In the 1950s, the introduction of two new drugs sparked a multibillion-dollar market for antidepressants. In fact, neither of these drugs was designed to treat depression, and at the time, many doctors and scientists believed psychotherapy was the only way to treat depression.
The first antidepressant drugs
The decades-long journey of discovery that followed completely changed our understanding of depression, raising questions that had not been considered before. One of the first two antidepressants was iproniazid, originally used to treat tuberculosis. In a 1952 trial, this drug not only treated tuberculosis but also improved the mood of patients who had been diagnosed with depression. In 1956, a Swiss doctor observed a similar effect when testing imipramine, a drug used for allergic reactions.
Both of these drugs affected a class of neurotransmitters called monoamines. This discovery led to the chemical imbalance theory, the idea that depression is caused by a deficiency of monoamines in the brain’s synapses. Drugs like iproniazid, imipramine, and others were thought to restore this balance by increasing the availability of monoamines in the brain.
However, these drugs targeted different types of monoamines, each acting on a range of receptors in the brain, which led to several side effects, including headaches, fatigue, and cognitive impairments such as difficulties with memory, thinking, and judgment.
New hope for antidepressants
In an effort to make the drugs more targeted and reduce side effects, scientists began studying existing antidepressants to identify which specific monoamines were most associated with improvements in treating depression. In the 1970s, several researchers converged on a common conclusion: the most effective antidepressants all seemed to act on one particular monoamine – serotonin.
This discovery led to the production of fluoxetine, also known as Prozac, in 1988. It was the first drug in a new class called selective serotonin reuptake inhibitors (SSRIs), which block the reabsorption of serotonin, making more serotonin available in the brain. Prozac not only worked effectively but also had fewer side effects compared to older antidepressants.
The makers of Prozac also worked to promote the drug by raising awareness about the dangers of depression to both the public and the medical community. As a result, many people came to understand that depression is a condition caused by mechanisms beyond an individual’s control, reducing the stigma and blame associated with the condition and encouraging more people to seek help.
In the 1990s, the number of people being treated for depression skyrocketed. Psychotherapy and other treatments faded into the background, and most people were treated solely with antidepressant drugs. However, since then, we have gained a more nuanced understanding of how to treat depression and what causes it.
Not everyone with depression responds to SSRIs like Prozac – some people respond better to drugs that affect other neurotransmitters, or they may not respond to medication at all. For many, a combination of psychotherapy and antidepressant drugs is more effective than either one alone.
While antidepressants alter monoamine levels within hours of taking the medication, patients typically do not feel the benefits until weeks later. And after stopping antidepressants, some patients may never experience depression again, while others relapse.
Today, we recognize that we do not know exactly what causes depression, or why antidepressants work. The chemical imbalance theory is at best an incomplete explanation. The fact that nearly all antidepressants act on serotonin does not mean serotonin deficiency is the cause of depression. To make it clearer, consider a simple example: steroid creams can treat rashes caused by poison ivy, but that does not mean steroid deficiency is the cause of the rash.
We still have a long way to go in understanding this disease. However, in the meantime, we have effective tools to treat depression.
Watch the full video content HERE.
Read more:
