Depression has often been described as a “chemical imbalance.” This description is helpful in that it shifts the view of depression from a moralizing, personal stance into a medical model, and it can help encourage people to receive treatment. However, the “chemical imbalance” model is outdated and inaccurate.
The chemical imbalance theory started in the middle of the 20th century. The discovery of biologic treatments for some mental disorders in the early 20th century (penicillin for syphilis-induced general paresis of the insane and nicotinamide for pellagra) tantalized the field with the possibility of a cure for major psychiatric disorders like depression and schizophrenia. In the early 1950s, three drugs emerged that were crucial to understanding depression: reserpine, a calming agent and antihypertensive medication that caused depression in some people; iproniazid, a newly discovered treatment for tuberculosis that was incidentally discovered to cause euphoria; and imipramine, which alleviated depressive symptoms.
Researchers spent the next decade attempting to identify how these three drugs affected people’s moods. With the technology available at that time, researchers discovered that the levels of certain chemical compounds were lower in fluid samples from people with depression. In the mid-late 1960s, several researchers consolidated the scientific evidence and proposed a theory that depression was caused by a deficiency or decrease in one or all of these chemicals. Thus, the “monoamine hypothesis” was born.
This theory inspired the development of selective-serotonin reuptake inhibitors, which are now among the most prescribed medications in the world due to their benefits for anxiety and depression. Their introduction of zimelidine and fluoxetine (brand name Prozac) in the 1980s, revolutionized the treatment of depression because the drugs were safer than older antidepressants, which could be fatal in overdose.
The chemical imbalance theory is important in the history of psychiatry. However, researchers at that time were limited by the scientific tools that were available. Scientific advances have allowed for a more comprehensive understanding of depression. The monoamine deficiency model is not supported by current research. Instead, current research emphasizes the balance of chemical activity overall, as well as the differing roles of various serotonin receptors. Other approaches, including genomics, immune factors and inflammation, functional neurobiology, and stress-induced changes are important as well. Scientists have yet to figure out how these interact with psychological and social factors, though there are models of how environmental stress can cause important changes in the brain.
The original focus on monoamine deficiency as the primary underlying cause of depression has faded. Rather, today it is treated as a likely characteristic of people who are depressed. Right now, there is no simple explanation for why depression happens. Many different biological changes occur in the depressed brain. It is likely that there are many pathways to depression, just as there are many different types or experiences of depression.
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