Fight Aging!

Metformin is one of the known calorie restriction mimetics amongst drugs presently in use by the medical establishment. A calorie restriction mimetic is a drug that can reproduce some of the beneficial changes to metabolism exhibited during the practice of calorie restriction, which hopefully in turn leads to improved health and extended healthy life span.

Metformin has been shown to modestly increase maximum life span in mice, though by much less than is possible through calorie restriction:

chronic treatment of female outbred SHR mice with metformin (100 mg/kg in drinking water) slightly modified the food consumption but decreased the body weight after the age of 20 months, slowed down the age-related switch-off of estrous function, increased mean life span by 37.8%, mean life span of last 10% survivors by 20.8%, and maximum life span by 2.8 months (+10.3%) in comparison with control mice.

In human medicine, metformin is primarily used as an anti-diabetic treatment, which has led to speculation as to just how much of the calorie restriction effect on health and longevity is due to changes in insulin metabolism - such changes made directly in genetically engineered laboratory animals have been shown to significantly affect longevity as well.

Here, however, I will point you towards a paper that shows much of the effect of metformin to reside in the mitochondria, the cell's power plants. Regular readers will by now know that our mitochondria are very important determinants of aging and longevity, and the accumulated damage suffered by mitochondria - caused by the reactive oxygen species they produce as a consequence of their operation - produces some fraction of the aging process. These reactive oxygen species include hydrogen peroxide, H2O2, and, as it turns out, metformin reduces the rate at which H2O2 is produced by mitochondria without otherwise impairing their operation:

In conjunction with improved glycemic control, metformin treatment reduced H(2)O(2) emission in muscle from obese rats to rates near or below those observed in lean rats ... Surprisingly, metformin treatment did not affect basal or maximal rates of O(2) consumption in muscle from obese or lean rats. ... These findings suggest that therapeutic concentrations of metformin normalize mitochondrial H(2)O(2) emission by blocking reverse electron flow without affecting forward electron flow or respiratory O(2) flux in skeletal muscle.

Since I'm not greatly in favor of efforts that only slow aging, I see this sort of research as more in the way of a confirmation of the importance of mitochondrial damage - and the need to put more resources towards mitochondrial repair with the aim of reversing the effects of aging.

Kane DA, Anderson EJ, Price JW 3rd, Woodlief TL, Lin CT, Bikman BT, Cortright RN, & Neufer PD (2010). Metformin selectively attenuates mitochondrial H2O2 emission without affecting respiratory capacity in skeletal muscle of obese rats. Free radical biology & medicine, 49 (6), 1082-7 PMID: 20600832