In this era of mass consumption of supplements and foods hawked as medicinal, we are bombarded by "healthspeak", a language that few understand. Antioxidant, free radical, and oxidative stress are prime examples of mystery expressions. Every field develops its own terminology in an attempt to create precise and agreed upon meanings to facilitate the communication of complicated ideas. Such technical jargon may be used by professionals in its field of origin or in the culture at large as a means to gloss over what is poorly understood, language masquerading as comprehension. It can provide a false sense of mastery, an attempt at reassuring ourselves that we know what's going on. But the most basic questions expose our ignorance. Ask anyone what an antioxidant is, if you want to have some fun.
In order to tell you why you should throw out your vitamins, we need to go over some of the language and science in that arena. I promise to make it as painless as possible.
As you may have guessed oxidation has to do with oxygen. It so happens that oxygen is both necessary for life and extremely toxic. The tragic cases of blindness in premature infants in the 1940s caused by high oxygen levels in the newly invented incubators gave us a taste of oxygen's destructive potential. The discovery of superoxide dismutase (SOD) in 1969, an agent that protects against oxygen damage and is found in almost all aerobic cells, marked the beginning of a vibrant field dedicated to the study of oxygen's effect on cell signaling, disease and ageing.
You might wonder how we came to experience oxygen as both vital and deadly. The answer is simple. There was no oxygen in the earth's atmosphere when the earliest life forms developed. 2.45 billion years ago blue-green algae evolved from the primordial ooze with the capacity to use sunlight, water and carbon dioxide to produce carbohydrates and oxygen, a process known as photosynthesis.
It then took 1 billion years (the "boring billion") for the oxygen levels to get high enough to enable the evolution of animals. There was a significant advantage in utilizing oxygen metabolically to generate energy, but it came with a price.
Oxygen's structure is unstable (its outer ring lacks a full set of electrons) and makes it want to react with almost anything in its vicinity. In doing so it destabilizes its neighbor. This can cause all sorts of damage to proteins, including DNA/RNA, and is considered a major cause of ageing and disease. Every compound, including oxygen, that can accept electrons is an oxidant or oxidizing agent. These oxidants are often referred to as "radicals". On the other hand, any agent that can donate electrons is an antioxidant or reducing agent.
So with the advent of an oxygen-rich atmosphere, organisms had to develop defenses against these new noxious oxidizing agents. Two of the most important antioxidants that our bodies manufacture are superoxide dismutase (SOD) and glutathione peroxidase, names you'll see bandied about in many health foods/products. However, despite nature's defense systems, some oxidative damage is always occurring.
Enter the antioxidant vitamins, center stage. Theoretically, it makes perfect sense. If oxidative damage is a common cause of disease and ageing, antioxidant vitamins, like C and E, should help. Unfortunately, these vitamins have been a disappointment. They work beautifully in the laboratory, in test tube experiments, but not in animal studies. This has had no impact on antioxidant vitamin sales, the most popular nutraceutical.
But it gets worse. In 2009 Ristow et al. published a stunning report in the Proceedings of the National Academy of Sciences entitled, "Antioxidants prevent health-promoting effects of physical exercise in humans" that turned everything on its head. Exercise, the most effective defense against obesity and type 2 diabetes (the acquired type associated with excess weight), exerts its therapeutic effects by increasing insulin sensitivity. In fact, exercise is more effective than medication in preventing type 2 diabetes in high risk individuals.
For years it had been believed that exercise (contracting muscle fibers) caused oxidative damage. Ristow's lab demonstrated that exercise-induced oxidation actually plays an essential role in promoting insulin sensitivity. These changes are eliminated by daily consumption of the antioxidant vitamins C (500mg twice/day) and E (400IU/day). That is to say, C and E appear to block one of the most important beneficial effects of exercise on metabolism.
This suggests that oxidative stress, something we thought was bad, is necessary to promote the production of our innate defense mechanisms. Interestingly, the use of antioxidants in type 2 diabetes is associated with increased hypertension and with overall mortality in the general population. How do we make sense of this?
The repeated exposure to sub-lethal doses of stress results in greater stress resistance. This adaptive phenomenon is called hormesis. Such exposure has been shown to improve immune responses, decrease tumor formation and significantly slow ageing.
It is not outlandish to wonder whether antioxidant vitamins are actually contributing to the diabetes epidemic. The fact that a diet rich in vegetables (a source of many antioxidants) decreases the risk of type 2 diabetes may be true despite vegetables antioxidant content.
If all the vitamins were thrown into the sea, it would be all the better for mankind and all the worse for the fishes.