Among 260 first-episode psychosis patients, early cannabis use and a specific BDNF gene variant independently predicted younger age at psychosis onset, with early cannabis use significantly associated with male gender.
Read this if you are interested in how genetics and cannabis use interact to influence psychosis risk and timing.
Early cannabis use and BDNF gene variant independently predicted younger psychosis onset
What the researchers found
This study investigated whether cannabis use and two genes (COMT Val158Met and BDNF Val66Met) interact to influence when psychosis first appears.
Among 260 Caucasian first-episode psychosis patients, two factors independently predicted younger age at psychosis onset: early cannabis use and carrying the met-allele of the BDNF Val66Met polymorphism.
The BDNF finding is significant because BDNF (brain-derived neurotrophic factor) is critical for brain development and neural plasticity. The met variant reduces BDNF secretion, which could make the developing brain more vulnerable to environmental insults like cannabis.
The COMT gene variant, which has been extensively studied in relation to cannabis and psychosis, did not significantly predict age of onset in this sample.
Notably, early cannabis use was significantly associated with male gender, consistent with the well-documented pattern of earlier and heavier cannabis use among males. This sex-specific pattern may contribute to the earlier psychosis onset often seen in men.
Why it matters
This study identifies a specific gene-environment interaction that influences when psychosis appears. If BDNF met-carriers are more vulnerable to cannabis-induced acceleration of psychosis, this could enable genetic risk stratification for cannabis use.
The numbers in context
260 first-episode psychosis patients. Early cannabis use and BDNF met-allele independently predicted younger age at psychosis onset. Early cannabis use significantly associated with male gender. COMT was not significant.
How the study worked
Cross-sectional study of 260 Caucasian first-episode psychosis patients. COMT Val158Met and BDNF Val66Met polymorphisms were genotyped. Early cannabis use, demographics, and age at psychosis onset were assessed. Logistic regression analyzed factors associated with early cannabis use and age at onset.
What this study cannot tell us
Cross-sectional design cannot prove the BDNF variant and cannabis cause earlier psychosis rather than correlating with other factors. The study included only Caucasian patients, limiting ethnic generalizability. Cannabis potency and frequency were not detailed. The sample size may be underpowered for detecting gene-gene interactions.
How to read the evidence
Cross-sectional genetic association study in first-episode psychosis patients. Moderate because of adequate sample size and replication of known associations, but cross-sectional design limits causal inference.
When this study was published
Published in 2017.
The bigger picture
The interaction between genetic vulnerability (BDNF met variant) and environmental exposure (early cannabis use) exemplifies how precision psychiatry might approach cannabis risk. Rather than universal warnings, genetic testing could identify individuals at specific risk for cannabis-accelerated psychosis.
Questions still open
- Would BDNF met-carriers who avoid cannabis still develop psychosis at the same age? Could BDNF-targeted therapies protect against cannabis-induced psychosis risk? Do other neurotrophic factor genes show similar interactions with cannabis?
Common questions
Does cannabis cause earlier psychosis?
Does genetics affect cannabis-psychosis risk?
Read the original research
Cannabis use, COMT, BDNF and age at first-episode psychosis.
Psychiatry research, 250, 38-43
Citation
Mané, Anna; Bergé, Daniel; Penzol, Maria Jose; Parellada, Mara; Bioque, Miquel; Lobo, Antonio; González-Pinto, Ana; Corripio, Iluminada; Cabrera, Bibiana; Sánchez-Torres, Ana Maria; Saiz-Ruiz, Jerónimo; Bernardo, Miguel. (2017). Cannabis use, COMT, BDNF and age at first-episode psychosis.. Psychiatry research, 250, 38-43. https://doi.org/10.1016/j.psychres.2017.01.045
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