The association between marijuana, also known as cannabis, and schizophrenia is historically fraught. In the 1960s and 1970s, scientists thought that smoking cannabis could trigger psychosis in anyone. Recent studies indicate that the risk is higher when the drugs are used by people under the age of 21, a time when the human brain is developing rapidly and is particularly vulnerable. People with any biological predisposition towards schizophrenia are at the highest risk, with previous studies stating that it is impossible to accurately identify this predisposition beforehand.
Now, a new study from researchers at University of Toronto shows that male teens who experiment with cannabis before age 16, and have a high genetic risk for schizophrenia, show a different brain development trajectory than low risk peers who use cannabis. The team state that the discovery, made from a combined analysis of over 1,500 youth, contributes to a growing body of evidence implicating cannabis use in adolescence and schizophrenia later in life. The study is published in the journal JAMA Psychiatry.
Previous studies show that adolescence is a period of vulnerability with regard to the emergence of psychotic disorders, especially in boys. Environmental influences on the continuing maturation of neural circuits during adolescence are of great interest to the global medical community. Based on this and the given the solid epidemiologic evidence supporting a link between cannabis exposure during adolescence and schizophrenia, the researchers investigated whether the use of cannabis during early adolescence (by 16 years of age) is associated with variations in brain maturation as a function of genetic risk for schizophrenia.
The current study used observations from three large samples of typically developing youth in Canada and Europe. The lab examined data from a total of 1,577 participants (aged 12 – 21 years, 57% male / 43% female), that included information on cannabis use, brain imaging results, and polygenic risk score for schizophrenia. The data came from the Saguenay Youth Study in Quebec (Canada), the Avon Longitudinal Study of parents and Children in the U.K., and the IMAGEN Study in the U.K., Germany, France and Ireland.
Data findings suggest that cannabis use might interfere with the maturation of the cerebral cortex in male adolescents at high risk for schizophrenia by virtue of their polygenic risk score. Results show that their brains showed lower cortical thickness compared with low-risk male participants and low-or-high risk female participants who used the drug. The group note that more research is needed to determine whether lower cortical thickness actually increases the probability of schizophrenia in at-risk males later in life.
The team state that it is too early to classify schizophrenia as either a neurodevelopmental (impairment of the growth and development of the brain) or a neurodegenerative (progressive loss of structure or function of neurons) disorder, as both seem to occur over the course of the illness. However, the group go on to conclude that research strongly suggests the emergence of schizophrenia is a result of both genetic and environmental factors.
The researchers surmise that the study shows the importance of understanding environmental influences on the developing brain in early life as this can have important implications for brain health through the lifespan. For the future the lab now plan to investigate the link between smoking cannabis later in life with a raised schizophrenia risk.