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	<title>Michael Fossel</title>
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	<link>http://www.michaelfossel.com/blog</link>
	<description>Michael is a Fellow of the American College of Emergency Physicians</description>
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		<title>2011 update</title>
		<link>http://www.michaelfossel.com/blog/?p=25</link>
		<comments>http://www.michaelfossel.com/blog/?p=25#comments</comments>
		<pubDate>Thu, 30 Dec 2010 15:50:39 +0000</pubDate>
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		<description><![CDATA[My newest book, &#8220;Immortality Edge&#8221;, coauthored by Greta Blackburn and David Woynarowski is a combined look at diet, exercise, lifestyle, meditation, and other approaches. It is not intended to give advice on how to lengthen telomeres, so much as to slow down their loss; not so much aimed at reversing aging, as slowing the process [...]]]></description>
			<content:encoded><![CDATA[<p>My newest book, &#8220;Immortality Edge&#8221;, coauthored by Greta Blackburn and David Woynarowski is a combined look at diet, exercise, lifestyle, meditation, and other approaches. It is not intended to give advice on how to lengthen telomeres, so much as to slow down their loss; not so much aimed at reversing aging, as slowing the process by everyday means.</p>
<p>For those of you interested in actually reversing the process, consider contacting TA Sciences, who have a commercially available telomerase activator. There are at least two (perhaps three) other know public sources, but some questions have been raised (and remain unanswered) regarding regarding patent infringement and efficacy of the available compounds. To be fair, the question of efficacy has also been raised with regard to TA Sciences&#8217;s product, TA65, but there is both laboratory data and some initial human clinical data supporting the efficacy of this compound. How well TA65 will bear up under long term scrutiny remains to be seen, but the initial data is supportive and consistent with what is known of both human aging and human pathology. For example, we know that human aging generally takes decades to occur and there is some a priori reason to suggest that reversing the process might take a similar time course, rather that merely a few months. In reality, we might expect that some processes (e.g., immunce rejuvenation) should proceed faster than other processes (e.g., changes in the coronary arteries or joint surfaces) and this expectation is consistent with the current data.</p>
<p>For those of you who are interested in other sources (whether proven or not), you might try the following:<br />
  www.revgenetics.com<br />
  www.terraternal.com</p>
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		<title>Dr. Michael Fossel Discusses &#8220;Reversing Human Aging&#8221;</title>
		<link>http://www.michaelfossel.com/blog/?p=12</link>
		<comments>http://www.michaelfossel.com/blog/?p=12#comments</comments>
		<pubDate>Mon, 14 Dec 2009 08:50:16 +0000</pubDate>
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		<description><![CDATA[Dr. Michael Fossel, M.D., Ph.D., gave a presentation on &#8220;Reversing Human Aging&#8221; at the National Institutes of Health&#8217;s Natcher Center on April 16, 1996. The presentation was sponsored by the Smithsonian Institution&#8217;s Smithsonian Associates. LES members and subscribers were notified of the talk, and a number of LES members attended. For years, Dr. Fossel has [...]]]></description>
			<content:encoded><![CDATA[<p>Dr. Michael Fossel, M.D., Ph.D., gave a presentation on &#8220;Reversing Human Aging&#8221; at the National Institutes of Health&#8217;s Natcher Center on April 16, 1996.  The presentation was sponsored by the Smithsonian Institution&#8217;s Smithsonian Associates.  LES members and subscribers were notified of the talk, and a number of LES members attended.<span id="more-12"></span></p>
<p>For years, Dr. Fossel has studied progeria and related accelerated aging syndromes.  He is convinced that the evidence from these</p>
<p>diseases, together with the fact that germ cells and cancer cells do not age, indicates that aging is a regulated process, that is, a</p>
<p>function of gene expression, and not a function of &#8220;wear and tear.&#8221;  His recent book, &#8220;Reversing Human Aging,&#8221; reviews recent research into &#8220;telomere&#8221; that identifies a mechanism for the regulation of aging.</p>
<p>This research shows that telomere, or &#8220;nonsense&#8221; DNA at the end of each chromosome, is shortened with each cell division in dividing</p>
<p>cells.  Telomere functions like the tip of a shoelace.  Snip off the tip bit by bit, and eventually the shoelace will unravel.  Once</p>
