I.F., exercise, and longevity

I.F. update.
I love this eating plan. On fast days I pretty much forget about food (unless I've had a high-intensity workout, in which case I might have a little protein to take vitamins with). But the overall flexibility is great, and I feel no negative effects at all during workouts. And that wierds me out, just a bit. Here's a bit of research on a tangential subject:
###


New Clue Into How Diet And Exercise Enhance
Longevity

*Science Daily —* The traditional
prescriptions for a healthy life--sensible diet, exercise and weight
control--extend life by reducing signaling through a specific pathway in the
brain, according to Howard Hughes Medical Institute researchers who
discovered the connection while studying long-lived mice.

They said their findings underscore the importance of maintaining a healthy
lifestyle and may also offer promising research directions for understanding
and treating diabetes and Alzheimer's disease.

Howard Hughes Medical Institute investigator Morris F. White and his
colleagues published their findings in the July 20, 2007, issue of the
journal Science. Akiko Taguchi and Lynn Wartschow in White's laboratory in
the Division of Endocrinology at Children's Hospital Boston and Harvard
Medical School were co-authors of the research article.

In their experiments, the researchers sought to understand the role of the
insulin-like signaling pathway in extending lifespan. This pathway governs
growth and metabolic processes in cells throughout the body. The pathway is
activated when insulin and insulin-like growth factor-1 switch on proteins
inside the cell called insulin receptor substrates (Irs).

Other researchers had shown that reducing the activity of the pathway in
roundworms and fruitflies extends lifespan. Despite those tantalizing clues,
White said, "The idea that insulin reduces lifespan is difficult to
reconcile with decades of clinical practice and scientific investigation to
treat diabetes."

"In fact, based on our work on one of the insulin receptor substrates, Irs2,
in liver and pancreatic beta cells, we thought more Irs2 would be good for
you," said White. "It reduces the amount of insulin needed in the body to
control blood glucose, and it promotes growth, survival and insulin
secretion from pancreatic beta cells.

In earlier work, the researchers had found that knocking out both copies of
the Irs2 gene in mice reduces brain growth and produces diabetes due to
pancreatic beta cell failure. However, in the new study, when the
researchers knocked out only one copy of the gene, they found the mice lived
18 percent longer than normal mice.

Because reducing insulin-like signaling in the neurons of roundworms and
fruitflies extends their lifespan, the researchers decided to examine what
would happen when they knocked out one or both copies of the Irs2 gene only
in the brains of mice.

Mice lacking one copy of the Irs2 gene in brain cells also showed an 18
percent longer lifespan, and the near complete deletion of brain Irs2 had a
similar effect. "What's more, the animals lived longer, even though they had
characteristics that should shorten their lives--such as being overweight
and having higher insulin levels in the blood," said White.

However, both sets of Irs2 knockout mice exhibited other characteristics
that marked them as healthier, said White. They were more active as they
aged, and their glucose metabolism resembled that of younger mice. The
researchers also found that after eating, their brains showed higher levels
of superoxide dismutase, an antioxidant enzyme that protects cells from
damage by highly reactive chemicals called free radicals.

"Our findings put a mechanism behind what your mother told when you were
growing up--eat a good diet and exercise, and it will keep you healthy,"
said White. "Diet, exercise and lower weight keep your peripheral tissues
sensitive to insulin. That reduces the amount and duration of insulin
secretion needed to keep your glucose under control when you eat. Therefore,
the brain is exposed to less insulin. Since insulin turns on Irs2 in the
brain, that means lower Irs2 activity, which we've linked to longer lifespan
in the mouse."

White and his colleagues are planning their next studies to better
understand how healthy aging and lifespan are coordinated by Irs2 signaling
pathways in the body and the brain. White speculated that the insulin-like
signaling pathway in the brain might promote age-related brain diseases.

"We are beginning to appreciate that obesity, insulin resistance, and high
blood insulin levels are connected to Alzheimer's disease, Huntington's
disease, and dementias in general," he said. "It might be that, in people
who are genetically predisposed to these diseases, too much insulin
overactivates Irs2 in the brain and accelerates disease progression. Thus,
insulin resistance and higher insulin levels might be the environmental
influences that promote these diseases," he said.

*Note: This story has been adapted from a news release issued by Howard
Hughes Medical Institute.*

--
Claudiney Morais
Rio de Janeiro - RJ