There has long been a hypothesis that a starvation diet can extend lifespan.
The only way it was really shown was by weaning mice on such a diet - and that isn't really ethical for human babies. And it doesn't work in the wild, because dietary restriction compromises the immune system’s ability to fight off disease and reduces the muscle strength necessary to flee a predator. Most animals don't live long enough to catch 'old age' diseases like cancer and the late-life pathologies that humans do.
A new paper in BioEssays also finds that consuming a diet very low in nutrients can extend lifespan in laboratory animals. Some studies have found that severely restricted food intake reduces the incidence of diseases of old age, such as cancer, which leads to extrapolations about the increase in lifespan. Despite cancer in 3,000 year old skeletons, the notion that cancer is caused by the modern lifestyle persists. The fact remains that the longer you stay alive, the more your chances of cancer increase.
“This effect has been demonstrated in laboratories around the world, in species ranging from yeast to flies to mice. There is also some evidence that it occurs in primates,” says lead author, Dr, Margo Adler, an evolutionary biologist at UNSW Australia. “But we think that lifespan extension from dietary restriction is more likely to be a laboratory artefact.
Dietary restriction also leads to increased rates of cellular recycling and repair mechanisms in the body, says Adler.
The new hypothesis is that this effect evolved to help animals continue to reproduce when food is scarce; they require less food to survive because stored nutrients in the cells can be recycled and reused. It is this effect that could account for the increased lifespan of laboratory animals on very low-nutrient diets, because increased cellular recycling reduces deterioration and the risk of cancer.
“This is the most intriguing aspect, from a human health stand point. Although extended lifespan may simply be a side effect of dietary restriction, a better understanding of these cellular recycling mechanisms that drive the effect may hold the promise of longer, healthier lives for humans,” Adler says.
It may be possible in future, for example, to develop drugs that mimic this effect.
Citation: M. I. Adler, R. Bonduriansky, ‘Why do the well-fed appear to die young?’ BioEssays, DOI: 10.1002/bies.201300165.
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