<p>telomere in a dividing cell becomes too short, the cell unravels, that is, it ceases to divide, senesces, and dies.</p>
<p>This explains why we have limited life spans, why calorie restriction and other methods that slow down metabolism and cell division may extend life, and why progeria victims have short lives (they are born with already-shortened telomere).  Why, then, don&#8217;t we just stay young and healthy, then drop like rocks at our appointed time?  The answer is that on each chromosome the regulatory genes are located near the tips, that is, near the telomere, and the expression of these regulatory genes is influenced by telomere length.  With each division beyond a certain point, the regulatory genes in dividing cells get a little more out of whack.</p>
<p>Germ cells and cancer cells are the exception.  They are immortal because they produce an enzyme, telomerase, that replaces the telomere that otherwise would be lost in each division.  It doesn&#8217;t restore already lost telomere, but it prevents further losses.</p>
<p>Organisms with telomere-limited cells have a survival advantage because damaged or mutated telomere-limited cells die off before they can kill the organism.  Cancer, in which telomerase production is turned on, is the exception.</p>
<p>Although gene expression leads to cell disfunction after numerous divisions, changes in gene expression early in life are important to</p>
<p>individual development, maturation, and reproduction.  Telomere may be involved in the master &#8220;clock&#8221; that regulates both maturational and senescent changes in gene expression.  (Death, then, would be the inadvertent byproduct of the continued ticking of the &#8220;clock&#8221; after maturation and reproduction had been taken care of.)</p>
<p>Unfortunately, achieving immortality is not simply a matter of introducing telomerase into normal cells.  First, some types of cells</p>
<p>do not divide (heart muscle or brain cells, for instance).  Second, many potentially cancerous cells fail to become immortal and die off</p>
<p>because they do not also become telomerase-producing.  Introducing telomerase wholesale would enable runaway mutant cells to divide indefinitely.</p>
<p>Perhaps some day we will be able to enable normal cells to produce telomerase and to limit telomerase production in abnormal cells.</p>
<p>Right now, research into telomerase inhibition (cancer control) is ahead of research into telomerase induction.</p>
<p>Dr. Fossel cautions that advances in telomerase induction may not significantly extend lives right away.  There are still too many other things &#8212; viruses, bacteria, trauma, poison, genetic errors &#8212; that can happen to bodies.</p>
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		<title>Reversing human aging: it&#8217;s time to consider the consequences.</title>
		<link>http://www.michaelfossel.com/blog/?p=11</link>
		<comments>http://www.michaelfossel.com/blog/?p=11#comments</comments>
		<pubDate>Mon, 14 Dec 2009 08:49:28 +0000</pubDate>
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		<description><![CDATA[Science may soon be able to slow, stop, or even reverse the aging process in humans. What will happen when people can live on and on for centuries? Within the next two decades we will extend the healthy human life-span indefinitely and, in doing so, alter human culture forever. Our maximum life-spans will not have [...]]]></description>
			<content:encoded><![CDATA[<p>Science may soon be able to slow, stop, or even reverse the aging process in humans. What will happen when people can live on and on for centuries?</p>
<p>Within the next two decades we will extend the healthy human life-span indefinitely and, in doing so, alter human culture forever.<span id="more-11"></span></p>
<p>Our maximum life-spans will not have become infinite, but indefinite: uncertain and unknown. The social consequences of extended life-spans are also unknown but likely to be explosive. The increase of healthy life-spans to perhaps double or more our current spans will trigger social changes greater perhaps than any since those that followed the invention of agriculture more than 10,000 years ago.</p>
<p>The changes will largely be positive, particularly the prevention of individual suffering from the diseases and fears associated with aging. But the changes will also be disruptive and detrimental to our culture and to our personal lives. Societal change, even when the outcome is favorable, always presents challenges. Peace on earth would put soldiers out of work; curing heart disease would require retraining for cardiologists. No matter the innovation &#8211; agriculture, sailing ships, the printing press, gunpowder, industrialization, the automobile, atomic energy &#8211; each one caused (and in some cases is still causing) disruption in the social order.</p>
