Maternal cannabis use disorder linked to higher autism risk in children, study finds

By Dr. Sanchari Sinha Dutta, Ph.D.Reviewed by Benedette Cuffari, M.Sc.May 23 2024

A study published in Psychiatry Research identifies a link between maternal cannabis use disorder and an increased risk of autism spectrum disorder (ASD). 

Study: Exposure to maternal cannabis use disorder and risk of autism spectrum disorder in offspring: A data linkage cohort study. Image Credit: NDAB Creativity / Shutterstock.com

Cannabis and ASD risk

ASD is a neurodevelopmental disorder characterized by persistent deficits in social communication and interaction abilities. Current estimates indicate that the global prevalence of ASD is 0.6%, with Australia reporting the highest prevalence of 1.7%. Multiple factors contribute to the pathogenesis of ASD, including genetics and environmental factors.

The use of cannabis has significantly increased over the past two decades due to the legalization of medicinal and recreational cannabis use, as well as shifts in illicit drug policies. In fact, cannabis has become the most commonly used illicit drug during pregnancy.   

The highest prevalence of cannabis use during pregnancy has been reported in the United States at 23%. Likewise, recent reports indicate that about 20% of pregnant women use cannabis in Australia.

Previous studies investigating the health outcomes of in-utero exposure to cannabis have found long-lasting effects on neurological development, including ASD. In the current study, scientists investigate the association between maternal cannabis use disorder (CUD) during pre-pregnancy, prenatal, and perinatal periods and the risk of ASD in exposed children.

Study design

The current study used data obtained from the New South Wales (NSW) Perinatal Data Collection (PDC), which includes information on an all-live birth cohort from January 2003 to December 2005. The dataset was linked with the Admitted Patients Data Collection (APDC) and outpatient visit records to obtain information on maternal CUD and offspring ASD.

The exposure variable of CUD and ASD, the outcome of interest, was identified using the 10^th international disease classification criteria. The primary study findings were adjusted for multiple confounding factors, including parental sociodemographic and socioeconomic status, smoking during pregnancy, maternal mental health disorders, maternal comorbidities, child gender, low birth weight, and prematurity at birth.

Important observations

Taken together, data on 222,534 mother-offspring pairs were analyzed, from whom a total of 1,441 children were diagnosed with ASD. Exposure to maternal pre-pregnancy, prenatal, and perinatal CUD were observed in 1.1%, 2.1%, and 2.6% of children with ASD, respectively.

Among children diagnosed with ASD, 32% were from poor socioeconomic backgrounds, 14% were exposed to prenatal smoking, 10% were born preterm, 9% had low birth weight, 2.4% were exposed to maternal prenatal depressive disorder, 1.9% were exposed to maternal prenatal opioid use disorder, and 1.9% were exposed to maternal prenatal anxiety disorder.

A significantly higher risk of ASD was observed among male children as compared to female children. However, maternal CUD was associated with an independent and persistently higher risk of ASD development in offspring, irrespective of their gender.

Mothers 20 years and younger also had a significantly greater risk of having children with ASD as compared to older mothers.

Association between maternal cannabis use disorder and ASD risk in offspring

A 3.5-times increased risk of ASD was observed among children born to mothers with prenatal CUD as compared to non-exposed offspring. Consistently significant associations were also observed between pre-pregnancy, during pregnancy, and perinatal CUD and the risk of ASD in offspring. All observed associations remained unchanged after adjusting for potential confounding factors.

Considering the interaction effect between maternal smoking and CUD, the analysis revealed that maternal smoking status can significantly influence the magnitude of the impact of prenatal CUD on ASD risk among offspring.

Conclusions

The current study finds that children exposed to maternal CUD during the prenatal period are at a 3.5 times greater risk of developing ASD as compared to non-exposed children. Moreover, male children appear at a greater risk of developing ASD than female children.

Mechanistic studies have shown that the psychoactive compound Δ9-tetrahydrocannabinol (THC) found in cannabis can readily pass through the placenta and fetal blood-brain barrier, thus highlighting the possibility of in-utero fetal exposure to cannabis and subsequent alterations in fetal brain development.

Maternal cannabis exposure has been found to alter human brain hippocampal functional connectivity, which, in turn, leads to alterations in fetal dorsolateral, medial, and superior frontal, insula, anterior temporal, and posterior cingulate connectivity. Fetal exposure to THC during pregnancy has also been shown to alter dopamine receptors, which significantly affects neurological development and impairs psychological development in offspring.

A comparatively higher risk of ASD observed in male children highlights the need for more research on gender-specific mechanisms for this disorder. Future studies should also address the impact of duration and timing of in-utero cannabis exposure on the risk of ASD in offspring.