Dose-dependent cannabis use, depressive symptoms, and FAAH genotype predict sleep quality in emerging adults: a pilot study

ABSTRACT

Background: Cannabis has been shown to affect sleep in humans. Findings from animal studies indicate that higher endocannabinoid levels promote sleep, suggesting that chronic use of cannabis, which downregulates endocannabinoid activity, may disrupt sleep. Objectives: This study sought to determine if past-year cannabis use and genes that regulate endocannabinoid signaling, FAAH rs324420 and CNR1 rs2180619, predicted sleep quality. As depression has been previously associated with both cannabis and sleep, the secondary aim was to determine if depressive symptoms moderated or mediated these relationships. Methods: Data were collected from 41 emerging adult (ages 18–25) cannabis users. Exclusion criteria included Axis I disorders (besides SUD) and medical and neurologic disorders. Relationships were tested using multiple regressions, controlling for demographic variables, past-year substance use, and length of cannabis abstinence. Results: Greater past-year cannabis use and FAAH C/C genotype were associated with poorer sleep quality. CNR1 genotype did not significantly predict sleep quality. Depressive symptoms moderated the relationship between cannabis use and sleep at a nonsignificant trend level, such that participants with the higher cannabis use and depressive symptoms reported the more impaired sleep. Depressive symptoms mediated the relationship between FAAH genotype and sleep quality. Conclusions: This study demonstrates a dose-dependent relationship between chronic cannabis use and reported sleep quality, independent of abstinence length. Furthermore, it provides novel evidence that depressive symptoms mediate the relationship between FAAH genotype and sleep quality in humans. These findings suggest potential targets to impact sleep disruptions in cannabis users.

KEYWORDS:

• Cannabis
• CNR1
• depressive symptoms
• FAAH
• sleep

Funding

This research was funded by the National Institute on Drug Abuse (NIDA; R03 DA027457) and the University of Cincinnati Center for Environmental Genetics Pilot Program (P30 ES06096). The researchers were also funded by NIDA (R01 DA030354) during manuscript preparation.

Additional information

Funding

This research was funded by the National Institute on Drug Abuse (NIDA; R03 DA027457) and the University of Cincinnati Center for Environmental Genetics Pilot Program (P30 ES06096). The researchers were also funded by NIDA (R01 DA030354) during manuscript preparation.