapestry of the synergies among various forms of "bystander damage" (injury, mutations, toxic insult, and oxidative damage) and the ways in which these can foreshadow diagnosable disease states. Oxidative damage remains a central player in the drama he unfolds, but now it shares the stage with several lesser-known, equally important accomplices: inflammation, damage during development, and the hazards of overnutrition. Finch's central thesis is wedded to a fundamental tenet of evolutionary biology: physiological adaptations for sustained health and reproduction involve evolutionary trade-offs. The growth and maintenance of reproductive and somatic tissues, for example, require hormones and growth factors (e.g., sex steroids and insulinlike growth factors) that also facilitate the proliferation of cancers and other pathological changes. Effective defenses against infection, injury, or stress--even during prenatal development--ignite a cascade of inflammatory factors, including cytokines and other peptides. This first wave of the innate immune response is followed by rapid proliferation of specialized cells and the release of a plethora of signaling molecules and oxidative by-products that can damage cells and macromolecules. Adding fuel to the fire is a diet too rich in animal fat, increasing exposure to pathogenic microbes and exacerbating inflammation. The book's cover features a photo of the "Venus of Willendorf," an exceedingly curvaceous, female stone effigy (~23,000 BCE). In a world of nutritional scarcity, she represented an unrealistic paragon of reproductive potential. Today, we consider a 1.65-m-tall woman of similar proportions--say, a body mass of 82 kg--to be obese (4), with clinically elevated risks for type 2 diabetes and cardiovascular disease. In his last and most provocative section, Finch proposes that increases in brain size and the human life span over the past million years occurred in concert with changing nutritional priorities, slower developmental rates, and a tolerance for inflammation in "dirty, invasive, and stingy" prehistoric environments. The integration of more meat into the human diet, he argues, provided protein needed for larger brains but involved new physiological and genetic trade-offs between fitness and liability for long-term damage. This scenario provides a satisfying rationale for why variants of some genes for metabolizing animal fat that are linked to a human predilection for atherosclerosis, some cancers, and the amyloid plaques characteristic of Alzheimer's disease (such as those of the ApoE gene family) are not shared by our closest primate relatives. The book provides an unparalleled synthesis of the burgeoning literature addressing the roles played by oxidative damage and inflammation in diseases of aging. Finch offers thorough discussions of methodologies and central constructs in aging research (including the search for better molecular biomarkers of aging) and a short primer of evolutionary aging theory--possibly not enough for some evolutionary biologists, but a sufficiently broad perspective for those wading into the field for the first time. Along with a catalog of experimental and genetic interventions in aging based on laboratory animal systems, he summarizes an exhaustive body of clinical literature, showcasing nutritional and pharmaceutical approaches that have potential for intervening in aging disease states by curtailing inflammation-induced damage. With the coupling of his expertise in neuroscience and clinical medicine to his keen interests in demography and comparative zoology, Finch arguably remains our most potent synthesizer of biology and gerontology. Here his writing conveys a sense of urgency not present in his classic Longevity, Senescence, and the Genome (5). A bit verbose and convoluted at times, The Biology of Human Longevity would have benefited from the attention of a copy editor half as ambitious as the author. That aside, the intellectual framework Finch provides in it will be intensely stimulating to both experts and newcomers in the field of aging. The book should attract notice from developmental biologists, anthropologists, and clinical researchers alike. |
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Aubrey de Grey on the Colbert Report contributed by member on 2008-02-12 |
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| Aubrey de Grey appeared on Stephen Colbert's show February 11th. This is a good sign that his work is now getting better coverage. | ||||||||
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General Article contributed by member on 2008-01-31 |
