One of the many ways in which FDA regulation corrupts research and development in medicine is the creation of a strong financial incentive to reuse existing drugs. It's much less expensive to obtain regulatory approval for a new marginal use of a drug already approved for other uses than it is to obtain regulatory approval for a completely new drug or other medical technology that might be far better. This discourages real progress in favor of something that only looks a little like progress: many of the existing stable of drugs are decades old, yet resources that might otherwise go to breaking new ground are instead poured into shoving these old square pegs into as many round holes as possible.
Given this it should be no great surprise to see that as work on the biology of calorie restriction has progressed, an increasing amount of time and money has been devoted to attempts to reuse existing drugs as calorie restriction mimetics - i.e. to find approved drugs that produce at least some of the same changes in metabolism, and with as few side-effects as possible. One of these drugs is metformin, but as I noted in a post earlier this year, it really isn't much to write home about, given that results from a range of studies are all over the map. It may or may not be useful or beneficial, and certainly doesn't show the clear benefits to health and life expectancy produced by calorie restriction itself:
Studies of the potential antiaging effects of antidiabetic biguanides, such as metformin, are still experimental for obvious reasons and their results are currently ambiguous.
Today I thought I'd direct your attention to a recent paper that shows metformin failing to do much for fly life spans:
The biguanide drug, metformin, commonly used to treat type-2 diabetes, has been shown to extend lifespan and reduce fecundity in C. elegans through a dietary restriction-like mechanism via the AMP-activated protein kinase (AMPK) and the AMPK-activating kinase, LKB1.
We have investigated whether the longevity-promoting effects of metformin are evolutionarily conserved using the fruit fly, Drosophila melanogaster. We show here that while feeding metformin to adult Drosophila resulted in a robust activation of AMPK and reduced lipid stores, it did not increase lifespan in either male or female flies. In fact, we found that when administered at high concentrations, metformin is toxic to flies. Furthermore, no decreases in female fecundity were observed except at the most toxic dose. Analysis of intestinal physiology after metformin treatment suggests that these deleterious effects may result from disruptions to intestinal fluid homeostasis.
Thus, metformin appears to have evolutionarily conserved effects on metabolism but not on fecundity or lifespan.
Nonetheless, money continues to flow for this and similar work.