<p>The degree to which any innovation alters society hinges not on how remarkable, expensive, or unexpected such innovation is, but rather on the degree to which it changes basic forces and assumptions in our lives and our society. Never before have we altered our basic assumption about maximum human life-span. The mean human life-span has changed radically within merely the last two centuries, from 25 years in the eighteenth century to 50 years in 1900, to 75 years now. This pattern reflects access to food, clean water, and basic medical care (such as immunizations and obstetrical care), and therefore defines much of what we mean by a &#8220;developed nation.&#8221; The fact that some developed nations (such as Japan and Sweden) have longer mean life-spans and less infant mortality than others (such as the United States) is often used as a telling criticism of the degree of social development, as though civilization itself were in some measure defined by health and life-span.</p>
<p>Throughout the course of history, however, we have never increased the maximum human life-span, estimated at 120 years. Some have extrapolated this historical precedent to its logical end, arguing that we will soon have mean life-spans of 100 or more, yet still age rapidly and die by 120. This extrapolation assumes that the maximum life-span cannot change &#8211; a reasonable assumption historically. No matter what the medical advance, we have never yet altered the maximum human life-span one year, let alone a decade. The mean life-span alters on a whim: a fastened seatbelt, a smoke detector, a clean well, or a tetanus shot. The maximum life-span has been beyond us, unalterable, fixed, and reliable.</p>
<p>Until now.</p>
<p>Already, scientists have extended the maximum life-span in two species: to twice normal in the fruit fly (Drosophila) and six times normal in the nematode worm (C. elegans). Extending the human life-span appears almost within reach.</p>
<p>Stopping and Reversing the Clock</p>
<p>We know that our cells age and die; recent discoveries suggest that they don&#8217;t have to. Cells have chromosomal clocks &#8211; called telomeres &#8211; that determine their life-spans, and they age and die as their clocks run down. But cancer cells</p>
<p>, for example, continually reset their clocks, allowing themselves to divide &#8211; and live &#8211; forever.</p>
<p>The telomere shortens as a cell divides because the cell fails to copy the tip of its chromosomes, where the telomere resides. Telomere &#8220;caps&#8221; are being built by researchers at the University of Texas that would essentially force the cell to always copy its telomere &#8211; and hence never shorten. The clock would never wind down, and the cell (and the person possessing it) would cease aging.</p>
<p>But we could also try for more than stopping the clock &#8211; we could reverse it. By adding telomerase &#8211; an enzyme, part protein and part RNA &#8211; we could relengthen the telomeres. &#8220;All&#8221; we would need to do is lengthen all 92 telomeres in each of our 100 trillion cells. It may be possible one day to produce a drug that gets each of our cells to treat its own 92 telomeres. Active research programs for telomerase inducer drugs are being conducted by the University of Texas&#8217;s Southwestern University Medical Center and by Cold Spring Harbor Laboratory on Long Island, New York, as well as by biotech and pharmaceutical firms.</p>
<p>We have no way of knowing what the maximum healthy life-span will become when we reextend human telomeres. We suspect that by using telomerase inducers we can probably extend the human life-span well beyond 120 years and that telomere manipulation should allow us to prevent most of the diseases we associate with aging: cancer (albeit by the reverse process of inhibiting telomerase), atherosclerosis</p>
<p>(and so most heart disease and strokes), osteoarthritis, Alzheimer&#8217;s, and most other diseases of aging.</p>
<p>Social Consequences</p>
<p>One social consequence of preventing aging will be a likely increase in the world population. A large world population is not inherently a bad thing. If the world population were only 1,000 people, would we have computers, immunizations, or even books? But at some level, high population does have liabilities that lower the quality of life. The optimal number of people depends on your assumptions about a number of variables, such as environmental damage, food supply and production, crime, war, disease, and overwhelming social &#8220;stresses&#8221; and their impact on the human condition.</p>
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