A number of studies have shown that restricting calories increases the lifespan of animals, but the biological basis for this has remained elusive. A new report hints that growth hormone, as well as insulin, are key factors in the life-extending effects of calorie restriction.
"The implication ... for pharmaceutical development would be that the signaling pathways of growth hormone and insulin may be logical targets for development of anti-aging medicine,"
Bartke's team tested whether growth hormone and insulin are tied to the life-extending effects of calorie restriction in a series of experiments with normal mice and mutant mice deficient in growth hormone.
The mutant mice do not express the receptor for growth hormone (and are therefore growth hormone resistant), have profoundly suppressed insulin levels, and are known to live longer and age more slowly than normal mice ... in sharp contrast to its effects in normal mice, calorie restriction failed to increase lifespan in mutant mice lacking growth hormone receptor.
Although it would be irresponsible to recommend that healthy people start using anti-diabetic drugs," said Bartke, "it is reasonable to suggest that treatment(s) causing an improvement in insulin sensitivity combined with modest reduction in insulin release would reduce risk of age-related disease and likely also delay aging.
Most interesting. Calorie restriction researchers are pulling at strands of the tangled knot of metabolic biochemistry - everything affects everything else. It is possible that an extra decade or two of healthy life span for even the most healthy and long-lived amongst us could result from present research into the biochemistry of calorie restriction. It's also possible that nothing of the sort will materialize prior to this line of research being rendered obsolete by the advance of much more aggressive approaches to tackling aging.
It seems to me that metabolic research cannot be more than a stepping stone to far better ways of extending the healthy human life span. Scientists should already be striding beyond these studies to tackle the repair of age-related damage in a more direct manner.