Since the 1960s, researchers have hypothesized that disruptions in the serotonin neurotransmitter system are the cause of major depression. However, despite the abundance of evidence, it was indirect. In point of fact, a recent in-depth review of all of the previous studies came to the conclusion that there was insufficient evidence to back up the “Serotonin Deficiency hypothesis.” Not so fast, according to a new study that provides direct evidence of impaired serotonin release in depression patients’ brains.
The study was published recently in the journal Biological Psychiatry.
Depression is one of the mental illnesses and disabilities that affect most people worldwide. Even though there is no direct evidence that the brain of a depressed person has disrupted serotonin signaling, most depression medications work by increasing extracellular serotonin, also known as 5-hydroxytryptamine (5-HT). Antidepressants only work for about half of patients, and fewer than 30% go into total remission. A deeper comprehension of the dynamics of 5-HT in depression could direct more efficient treatments.
“Our thinking about the role of the Serotonin Deficiency hypothesis in depression has evolved significantly over the past decade. We once thought that serotonin changes could account for the entirety of depression. The current study provides important new support for further exploration of the role of serotonin in depression.
“Our pondering the job of serotonin in gloom has advanced altogether throughout the last 10 years. We once believed that changes in serotonin could be the entire cause of depression.” The current study offers significant new support for expanding our understanding of the role that serotonin plays in depression.
Lead author David Erritzoe, MRCPsych, Ph.D., stated,
“The results suggest reduced serotonin (release) functioning in depression. This study used a new and more direct method to measure the Serotonin Deficiency hypothesis in the living human brain.”
At the outset, the two groups did not significantly differ. However, participants with depression did not exhibit a significant decrease in binding potential, indicating that they had a reduced capacity for serotonin release in important brain regions.
Serotonin release capacity deficits did not correlate with depression severity, according to the study.
Notably, none of the patients had ever taken antidepressants, and 11 of the 17 had never done so. This suggests that low serotonin release capacity is a sign of depression rather than a side effect of antidepressants.
Sadness is a diverse problem that might have numerous causes, and different subtypes may include various synapse frameworks. It is unlikely that serotonergic dysfunction can explain all of this disorder’s clinical features. However, this study demonstrates that unmedicated depression suffers from serotonergic deficits.
“It has taken our field over 20 years to develop a method that enables the measurement of serotonin release in the living human brain,” stated Eugenie Rabiner, MBBCh, FCPsych SA, senior author at Invicro. I trust that we can involve this procedure in the future to investigate the various side effects of sorrow, as well as serotonergic shortfalls tracked down in different circumstances, like Parkinson’s sickness.”
An example: Depression Impairs the Release of Serotonin from the Brain:
David Erritzoe, Beata R. Godlewska, Gaia Rizzo, Graham E. Searle, Claudio Agnorelli, Yvonne Lewis, Abhishekh H. Ashok, Alessandro Colasanti, Iro Boura, Chloe Farrell, Hollie Parfit, Oliver Howes, Jan Passchier, Roger N. Gunn, David J. Nutt, Philip J. Cowen, Gitte K