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| I thought this was a oool article- esp. where it mentions telomerase inducers being near clinical trials (to effectively -reverse- aging in tissues). Anton B, Vitetta L, Cortizo F, Sali A. Can we delay aging? The biology and science of aging. Ann N Y Acad Sci. 2005 Dec;1057:525-35. Review. PMID: 16399917 Abstract Long before the fountain of youth, mankind has had an interest in staying young. As we move into the 21st century, that interest has not only continued, but it has become an obsession. While no one can really prevent normal, chronological aging, there are things we can do to slow down "pathological aging." After all, aging is about accelerated inflammation, depletion, and wear and tear. With the marked increase in life expectancy and life span, clinicians need to be aware of the effects of aging on the provision of treatment modalities. Appropriate interventions individualized to the patient can help to "compress morbidity" by shortening the period of functional decline common in old age. Therefore, the "health span" will come closer to matching the life span. Disease and disuse are far more likely explanations for functional decline and the onset of common chronic conditions in older persons than is "tru" natural or normal aging. Regardless of your genetic inheritance, you can accelerate aging by lifestyle choices and environmental conditions to which you expose your genes. There are even ways to reverse the problems associated with aging. Getting older does not have to mean growing older. Welcome to the world of preventative gerontology, better known as anti-aging medicine! Until quite recently, the notion of reversing human aging was mere fantasy, absent of any scientific support. Throughout history, going as far back as the Epic of Gilgamesh 4700 years ago, we have dreamed of being able to cure aging and the diseases that accompany it; but every claim of a "fountain of yout" has proven to rely on nothing more than false hopes and-more often than not-an urge to profit at the expense of the gullible. The fact that we never really understood aging made it extremely unlikely that we could learn to slow, prevent, or reverse the process. HISTORY AND AGING Today, we stand at a unique point in history, much like where we were in 1870 with regard to infectious disease. At that time, few had heard of Pasteur or Koch, and well-known scientists ridiculed the idea of microbes being dangerous or causing disease. Time passed, however, and, once ridiculed or not, we now take the concept of infectious disease for granted. In fact, much of what is good about modern medical care-sterile technique, antibiotics, immunizations, for example-derives from this single, powerful conceptual revolution that began 135 years ago. Before we came to grips with the fact that microscopic creatures could harm and even kill us, effective intervention in most common diseases was also fantasy. In those days, treatment for tetanus infection- "lockjaw"-was a matter of early cauterization to remove "devitalised tissu" (using a red-hot iron rod or boiling oil), amputation (without anaesthesia) if things got worse, followed finally by hope and prayer, though nothing really improved the deadly outcome. We think of malaria, cellulitis, tetanus, pneumonia, and yellow fever as a short list of infectious diseases; to the physicians of those times, each of these diseases was independent and unique, without shared mechanism and without hope of effective treatment. Today, we have much the same conception (and misconceptions) of aging and age-related diseases. We think of cancer, atherosclerosis, osteoporosis, osteoarthritis, skin aging, and immune senescence as all unrelated, except chronologically. You get these diseases as you get older, not because they have anything in common, but "just because you get older" Even pathologists rarely consider common mechanisms, cellular events that link each of these diseases at the genetic level. After all, what could osteoarthritis and atherosclerosis, aging skin and Alzheimer's possibly have to do with one another except that they happen to old people? Yet, not only do they have a great deal in common, but also it is precisely this common thread that will allow effective intervention both in age-related diseases and in aging itself. THEORIES OF AGING Many theories of aging have been proposed, yet science has not produced a universal theory of aging. Why do we age? Current theories of aging at the cellular and molecular level generally revolve around two themes: aging is programmed, and aging is accidental. To better understand the process of aging we need to focus on the differences between "normal" aging and "pathologica" aging. Pathological aging is the aging process that is brought on by the presence of disease, such as adult-onset diabetes or arthritis, and that may later bring on cardiovascular disease or osteoporosis. This is not considered normal aging. These conditions are due to heredity or lifestyle. However, developing cataracts is considered normal aging, because if you live long enough, you will develop them. Every time the earth circles the sun, we are one year older chronologically, yet we know that the rate at which people age biologically varies widely. The loss of muscle tone, circulation, immune capacity, skin elasticity and joint flexibility, for example, occurs much more quickly in some people than in others. This is due to gene expression. Genes do not change, but their expression does: Therefore, we are not prisoners of our genetic destiny. There is a level of plasticity in gene expression. There