Study Finds First Direct Evidence of Link Between Low Serotonin and Depression | The Depression
Scientists claim to have found the first direct evidence that people with depression have a reduced ability to release serotonin in the brain.
The results of a brain imaging study rekindle a debate within psychiatry over the so-called serotonin hypothesis in depression and challenge the conclusions of an influential review published in July which found “no clear evidence” that low levels of serotonin are responsible. The latest work, led by scientists at Imperial College London, has suggested that people with depression have a reduced serotonergic response.
“This is the first direct evidence that serotonin release is blunted in the brains of people with depression,” said Professor Oliver Howes, a consultant psychiatrist based at Imperial College and King’s College London, and co-author. “People have been debating this issue for 60 years, but it’s all based on proxy measures. It is therefore a very important step. »
The serotonin hypothesis arose from evidence from post-mortem brains and blood samples suggesting that a deficiency of serotonin may be involved in depression. The theory provides a plausible biological mechanism explaining the effectiveness of the main class of antidepressants, selective serotonin reuptake inhibitors (SSRIs), and is why the brain chemical is sometimes called the “happiness hormone”. .
However, there is not yet conclusive evidence that serotonin abnormalities are the underlying cause of depression and addressing this issue is considered crucial to providing better treatments. The latest paper adds weight to the idea that serotonin plays a role and demonstrates a new brain imaging technique that could pave the way to a better understanding of why SSRI drugs fail to help about 10 to 30 % patients.
“It’s the closest anyone has gotten so far,” Howes said. “It is difficult to measure these transmitters in the brains of living people. You can’t put a pipette in there and take a sample. It’s the closest we’re likely to come.
The study, published in the journal Biological Psychiatry, involved seventeen patients with major depressive disorder or depression related to Parkinson’s disease and 20 healthy volunteers. Participants received a PET scan that uses a radioactive tracer to reveal how much serotonin binds to certain receptors in the brain. They were then given a dose of amphetamine, which stimulates the release of serotonin, and scanned again. A reduced serotonin response was seen in depressed patients, the researchers found.
Professor Catherine Harmer, from the University of Oxford, who was not involved in the work, described it as an important discovery. “It’s really remarkable that they found evidence of lower serotonin release,” she said. Harmer said few in the field would now argue that all depression was the result of low serotonin, but the results were “very consistent with the idea that serotonin may play an important role.”
Others were more skeptical. Eiko Fried, a clinical psychologist at Leiden University, questioned whether the results were statistically robust. “The conclusions drawn by the authors are not commensurate with the evidence presented,” he said. “Statistical analyzes are inconsistent and do not establish ‘clear evidence’ for the serotonin depression theory.”
Joanna Moncrieff, professor of psychiatry at University College London who led the review which concluded there was no evidence that chemical imbalances in the brain cause depression, said the latest paper does not would not lead him to revise this point of view. She pointed to the size of the study and the fact that it was still measuring a proxy for serotonin as gaps. “This study does not provide compelling evidence that a serotonin abnormality is the cause or mechanism underlying depression, or one of the causes or mechanisms,” she said.
Howes said the findings should be replicated and further studies would be needed to determine whether differences in serotonin cause depression or result from disease. “It’s important because while current treatments help a lot of people, they don’t work for everyone,” he said. “For a lot of people, the first treatment doesn’t work, and some people don’t find any treatment that helps them.”