Depression holds sway worldwide, and it is one of the psychiatric disorders that can strike any group, age, or anytime.

During 2015–2018, 13.2% of Americans aged 18 and over reported taking antidepressant medication in the past 30 days. Antidepressant use was higher among women than men in every age group. Use increased with age in both men and women. Almost one-quarter of women aged 60 and over (24.3%) took antidepressants.

Over the past several decades, as antidepressant use increased, patients (and the healthcare profession) have believed that depression was due to “a chemical imbalance” of the neurotransmitter serotonin. With that thought in mind, researchers concocted numerous antidepressants to manipulate serotonin actions in a patient’s nervous system by enlisting a pattern of blocking (antagonist) or facilitating (agonist) the neurotransmitter’s exertion.

The belief in serotonin’s ability to control depression was further facilitated by flawed research that cherry-picked results, didn’t publish failed efforts on its behalf, and the marketing needs of pharmaceutical companies. To say that depression was produced by “a chemical imbalance” served several purposes.

The first factor was the wish of patients to believe they were victims of their biology, not their negative cognitions or lifestyle choices, or other factors. The second major factor was to produce blockbuster medications.

Prozac was incredibly successful (read “Listening to Prozac ”) because of efforts to promote it. Its problems, however, were understated or not stated at all during prescribing. After the introduction of Prozac into the pharmaceutical armamentarium, several groups of medications were based on similar theoretical beliefs with slight chemical changes.

Authors quickly jumped on the bandwagon and began producing books and articles that ingrained this chemical imbalance belief further. The writers offered ways to reverse it with foods, exercises, or natural products.

A New View of the Theory

Thanks to a meta-analysis research project, the cat may be out of the bag. But, after all these years and before this research, didn’t people wonder why their antidepressant wasn’t working? Was serotonin not the culprit it had been viewed as in the past?

And why did placebos work when antidepressants didn’t? The new effort at seeking out more about serotonin and whether it was the culprit in depression has been eye-opening.

Our comprehensive review of the major strands of research on serotonin shows there is no convincing evidence that depression is associated with, or caused by, lower serotonin concentrations or activity. Most studies found no evidence of reduced serotonin activity in people with depression compared to people without, and methods to reduce serotonin availability using tryptophan depletion do not consistently lower mood in volunteers.

While the review would seem to set the serotonin theory aside, there may still be individuals who could benefit from these medications. As one supervisor I had during my internship once told me, even a sample of ONE is sufficient for research. If someone, anyone, benefits, it’s the proper medication for them.

Dispensing millions of pills must surely hit one patient or more with a special need. Depression remains a serious, misunderstood disorder that ravages lives and results in suicide for too many. WHO notes that up to 280 million people worldwide suffer from depression.

In 2016, suicide ranked as the 10th leading cause of death among Americans. It is the second leading cause of death for those under 35.

Bringing some control over the illness/disorder remains a primary goal for anyone in healthcare because of the millions who suffer from depression and die because of the emotional pain it causes.