is a large paradigm shift that needs to occur in our thinking: aging is a disease that can be prevented or reversed. Changing variables that affect genes such as diet, lifestyle, and stress can have an impact on genetic expression. We age because our hormones decline; our hormones do not decline because we age. Here we need to remember that hormones are required to trigger genes in cells to manufacture the necessary proteins, peptides, and other hormones. Lower volumes will yield lower manufacture. The goal of anti-aging medicine is to increase the health span, not just the life span. After all, who would want to live longer with chronic debility or cognitive impairment? Anti-aging medicine consists of modalities and therapies involving diet, nutrition, exercise, destress, functional balance, system reserves, and a balance in anabolic to catabolic metabolism. Some of the familiar modalities of biochemistry and pathology associated with anti-aging medicine include glycation, inflammation, oxidation, methylation, endocrine deficiencies and imbalances, and decline of immunity. Aging is fundamentally a metabolic process. While clinicians deal constantly with the myriad symptoms of aging, the best results are not obtained until the underlying decrease in anabolic metabolism has been corrected. PATHOPHYSIOLOGY As humans age, all functions and characteristics are modified. However, there is no clear consensus about what aging actually is-what "naturall" occurs with the passage of time-versus the effects of disuse and disease. Optimal health management requires an understanding of aging processes that are assumed to be natural and inevitable and knowledge of the most accepted theories of how and why we age prematurely, usually due to many reversible risk factors. Although at present there is a significant emphasis on development of new technologies, especially in the area of human genomics and stem cell research, to provide greater clarity on genetic and cellular aging mechanisms, adaptation of traditional, allopathic, complementary, and alternative integrative modalities to reflect current understanding of the effects of aging and of how to postpone or prevent premature aging is now possible. Earlier studies attempted to identify the effects of natural or normal aging free of disease as distinct from the development of age-related diseases such as cancer, cardiovascular disease, diabetes, osteoporosis, and neurodegenerative diseases such as dementia and Alzheimer's disease. Results from such studies suggest that the effects of aging are extremely "plastic" and variable from person to person. McEwen's concept of the "allostatic load" suggests that each person's signature of aging is a result of interactions among genetic makeup, lifestyle, diet, and environmental challenges. Thus, a combination of holistic parameters can be used to assess cumulative physiologic and psychological challenges over the life span and to predict how today's health care practitioners will respond not only to new challenges such as management of age-related conditions and application of treatment modalities in old age, but also to longevity itself. Accordingly, a broader pattern of aging processes or biomarkers should be considered in determining how "wel" a particular person is aging and how to customize interventions to reduce the effect of a chronic condition, thereby preventing certain processes from leading to the development of one or more ailments that are more likely to appear in old age. Table 1 lists various physiologic biomarkers found more often with suboptimal aging. Another finding, from longitudinal studies, is that normal aging appears to be a phenomenon of gradual rather than precipitous change. Rapid decline is more likely to occur with the onset of a specific age-related pathologic process. TABLE 1. Biomarkers of aging ===================================== Loss of strength Reduced flexibility Decreased cardiovascular endurance Increased body fat (and resultant loss of lean muscle mass, or sarcopenia Reduced resting energy expenditure Lower kidney clearance Reduced cell-mediated immunity Increased hearing threshold Reduced vibratory sensation Compromised near visiion and dark accommodation Reduced taste and smell acuity Increased autoantibodies Altered hormone levels ===================================== Adapted from Evans and Rosenberg.17 OLD CELLS AND FREE RADICALS To understand the common mechanism, we need first to understand how aging occurs. To many, aging is simply a matter of wear and tear, often expressed in the scientific terminology of free radical damage to proteins and DNA or of reactive oxygen molecules and mitochondria. Some scientists view getting old as the same thing that happens to a car, as it gathers rust, loses power, and falls apart. The problem with the car analogy is that organisms are not cars. What car can continually repair itself for decades? You live in a body that actively resists wear and tear by continually repairing itself, replacing lost cells and damaged proteins, making new mitochondria and new molecules, fixing DNA, and remaking itself from top to bottom. And yet this body that continually repairs itself grows old. The problem lies in the fact that it stops repairing itself. There is always free radical damage, but older cells stop doing much about it. Every single one of your cells divided and ultimately came from two joined cells, one from each of your parents (with the mitochondria from your mother), whose cells in turn came from their parents, and so on back as far as life has been around. Following your cells (and their mitochondria) back through your maternal line, we quickly realize that you are part of a line of cells that is three and a half billion years old. You look pretty good, considering that free radical damage has been after your cells for several billion years. Why have those cells not aged and died? Perhaps the problem is not just free radical damage, but something about fertilization and having so many cells. But there are multicellular organisms that never age and single-celled organisms that do. In fact, the reason that your cells age is that they allow themselves to do so. Some cells, cancer cells or the germ cell lines that created you, never age. Other cells, such as most (though not all) of the cells of your body do age, although at varying rates. All of these cells-aging or not, at different rates or not-are exposed to free radical and other damage, yet only certain cells age. The difference is that aging cells slow down their repair (and other) processes, whereas cells that do not age continue to deal with the damage, quite literally forever. Let us look at what kinds of damage we are talking about, even just narrowing it down to free radical damage. Almost all (about 92%) of free radicals are made in your mitochondria. The first problem, then, is trying to avoid making free radicals. Unfortunately, since we need oxygen to survive, we cannott avoid making at least a few free radicals as we make ATP, the molecule that fuels almost everything in your cells. Worse yet, as your cells age, they make more and more free radicals for the same amount of ATP. In other words, your cells get sloppier as they get older. The second problem is keeping the free radicals away from things that you need. It is bad enough to make free radicals within the mitochondria, but the last thing you want is to expose your DNA and critical cell proteins to attack from these dangerous free radicals. Luckily, your cells (like all eukaryotic cells) hide the DNA in a safe place-the nucleus-and tries to keep the free radicals in another-the mitochondria. But as your cells get older, the lipid membranes begin to leak: the free radicals begin to escape from the mitochondria. The third problem is catching and breaking down those escaping free radicals. Your cells use vitamin E, superoxide dismutase, and a number of other mechanisms to deal with free radicals. Unfortunately, as you get older, all of these mechanisms become a bit less available. As a result, free radicals roam about more freely and do more damage in older cells than they did in younger cells. Finally, no matter how good your cells are otherwise, there is always some damage that your cells have to deal with. In the case of DNA, you repair it. In the case of everything else, you replace it. Unfortunately, as your cells age, all of this slows down, too. The result is a gradual increase in the likelihood of damaged DNA, proteins that do not work, and membranes that leak (as above). Together, these four problems are a guarantee that your cells will slowly fall apart and fail to work, resulting in tissues that do not work, a body that does not work-in other words, problems for you. The obvious question is what we might be able to do about any of this? You could try to fix any one of these problems. For example, you might use caloric restriction to limit the production of free radicals. Or you could increase your dietary vitamin E to help scavenge the ones that escape. Both of these and most other approaches deal with only a single part of the problem and, worse yet, with problems only after they have occurred. The best approach would be to deal with all of the problems, not just by "cleaning up after them" but by stopping the entire problem at the cause. But is there really a single place to intervene? GENES AND CELL REPAIR Curiously enough, all of the problems come together in one single place: gene expression. All of the changes listed above, and a lot of others, occur because the pattern of gene expression changes as we age. Your genes are just the same, but what they do certainly is not. Just as the difference between a muscle cell and a skin cell is in the pattern of gene expression, so, too, is the difference between a young cell and an old one. But what controls that pattern and, more importantly, can we do anything about it? The list of things that affect gene expression is enormous. Every cell affects its neighbors; and depleted hormones, diet, activity, infections, methylation, glycation, inflammation, and a host of other things affect gene expression. In fact, the list is practically infinite: almost everything affects gene expression to some