The hallucinogenic compound found in magic mushrooms could be used to treat depression.
A new study suggests that boosting the brain's connections may help people with depression break out of negative thinking.
Recent clinical trials have shown that the drug psilocybin may be an effective treatment for depression. In the new study, published Monday in the journal Nature Medicine, researchers looked at how the psychedelic works to improve peoples' moods. The team collected brain scans from about 60 patients who had participated in clinical trials for psilocybin therapy, and these brain scans revealed distinct changes in the patients' brain wiring that emerged after they took the drug.
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The first author of the study, Richard Daws, was a PhD student at Imperial College London. Studies suggest that people with high levels of well-being and cognitive function tend to have highly connected brains, but in people with depression, there is a brain characterized by segregation. He said that this sort of organization undermines the ability of the brain to switch between different mental states.
Hewa Artin, the chief resident of outpatient Psychiatry at the UC San Diego School of Medicine, was not involved in the study. Artin told Live Science in an email that additional studies will be needed to replicate results.
The FDA calls it a "breakthrough therapy" for severe depression.
The new study included 59 people, 16 of whom participated in one trial for the drug.
People with treatment-resistant depression were included in the first trial because they had tried various antidepressants in the past without feeling better. The patients in the trial received a 10-milligram dose of the drug and then an additional 25-milligram dose seven days later. The participants were monitored during each treatment session and had a chance to speak with a therapist after the session.
The researchers used a technique called fMRI, which measures changes in blood flow to different parts of the brain, to see how the patients' brains changed after treatment. The movement of blood through the brain shows which parts of the organ are active. The participants underwent fMRI scans prior to the start of therapy and one day after their 25-milligram dose; and their depressive symptoms were also assessed before and after treatment.
The brain networks of the patients became more integrated after the treatment as shown by the dynamic flow of blood between them. The changes correlated with long-term improvements in the patients.
The second trial was a randomized controlled trial that was considered the gold standard of clinical trials. Neither the participants nor the researchers knew which medication was given to which participant.
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The group took sugar pills throughout the trial and received two 25-milligram doses of the drug. The escitalopram group took daily escitalopram pills throughout the trial after receiving two 1-milligram doses of psilocybin.
Senior author Robin Carhart-Harris, who was the head of the Centre for Psychedelic Research at Imperial College London at the time of the study, said that the 1-milligram doses of psilocybin were a placebo. It would take three to five times that amount to make a difference, said Carhart-Harris, who is now director of the Psychedelics Division within the University of California, San Francisco.
The escitalopram group did not show any significant changes in brain connections, but the people who took the drug showed marked increases in brain network integration. Patients in the group of people who use the drug psilocybin had more improvements in their symptoms than those who took escitalopram.
It suggests that the way that conventional antidepressants work is not the same as the way that psilocybin works.
What is the mechanism? Carhart-Harris said it likely involves a structure on brain cells.
Serotonin 2A is a cannabinoid that plugs into the brain and stimulates it. Carhart-Harris said that certain regions of the cerebral cortex are involved in high-level cognitive functions. He theorizes that after exposure to psilocybin, the receptors undergo a kind of reset that brings their activity back to normal.
The action at the 2A receptor seems to be part of the picture of the mechanism of action.
Large-scale clinical trials with hundreds of patients will need to be conducted in order for the FDA to approve the therapy. 233 patients were included in the largest trial to date.
Carhart-Harris is involved in research at Imperial College London to see if there is a benefit to patients with other conditions. Carhart-Harris is studying how the benefits of the drug vary when it is combined with different forms of therapy.
Carhart-Harris said that the safety and efficacy of the drug used with the therapy rests on it. Carhart-Harris said that he might expect patients with treatment-resistant depression to have three to four dosing sessions in a year, in conjunction with therapy similar to what they used in their clinical trials.
It was originally published on Live Science.
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