Psychiatric clinicians are often asked to treat patients with evidence-based methods, but frequently the evidence we have to guide our practice does not reflect the reality we see every day in our offices. As such, we are often forced to make clinical decisions based on a minimum amount of evidence.
Currently, many of our patients are using cannabinoids, especially cannabidiol (CBD) to treat their own symptoms—ranging from insomnia, to anxiety, to depression. What evidence is there that this will help? What are the risks? What doses of CBD should they be using? What route? How will CBD interact with other medications? I’ll be exploring these questions in my talk “Confused about Cannabidiol: A Scientific and Rational Examination of its Risks and Benefits in Psychiatry” at Psych Congress in San Diego, California. Here, I will provide a preview of my talk.
A LONG HISTORY
The Cannabis plant was noted in the Chinese medical pharmacopeia nearly 5000 years ago and was a common component in Western patient medications of the 19th century, when it was used to treat insomnia, anxiety, and pain.1 The early, racially charged (it was at this time that the word “marijuana” was used to describe the plant so as to associate its use with vilified Mexican immigrants) efforts of the 1930s to eradicate the use of the plant, most famously by the propaganda film Reefer Madness, began the process of moving the substance out of the pharmacopeia and into the ranks of banned drugs. The Controlled Substances Act (CSA) of 1970 codified this ban, making research into the benefits of cannabis more difficult with its tautological definition of a Schedule I drug as being one that has “no medical use and has a high risk of abuse.”
Also at Psych Congress: MDMA Moving Closer to Therapeutic Use
At the time of its federal ban, the complexity of the cannabis plant was only just beginning to be understood, with the isolation of 9-tetrahydrocannabinol (THC), often described as the intoxicating component of cannabis, by Raphael Mechoulam in 1964.2 The presence of an endocannabinoid system in the mammalian body was unknown at the time, and the first of 2 endogenous cannabinoid receptors, CB1, was only just discovered in 1990.3,4
A CRITICAL BODILY SYSTEM
Before discussing exogenous cannabinoids, I will first review how the mammalian central nervous system expresses endocannabinoid receptors. The endocannabinoid system is critical in fine-tuning multiple other neurotransmitter systems. While most neurotransmission is anterograde, that is, a message is passed from presynaptic neuron to postsynaptic neuron, the endocannabinoids function more like salmon swimming upstream. Unlike the serotonergic or dopaminergic systems that largely propagate a signal downstream, the endocannabinoid system is a retrograde signaling mechanism.5 Another metaphor for retrograde signaling is what occurs when people move boxes in a “bucket brigade” from a house to a moving truck too quickly. When the last person in the line, whose job it is to stack the boxes in the truck, calls out “slow down” and that message is passed down the line, this is a kind of retrograde signaling.