degree in a cell somewhere in your body. Even the much smaller list of things that control the change in pattern of gene expression between young cells and old ones is remarkably long. Luckily, however, we know of one thing that appears to be the major controlling of that change-namely, the telomere. The telomere is a long piece of DNA at the end of each one of your chromosomes. Because of the way DNA is replicated, every time one of your cells divides, it loses a small part of its telomere. This gradual loss causes a change in the proteins around the telomere, which in turn causes an indirect change in gene expression throughout the rest of the chromosome. The overall result is simple: every time your cells divide, they get a little bit older. Although some of your cells-nerve and muscle cells, for example-do not divide very often, this does not protect them. In each case the cells that do not divide (and so do not age much) are dependent on cells that divide quite a bit. In the case of heart muscle cells, for example, it is not the heart that ages, but the arteries supplying the heart. In the coronary arteries that supply the heart muscle, the cells lining the vessels-the vascular endothelial cells-not only divide, but do so all the more in the face of smoking, high blood pressure, diabetes, and other things known to cause atherosclerosis. In short, the reason that most cardiac risk factors cause heart attacks is that they make the cells that line your arteries divide and age. In each organ, we can trace aging diseases to aging cells. In Alzheimer's disease, it is the microglia that appear to be the culprit. In arthritis, it is the chondrocytes that make up the cartilage in your joints. In your bones, the osteoblasts age, resulting in osteoporosis. In your immune system, the lymphocytes age and result in poor immune function. In your skin, the fibroblasts and keratinocytes age and result in thin and wrinkled skin. In every organ, in every tissue, in every disease, we find dividing cells, aging, changing, and failing. None of this would be of much importance if we could not prevent the failure; but, as it turns out, we can. The first study that showed we could prevent aging in cells came out only a few years ago. Since then, the same result has been repeated in a host of other laboratories and other cell types. At the cellular level, reversing aging is well within our current ability. None of us, however, are mere cells, but tissues, organs, and bodies-vast collections of cells, each cell with a specific function and each dependent upon all other cells. While we can reverse aging in cells, can we go further and reverse aging in tissues or entire organs? In a sense, we already have. We can now reset aging in "reconstitute" human skin. If we take a mouse and transplant human skin cells (keratinocytes and fibroblasts) onto it, the cells layer out and grow human skin. If we use young human cells, we get young human skin, with thick and deeply interdigitated layers, strongly bound together between the dermis and epidermis. If we use old human cells, we get old human skin, with thin and barely adherent layers, weakly bound between dermis and epidermis and prone to sloughing off at the least pull. But if we take old human cells and reset the pattern of gene expression, the result is, once again, young skin; the skin is thick, the layers have deep interdigitations, and the cells are typical of young skin both in terms of their gene expression and their histology. The age of your skin is not a matter of how old the cells are, but of how old the gene expression is. REVERSING AGING Just as the telomere is the key to the altered pattern of gene expression in aging cells, so, too, is it the key to resetting gene expression in cells and in reconstituted human skin. Here, as always, the question is not, what causes aging? but rather, what is the single most effective point to intervene in aging? The issue is not academic, but concrete. How can we most effectively and efficiently prevent or treat the diseases of aging? In treating arthritis, we could (and do) replace the affected joints, but this is painful, expensive, and not entirely effective. In treating heart disease, we could replace the heart itself, but this is not only painful and expensive, but remarkably risky as well. In treating the genes that underlie these and other age-related diseases, we could-just as with hips and hearts- replace the affected part. But just as in hips and hearts, so, too, with genes: why not simply make the normal part work the way it was intended to work? The difference between a young cell and an old cell is not the superoxide dismutase gene, nor should we replace this or other genes. The difference between a young cell and an old cell is that this and other genes are not being expressed in the right amounts and at the right times. All of this can, and has been, reset by using telomerase both in the laboratory and in reconstituted skin. The current question is, what is the best way to reset gene expression to that of normal young cells? We could replace the telomerase gene, which would then