It is a myth that dietary antioxidant supplementation can reliably extend life or even reliably do good things for general health. The weight of evidence strongly suggests that the results are either negligible or harmful. Oxidant molecules have many beneficial roles in addition to being damaging in large volumes, and most likely being involved in the progression of aging. They are used as signals in our tissue to spur maintenance processes essential in generating the benefits derived from exercise, for example.
It is possible to reliably extend life with antioxidants, but they have to be carefully designed molecules that target themselves to the mitochondria in our cells, where the most damaging and least necessary oxidants are generated. The types of antioxidant that you can buy in the store, such as those used in this study, don't go to where they can do some good in tissues and instead interfere with useful processes everywhere else:
While oxidative damage owing to reactive oxygen species (ROS) often increases with advancing age and is associated with many age-related diseases, its causative role in ageing is controversial. In particular, studies that have attempted to modulate ROS-induced damage, either upwards or downwards, using antioxidant or genetic approaches, generally do not show a predictable effect on lifespan.
Here, we investigated whether dietary supplementation with either vitamin E (α-tocopherol) or vitamin C (ascorbic acid) affected oxidative damage and lifespan in short-tailed field voles, Microtus agrestis. We predicted that antioxidant supplementation would reduce ROS-induced oxidative damage and increase lifespan relative to unsupplemented controls.
Antioxidant supplementation for nine months reduced hepatic lipid peroxidation, but DNA oxidative damage to hepatocytes and lymphocytes was unaffected. Surprisingly, antioxidant supplementation significantly shortened lifespan in voles maintained under both cold (7 ± 2°C) and warm (22 ± 2°C) conditions. These data further question the predictions of free-radical theory of ageing and critically, given our previous research in mice, indicate that similar levels of antioxidants can induce widely different interspecific effects on lifespan.