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"We are on the verge of a revolution in medicine: understanding, treating, and ultimately preventing the causes of degenerative aging. But medical revolutions only happen if we all stand up in support of funding and research. We did it for cancer. We're doing it for Alzheimer's. We can do it for aging - and create an era of longer, healthier lives!"
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Calorie Restriction
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   Daily News             

A Reminder that Fat Doesn't Just Sit There
September 02 2010   |   Permanent Link
Excess fat tissue in your body actively works to change your metabolism, and largely for the worse. Here's a reminder of that fact: "Scientists are reporting new evidence that the fat tissue - far from being a dormant storage depot for surplus calories - is an active organ that sends chemical signals to other parts of the body, perhaps increasing the risk of heart attacks, cancer, and other diseases. They are reporting discovery of 20 new hormones and other substances not previously known to be secreted into the blood by human fat cells and verification that fat secretes dozens of hormones and other chemical messengers. ... [Researchers] note that excess body fat can contribute to heart disease, diabetes, cancer and other diseases. Many people once thought that fat cells were inert storage depots for surplus calories. But studies have established that fat cells can secrete certain hormones and other substances much like other organs in the body. Among those hormones is leptin, which controls appetite, and adiponectin, which makes the body more sensitive to insulin and controls blood sugar levels. However, little is known about most of the proteins produced by the billions of fat cells in the adult body."

New York Times on Sarcopenia
September 02 2010   |   Permanent Link
The mainstream press notices sarcopenia: "Bears emerge from months of hibernation with their muscles largely intact. Not so for people, who, if bedridden that long, would lose so much muscle they would have trouble standing. Why muscles wither with age is captivating a growing number of scientists, drug and food companies ... Comparisons between age groups underline the muscle disparity: An 80-year-old might have 30 percent less muscle mass than a 20-year-old. And strength declines even more than mass. Weight-lifting records for 60-year-old men are 30 percent lower than for 30-year-olds; for women the drop-off is 50 percent. With interest high among the aging, the market potential for maintaining and rebuilding muscle mass seems boundless. Drug companies already are trying to develop drugs that can build muscles or forestall their weakening ... In addition, geriatric specialists, in particular, are now trying to establish the age-related loss of muscles as a medical condition under the name sarcopenia. ... But with sarcopenia still not established as a treatable condition, 'there is no real defined regulatory path as to how one would get approved in this area.'" When you live under a regime in which all that is not permitted is forbidden, it should be no surprise that progress is slow and expensive. One of the best things that could happen for medicine in this modern age is to tear down the FDA and other similar regulatory bodies.

An Alternate View of the Aging Immune System
September 01 2010   |   Permanent Link
The mainstream view of aging in the adaptive immune system is that too many memory T cells exist, uselessly specialized and using up limited resources that should be devoted to the naive T cells needed to tackle new threats. An alternative (and not mutually exclusive) theory is presented in this paper: that memory cell populations are failing in old age, meaning that acquired immunity vanishes. "Evidence is accumulating that old individuals are more susceptible to infection with organisms to which they were previously immune, indicating that there might be a limit to the persistence of immune memory. The prevailing concept is that defects in memory T-cell populations result from inexorable end-stage differentiation as a result of repeated lifelong antigenic challenge. We discuss here mechanisms that might constrain the persistence of memory T cells and consider whether humans will suffer from memory T-cell exhaustion as life expectancy increases." Whether or not this in fact occurs, the proposed therapies would look much the same as for other immune system issues known to occur with aging: destroy the old, misconfigured, damaged immune cells and replace them with new cells grown from the patient's stem cells.

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