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Federal government websites often end in. The site is secure. Preview improvements coming to the PMC website in October Learn More or Try it out now. There is compelling evidence that children exposed to high levels of prenatal stress are at risk for a host of adverse health outcomes [ 1 , 2 , 3 , 4 , 5 , 6 , 7 ].
Prenatal maternal stress PNMS increases fetal exposure to stress biomarkers e. This confers lasting susceptibility to health complications in the child [ 2 , 4 , 5 , 6 ] and potentially transgenerational risks through epigenetic programming [ 8 , 9 , 11 ].
Consequently, many scholars have underscored the need to evaluate for sex-dependent effects in PNMS programming models [ 12 , 13 , 15 , 16 , 17 , 18 ]. The potential sex-dependent nature of PNMS programming is intuitive given well-established sex differences in human embryonic and fetal development [ 19 , 20 ]. The placenta is sexually dimorphic both in terms of its biological makeup [ 15 , 20 ] and its adaptations within the intrauterine environment [ 12 , 15 , 16 , 20 , 21 ].
Female and male fetuses generally employ different evolutionary strategies to optimize fitness. Males invest heavily in growth but are less adaptable to environmental challenges in utero. In contrast, female fetuses are more responsive to environmental stress signals and are better able to adapt to prenatal insults e. The female fetus is also better protected from inflammatory processes that could compromise viability [ 13 , 16 ].
Thus, females are better positioned to survive suboptimal intrauterine conditions, whereas males are more susceptible to severe consequences of intrauterine adversity e. However, the female viability advantage appears to come with increased vulnerability to less severe but lasting health complications e.