express normal telomerase, reset the genes, and rejuvenate normal cell function. Even better, however, would be to control the existing telomerase gene in each of your cells, turning it on and off as needed. This is the role of a telomerase inducer currently under development. Either of these techniques-inserting another copy of the normal telomerase gene or using a telomerase inducer-should do the trick. Gene insertion has already been used in other contexts, and human trials using telomerase are not far off. Using this technique, a gene gun can be used to fire millions of copies of the human telomerase gene (hTERT) into human skin. While the "tak" for this technique is normally fairly low, it would be sufficient. Dermal and epidermal cells would take up the hTERT gene and begin expressing it, resetting gene expression and returning to normal young adult cell function. Current plans call for attempting this in four different types of patient: those with Fanconi's anemia, those with dyskeratosis congenita, normal older patients in a wound care center, and children with Hutchinson-Gilford progeria. In the first two diseases, patients are known to have difficulty maintaining normal telomere function. In Hutchinson-Gilford progeria, the cells lose telomere length early in life, at least in the blood vessels, skin, hair follicles, and joints. The result is that these children have atherosclerosis, thin skin, little hair, and arthritis, usually dying by age 13 of a heart attack or stroke. Small wonder we might want to try fixing the problem! In the case of normal older patients, we may try inserting a normal hTERT gene into the skin, particularly around the pressure sores these patients typically have. These are the result of poor innervation (so the patient is often unaware of sitting on them for hours), poor circulation (so they easily get infected and have a poor oxygen supply), and poor skin function (so the cells are slow to divide and heal the lesion). If we can repopulate the skin with healthy cells, the sores may heal more quickly and fully than is normally the case in the elderly. The real question, however, is, what happens if we try these approaches in normal, older patients even without skin sores? Moreover, we could try a similar approach in coronary arteries (the cause of heart disease), glial cells in the brain (which may underlie Alzheimer's dementia), chondrocytes in the joints (which cause osteoarthritis), osteoblasts in the bones (which fail in osteoporosis), lymphocytes in the blood (which cause immune aging), and other sites. Both these trials and trials using telomerase inducers are likely to begin within the next few years. Only when we are finally able to intervene in the fundamental causes of aging-the altered pattern of gene expression that permits your cells to finally succumb to free radicals and a host of other problems-will we finally be able to reverse human aging and prevent the suffering that accompanies the diseases of aging. ENDOCRINOLOGY Aging is also regarded by many physicians and scientists as a manifestation in hormone levels over the course of adulthood. In longevity medicine, we are trained that with aging all our organs and glands are shrinking. Even our skin is shrinking. In addition, we are losing bone and about one-half pound of muscle a year. Not merely limited to menopause, andropause (male menopause), somatopause (adult growth hormone deficiency), and other sex hormone related diseases, hormones are now implicated in conditions such as obesity, osteoporosis, fibromyalgia, chronic fatigue syndrome, cancer, attention deficit, and more. Conventional medicine treats only severe hormone depletion, ignoring the mild and moderate deficiencies; whereas the anti-aging medicine model focuses on mild, moderate, and severe deficiencies. It stands to reason that symptoms and severity of symptoms will be proportional to the level of deficiency for each hormone. Only recently has the science of endocrinology started focusing on advanced testing methods, taking into account reference ranges based on age as well as gender, free or bioavailable hormone levels versus bound hormone levels, and ratios between major antagonistic hormones to titrate patients and achieve an optimum balance. Titration and optimum balance have been used with thyroid and insulin hormones, but strangely enough this concept has not been universally applied to all other hormones in conventional medicine until now. In order to adequately address hormone decline in our adult patients, anti-aging physicians must first understand the hormonal cascade, an intricate interplay between the signals, pathways, and production and delivery systems that are responsible for our youthful hormonal state. The hormonal cascade involves estrogen, progesterone, testosterone, thyroid hormone, dehydroepiandrosterone (DHEA), cortisol, human growth hormone (hgh), and melatonin. Second, anti-aging physicians must be able to readily identify symptoms of hormone-related decline in our adult patients. On a related note, we must also be familiar with the laboratory tests that are able to objectively