Psilocybin is a controlled substance within the UK, being labelled as a Class A drug. Our article is intended as an educational overview of current research, not medical advice. Nor does it advocate for the growing of magic mushroom spores. We strongly recommend against growing magic mushroom spores as this is illegal, and to stick to the laws and regulations within your country. This article sets out to acknowledge the recent increase in global clinical research (FDA breakthrough therapy designation in the US, UK trials at Imperial College London, etc.) as well as discuss these studies and the potential effects of Psilocybin in the brain.
Despite it’s label as a Class A substance, research has been carried out on the naturally occurring psilocybin compound found in certain mushroom species. This compound has received a strong amount of public interest recently due to its potential effects on the mind in treating various mental health conditions where other drugs or therapies have failed. It has shown a promising positive effect in treating treatment-resistant depression, end-of-life anxiety and alcohol dependence. It is important to note that at the time of writing this article there is no definitive answer on whether this compound will be of use to the medical community.
Psilocybin and Psilocin
Psilocybin and Psilocin are similar in name, which makes it incredibly easy for people to mistake one for the other. It is important to note the difference in order to understand it’s influence on our mind and to prevent misinformation.
Psilocybin is a prodrug, meaning it is inactive until the body works to metabolise it. Once this is ingested, the body will work on it to convert it into Psilocin. It gets broken down by enzymes in the digestive system, which remove a phosphate group from the psilocybin. This chemical process is what converts the psilocybin into psilocin. Think of the psilocybin as an uncut key which is useless on its own. Once the key cutter (the enzymes) work on it, and “cut” it into psilocin, it can then produce the effects observed in research.
Psilocin is the compound which actually crosses that blood-brain barrier and interacts with your serotonin receptors. This is structurally similar to serotonin, which is why it binds so well to serotonin receptors in your brain. This process is well-documented in pharmacological research, in both human and animal studies.
The bodies processes to break down the Psilocybin into Psilocin work with such speed and efficiency that the effects of psilocybin tend to come on within 20-40 minutes in a clinical setting. Psilocin is eventually eliminated from the body by the process of metabolism within the liver, where it is then excreted through the urine. This process typically takes 4-6 hours, by this time the effects of this compound will be gone.
The effects on your brain
Psilocin mainly interacts with the serotonin (5-HT2A) receptors in the brain which can change the way your brain signals in regions related to mood, perception and cognition. It can also interact with other serotonin receptors, but this area is understudied therefore we lack proper understanding at this time.
Current research shows that psilocybin reduces the activity in the default mode network. The default mode network is the part of the brain’s infrastructure linked to self-referential thought and rumination. At the same time as dampening this network, it also increases the crosstalk between regions of the brain which would typically not communicate. Some scientists would describe this as the “loosening” of your typical, day to day rigid thought patterns. fMRI scans at the Imperial College London were key in showing these connectivity changes in action.
In clinical studies, users would report heightened sensory perception, an altered sense of time and feelings of interconnectedness with others, themselves and the universe. Other mood effects include reductions in negative thought loops and emotional openness in supervised trials. There were also reports of transient anxiety, nausea and challenging experience via “bad trips”. The findings mentioned come from controlled studies, not general reports.
Mental Health Application
Trials such as these have seen a boom in interest for psilocybin-assisted therapies for depression, anxiety and addiction. There are several promising clinical trials at the time of writing this which are in Phase II/III research which may yet provide further evidence for the positive use of this compound.
The long-term effects of Psilocybin are yet to be fully comprehended as there have been little to no studies for this. There also remain questions about the optimal dosage, set and setting and how to integrate the experience into therapy. It must be noted that psilocybin is not risk-free and still remains highly restricted. Phase III studies will shed more light on this topic, but regulatory approval is still a long way off and due to the reputation of magic mushrooms, any positive application of Psilocybin may face a lot of red tape before use in medical settings.
Disclaimer
This article provides a summary of current research into psilocybin. It is not medical advice. Psilocybin remains a controlled substance in the UK and should not be consumed outside of approved scientific research.
Sources:
Cahart-Harris RL, et al. (2012). Neural correlates of the psychedelic state as determined by fMRI studies with psilocybin. PNAS, 109(6): 2138-2143.
Cahart-Harris RL, et al. (2016). Psilocybin with psychological support for treatment-resistant depression: an open-label feasibility study. Lancet Psychiatry, 3(7): 619-627.
Davis AK, et al. (2021). Effects of psilocybin-assisted therapy on major depressive disorder: a randomized clinical trial. JAMA Psychiatry, 78(5): 481-489.
Griffiths RR, et al. (2016). Psilocybin produces substantial and sustained decreases in depression and anxiety in patients with life-threatening cancer. Journal of Psychopharmacology, 30(12): 1181-1197.
Johnson MW, Garcia-Romeu A, Griffiths RR. (2014). Long-term follow up of psilocybin-facilitated smoking cessation. American Journal of Drug and Alcohol Abuse, 40(1): 43-49
