There are a great many ways to influence cellular metabolism to modestly slow the pace of aging, but few of them are of lll that much interest from a practical point of view, as a basis for therapies that might meaningfully extend human life spans. If an approach involves improvements in mitochondrial function and less than a 10% increase in life span in a short-lived species such as flies, as is the case here, then it is only of academic interest to scientists who closely study the intersection between metabolism and degenerative aging. Improvements in life span in short-lived species achieved in this manner, via changes in mitochondrial function, scale down dramatically when the same approach is tried in longer-lived species. Thus this method of slowing aging is unlikely to be any better for human health than the well-described outcomes of eating somewhat less or exercising somewhat more.
One approach to identify new traits responsible for aging is to compare how these traits change with age in control and long-lived animals of the same species. For example, centenarians have a distinctive epigenetic profile compared to an age-matched control population. Similarly, we previously showed that flies
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