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Calorie Restriction Leads Scientists to Molecular Pathways That Slow Aging, Improve Health
Science Daily (Apr. 15, 2010) —
Organisms from yeast
to rodents to humans all benefit from cutting calories. In
less complex organisms, restricting calories can double or
even triple lifespan. It's not yet clear just how much
longer calorie restriction might help humans live, but those
who practice the strict diet hope to survive past 100 years old.
In a review article in the April 16 edition of Science,
nutrition and longevity researchers at Washington University
School of Medicine in St. Louis, University College in London and
the Andrus Gerontology Center at the University of Southern
California, report that calorie restriction influences the same
handful of molecular pathways related to aging in all the animals
that have been studied.
Aware of the profound influence of calorie restriction on
animals, some people have cut their calorie intake by 25 percent
or more in hopes of lengthening lifespan. But first author Luigi
Fontana, MD, PhD, is less interested in calorie restriction for
longer life than in its ability to promote good health throughout
life.
"The focus of my research is not really to extend lifespan to 120
or 130 years," says Fontana, research associate professor of
medicine at Washington University and an investigator at the
Istituto Superiore di Sanità in Rome, Italy. "Right now, the
average lifespan in Western countries is about 80, but there are
too many people who are only healthy until about age 50. We want
to use the discoveries about calorie restriction and other
related genetic or pharmacological interventions to close
that 30-year gap between lifespan and 'healthspan. '
However, by extending healthy lifespan, average lifespan
also could increase up to 100 years of age."
Fontana and his co-authors write about how cutting calorie intake
between 10 percent and 50 percent decreases the activity of
pathways involving insulin-like growth factor (IGF-1), glucose
and TOR (target of rapamycin), and considerably increases
lifespan in animals.Genetic mutations involved in those
pathways have the same effect. Those animals have far fewer
problems with diseases related to aging, such as cancer,
cardiovascular disease and cognitive problems.
"About 30 percent of the animals on calorie restriction die at an
advanced age without any diseases normally related to aging,"
Fontana says. "In contrast, among animals on a standard diet, the
great majority (94 percent) develop and die of one or more
chronic diseases such as cancer or heart disease. In 30
percent to 50 percent of the animals on calorie
restriction, or with genetic mutations in these
aging-related pathways, healthspan is equal to lifespan.
They eventually die, but they don't get sick."
Unfortunately, many humans are moving in the opposite direction.
As obesity reaches epidemic rates in Western countries, Fontana
says rather than closing the 30-year gap between healthspan and
lifespan, the gap is likely to grow. It's even possible lifespan
may decrease as people develop preventable diseases such as
atherosclerosis, type 2 diabetes and certain forms of cancer.
Those growing rates of obesity are a reason some scientists think
calorie restriction will never catch on, regardless of its
potential benefits. But, Fontana says, if researchers who study
nutrition and aging can understand how calorie restriction
lengthens life and makes people healthier, it may be possible to
develop less drastic interventions or medicines that influence
pathways affected by calorie restriction and help keep people
healthy as they get older.
Among people now practicing calorie restriction, he says side
effects include reduced libido because calorie restriction
reduces testosterone levels. They also tend to become cold
more quickly because their thermal regulation changes as
their metabolism slows and their core body temperature
drops.
Fontana says as calorie restriction research advances on many
fronts, it's becoming clear that dietary advice once based on
epidemiological data now makes sense from a molecular point of
view. In the past, dietitians might recommend more fruits and
vegetables or less meat and more whole grains. They based that
advice on studies showing people who ate more vegetables or fewer
animal products tended to have less cardiovascular disease.
"Now we have moved from epidemiology to molecular biology," he
says. "We know that certain nutrients, as well as lower calorie
intake, can influence IGF-1 and other pathways. Soon we hope to
be able to use that knowledge to help people live longer
and healthier lives.
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Key Protein May Explain The Anti-aging And Anti-cancer Benefits Of D
Posted by: "Domingo" dpichardo3@verizon.net harrygton_oliver
Tue Dec 21, 2010 5:18 am (PST)
http://www.scienced aily.com/ releases/ 2009/05/09052208 1214.htm
<http://www.scienced aily.com/ releases/ 2009/05/09052208 1214.htm>
Key Protein May Explain The Anti-Aging And Anti-Cancer
Benefits Of Dietary Restriction
ScienceDaily (May 26, 2009) — A protein that plays a
key role in tumor formation, oxygen metabolism and
inflammation is involved in a pathway that extends lifespan
by dietary restriction. The finding, which appears in the
May 22, 2009 edition of the online journal PLoS Genetics,
provides a new understanding of how dietary restriction
contributes to longevity and cancer prevention and gives
scientists new targets for developing and testing drugs that
could extend the healthy years of life.
The protein is HIF-1 (hypoxia-inducible factor 1). It helps cells
survive by "turning on" when oxygen levels are low. HIF-1 is also
active in some forms of human cancer. HIF-1 overexpression is
frequently detected in solid tumors; inhibition of HIF-1 has been
proved to be an efficient way to prevent cancer growth. Now,
scientists at the Buck Institute for Age Research have shown that
HIF-1 is also a key player in dietary restriction. HIF-1 is
involved in a molecular pathway known to regulate cell growth and
metabolism in response to nutrients and growth factors.
"Previous studies on HIF-1 have mainly focused on its roles in
oxygen metabolism and tumor development" , said Buck faculty
member Pankaj Kapahi, PhD, lead author of the study.
Kapahi says the study encourages the investigation of HIF-1 in
nutrient sensing pathways. "The data in this study also points to
HIF-1 as a likely target for regulating the protective effects of
dietary restriction in mammals," said Kapahi.
"Dietary restriction is one of the most robust methods for
extending lifespan and delaying age-related disease among various
species."
Kapahi says the molecular mechanisms involved in how dietary
restriction slows cancer and extends lifespan have been largely
unknown. "This study gets us closer to understanding that process
and gives us better targets for both designing and testing drugs
which could mimic the effects of dietary restriction in humans,"
said Kapahi.
The research involved nematode worms that were genetically
altered to both under and over-express HIF-1. The animals, which
are the most-often used model to study aging, were fed different
diets. Animals that were designed to over-express HIF-1 did not
get the benefit of lifespan extension even though their diets
were restricted. Animals that under-expressed HIF-1 lived
longer, even when they had a nutrient-rich diet.
Furthermore, it was found that the lifespan extension
resulting from dietary restriction required activity in
signaling pathways in the endoplasmic reticulum, the part
of the cell involved in processing and the proper folding of
proteins. This finding supports the theory that aging stems from
the effects of misfolded proteins and opens up a rich area of
investigation to examine the mechanisms by which stress in the
endoplasmic reticulum affects lifespan.
Other Buck Institute researchers involved in the study include Di
Chen, and Emma Lynn Thomas. The work was supported by the Ellison
Medical Foundation, the Larry L. Hillblom Foundation, the
American Federation for Aging Research, the Bill and Rita
Haynes Foundation, and the National Institute on Aging.
http://www.sciencedaily.com/releases/2010/04/100415141123.htm
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