Potential Biological Mechanisms Linking Prenatal Cannabis Exposure to Neurodevelopmental OutcomesPotential Biological Mechanisms Linking Prenatal Cannabis Exposure to Neurodevelopmental Outcomes Prenatal cannabis exposure has been associated with an increased risk of mental health problems in children and adolescents. However, the underlying biological mechanisms responsible for this association remain unclear. A recent study published in Nature Mental Health sheds light on some of these potential mechanisms. Researchers found that cannabis exposure in the womb can impact the developing brain, affecting neurobiological processes that may contribute to later behavioral problems. These potential mechanisms include: * Altered gene expression: Cannabis exposure can alter gene expression, influencing the development and function of neural circuits involved in mental health. * Disrupted neurogenesis: Cannabis exposure may impair neurogenesis, the process by which new neurons are created. This could lead to a reduction in brain volume and impaired neural function. * Abnormal neuroinflammation: Cannabis exposure can trigger neuroinflammation, a process involving the activation of immune cells in the brain. Chronic neuroinflammation has been linked to mental health disorders. * Changes in neurotransmitter systems: Cannabis exposure can affect neurotransmitter systems, such as the endocannabinoid system, which plays a crucial role in mood regulation and cognition. Confounding Factors and Research Considerations Unraveling the long-term effects of prenatal cannabis exposure is challenging due to the presence of confounding factors that can influence mental health and behavior. These factors include: * Socioeconomic status: Families that use cannabis during pregnancy may also have other socioeconomic challenges that could impact child development. * Substance abuse disorders: Parents who use cannabis during pregnancy may also have substance abuse disorders, which can contribute to behavioral problems in children. * Genetic factors: Individual genetic predispositions can interact with cannabis exposure, influencing neurodevelopmental outcomes. Future Research Directions Further research is needed to investigate the potential biological mechanisms linking prenatal cannabis exposure to neurodevelopmental outcomes. Longitudinal studies that follow children exposed to cannabis in the womb over time can help establish causal relationships. Additionally, animal models can provide insights into the neurobiological consequences of prenatal cannabis exposure. By understanding the biological mechanisms involved, researchers can develop targeted interventions to mitigate the potential risks of prenatal cannabis exposure and promote healthy child development.
Scientists are trying to understand how cannabis might affect long-term neurodevelopment when humans are exposed to it in the womb. Previous work by Washington University in St. Louis researchers Sarah Paul and David Baranger in the Behavioral Research and Imaging Neurogenetics (BRAIN) lab led by Ryan Bogdan found links between prenatal cannabis exposure and potential mental health problems in childhood and adolescence, but potential biological mechanisms that might explain this association were unclear.
In In a study published this month in Nature Mental Health, Bogdan, Dean’s Distinguished Professor of Psychological & Brain Sciences in Arts & Sciences, and senior scientist Baranger outline some of those potential mechanisms, the intervening biological steps that may play a role in how prenatal cannabis exposure leads to behavioral problems later in life.
“We see evidence that cannabis exposure can impact the developing brain, which is consistent with associations with mental health,” Baranger said.
Trying to figure out the long-term effects of cannabis exposure during pregnancy is not an easy knot to untangle. There are many confounding factors that influence mental health and behavior. Nat. Mental Health (2024). https://doi.org/10.1038/s44220-024-00281-7
The research reported in this press release was supported by R01DA54750 (RB, AA). Additional funding included: DAAB (K99AA030808), APM (T32DA015035), AJG (DGE-213989), SEP (F31AA029934), ASH (K01AA030083), ECJ (K01DA051759; BBRF Young Investigator Grant 29571), CER (R01DA046224), AA (R01DA54750), RB (R01DA54750, R21AA027827, U01DA055367). Data for this study were provided by the Adolescent Brain Cognitive Development (ABCD) Study, which was funded by awards U01DA041022, U01DA041025, U01DA041028, U01DA041048, U01DA041089, U01DA041093, U01DA041106, U01DA041117, U01DA041120, U01DA041134, U01DA041148, U01DA041156, U01DA041174, U24DA041123, and U24DA041147 from the NIH and additional federal partners (https://abcdstudy.org/federal-partners.html). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.
