A new study published in the journal Biological Psychiatry revealed that the slow capacity to release serotonin was linked to depression among people. 

The findings revive a 50-year-old debate that researchers have dubbed the serotonin hypothesis, which considers that diminished activity of serotonin pathways plays a causal role in the pathophysiology of depression. 

This particular study, which was conducted at the Imperial College of London shows, that people with depression have a decreased response to the release of serotonin.

"This is the first direct evidence that the release of serotonin is blunted in the brains of people with depression," said Prof Oliver Howes, a consultant psychiatrist based at Imperial College and King’s College London and a co-author.

"People have been debating this question for 60 years, but it’s all been based on indirect measures. So this is a really important step."

The hypothesis emerged from studies conducted on postmortem brains and blood samples that suggested low quantities of serotonin could be responsible for higher incidences of depression.

The theory further offers a plausible biological mechanism for how the principal class of antidepressant drugs, namely selective serotonin reuptake inhibitors, works effectively well.

Yet, evidence is required to support the claim that serotonin abnormalities are the principal cause of depression, and tackling this question may benefit the provision of better treatments.

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This study contributes to the debate by showing how serotonin plays a crucial role via new brain imaging techniques that could unfold new ways of understanding why SSRI drugs failed to help an estimated 10% to 30% of patients.

"It’s the closest anyone has been able to get so far,” said Howes. “It’s hard to measure these transmitters in the brains of living people. We can’t put a pipette in there and take a sample. This is the closest we’re likely to come."

The study included the participation of seventeen patients with major depressive disorder or depression linked to Parkinson’s disease and 20 healthy volunteers for comparative purposes.

PET scans were conducted on participants using a radioactive tracer to determine quantities of serotonin that were released to receptors in the brain.

After participants were given a certain dose of amphetamines to stimulate serotonin release, their brains were scanned again and showed that response to the release of serotonin was slower in depressed patients. 

Prof Catherine Harmer, of the University of Oxford, who was not involved in the work, said, "It’s really noteworthy that they found evidence for lower serotonin release," adding that a few would now argue that depression is always a result of low serotonin. 

Harmer said that few in the field would say that depression was the outcome of low serotonin, but the results were "very much in line with the idea that serotonin may play an important role."

Others rather expressed skepticism. Eiko Fried, a clinical psychologist at the University of Leiden, said, "The conclusions the authors draw are not proportional to the evidence presented."

"The statistical analyses are inconsistent and do not … establish ‘clear evidence’ for the serotonin theory of depression."

On her part, Joanna Moncrieff, professor of psychiatry at University College London, said, “This study does not provide convincing evidence that a serotonin abnormality is the cause or mechanism underlying depression, or one of the causes or mechanisms."

Howes said the results further studies to fully back the results and determine whether any serotonin differences cause depression or arise from the condition.

"It’s important because whilst current treatments do help a lot of people they don’t work for everyone,” he said.

"For large numbers of people the first treatment doesn’t work and some people can’t find any treatment that helps."

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