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This hypothesis, referred to as the monoamine hypothesis, grew primarily out of two main observations made in the 1950s and ’60s.14 One was seen in patients being treated for tuberculosis who experienced mood-related side effects from the antitubercular drug iproniazid, which can change the levels of serotonin in the brain. Another was the claim that reserpine, a medication introduced for seizures and high blood pressure, depleted these chemicals and caused depression—that is, until there was a fifty-four person study that demonstrated that it resolved depression.15 From these preliminary and largely inconsistent observations a theory was born, crystallized by the work and writings of the late Dr. Joseph Schildkraut, who threw fairy dust into the field in 1965 with his speculative manifesto “The Catecholamine Hypothesis of Affective Disorders.”16 Dr. Schildkraut was a prominent psychiatrist at Harvard who studied catecholamines, a class of naturally occurring compounds that act as chemical messengers, or neurotransmitters, within the brain. He looked at one neurochemical in particular, norepinephrine, in people before and during treatment with antidepressants and found that depression suppressed its effectiveness as a chemical messenger. Based on his findings, he theorized broadly about the biochemical underpinnings of mental illnesses. In a field struggling to establish legitimacy (beyond the therapeutic lobotomy!), psychiatry was desperate for a rebranding, and the pharmaceutical industry was all too happy to partner in the effort. This idea that these medications correct an imbalance that has something to do with a brain chemical has been so universally accepted that no one bothers to question it or even research it using modern rigors of science. According to Dr. Joanna Moncrieff, we have been led to believe that these medications have disease-based effects—that they’re actually fixing, curing, correcting a real disease in human physiology. Six decades of study, however, have revealed conflicting, confusing, and inconclusive data.17 That’s right: there has never been a human study that successfully links low serotonin levels and depression. Imaging studies, blood and urine tests, postmortem suicide assessments, and even animal research have never validated the link between neurotransmitter levels and depression.18 In other words, the serotonin theory of depression is a total myth that has been unjustly supported by the manipulation of data. Much to the contrary, high serotonin levels have been linked to a range of problems, including schizophrenia and autism.19 Paul Andrews, an assistant professor
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Kelly Brogan (A Mind of Your Own: The Truth About Depression and How Women Can Heal Their Bodies to Reclaim Their Lives)