Occasionally during my love affair with marijuana I would experience perceptual disruptions profound enough to freak me out. One time I was driving along a crowded road when my car seemed a little wobbly and then listed towards the centre, an alarming thud-thud emanating from the back end. In the middle of a densely populated spot without a hard shoulder, I crept slowly across a few lanes of traffic and pulled to a stop. Concentrating very hard, I got out of the car to assess and hopefully change the flat tyre. I rarely got paranoid from smoking weed; neither did it typically make me sleepy. Instead, I was among the lucky ones, as the drug made everyday activities such as gardening, waiting on tables and talking to my family bearable if not interesting. So I was shocked and embarrassed to find, after a few minutes of close inspection amid the honking horns, that there was nothing wrong with the car.
At the time I took hallucinations as evidence of a good score. Now, as an ex-smoker and neuroscientist whose focus is addictive drugs, I know that my resilient response to this stressful experience was contingent on having a neurotypical brain. Neural pathways are forged by finely orchestrated signals for synapse growth and pruning; disruptions can result in atypical neural connections that increase the risk of psychosis. The liability may be unmasked by environmental conditions that can essentially be reduced to an ambiguous but well-recognised bogeyman: stress.
A new study in the Lancet Psychiatry journal has attempted to shed light on the relationship between cannabis and psychosis. The authors assessed symptoms such as trouble telling the difference between real and unreal experiences, having false ideas about what is taking place, or who one is, nonsense speech, lack of emotion, and social withdrawal – all core features of the debilitating disorder schizophrenia. Replicating and extending earlier studies, the authors were able to connect cannabis use to increased risk for psychosis.
As anyone who has ever taken a general psychology course well knows, correlation does not mean causation. We would need an experiment to prove this link unequivocally – for example, taking a large group of people and randomly assigning them to using and non-using groups, following them for a number of years and then assessing them for psychotic symptoms. Obviously, that would be unethical. Nevertheless, this study strongly supports the notion that schizophrenia can be precipitated by consuming weed, with high-potency strains a particular concern.
This drug is an increasingly ubiquitous part of modern, socially liberal life. A majority of Americans think it is at least harmless, if not beneficial. The plant contains more than 100 pharmacologically active compounds, called cannabinoids. Of these, the two of primary interest to researchers and consumers are delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD).
In 1964 we learned that THC is responsible for the drug’s recreational high. Two key discoveries followed. First, THC produces its effects (perceptual distortions, changes in thinking and euphoria, for example) by interacting with a particular class of cell receptors. These CB1 receptors are present in virtually every synapse – the point at which brain cells convey information to each other. Such wide distribution indicates that they play a critical role in most, if not all, brain activity. That’s not because we evolved to enjoy smoking weed. It’s because those plants happen to mimic signalling molecules found in our bodies – endocannabinoids – just like morphine mimics our endorphins. It seems that one role of endocannabinoids is to help highlight especially important communication. When something meaningful happens, the release of these molecules helps ensure that relevant circuits in the brain take note.
The primary difference between THC and our brain’s own cannabinoids is dosing. Neurotransmission occurs in a targeted, local manner appropriate to specific demands. After using cannabis, all brain circuits are flooded with THC, so the process of sorting meaning from the mundane is disrupted. Everyday occurrences such as eating a meal, listening to music, watching television or driving a car become soaked with import. For someone with hearty neural connections who is resilient to stress, this can be a real treat, but for those whose ability to cope and sort is naturally less robust, including those with a susceptibility schizophrenia, it can be a threat.
Well designed, placebo-controlled studies on cannabis are still lacking. In particular, we need more research to distinguish between the effects of THC and those of CBD. The latter compound counteracts the effects of THC and has therapeutic promise for a number of health conditions. There seems no reason therefore not to make CBD widely available, but plenty to suggest careful consideration before embracing THC.
We are swept up in a backlash against overly restrictive and unscientific regulation of cannabis. While it is well past time to loosen restrictions, promote research and consider the data that emerges, the Lancet study provides evidentiary warning about the inherent dangers – to some – of our quest to mitigate reality.
Most societies take it upon themselves to provide appropriate assistance for those with disability; they ought also to take reasonable measures to prevent those disabilities occurring, when possible. Addiction and psychosis are similar in that they are the result of biological vulnerability combined with a stressful environment. Some are more predisposed than others, and this should provoke ethical and moral obligation – particularly from those of us who are not at risk – to protect the unlucky ones for whom the use of cannabis may be permanently detrimental.