The area of cellular metabolism surrounding growth hormone, IGF-1, and insulin is arguably the most studied set of mechanisms linking the operation of metabolism and the pace of aging. It is impacted by calorie restriction, an intervention that reliably slows aging. The longest lived engineered mice are those in which growth hormone signaling is disabled, and there is an equivalent human population with a similar inherited mutation to study. Many of the early attempts at producing long-lived nematode worms involved manipulation of IGF-1/insulin signaling. A greater number of centenarians than younger individuals appear to have favorable IGF-1/insulin signaling, suggesting some survival advantage.
But is this of any practical use when it comes to producing therapies that treat aging and meaningfully lengthen human life spans? After going on for thirty years of study, one has to think that the answer might be no. There is no way forward to radical life extension of decades and restored youth via mimicking calorie restriction, or trying to make metabolism more like that of long-lived people. Most people with the same biochemistry as centenarians die long before reaching that point – the survival advantage