Skip to content

Abstract Search

Mental Health

Perinatal Cannabis Use Disorder and Risk of Disruptive Behavioral Disorders in Offspring: A Linked Data Cohort Abay Tadesse* Abay Tadesse Berihun Assefa Dachew Kim Betts Getinet Ayano Rosa Alati

Abstract
Background: In-utero exposure to cannabis might be linked to a higher risk of disruptive behavioural disorders (DBD), including conduct and oppositional disorders during childhood and adolescence. However, existing evidence relies on maternal self-reporting of cannabis use during pregnancy. To address this limitation, both the exposure (cannabis use disorder) and outcomes of interest (DBD) were validated using diagnostic tools, specifically the International Classification of Diseases-Australian Modification (ICD-10-AM) classification system.

Objective: This study aimed to examine the associations between prenatal cannabis use disorder (CUD) and DBD in offspring using a large-scale cohort study.

Methods: This population-based cohort study was conducted by participating 222,534 mother-offspring pairs using linked data derived from health data registries in New South Wales (NSW), Australia. The data were sourced from the Perinatal Data Collection (PDC), covering all live birth cohorts from January 2003 to December 2005. This dataset was linked to the NSW Admitted Patient Data Collection (APDC) and Ambulatory Mental Health Data collections (AMB-MH) using unique identifications for mothers and offspring. The exposure variable (CUD) and the occurrence of DBD in offspring, the primary outcomes of interest, were identified through the ICD-10-AM criteria (coded as F12.0-F12.9 and F91.0-F91.9, respectively). Associations were examined using Generalized Linear Models (GLMs) with a binomial family regression model to estimate relative risks. Additionally, gender-specific sensitivity analyses were carried out.

Results: After adjusting for pertinent confounding factors, we observed a five-fold rise in the risk of disruptive behavioural disorders in children exposed to prenatal CUD [RR = 4.87 (95% CI 3.43 – 6.93)] compared to non-exposed offspring. In our stratified analyses, a significant gender difference was observed; female offspring has a slightly higher risk of DBD than their male counterparts [RR = 5.20 (95% CI 2.80, 9.60) versus RR = 5.01 (95% CI 3.26, 7.69)].

Conclusion: This study shows that maternal prenatal CUD is linked to a higher risk of DBD in offspring, with a stronger risk in female offspring. Further research is needed to understand these gender-specific effects and the relationship between maternal CUD and DBD risk in children.