Healthy Life Extension

When Will You Die?

posted on May 24, 2011

Dear Future Centenarian,

That’s the question that made the news last week, instead of the question “How can you extend your active lifespan?”

The airwaves in Europe, the U.S., and likely around the world were abuzz with the dramatic announcement coming out of Spain about "The New Test That Tells You How Long You'll Live!" That new test, of course, is the measure of telomere lengths, not so new, actually. But the announcement described the real breakthrough that Dr. Maria Blasco's lab and new telomere measurement company, Life Length, SL, in Spain, has made to measure the shortest telomeres, which is really the critical measure, as opposed to the more commonly measured average telomere length.

Telomeres are the protective tips of your chromosomes that shorten each time your cells divide. Some researchers believe many diseases can be avoided, and healthy lifespans can be extended by lengthening the shortest telomeres, thus “resetting the aging clock.”

As I scanned the many TV and press reports, some were quite positive and optimistic about the news. Others frankly missed the mark, essentially giving the [untrue] message: "Why should I have my telomeres measured, since there's nothing I can do to affect or improve my telomere length anyway? My (telomere) fate and lifespan are sealed."

If you’ve read the new book, The Immortality Edge, you know there are in fact many proven actions that can not only slow down the rate of telomere shortening (thus slowing down your aging process), but also to re-lengthen telomeres (with the goal of actual age reversal.)

The media focused on scare tactics like "Do you really want to know when you will die?" and "Why bother knowing? After all, you were BORN with telomeres of a certain length, and there’s nothing you can do..."  

You get the picture.

Much of the dialogue and “controversy” in some circles in the field of telomeres revolves around the question: "OK, if short telomeres are “bad”, will it really help me if I can lengthen my telomeres?"

There is a wealth of data from many of the leading telomere biologists supporting a "yes" answer to that question. But the other vitally important point that is missed with this question, and for which I know of no controversy among the experts. It’s that: there are many ways, and absolute benefit, to slowing the rate of telomere shortening and telomere loss—essentially slowing down your rate of aging—through the targeted actions detailed in the book. These include: exercise; multiple stress management techniques like yoga, meditation, even deep breathing; nutrition and targeted nutritional supplementation.

As Nobel Laureate Elizabeth Blackburn has stated, "Correct telomere maintenance is critical." And as you know, many of those news reports last week were indeed wrong: there are ways to maintain, even increase, your telomere length. And you are out there doing it! Right?

For information on emerging telomere maintenance and lengthening compounds, go to: http://www.maxlife.org/telomeres/.  

To your good health, with longer telomeres! 

Long Life,
David Kekich
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LATEST HEADLINES FROM FIGHT AGING!

ALCOR VIDEO LIBRARY UPDATED Thursday, May 19, 2011 http://www.fightaging.org/archives/2011/05/alcor-video-library-updated.php
From Alcor News: "The Alcor Video Library has recently added new material. It now includes a short Video Tour of Alcor Facility and five complete presentations from the 2006 Alcor Conference. The video quality has also been significantly upgraded. The Limitless Future (28-minutes). Alcor documentary video (2005).

Discover how leading-edge science at the Alcor Life Extension Foundation is getting closer to making the dream of a vastly extended lifespan come true and how our notion of "death" is shifting. Includes interviews with world-renowned scientists including Dr. Aubrey de Grey, [explaining] how life can be cryopreserved on the verge of death and then revitalized, giving us a second chance at a long and productive life, and Dr. Ralph Merkle, Distinguished Professor of Computing at Georgia Tech, exploring how molecular-sized machines will be able to repair damage to your body from aging or the devastating effects of cancer and other illnesses, including frostbite." You might also take a look at some of the other videos linked in the post, such as a presentation on the economics of longevity: "In this talk, Dr. Friedman shares his insights into the many potential consequences of an extended lifespan.
He asks provocative questions about the future of the family unit, a typical career path, and the economic outlook for society as a whole."

MORE HEART PATCHING Thursday, May 19, 2011 http://www.fightaging.org/archives/2011/05/more-heart-patching.php
Patching a damaged heart is on the agenda again, with nanoscale-featured scaffold material this time: "When you suffer a heart attack, a part of your heart dies. Nerve cells in the heart's wall and a special class of cells that spontaneously expand and contract - keeping the heart beating in perfect synchronicity - are lost forever. [At present] surgeons can't repair the affected area [but the] best approach would be to figure out how to resuscitate [it]. Scientists turned to nanotechnology. In a lab, they built a scaffold-looking structure consisting of carbon nanofibers and a government-approved polymer.

Tests showed the synthetic nanopatch regenerated natural heart tissue cells ­- called cardiomyocytes - as well as neurons. In short, the tests showed that a dead region of the heart can be brought back to life.. The engineers employed carbon nanofibers, helical-shaped tubes with diameters between 60 and 200 nanometers. The carbon nanofibers work well because they are excellent conductors of electrons, performing the kind of electrical connections the heart relies upon for keeping a steady beat. In tests with the 200-nanometer-diameter carbon nanofibers seeded with cardiomyocytes, five times as many heart-tissue cells colonized the surface after four hours than with a control sample consisting of the polymer only. The scaffold works because it is elastic and durable, and can thus expand and contract much like heart tissue. It's because of these properties and the carbon nanofibers that cardiomyocytes and neurons congregate on the scaffold and spawn new cells, in effect regenerating the area."

