A new study suggests that serotonin deficiency, which was previously thought to be a primary cause of depression, may not be as influential on the condition as doctors initially thought. This link between serotonin levels and the development of depression was advocated in the late 1980s when serotonin was considered as the "signaling molecule" that was used centrally to gauge depression treatment. During this period, Prozac became the antidepressant of choice since it worked by boosting the levels of serotonin in the brain to combat depression.
Antidepressant researcher and chairperson of the Pharmacology Department at the University of Texas Health Science Center, Alan Frazer, believes that there is no sound evidence to support this theory, and that it was mostly the popularity of Prozac at that time that was responsible for driving the widespread speculation on serotonin. "I don't think there's any convincing body of data that anybody has ever found that depression is associated to a significant extent with a loss of serotonin." Similarly, Dr. Joseph Coyle from the Harvard Medical School's Neuroscience department says that, "Chemical imbalance is sort of last century thinking. It's much more complicated than that. It's really an outmoded way of thinking." Up-to-date studies have now shown that 60 to 70% of depressed patients show no significant response to Prozac or other similar drugs.
A research team from the VA Medical Center and the Wayne State University School of Medicine conducted a study to determine the role of serotonin in depression by observing animal subjects that were unable to produce serotonin. They found that the subjects showed increased tendencies towards aggression and compulsivity, but no symptoms of depression. When subjected to stress, the animals that lacked serotonin responded similarly to antidepressant medication as the ones with normal serotonin levels, leading researchers to conclude that serotonin is not a dominant factor in depression.
