I post often on examples of scientific inquiry in action. I think it is an important way to see how science works while searching for answers. The process is not a simple one, but after a solution is found it can often be presented as obvious. But while trying to find answers it is quite difficult.
How Prozac sent the science of depression in the wrong direction
But the success of Prozac hasn’t simply transformed the treatment of depression: it has also transformed the science of depression. For decades, researchers struggled to identify the underlying cause of depression, and patients were forced to endure a series of ineffective treatments. But then came Prozac. Like many other antidepressants, Prozac increases the brain’s supply of serotonin, a neurotransmitter. The drug’s effectiveness inspired an elegant theory, known as the chemical hypothesis: Sadness is simply a lack of chemical happiness. The little blue pills cheer us up because they give the brain what it has been missing.
There’s only one problem with this theory of depression: it’s almost certainly wrong, or at the very least woefully incomplete. Experiments have since shown that lowering people’s serotonin levels does not make them depressed, nor does it does not make them depressed, nor does it worsen their symptoms if they are already depressed.
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In this sense, Prozac is simply a bottled version of other activities that have a similar effect, such as physical exercise.
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It is jarring to think of depression in terms of atrophied brain cells, rather than an altered emotional state. It is called “depression,” after all. Yet these scientists argue that the name conceals the fundamental nature of the illness, in which the building blocks of the brain – neurons – start to crumble. This leads, over time, to the shrinking of certain brain structures, like the hippocampus, which the brain needs to function normally.
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