TOWARDS TREATMENTS FOR AGE-RELATED MUSCLE LOSS Wednesday, May 18, 2011 http://www.fightaging.org/archives/2011/05/towards-treatments-for-age-related-muscle-loss.php
Stem cell therapies are one theoretical path towards therapies for sarcopenia, the loss of muscle mass and strength with age. Here, researchers have discovered "the mechanism that causes stem cells in the embryo to differentiate into specialised cells that form the skeletal muscles of animals' bodies. The field has the potential to revolutionize medicine by delivering therapies to regenerate tissue damaged by disease or injury. Differentiation happens soon after fertilization, when embryonic cells are dividing rapidly and migrating as the animal's body takes shape.

The scientists investigated the effect of a known signaling pathway called NOTCH on muscle differentiation. They found that differentiation of stem cells to muscle was initiated when NOTCH signaling proteins touched some of the cells. These proteins were carried by passing cells migrating from a different tissue - the neural crest - the progenitor tissue of sensory nerve cells. Muscle formation in the target stem cells occurred only when the NOTCH pathway was triggered briefly by the migrating neural crest cells. This kiss-and-run activation of a pathway is a completely novel mechanism of stem cell specification which explains why only some stem cells adopt a muscle cell fate. The team would now focus on unraveling the mechanisms of embryonic muscle cell differentiation at the molecular level as a necessary step to regulating regeneration of the muscles in human patients."

STEM CELLS REVERSE PARKINSON'S IN RATS Tuesday, May 17, 2011 http://www.fightaging.org/archives/2011/05/stem-cells-reverse-parkinsons-in-rats.php
Promising news: "A team of researchers [has] now compared the ability of cells derived from different types of human stem cell to reverse disease in a rat model of Parkinson disease and identified a stem cell population that they believe could be clinically relevant. Parkinson disease results from the progressive loss of a specific subpopulation of nerve cells. Current treatments provide only relief from the symptoms of the disease and cannot reverse the nerve cell loss. Stem cells are considered by many to be promising candidate sources of cells to reverse nerve cell loss in individuals with Parkinson disease through their ability to regenerate and repair diseased tissues.

There are two types of stem cell considered in this context: embryonic stem (ES) cells, which are derived from early embryos; and induced pluripotent stem (iPS) cells, which are derived by reprogramming cells of the body such that they have the ability to generate any cell type. In turn, cells of the body can be reprogrammed to become iPS cells in one of two ways: the reprogramming proteins can be transferred directly into the cells (protein-based iPS cells) or viruses can be used to deliver to the cells the genetic information necessary for producing the reprogramming proteins (virus-based iPS cell). [Researchers] found several problems with cells derived from virus-based human iPS cells that precluded their use in the Parkinson disease model but found that nerve cells derived from protein-based human iPS cells reversed disease when transplanted into the brain of rats modeling Parkinson disease. They therefore conclude that protein-based human iPS cells could be used in the treatment of individuals with Parkinson disease."

MORE RETINAL REGENERATION Tuesday, May 17, 2011 http://www.fightaging.org/archives/2011/05/more-retinal-regeneration.php
From EurekAlert!: researchers "are the first to regenerate large areas of damaged retinas and improve visual function using IPS cells (induced pluripotent stem cells) derived from skin. While other researchers have been successful in converting skin cells into induced pluripotent stem cells (iPSCs) and subsequently into retinal neurons, we believe that this is the first time that this degree of retinal reconstruction and restoration of visual function has been detected. Today, diseases such as retinitis pigmentosa (RP) and age-related macular degeneration (AMD) are the leading causes of incurable blindness in the western world. In these diseases, retinal cells, also known as photoreceptors, begin to die and with them the eye's ability to capture light and transmit this information to the brain.

Once destroyed, retinal cells, like other cells of the central nervous system have limited capacity for endogenous regeneration. Stem cell regeneration of this precious tissue is our best hope for treating and someday curing these disorders. [Researchers] harvested skin cells from the tails of red fluorescent mice. They used red mice, because the red tissue would be easy to track when transplanted in the eyes of non-fluorescent diseased mice. The group generated red fluorescent IPSCs, and, with additional chemical coaxing, precursors of retinal cells. Within 33 days the cells were ready to be transplanted and were introduced into the eyes of a mouse model of retina degenerative disease. Within four to six weeks, the researchers observed that the transplanted 'red' cells had taken up residence in the appropriate retinal area (photoreceptor layer) of the eye and had begun to integrate and assemble into healthily looking retinal tissue."

N-GLYCAN PROFILES AND INHERITED LONGEVITY Monday, May 16, 2011 http://www.fightaging.org/archives/2011/05/n-glycan-profiles-and-inherited-longevity.php
Some people can live moderately longer than others due to differences in their genes that enhance the ability of a good lifestyle to extend life, or blunt the tendency for a bad lifestyle to shorten life. In this age of biotechnology it is only a matter of time before all the biochemical differences between naturally longer-lived and shorter-lived human lineages are uncovered: "The development of medical interventions for the preservation of disease-free longevity would be facilitated by markers that predict healthy aging. Altered protein N-glycosylation patterns have been found with increasing age and several disease states.

Here we investigate whether glycans derived from the total glycoprotein pool in plasma mark familial longevity and distinguish healthy from unhealthy aging. Total plasma N-glycan profiles of 2396 middle aged participants in the Leiden Longevity Study (LLS) were obtained. After normalization and batch correction, several regression strategies were applied to evaluate associations between glycan patterns, familial longevity, and healthy aging. Two N-glycan features (LC-7 and LC-8) were identified to be more abundant in plasma of the offspring of long-lived individuals as compared to controls. Furthermore, a decrease in levels of LC-8 was associated with the occurrence of myocardial infarction, indicating that plasma glycosylation patterns do not only mark familial longevity but may also reflect healthy aging. In conclusion, we describe two glycan features, of which increased levels mark familial longevity and decreased levels of one of these features mark the presence of cardiovascular disease."

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