The science behind many anti-depressant medications appears to be “backwards”, say the authors of a new study that challenges the prevailing ideas about the nature of depression and some of the world’s most commonly prescribed medications.
The study, published in the journal Neuroscience & Biobehavioral Reviews, reviews existing research on the theory that has dominated nearly 50 years of depression research: that depression is related to low levels of serotonin in the gaps between cells in the brain.
The low-serotonin theory is the basis for commonly prescribed anti-depressant medications called selective serotonin re-uptake inhibitors, or SSRIs, which keep the neurotransmitter’s levels high by blocking its re-absorption into the cells that release it.
Those serotonin-boosting medications could actually make it harder for patients to recover, especially in the short term, says lead author Dr. Paul Andrews, an assistant professor of Psychology, Neuroscience & Behavior at McMaster University in Ontario, Canada.
“It’s time we rethink what we are doing,” says Dr. Andrews. “We are taking people who are suffering from the most common forms of depression, and instead of helping them, it appears we are putting an obstacle in their path to recovery.”
When depressed patients on SSRI medication do show improvement, it appears that their brains are actually overcoming the effects of anti-depressant medications, rather than being assisted directly by them. Instead of helping, the medications appear to be interfering with the brain’s own mechanisms of recovery.
“We’ve seen that people report feeling worse, not better, for their first two weeks on anti-depressants,” notes Dr. Andrews. “This could explain why.”
It is currently impossible to measure exactly how the brain is releasing and using serotonin, the researchers say, because there is no safe way to measure it in a living human brain. Instead, scientists must rely on measuring evidence about levels of serotonin that the brain has already metabolized, and by extrapolating from studies using animals.
The best available evidence appears to show that there is more serotonin being released and used during depressive episodes, not less, the authors say. The paper suggests that serotonin helps the brain adapt to depression by re-allocating its resources, giving more to conscious thought and less to areas such as growth, development, reproduction, immune function, and the stress response.
In previous research, Dr. Andrews and his colleagues had questioned the effectiveness of anti-depressants even for their prescribed function, finding that patients were more likely to suffer relapse after going off their medications as their brains worked to re-establish equilibrium.
With even the intended function of anti-depressants in question, Dr. Andrews says it is important to look critically at their continuing use. However, by no means should any patient stop taking their medication without consulting a doctor first. Research has shown that between half to two-thirds of depressed patients experience long-term symptom improvement when anti-depressants are used correctly, and combination drug therapies can help those who do not experience relief with a single medication.
It’s also important to point out that serotonin is only one of the brain chemicals implicated in depression, and that the disorder is not a simple matter of one chemical being too low and another too high. Many chemicals are involved, working both inside and outside nerve cells. There are millions, even billions, of chemical reactions that make up the dynamic system that is responsible for your mood, perceptions, and how you experience life.
With this level of complexity, you can see how two people might have similar symptoms of depression, but the problem on the inside, and therefore what treatments will work best, may be entirely different.