It is so rare that we see a medical study that is controlled, reasonably-sized, and actually shows a mechanism for a process. The usual paper these days seems to need 100,000 participants to find a statistically significant result, about whose mechanism the authors speculate at length without any actual data to support their pontifications.
The recent study (Ristow, M., Zarse, K., Oberbach, A., Klöting, N., Birringer, M., Kiehntopf, M., Stumvoll, M., Kahn, C.R., and Blüher, M., 2009. Antioxidants prevent health-promoting effects of physical exercise in humans. PNAS published online before print May 11, 2009, doi:10.1073/pnas.0903485106), because of its scientific rigor, should be received as another blow to the supplement-obsessed, along with the recent gargantuan mega-study that failed to find any benefits to vitamin use in post-menopausal women, despite its ridiculously large data set.
The Ristow et al. study, in contrast, measured the physiological effects of antioxidant vitamins (C and E) in 40 males, half of which were given placebo vitamins. Simply put, this was the theory behind the study: exercise (i.e. higher metabolism) creates reactive oxygen species (ROS), including those insidious compounds known as “free radicals,” which have been popularly linked in recent years to aging. On the one hand, exercise clearly is beneficial for health, but on the other hand, antioxidants (such as vitamins C and E) bind with free radicals and prevent them from doing the damage we assume they are doing. So the question was whether taking vitamins C and E affected the physiology of exercise, and whether that effect was beneficial or not.
The use of antioxidants has been promoted for years to prevent disease and slow inevitable decline. The problem is, recent accumulating data suggests that vitamin E does not protect against disease and sometimes might even promote it. Once again, our overly simplistic assessment of a compound’s function in the human body has led us to believe we can easily alter that function to our benefit.
It is the assumption that free radicals only do us damage that is challenged by the results of the study. The vitamins did what they were supposed to do; they reduced oxidative stress in exercising individuals. But this meant that they interfered with a necessary process that is naturally set in motion by exercise, improving insulin sensitivity – i.e. better glucose metabolism. In the long run this natural process, driven by ROS, keeps metabolism functioning properly and helps to prevent problems such as type 2 diabetes (a disorder characterized by insulin resistance – i.e. poor glucose metabolism). The vitamins also prevented a normal post-exercise increase in the hormone adiponectin, which is involved with breaking down fats; normally, higher levels are correlated with lower body fat.
The authors conclude that ROS have the important function of activating key genes affecting metabolism; they are an integral part of the positive physiological response to exercise. Blocking these compounds with commonly ingested amounts of antioxidants reduces drastically some of the important health benefits of exercise. The lesson here is that free radicals are not just trash molecules that do nothing but harm us. There is probably much more to their function than we yet understand.
In fact, there is much more to almost any compound utilized by the human body than we currently understand, and none of these compounds work in a vacuum. It’s time for the reductionists to stop telling us there is a magic pill to cure our woes. Our bodies evolved to eat living plants and animals, not processed collections of laboratory-derived compounds, and to walk as our primary mode of transportation, not drive.
And as a final note to the skeptical supplementers out there: don’t confuse a study like this with the giant mega-analyses that are based on self-reported data. This was a rigorous scientific study that produced a reliable result, and a pretty good understanding of its mechanism. Never listen to anyone who says that a medical study is no good because its sample size is small; on the contrary, huge sample sizes often produce spurious statistical effects, so a statistical difference found in a well designed study of low sample size is much more likely to be biologically significant.