Al-Huda
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Newsletter for July 2011
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Eat Less, Live Healthier and Longer,
but Preserve the Meaning of Life and Death
Calorie restriction, involves eating about 30 percent fewer
calories than normal while still getting adequate amounts of
vitamins, minerals and other nutrients. Aside from direct
genetic manipulation, calorie restriction is the only strategy
known to extend life consistently in a variety of animal species
In the last year, calorie-restricted diets have been shown in
various animals to affect molecular pathways likely to be
involved in the progression of Alzheimer's disease, diabetes,
heart disease, Parkinson's disease and cancer. Earlier this
year, researchers studying dietary effects on humans went so far
as to claim that calorie restriction may be more effective than
exercise at preventing age-related diseases.
The findings cast doubt on long-held scientific and cultural
beliefs regarding the inevitability of the body's decline. They
also suggest that other interventions, which include new drugs,
may retard aging even if the diet itself should prove
ineffective in humans. One leading candidate, a newly
synthesized form of resveratrol -- an antioxidant present in
large amounts in red wine -- is already being tested in
patients. It may eventually be the first of a new class of
anti-aging drugs. Extrapolating from recent animal findings, Dr.
Richard A. Miller, a pathologist at the University of Michigan,
estimated that a pill mimicking the effects of calorie
restriction might increase human life span to about 112 healthy
years, with the occasional senior living until 140, though some
experts view that projection as overly optimistic.
In almost every instance, the subjects on low-calorie diets have
proven to be not just longer lived, but also more resistant to
age-related ailments.
"In mice, calorie restriction doesn't just extend life span,"
said Leonard P. Guarente, professor of biology at the
Massachusetts Institute of Technology. "It mitigates many
diseases of aging: cancer, cardiovascular disease,
neurodegenerative disease. The gain is just enormous."
Researchers at Louisiana State University reported in April in
The Journal of the American Medical Association that patients on
an experimental low-calorie diet had lower insulin levels and
body temperatures, both possible markers of longevity, and fewer
signs of the chromosomal damage typically associated with aging.
These studies and others have led many scientists to believe
they have stumbled onto a central determinant of natural life
span. Animals on restricted diets seem particularly resistant to
environmental stresses like oxidation and heat, perhaps even
radiation. "It is a very deep, very important function," Dr.
Miller said. Experts theorize that limited access to energy
alarms the body, so to speak, activating a cascade of
biochemical signals that tell each cell to direct energy away
from reproductive functions, toward repair and maintenance. The
calorie-restricted organism is stronger, according to this
hypothesis, because individual cells are more efficiently
repairing mutations, using energy, defending themselves and
mopping up harmful byproducts like free radicals.
"The stressed cell is really pulling out all the stops" to
preserve itself, said Dr. Cynthia Kenyon, a molecular biologist
at the University of California, San Francisco. "This system
could have evolved as a way of letting animals take a timeout
from reproduction when times are harsh."
In a series of studies, Dr. Kenyon, of the University of
California, San Francisco, has created mutant roundworms that
live six times longer than normal, largely because of a mutation
in a single gene called daf-2. The gene encodes a receptor on
the surface of cells similar to a receptor in humans that
responds to two important hormones, insulin and the insulin-like
growth factor 1 or IGF-1.
Insulin is necessary for the body to transport glucose into
cells to fuel their operations. Dr. Kenyon and other researchers
suggest that worm cells with mutated receptors may be "tricked"
into sensing that nutrients are not available, even when they
are. With its maintenance machinery thereby turned on high, each
worm cell lives far longer -- and so does the worm.
Many experts are now convinced that the energy-signaling
pathways that employ insulin and IGF-1 are very involved in
fixing an organism's life span. Some researchers have even
described Type 2 diabetes, which is marked by insensitivity to
the hormone insulin, as simply an accelerated form of aging.
In yeast, scientists have discovered a gene similar to daf-2
called SIR2, that also helps to coordinate the cell's defensive
response once activated by calorie restriction or another
external stressor. The genes encode proteins called sirtuins,
which are found in both plants and animals.
A mammalian version of the SIR2 gene, called SIRT1, has been
shown to regulate a number of processes necessary for long-term
survival in calorie-restricted mice.
Scientists are now trying to develop synthetic compounds that
affect the genes daf-2 and SIRT1.
Several candidate drugs designed to prevent age-related
diseases, particularly diabetes, are on the drawing boards at
biotech companies. Sirtris Pharmaceuticals, in Boston, already
has begun testing a new drug in patients with Type 2 diabetes
that acts on SIRT1 to improve the functioning of mitochondria,
the cell's energy factories.
While an anti-aging pill may be the next big blockbuster, some
ethicists believe that the all-out determination to extend life
span is veined with arrogance. As appointments with death are
postponed, says Dr. Leon R. Kass, former chairman of the
President's Council on Bioethics, human lives may become less
engaging, less meaningful, even less beautiful.
Dr. Kass recently wrote. "Mortality makes life matter."
Excerpted from: One for the Ages: A Prescription That May Extend
Life
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