Overview
The framework of a “chemical imbalance” is a popular one used to conceptualize neurobiological changes that provide the physiological basis for disorders like Major Depressive Disorder (MDD) or Substance Use Disorder (SUD), but the scientific community generally considers it to be an oversimplified model that overlooks neural connectivity and neuroplasticity.
History and Etymology
As with many models of health and anatomy that become embedded in the public consciousness, the notion of a chemical imbalance as the root cause of mental health disorders was fueled by marketing campaigns. From the 1950s to the 1960s, clinicians who prescribed medications to address infections like tuberculosis or chronic conditions like high blood pressure noticed that they also improved patients’ moods. Joseph Schildkraut formally proposed a framework for depression in 1965 that claimed a deficiency in monoamine neurotransmitters (such as norepinephrine and serotonin) was a cause for depression. After all, it seemed pretty straightforward and logical to conclude that if a medication raised the level of a neurotransmitter while improving mood, then a deficiency of that neurotransmitter was related to the low mood. When Selective Serotonin Reuptake Inhibitors (SSRIs) like Prozac, Zoloft, and Paxil were created, pharmaceutical companies rolled out marketing campaigns that used the model of a chemical imbalance to explain their mechanisms. The model was also used by public health advocates to address the stigma of mental health conditions being problems of morality or character without a physiological basis. However, by the early 2000s, the scientific community had accumulated ample evidence that people with depression did not actually have a measurable chemimcal deficiency in the brain. Antidepressants appeared to work by promoting other factors in the brain involved with repair and growth through flooding the brain with neurotransmitters.