How does psychosis arise (part 1)

I want to get back to Basia’s question: why do people become psychotic? The honest answer is, ‘no one knows’, or as my father (who was a physician-scientist) used to say, ‘if I knew the answer to that I would win the Nobel Prize’. But there are certainly a number of useful ways to think about how psychosis arises.

It’s interesting that western science (including neuroscience) and the contemplative sciences (like Buddhism) share the view that events and conditions arise as a result of previous events and conditions. It’s called cause and effect. So the answer to why or how something happened involves identifying a set of factors that interacted over time.

Western and Eastern thought also agree that cause and effect is very complex; a web of constantly changing, interacting phenomena. Multi-factorial interactions are the name of the game for any explanatory model.

A prime example is the ‘Stress-Vulnerability’ model that is commonly used in psychiatry and neuroscience (and in western medicine in general). The idea is that each person has some particular degree of vulnerability to develop (in this case) psychosis. Some people are very vulnerable. Others have a very low vulnerability. The key point is that there is an interaction between whatever vulnerability there is and the degree of stress that they have encountered over time (including the present). High vulnerability and high stress makes it very likely that psychosis will manifest, much more so than if there is, for example, high vulnerability and low stress.

In the Stress-Vulnerability model, stress refers to any environmental factor (psychosocial, physical or chemical). So this model is basically pointing out the interaction of ‘nature’ (biological vulnerability) and ‘nurture’ (environmental exposure),

I found the model is useful in clinical practice. We worked with a young man who smoked a lot of marijuana (for months) and became psychotic. We showed him research data indicating that using marijuana increases a person’s risk of psychosis. His questions was, “I have three friends who smoked even more than me, but they didn’t become psychotic; how come”? Our answer was, ‘because you are more vulnerable to the chemical stress that marijuana represents”.

He wasn’t convinced, of course, but he did ask the obvious next question; ‘why am I more vulnerable’? Good question; perhaps we should rephrase Basia’s question to be: why do some people become psychotic and others don’t? I’ll take a shot at that in ‘part 2’ (stay tuned).