confirm, or rule out, hormone imbalances. TESTING PROGRAMS A series of all-encompassing testing and analysis programs are designed specifically to determine the body's rate of aging, alleviate symptoms of aging, and return your body to a healthier state of functioning. As you age, your "cellular sou "-the molecules, nutrients, and chemicals that circulate in and among the cells of the body and determine your genetic potential-becomes deficient in various nutrients and minerals. This can cause a breakdown in functions throughout the body and, over time, promote accelerated aging. Each individual body responds differently to the aging process and therefore has different requirements. Treatment programs and protocols are based on assessing the patient's current status and determining if the patient falls in one of the following categories: accelerated aging, premature aging, normal aging, reduced aging. Programs are designed to help patients progress from accelerated aging to reduced aging. Based on one's individual needs, the anti-aging practitioner can then design a customized treatment regimen to address the specific symptoms. Remarkable breakthroughs in modern science indicate that aging can be effectively managed with the application of new options including hormonal replacement therapy, nootropics, and brain entrainment techniques. These therapy programs use these approaches, combined with comprehensive lab tests (blood, skin, saliva, and urine), diet, exercise, nutrition, and high-tech meditation, to alleviate aging symptoms. Augmenting the body's ability to repair DNA damage, stimulating the immune system, and keeping the neurohormonal centers of the nervous system functioning are key components in retarding age. Some of the documented outward effects of longevity programs include measurable improvements in mental speed, clarity of thought, skin tightness, sexual function, plus a general improvement of energy levels. Ongoing research in the field of longevity includes the use of nutrient precursors and hormonal precursors to augment the body's ability to make more of its own hormonal compounds as well as to limit DNA damage. Some doctors feel that the essence of all anti-aging treatment centers on protecting DNA from damage and augmenting its ability to repair itself and produce the key peptides and proteins that are responsible for all cell growth and regeneration. Others consider accelerated aging a nutritional deficiency syndrome. TREATMENT PROGRAMS With the onset of the 21st century, it is apparent that we stand on the horizon of a revolution in anti-aging therapies and technologies. One of the most promising techniques that within the next 5-10 years will allow us to markedly expand the quality of health and human longevity is the concept of stem cell treatments. Recent advances by major corporations, both private and public, have documented that we are already capable of taking what are termed stem cells from an individual and selectively copying these cells along with their DNA components to restore the rejuvenative properties that our bodies lose as we age. This revolutionary technology of therapeutically cloning our own cells and giving them back to our cells will allow us to selectively focus on the components that deteriorate with the aging process, uniquely for each individual. We all inherited certain genetic weaknesses-some a poor immune system, some a poor nervous system, some a poor cardiovascular system. With these new technologies we will be able to selectively restore these faulty genetic mechanisms. |
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Reverse Engineering of Rat Brain Component Completed contributed by member on 2008-01-23 |
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http://www.guardian.co.uk/technology/2007/dec/20/research.it In case you hadn't heard - Henry Markram and lab formally announced completion of phase one of their Blue Brain project. They created a full simulation of a rat neocortical column - a tiny but repeating part of a rat's brain, with 10,000 neurons and 30 million synapses. Check out the mind-blowing videos at http://ditwww.epfl.ch/cgi-bin/EPFLTV/home.pl?page=channel_one&lang=2&connected=0&channel_id=29 Now onward, toward full human brain emulation... |
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Links Discussed At last Meeting contributed by member on 2008-01-23 |
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| Florida Dept. of Motor Vehicles emergency contact setup page. Apparently not many people know this exists. It sets it up so in case of emergency when the police run your ID or driver's license they get 2 emergency contacts right away. Go to the page and fill out the info...it only takes a minute. https://www6.hsmv.state.fl.us/dlcheck/findcustomer Latest alarms systems update from Ben Best http://www.benbest.com/cryonics/alarms.html#2007 Active/Passive Cooling Garments http://www.cszmedical.com/products/localizedcold/index.htm Very professional looking equipment but no prices given http://polarsoftice.com/softiceactivevest.html Not as professional but at least they give prices. http://coolzoneproducts.com/_wsn/page2.html Less expensive than polarsoftice including a cooling helmet for $15 |
