Prozac - a new defense

Head fake
How Prozac sent the science of depression in the wrong direction
By Jonah Lehrer
July 6, 2008

One of the first cracks in the chemical hypothesis of depression came from a phenomenon known as the "Prozac lag." Antidepressants increase the amount of serotonin in the brain within hours, but the beneficial effects are not usually felt for weeks.

This led neuroscientists to wonder if something besides serotonin might be responsible. Duman, for instance, began to study a class of proteins known as trophic factors, which help neurons grow and survive. Trophe is Greek for nourishment; what sunlight and water do for trees, trophic factors do for brain cells. Numerous studies had shown that chronic stress damages the brain by suppressing the release of trophic factors. In a series of influential papers published earlier this decade, Duman demonstrated that the same destructive hallmark is seen in depression, so that our neurons are deprived of what they need.

"The mental illness occurs when these stress mechanisms in the brain spiral out of control," he says.

Once that happens, the brain begins to shut itself down, suppressing all but the most essential upkeep. Not only do neurons stop growing, but the brain seems to stop creating new cells. A 2003 study, led by Columbia University neuroscientist Rene Hen, found that when the birth of new brain cells was blocked with low doses of radiation in "depressed" rats, antidepressants stopped working.

A recent study by Italian researchers, published in the journal Science, helps to reveal another mechanism by which antidepressants reverse the damage of depression. The scientists were interested in seeing if fluoxetine, the active ingredient of Prozac, could increase the potential of brain cells in the adult rat. They studied animals with severe cases of "lazy eye," a condition characterized by poor vision in one eye due to underdevelopment of the visual cortex. The scientists showed that fluoxetine gave brain cells the ability to take on new roles and form new connections, which erased the symptoms of the disorder.

"The drug appears to make brain cells quite young," says Jose Vettencourt, a lead author. The scientists are currently repeating the experiment with humans, raising the possibility that fluoxetine will soon be used to treat lazy eye and related conditions.

In fact, many scientists are now paying increased attention to the frequently neglected symptoms of people suffering from depression, which include problems with learning and memory and sensory deficits for smell and taste. Other researchers are studying the ways in which depression interferes with basic bodily processes, such as sleeping, sex drive, and weight control. Like the paralyzing sadness, which remains the most obvious manifestation of the mental illness, these symptoms are also byproducts of a brain that's literally withering away.

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