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The endocannabinoid and stress hormone systems interact in complex ways to influence psychosis risk

Systematic ReviewModerate evidence
The takeaway

A systematic review of 41 studies found the endocannabinoid and HPA stress systems show interconnected alterations in psychosis, with THC affecting the stress axis and childhood trauma affecting endocannabinoid signaling.

People interested in the biological mechanisms linking cannabis use, stress, and psychosis risk.

Bidirectional interaction between endocannabinoid and stress systems in psychosis

What the researchers found

Both systems show independent contributions to psychosis risk, but they also interact bidirectionally: cannabis use affects endocannabinoid tone, stress exposure alters the HPA axis, and crucially, THC also affects the HPA axis while childhood trauma affects endocannabinoid signaling, revealing cross-system perturbation.

Why it matters

The stress-diathesis model and cannabinoid hypothesis of schizophrenia have been studied independently. This review reveals they are deeply interconnected, suggesting that cannabis risk for psychosis cannot be understood without considering stress, and vice versa.

The numbers in context

41 studies reviewed. 9 HPA-related biological studies. 2 endocannabinoid-related biological studies. 29 environmental-measure studies. 1 genetic study. CNR1 genetic variation identified as a cross-system factor.

How the study worked

PRISMA-compliant systematic review searching PubMed, Web of Science, and Scopus. 41 eligible studies extracted, including biological interventional and non-interventional studies, environmental-measure studies, and genetic studies examining the interplay of HPA and endocannabinoid systems in psychosis.

What this study cannot tell us

Heterogeneous study designs limit direct comparisons. Many included studies measured environmental factors (cannabis use, stress) rather than biological endocannabinoid or HPA markers. The mechanistic evidence is stronger for within-system than cross-system effects.

How to read the evidence

PRISMA-compliant systematic review synthesizing 41 studies. Evidence is consistent but mostly correlational, with limited interventional data for cross-system effects.

When this study was published

Published in 2024 in Current Neuropharmacology.

The bigger picture

Understanding psychosis risk requires looking at the interplay between genetic vulnerability, cannabis use, stress exposure, and biological systems. This review argues for a unified model rather than studying cannabis and stress as separate risk factors.

Questions still open

  • Could interventions targeting both the HPA axis and endocannabinoid system simultaneously reduce psychosis risk? Does the timing of stress relative to cannabis exposure matter for the cross-system interaction? Are there genetic profiles that make the interaction particularly dangerous?

Common questions

How do cannabis and stress interact to affect psychosis risk?
This review found the two systems work in both directions: THC directly affects stress hormones, while stressful experiences like childhood trauma alter the endocannabinoid system. Both pathways independently and together contribute to psychosis risk.
Can you separate cannabis risk from stress risk for psychosis?
This review suggests not easily. The endocannabinoid system and stress response system are so interconnected that cannabis use in the context of stress may be more risky than either factor alone.

Read the original research

Biobehavioral Interactions between Endocannabinoid and Hypothalamicpituitary- adrenal Systems in Psychosis: A Systematic Review.

Current neuropharmacology, 22(3), 495-520

Citation

Colizzi, Marco; Bortoletto, Riccardo; Antolini, Giulia; Bhattacharyya, Sagnik; Balestrieri, Matteo; Solmi, Marco. (2024). Biobehavioral Interactions between Endocannabinoid and Hypothalamicpituitary- adrenal Systems in Psychosis: A Systematic Review.. Current neuropharmacology, 22(3), 495-520. https://doi.org/10.2174/1570159X21666230801150032

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