There is evidence from several prospective studies that stress during pregnancy can affect the behavioural, emotional and cognitive development of the fetus and the child. Animal models suggest that this may be mediated via the HPA axis. Interventions to reduce stress in pregnant women are now a priority. Large prospective studies are providing increasing independent evidence that maternal stress/anxiety during pregnancy can affect fetal brain development, having adverse effects on the child's emotional, behavioural and cognitive development. It is suggested that the function of fetal programming is linked with a predictive adaptive response. Environmental influences on the mother are preparing the child in her womb for the external environment it is likely to inhabit. This is different from the genetic changes and mutations which will be effective for many generations. These affect circadian rhythm including sleep habit, and other aspects including laterality and sexuality. Their seriousness is now well enough established to feature in an American Child Health strategic plan 2005–10. Animal studies have provided a basis for human studies. Antenatal maternal stress in rats leads to anxiety in the offspring. It can alter laterality – right-handedness etc – and sexuality, and disrupt the circadian rhythm including sleep pattern. Prenatal stress reduces the animal's later negative feedback, the calming effect of Cortisol, by reducing the Cortisol receptors in the hippocampus. In monkeys likewise, maternal prenatal stress leaves the offspring with a lower attention span and more anxiety. There are greater Cortisol responses, and imaging also reveals more dopamine receptors to be affected by that stress neurotransmitter. So there is objective evidence of mammalian prenatal stress effects on offspring. In a group of anxious mothers, a simple arithmetic exercise met with a rise in fetal heart-beat, showing that maternal stress clearly affects the fetus. Dr Glover's human research has made use of the ALSPAC community study program. The strongest effects discerned of maternal prenatal stress on the offspring were on behavioural and emotional problems. The strength of effect was stronger from stress at 32 weeks prenatally than 18 weeks, and resulted in double the levels of the offspring's hyperactivity, and emotional and conduct disorders. The children of anxious mothers in late pregnancy had high waking level of Cortisol. In a separate study her group has shown that prenatal stress can affect the child's cognitive development also. In this study it was stress due to relationship problems with the partner, particularly emotional cruelty and separation, which had the largest effect on the child. Studies show that stress acts on the hypothalamus to produce corticotrophin releasing hormone, which in turn acts on the pituitary gland to produce adreno-corticotrophic hormone. This stimulates the adrenal gland to secrete Cortisol for negative feedback to the hippocampus to stabilise the system. Yet both maternal and fetal Cortisol are a positive stimulus on placental CRH. These results suggest the importance of detecting and treating affective disorder and relationship stress during pregnancy, both for the direct benefit to the mother herself, and particularly to help reduce later development of behavioural and other problems in children.
Maternal stress during pregnancy alters fetal cortico-cerebellar connectivity in utero and increases child sleep problems after birth
