The recent death of comedian and actor, Robin Williams has brought new attention and focus to the problem of mental depression. Williams, who committed suicide at age 63, had suffered from deep mental depression for years, likely related to his history of drug and alcohol abuse. Depression is perhaps the most common mental illness, affecting approximately 3 to 10% of the worldwide population. Those with chronic medical disorders show even higher rates of depression, with a range of 22 to 46%. In the United States, depression is the main cause of disability, or the ability to function in life normally for persons aged 15 to 44. While we know that depression is a widespread disorder, the precise causes are still argued among medical researchers.
The initial hypothesis as to the root cause of depression was offered in 1965. At that time, certain drugs used to treat high blood pressure and other ills were shown to be also associated with the onset of depression. These drugs appeared to lower brain chemicals involved in the transmission of nerve messages within the brain, known as neurotransmitters. When the activity of these endogenous brain chemicals declined, brain activity slowed, resulting in depression. The primary neurotransmitters involved in this process were norepinephrine, serotonin, and dopamine. While this new hypothesis, known as the monoamine hypothesis, since the neurotransmitters involved were all categorized as monoamines, appeared to succinctly answer the question of precisely what caused depression, in reality, several other aspects of depression that occur may have other causes.
More recent research, for example, has implicated another brain chemical as being a major player in depression. This new cause involves glutamate, which is synthesized in the brain from the amino acid, glutamic acid. This doesn't mean that consuming a protein source that contains glutamic acid will bring on depression. It's not so much the glutamate in the brain that is the problem, but rather the way it interacts with a certain brain receptor called the NMDA receptor. When glutamate builds up in the brain, it interacts with this receptor, causing depression. As a point of interest, an excess of glutamate also occurs in the course of a stroke and is considered the major arbiter of brain damage that happens after a stroke. Researchers found the depression link of glutamate when they provided a drug that blocks the glutamate interaction with NMDA brain receptors. Doing so resulted in rapid antidepressant effects. As a result, drug companies are now pursuing this promising avenue of research for the treatment of depression. Drugs that modulate glutamate release in the brain would have the advantage of working much faster than existing antidepressant drugs, most of which don't begin to produce results until after 4-6 weeks on average. On the other hand . . .