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Central Florida Life Extension Meetup Group contributed by member on 2008-01-23 |
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| We had our fourth successful Life Extension / Alcor Meetup on Tuesday night. Changes to the website have been made including a user login and member info pages. Due to spam only members will be allowed to post articles or leave comments. In addition to protect member privacy only logged in members will be able to see the names of article posters. Otherwise the word 'member' will appear next to the article headline. |
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Cryonics Institute releases vitrification formula contributed by member on 2007-02-25 |
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| The Cryonics Institute announced on February 23rd that they are releasing the formula for their vitrification mixture to the public. To date this formula has been used on two patients. They stated legal reasons relating to their patent application as the reason for the disclosure. The hope is to prevent others from stopping them the use of their own formula. | ||||||||
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Advances in Limb Regeneration Research contributed by member on 2007-02-20 |
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| Regrowing fingertips now seems very likely with a new product by Acell Inc. Trials with Iraq veterans is now underway in Texas. Currently Acell Inc. is only marketing their product to vets but they have been approved by the FDA for human clinical trials as medical devices. Acell uses acelluar tissue from pig bladders as a resorbable scaffolding for tissue regeneration. It has been used in animals for myocardial repair, musculotendinous and ligamentous repair and urinary incontinence. Some people haven't waited for the clinical trials and have successfully used the vet products.
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Aubrey de Grey to speak at Edmonton Aging Symposium contributed by member on 2007-02-20 |
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| To be held March 30-31st in Edmonton Canada. Registration fees are reasonable ($55 to $340 depending on student / professional status and days attended). Besides Aubrey some of the speakers and their topics: Michael West PhD. (ACT) Therapeutic Cloning and Tissue Engineering Tarek El-Bialy PhD. (University of Alberta) Ultrasound Induced Bone and Tooth Growth Hasan Uludag PhD. (University of Alberta) Scaffolds, Growth Factors and Tissue Constructs Luigi Fontana MD PhD (Washington University) Caloric restriction |
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$95 Registration Fee extended thru March for SA Conference contributed by member on 2007-02-17 |
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| Some of the highlights will include: . First-ever public information about a new, heavily-funded research program to achieve true whole-body vitrification in mammals, including, eventually, humans. . Full details about liquid ventilation technology, which promises to increase radically the rate of cooling of cryonics patients after cardiac arrest in order to reduce ischemic and other damage to the brain. . Two new systems for administering cardiopulmonary support during cryonics standby/stabilization work. . Details of intermediate temperature storage systems for cryonics patients, promising to reduce or eliminate cracking during the cryopreservation process. . News of recent developments at the Cryonics Institute, Alcor Foundation, and the American Cryonics Society. Representatives of all three organizations are on the program. . Valuable information about Personal Revival Trusts to provide additional funding for long-term care of cryonics patients, research to revive patients, and assets for your own personal use if and when you are revived. . Guided tours of the Suspended Animation facility. Speakers will include (in alphabetical order) Ben Best (CEO, Cryonics Institute) Aschwin de Wolf (Cryopreservation Protocol Director, Suspended Animation) Gregory M. Fahy, PhD (Chief Scientific Officer, 21st Century Medicine) Steve Harris, MD (Scientific Director, Critical Care Research) Rudi Hoffman (Life Insurance and Financial Advisor) Tanya Jones (COO, Alcor Life Extension Foundation) Saul Kent (CEO and Director, Suspended Animation) Charles Platt (representing Suspended Animation) Michael Riskin, CPA (Chairman of the Board, Alcor Life Extension Foundation) Steve Van Sickle (Executive Director, Alcor Life Extension Foundation) Brian Wowk, PhD (Senior Scientist, 21st Century Medicine) Jim Yount (CEO, American Cryonics Society) |
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Book Review: The Immortal Cell by Michael West contributed by member on 2007-02-15 |
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 The Immortal Cell: One Scientist's Quest to Solve the Mystery of Human Aging
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