No abstract

Despite long-standing interest in the role of sex on human development, the functional consequences of fetal sex on early development are not well understood. Here we explore the gestational origins of sex as a moderator of development. In accordance with the focus of this special issue, we examine evidence for a sex differential in vulnerability to prenatal and perinatal risks. Exposures evaluated include those present in the external environment (e.g., lead, pesticides), those introduced by maternal behaviors (e.g., alcohol, opioid use), and those resulting from an adverse intrauterine environment (e.g., preterm birth). We also provide current knowledge on the degree to which sex differences in fetal neurobehavioral development (i.e., cardiac and motor patterns) are present prior to birth. Also considered are contemporaneous and persistent sex of fetus effects on the pregnant woman. Converging evidence confirms that infant and early childhood developmental outcomes of male fetuses exposed to prenatal and perinatal adversities are more highly impaired than those of female fetuses. In certain circumstances, male fetuses are both more frequently exposed to early adversities and more affected by them when exposed than are female fetuses. The mechanisms through which biological sex imparts vulnerability or protection on the developing nervous system are largely unknown. We consider models that implicate variation in maturation, placental functioning, and the neuroendocrine milieu as potential contributors. Many studies use sex as a control variable, some analyze and report main effects for sex, but those that report interaction terms for sex are scare. As a result, the true scope of sex differences in vulnerability is unknown.

The relation of observed emotional reactivity and regulation in infancy to executive function in early childhood was examined in a prospective longitudinal sample of 1,292 children from predominantly low-income and rural communities. Children participated in a fear eliciting task at ages 7, 15, and 24 months and completed an executive function battery at age 48 months. Results indicated that the relation of child negative emotional reactivity at 15 months of age to executive functioning at 48 months of age was dependent on observed emotion regulation. High levels of executive function ability were observed among children who exhibited high levels of emotional reactivity and high levels of the regulation of this reactivity. In contrast, low levels of executive function ability were observed among children who exhibited high levels of reactivity but low levels of regulation. Among children exhibiting low levels of emotional reactivity, emotion regulation was unrelated to executive functioning. Moreover, emotionally reactive infants exhibiting high levels of emotion regulation were more likely to have primary caregivers who exhibited high levels of positive parenting behavior in a parent-child interaction task. Results provide support for a neurobiologically informed developmental model in which the regulation of emotional arousal is one mechanism whereby supportive environments are associated with higher levels of self-regulation ability for highly reactive infants. Findings are discussed with implications for differential susceptibility and biological sensitivity theories of child by context interaction.

The present study examined infant negativity and maternal symptomatology by term status in a predominately low-income, rural sample of 132 infants (66 late-preterm) and their mothers. Late-preterm and term infants were group-matched by race, income, and maternal age. Maternal depression and anxiety symptoms were measured with the Brief Symptom Inventory 18 (BSI-18) when infants were 2 and 6 months of age. Also at 6 months, infant negativity was assessed by global observer ratings, maternal ratings, and microanalytic behavioral coding of fear and frustration. Results indicate that after controlling for infant age, late-preterm status predicted higher ratings of infant negativity by mothers, but not by global observers or microanalytic coding, despite a positive association in negativity across the three measures. Further, mothers of late-preterm infants reported more elevated and chronic co-morbid symptoms of depression and anxiety, which in turn, was related to concurrent maternal ratings of their infant’s negativity. Mothers response to late-preterm birth and partiality in the assessment of their infant’s temperament is discussed.