In the end I do not think caloric
restriction will work well as typically attempted. After all this ability to improve one’s
lifespan also is a natural result of not been overweight in the first
place. My own answer to the problem has
been my previously described ‘Arclein Diet’ in which I take advantage of the
body’s own inclinations to trick it into only eating the calories needed on a
weekly basis, without risking the triggering of any of its natural responses to
an occasional lack of food.
For the record I have lost a full
forty pounds in a little over twelve months and my body is preparing to shed
another five or so. I have done this
while never feeling particularly hungry unless I overstay my fast day.
I doubt that the benefits of
fasting will justify a drug based protocol and hopefully it does not come to
that.
Live Longer With Fewer Calories? Key Enzyme Involved in Aging Process
Found
ScienceDaily (Oct. 31, 2011) — By consuming fewer calories, aging
can be slowed down and the development of age-related diseases such as cancer
and type 2 diabetes can be delayed. The earlier calorie intake is reduced, the
greater the effect. Researchers at the University of Gothenburg
have now identified one of the enzymes that hold the key to the aging process.
"We are able to show that caloric restriction slows down aging
by preventing an enzyme, peroxiredoxin, from being inactivated. This enzyme
is also extremely important in counteracting damage to our genetic
material," says Mikael Molin of the Department of Cell and Molecular
Biology.
By gradually reducing the intake of sugar and proteins, without
reducing vitamins and minerals, researchers have previously shown that monkeys
can live several years longer than expected. The method has also been tested on
everything from fishes and rats to fungi, flies and yeasts with favourable
results. Caloric restriction also has favourable effects on our health and
delays the development of age-related diseases. Despite this, researchers in
the field have found it difficult to explain exactly how caloric restriction
produces these favourable effects.
Using yeast cells as a model, the research team at the University of Gothenburg has successfully identified
one of the enzymes required. They are able to show that active peroxiredoxin 1,
Prx1, an enzyme that breaks down harmful hydrogen peroxide in the cells, is
required for caloric restriction to work effectively.
The results, which have been published in the journal Molecular
Cell, show that Prx1 is damaged during aging and loses its activity. Caloric
restriction counteracts this by increasing the production of another enzyme,
Srx1, which repairs Prx1. Interestingly, the study also shows that aging can be
delayed without caloric restriction by only increasing the quantity of Srx1 in
the cell. Repair of the peroxiredoxin Prx1 consequently emerges as a key
process in aging.
"Impaired Prx1 function leads to various types of genetic defects
and cancer. Conversely, we can now speculate whether increased repair of Prx1
during aging can counteract, or at least delay, the development of
cancer."
Peroxiredoxins have also been shown to be capable of preventing
proteins from being damaged and aggregating, a process that has been linked to
several age-related disorders affecting the nervous system, such as Alzheimer's
and Parkinson's. The researchers are accordingly also considering whether
stimulation of Prx1 can reduce and delay such disease processes.
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