Spark

by John J. Ratey

OUT OF THE TUNNEL Science has come a long way since our search for the single culprit began, and the decades’ worth of research generated from the monoamine hypothesis has taught us volumes about the biology of emotions. The closer we get to the cause of depression, the more complex it appears. When we began, everyone was fairly certain that the problem was an imbalance of neurotransmitters at the synapses. Now we know for certain that it’s not so simple. Ironically, I think this is precisely why exercise has yet to be embraced as a medical treatment. It doesn’t simply raise serotonin or dopamine or norepinephrine. It adjusts all of them, to levels that, we can only presume, have been optimally programmed by evolution. The same goes for exercise’s effect on BDNF, IGF-1, VEGF, and FGF-2, which provide the building material and oversight for the construction of new connections and neurons. In short, exercise affects so many variables in the brain that its nigh impossible to isolate its effect as we’d like—in the name of hard science. But the evidence is there, from the action of microscopic molecules to massive surveys of tens of thousands of people over the years. Yes, exercise is an antidepressant. But it is also much more.