WASHINGTON (Reuters) - Scientists have known for seven decades that mice, dogs, fruit flies and other animals given diets bordering on starvation tended to live up to 40 percent longer than their better-fed cousins.
Now they think they know why.
They identified a gene in roundworms on Wednesday that directly links calorie restriction to longer lifespan.
The researchers, led by Andrew Dillin of the Salk Institute for Biological Studies in La Jolla, California, said a gene called pha-4 plays a role in gut development in embryonic worms but in adults is associated with calorie-restricted longevity.
Dillin said it is unclear whether similar genes may play a similar role in humans.
People have three genes very much like the worm’s pha-4. They are related to glucagon, a pancreatic hormone that increases blood sugar concentration and maintains the body’s energy balance, particularly during fasting, they said.
Pinpointing the worm gene might open the door to drugs that imitate the effects of calorie restriction and could allow people to live longer without following such a severely restrictive diet, the researchers report in this week’s issue of the journal Nature.
“We don’t know yet whether or not dietary restriction will increase longevity in humans,” Dillin said in a conference call with reporters. Experts are testing the diets in monkeys.
“There are several people that are actively doing this voluntarily,” Dillin added.
“But there is a primate study that’s going on that’s around 35 years into it, and it looks like the primates are going to respond very well to reduced food intake and actually live longer.”
Dillin said it usually takes a 50 to 70 percent reduction in normal food intake to yield longer lifespan in animals.
“If you reduce food too much, you’re going to go toward starvation and actually live shorter,” Dillin said.
“If you overeat -- have the Big Mac diet, high-calorie content -- you’re going to come to obesity and have a short life span as well. So dietary restriction is really a sweet spot in between the two.”
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