The most convincing proof of psilocybin’s mechanism of action comes from a double-blind, randomized controlled trial, which is the gold standard of clinical studies. This study was the first to compare a group of depressed people taking psilocybin to those taking the antidepressant medication escitalopram. The trial’s results were contrasted with other fMRI findings from a recent clinical trial and further analyzed using MRI brain scans.
One day following the initial psilocybin dose, fMRI measurements showed an overall increase in connection between the major brain networks, which is generally decreased in people with severe depression.
The default mode network was simultaneously made smaller while connectivity to other networks was more robust, supporting earlier, smaller experiments.
Some persons saw a more significant increase in connectedness than others after the dose. However, the investigations revealed that six months later, the symptoms improved most for those whose network connections had increased the most.
Six weeks into therapy, however, there was no difference in the connection between the default mode and other brain networks in the brains of escitalopram users. Escitalopram might result in modifications in the future. However given that psilocybin’s antidepressant impact kicks in quickly, it might be the best option for those who do not respond to currently available antidepressants. [8]
According to the study, psilocybin and escitalopram exert different effects on the brain’s “serotonergic 5-HT2A receptors,” with psilocybin having a more concentrated effect. These receptors, which are active in all networked brain regions, including the default mode network, are triggered by serotonin. We already know that psilocybin’s amount of binding to these receptors causes psychedelic effects. However, it is still unknown precisely how their activation affects network connectivity. [9]
Read About: How Diet Can Affect Mood, Cognition, And Sleep