A review of 13 studies found that genetic variations in dopamine-related genes (especially COMT) modulated how cannabis impairs working memory, attention, and other cognitive functions.
Read this if you want to understand why cannabis affects some people's thinking more than others.
COMT Val allele carriers showed greater cognitive impairment from cannabis
What the researchers found
Researchers systematically reviewed 13 studies examining how genetic variations influence the cognitive effects of cannabis use. The most consistent finding involved the COMT gene, which regulates dopamine breakdown in the prefrontal cortex.
People with the Val variant of the COMT gene showed greater impairment in working memory, verbal and visual memory, and sustained attention during cannabis intoxication compared to those with the Met variant. The COMT gene also modulated sustained attention effects during regular cannabis use, not just acute intoxication.
Several other genes showed potential modulatory effects: the CNR1 gene (encoding the CB1 receptor), the AKT1 gene (involved in dopamine signaling), the DBH gene (involved in norepinephrine synthesis), and the serotonin transporter gene (5-HTT/SLC6A4).
The review noted that most of these genes are also linked to schizophrenia risk, suggesting that the genetic factors determining how cannabis affects cognition may overlap with those determining vulnerability to cannabis-related psychosis.
Why it matters
Not everyone responds to cannabis the same way cognitively. Understanding the genetic basis of these differences could eventually enable personalized risk assessment, identifying individuals who are most vulnerable to cannabis-related cognitive impairment before they experience it.
The numbers in context
13 studies included. Key gene: COMT Val allele associated with greater cognitive impairment during intoxication. Other modulatory genes identified: CNR1, AKT1, DBH, 5-HTT/SLC6A4. Cognitive domains affected: working memory, verbal memory, visual memory, sustained attention.
How the study worked
Systematic search of PubMed, Web of Science, and ScienceDirect databases for studies measuring neurocognition and assessing genotypes in the context of cannabis use. Thirteen articles meeting inclusion criteria were reviewed.
What this study cannot tell us
Only 13 studies were available, limiting the ability to draw firm conclusions. Most studies were small and used different cognitive assessments. Gene-gene interactions were not addressed. Environmental factors that interact with genetics were largely unexplored. Replication of findings across studies was limited.
How to read the evidence
This is a systematic review of a small but emerging literature, providing moderate evidence for gene-cannabis interactions on cognition.
When this study was published
Published in 2018. Pharmacogenomics of cannabis response is still a developing field.
The bigger picture
The overlap between genes that modulate cannabis cognitive effects and genes linked to schizophrenia provides a molecular bridge between cannabis use and psychosis risk. Understanding these shared genetic pathways could clarify the mechanisms linking cannabis to psychosis and help identify who is most at risk.
Questions still open
- Could genetic testing guide personalized advice about cannabis use? Do the same genetic variants that increase cognitive vulnerability also increase psychosis risk? Would gene-cannabis interaction research benefit from larger genome-wide association approaches?
Common questions
Do genes affect how cannabis impacts your thinking?
Are these the same genes linked to schizophrenia?
Read the original research
The effect of interactions between genetics and cannabis use on neurocognition. A review.
Progress in neuro-psychopharmacology & biological psychiatry, 82, 95-106
Citation
Cosker, E; Schwitzer, T; Ramoz, N; Ligier, F; Lalanne, L; Gorwood, P; Schwan, R; Laprévote, V. (2018). The effect of interactions between genetics and cannabis use on neurocognition. A review.. Progress in neuro-psychopharmacology & biological psychiatry, 82, 95-106. https://doi.org/10.1016/j.pnpbp.2017.11.024
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