Studies show associations between prenatal maternal stress (PNMS) and child autism, with little attention paid to PNMS and autism in young adulthood. The broad autism phenotype (BAP), encompassing sub-clinical levels of autism, includes aloof personality, pragmatic language impairment and rigid personality. It remains unclear whether different aspects of PNMS explain variance in different BAP domains in young adult offspring. We recruited women who were pregnant during, or within 3 months of, the 1998 Quebec ice storm crisis, and assessed three aspects of their stress (i.e., objective hardship, subjective distress and cognitive appraisal). At age 19, the young adult offspring (n = 33, 22F / 11M) completed a BAP self-report. Linear and logistic regressions were implemented to examine associations between PNMS and BAP traits. Up to 21.4% of the variance in BAP total score and in BAP three domains tended to be explained by at least one aspect of maternal stress, For example, 16.8% of the variance in aloof personality tended to be explained by maternal objective hardship; 15.1% of the variance in pragmatic language impairment tended to be explained by maternal subjective distress; 20.0% of the variance in rigid personality tended to be explained by maternal objective hardship and 14.3% by maternal cognitive appraisal. Given the small sample size, the results should be interpreted with caution. In conclusion, this small prospective study suggests that different aspects of maternal stress could have differential effects on different components of BAP traits in young adults.

Prenatal maternal stress and mental health problems are known to increase risk for developmental psychopathology in offspring, yet pathways leading to risk or resiliency are poorly understood. In a quasi-experimental design, we prospectively examined associations between disaster-related prenatal stress, maternal mental health symptoms, and infant temperament outcomes. Mothers who were pregnant during Hurricane Harvey (N = 527) reported on objective hardships (e.g., loss of belongings or income, evacuation, home flooding) related to the storm and subsequent mental health symptoms (anxiety/depression, posttraumatic stress) across time. At a postpartum assessment, mothers reported on their infant’s temperament (negative affect, positive affect, orienting/regulatory capacity). Greater objective hardship indirectly predicted higher levels of infant orienting/regulatory capacity through its association with increased maternal posttraumatic stress symptoms. Greater objective hardship also indirectly predicted higher levels of infant negative affect through its association with increased maternal anxiety/depression symptoms across time. Our findings suggest a psychological mechanism linking prenatal stress with specific temperamental characteristics via maternal mental health symptoms. Findings point to the importance of high-quality assessment and mental health services for vulnerable women and young children.

Numerous studies have shown associations between maternal stress and poor birth outcomes, but evidence is unclear for causal inference. Natural disasters provide an opportunity to study effects of quasi-randomized hardship with an accurate measure of onset and duration. In a population-based quasi-experimental study, we examined the effect of maternal exposure to the January 1998 Québec ice storm on birth outcomes by comparing pregnant mothers who lived in an area hard hit by the ice storm with those in two unaffected regions. In a total of 147,349 singleton births between 1995 and 2001, we used a difference-in-differences method to estimate the effects of the ice storm on gestational age at delivery (GA), preterm birth (PTB), weight-for-gestational-age z-scores (BWZ), large for gestational age (LGA), and small for gestational age (SGA). After adjusting for maternal and sociodemographic characteristics, there were no differences between the exposed and the unexposed mothers for birth outcomes. The estimated differences (exposed vs. unexposed) were 0.01 SDs (95% CI: −0.02, 0.05) for BWZ; 0.10% point (95% CI: −0.95%, 1.16%) for SGA; 0.25% point (95% CI: −0.78%, 1.28%) for LGA; −0.01 week (95% CI: −0.07, 0.05) for GA; and 0.16% point (95% CI: −0.66%, 0.97%) for PTB. Neither trimester-specific nor dose–response associations were observed. Overall, exposure to the 1998 Québec ice storm as a proxy for acute maternal stress in pregnancy was not associated with poor birth outcomes. Our results suggest that acute maternal hardship may not have a substantial effect on adverse birth outcomes.

The 5-HTTLPR polymorphism of the serotonin transporter has been shown to play a role in autism spectrum disorders (ASD). Moreover, disaster-related prenatal maternal stress (PNMS) has also been shown to be associated with ASD. However, no study to date has examined whether these two factors, either individually or in combination, are predictive of ASD traits in the same sample. We hypothesized that children, particularly boys, with the LL genotype exposed to high levels of disaster-related PNMS would exhibit higher levels of ASD traits compared to boys with the LS or SS genotypes and girls regardless of genotype. Genotype and ASD levels obtained using the Australian normed Autism Spectrum Rating Scales – Short Form were available for 105 30-month-old children exposed to varying levels of PNMS following the 2011 Queensland Flood. For boys, higher ASD traits were associated with the 5-HTTLPR LL genotype in combination with either a negative maternal appraisal of the flood, or high levels of maternal composite subjective stress, PSTD-like or peritraumatic dissociation symptoms. For girls, maternal peritraumatic dissociation levels in combination with the 5-HTTLPR LS or SS genotype were associated with higher ASD traits. The present findings are the first to demonstrate that children’s genotype moderates effects of disaster-related PNMS on ASD traits, with different pattern according to child sex.

It is possible that findings suggesting a link between prenatal maternal stress (PNMS) and anxiety symptoms in offspring are confounded by postnatal and/or shared mother–child heritability effects. Following exposure to a natural disaster, the Queensland Flood Study investigated the unique and additive effects of various types of disaster-related PNMS (objective hardship, cognitive appraisal, and subjective distress) on childhood anxiety symptomatology (internalizing and/or anxiety symptom measures). Timing of flood exposure during pregnancy and child sex were examined as potential moderators. After controlling for maternal psychosocial factors, greater objective hardship as a result of the floods was significantly associated with greater anxiety symptoms (N = 114) and marginally associated with greater internalizing behaviors (N = 115). Earlier timing of the flood in pregnancy was associated with greater anxiety symptoms. No such associations were found between any PNMS measure and teacher-rated child internalizing behaviors (N = 90). Sex and timing did not moderate associations. Our findings suggest that, in isolation, increased maternal hardship due to exposure to an independent stressor, during pregnancy, may have a programming effect on childhood anxiety symptoms.

Prenatal maternal stress (PNMS) has been associated with postnatal behavioral alterations that may be partly explained by interactions between the hypothalamic–pituitary–adrenal (HPA) and hypothalamic–pituitary–gonadal (HPG) axes. Yet it remains unclear whether PNMS leads to enduring HPA–HPG alterations in the offspring, and whether HPA–HPG interactions can impact behavior during development, in particular levels of aggression in childhood. Here we investigated the relationship between a marker for HPG axis function (baseline testosterone) and a marker for HPA axis response (cortisol area under the curve) in 11½-year-olds whose mothers were exposed to the 1998 Quebec ice storm during pregnancy (n = 59 children; 31 boys, 28 girls). We examined (a) whether the degree of objective or subjective PNMS regulates the testosterone–cortisol relationship at age 11½, and (b) whether this testosterone–cortisol relationship is associated with differences in aggressive behavior. We found that, at lower levels of subjective PNMS, baseline testosterone and cortisol reactivity were positively correlated; in contrast, there was no relationship between these hormones at higher levels of subjective PNMS. Cortisol response moderated the relationship between testosterone and aggression. These results support the notion PNMS may explain variance in fetal HPA–HPG interactions, and that these interactions may be associated with aggressive behavior in late childhood.