- NEW YORK (Reuters
Health) - While low-calorie diets have been linked to a longer lifespan
in both animals and humans, the reason for the association has been unclear.
Now researchers have evidence from studies in mice that cutting calories
shields brain cells from the decline that comes with aging.
- According to investigators at the University of Wisconsin-Madison,
the study suggests that calorie intake may help determine a person's risk
for degenerative brain diseases like Alzheimer's and Parkinson's disease.
- Cheol-Koo Lee and his colleagues report their findings
in the July issue of Nature Genetics. In experiments with mice, Lee's team
used a gene chip, a new type of gene-scanning technology, to rapidly determine
the activity of more than 6,000 genes in the animals' brain tissue.
- The researchers found that aging boosted the activity
of some genes and decreased it in others. As the mice aged, activity increased
in genes responsible for inflammation and the stress response--two key
factors related to cell damage. In addition, activity declined in genes
involved in repairing cell damage. Co-investigator Dr. Richard Weindruch
told Reuters Health that inflammation in the brain is believed to be related
to certain diseases such as Alzheimer's.
- Since it is known that animals live longer on restricted
diets, Weindruch said, his team expected that brain tissue from mice raised
on low-calorie diets would show fewer aging-related gene shifts. The researchers
had previously shown this to be true in mouse skeletal muscle.
- Indeed, when Weindruch and his colleagues compared elderly
mice raised on a low-calorie diet with those on a standard diet, they found
the calorie-deprived mice had maintained a more youthful balance of gene
- Exactly how calorie intake affects genes over a lifetime
is unknown, according to Weindruch. He said it is possible that restricting
energy intake results in basic changes in energy metabolism, which in turn
helps regulate gene activity.
- Weindruch also noted that a study in Parkinson's patients
has suggested that high calorie intake contributes to the risk for the
disease. ``These findings,'' he said, ``provide a link at the molecular
- SOURCE: Nature Genetics 2000;25:294-297.
Site Served by TheHostPros