Research is increasingly showing that maternal stress and anxiety during pregnancy can influence the long-term mental health of children. Recent animal studies and human evidence suggest that prenatal experiences may leave molecular “marks” on the developing brain, increasing vulnerability to anxiety disorders later in life.
A recent study reported that when pregnant mice were exposed to inflammation used as a proxy for stress, their male offspring showed anxiety-like behaviors as adults, such as avoiding open spaces.2
Brain analysis revealed hyper-reactivity in neurons of the ventral dentate gyrus, a region linked to threat assessment. Researchers found altered DNA methylation in thousands of genes, especially those regulating neuronal signaling. These epigenetic modifications appeared to make the brain more sensitive to danger, offering a possible mechanism by which prenatal stress can reprogram offspring’s stress response systems.
A review article, “Anxiety, depression and stress in pregnancy: implications for mothers and children”, compiles evidence from human cohorts. It shows that prenatal stress is associated with higher risks of behavioral and emotional difficulties in children.1
However, the review emphasizes limitations. Human studies often rely on peripheral tissues such as cord blood or placenta for DNA methylation analysis, which may not fully represent brain changes. Sample sizes are frequently small, and variability in defining stress or timing during pregnancy complicates findings. More longitudinal studies are needed to connect prenatal stress, epigenetic changes, and later outcomes.
Other studies suggest that late pregnancy may be a particularly sensitive period. For example, higher maternal anxiety in the third trimester has been linked to increased DNA methylation of the NR3C1 gene, which regulates the body’s stress hormone response. Some findings also suggest sex-specific effects, with male and female children showing different epigenetic responses to maternal stress.
Together, animal and human research points toward a model:
Prenatal adversity → epigenetic modifications → altered neural circuit function → elevated risk of anxiety.
Animal studies provide direct mechanistic evidence, while human studies show correlations. Key moderating factors include timing of exposure, sex of the fetus, and postnatal environment. Importantly, not all studies replicate these findings, and many effects are small, suggesting that prenatal stress is one of several influences on later anxiety.
The findings highlight the importance of maternal mental health during pregnancy. Supporting pregnant individuals with screening and interventions for stress, anxiety, or depression may have long-term benefits for children. However, because human evidence is not yet conclusive, epigenetic biomarkers are not ready for clinical use.
Future research will require large, longitudinal cohorts that combine prenatal assessments, epigenetic profiling, brain imaging, and behavioral follow-up. This integrated approach could clarify how molecular changes link prenatal environments to adult mental health.
While evidence is still emerging, research increasingly suggests that anxiety may have roots in prenatal life. Through epigenetic changes in stress-sensitive brain circuits, maternal stress and inflammation during pregnancy may shape vulnerability to anxiety decades later. These findings underline the value of maternal mental health support and the potential of epigenetics to explain how early life experiences influence adult wellbeing.
References
Schetter, Christine Dunkel, and Lynlee Tanner. “Anxiety, Depression and Stress in Pregnancy: Implications for Mothers, Children, Research, and Practice.” Current Opinion in Psychiatry 25, no. 2 (March 2012): 141–48. https://doi.org/10.1097/YCO.0b013e3283503680. PMCID: PMC4447112.
Nield, David. “Roots of Your Anxiety May Trace Back to a Time Before You Were Born.” ScienceAlert, September 25, 2025. https://www.sciencealert.com/roots-of-your-anxiety-may-trace-back-to-a-time-before-you-were-born
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