While postnatal psychological distress has been widely studied for many years, particularly with a focus on postpartum depression, symptoms of maternal depression, stress, and anxiety are not more common or severe after childbirth than during pregnancy [1]. In a recent meta-analysis of 28 articles regarding depression during pregnancy, Gavin et al. found that up to 13% of women experience depressive episodes at some point during pregnancy or within the first year postpartum [2]. Thus, a newer body of research has emerged aimed at identifying the effects of women’s antenatal psychological distress on fetal behavior and child development, and the biological pathways for this influence. These studies are in line with the growing body of literature supporting the “fetal origins hypothesis” that prenatal environmental exposures — including maternal psychological state–based alterations in in utero physiology — can have sustained effects across the lifespan.
The prenatal period is a critical time for neurodevelopment and is thus a period of vulnerability during which a range of exposures have been found to exert long-term changes on brain development and behavior with implications for physical and psychiatric health. For example, maternal consumption of essential fatty acids during pregnancy is linked to lower birth weight and decrements in cognitive and motor function, while fetal exposure to PCBs and methylmercury, via seafood in women’s diet, is linked to neurocognitive deficits [3].
While toxins have direct effects on the processes of neurogenesis, neuronal migration, cellular differentiation and synaptic refinement that are occurring during the prenatal period, there also is evidence for the interaction between these types of prenatal exposures and maternal psychosocial health. Risk of developmental delay in children exposed prenatally to tobacco smoke has been found to be much greater among those infants whose mothers also experienced material hardship during pregnancy[3]. This finding is consistent with extensive epidemiological research on birth cohorts from the Dutch Hunger Winter of 1944 based on offspring of women who were pregnant at the time when food intake was reduced to 500 – 1500 kcal per day during WWII. In a series of studies, Brown and colleagues have shown that fetal development during this period is associated with a two–fold increased risk for schizophrenia, schizoid/schizoptypal personality disorder, as well as comparable risk for major affective disorders in adulthood [4]. Two interpretations regarding the causal mechanisms of these effects have been suggested: 1) deficiency in many micro– and macronutrients, such as folate and/or overall calorie nutrition could directly alter brain development or 2) maternal stress, secondary to famine, could have neurotoxic effects on brain regions relevant to mental illness. Though these mechanisms are not mutually exclusive and could both contribute to the increased risk of psychopathology observed in these studies, there are extensive studies on prenatal stress in animals that provide support for the latter interpretation and largely rule out genetic factors for the prenatal stress effects [5].
Clinical studies link pregnant women’s exposure to a range of traumatic, as well as chronic and common life stressors (i.e., bereavement, daily hassles, and earthquake), to significant alterations in children’s neurodevelopment, including increased risk for mixed handedness, autism, affective disorders, and reduced cognitive ability[6]. More recently, maternal antenatal anxiety and/or depression have been shown to predict increased risk for neurodevelopmental disorders in children, and to confer risk for future mental illness. Reports show that elevated levels of antenatal depression and anxiety are associated with poor emotional adjustment in young children [7]. The impact of women’s anxiety (and/or depression) during pregnancy has been found to extend into childhood and adolescence, as well as to affect the hypothalamic-pituitary-adrenal (HPA) axis, predicting attention deficit hyperactivity disorder (ADHD) symptoms in 8–9 year old children [8]as well as alterations in HPA axis activation in 4 month olds in our laboratory [9] and in 10 [10], and 14–15 year olds [11]. The majority of these studies have controlled for women’s postnatal mood, as well as other demographic factors, yet the possibility that the women’s’ antenatal mood is a marker for qualities in the postnatal environment that affect child development cannot be ruled out. What these data suggest is that, in addition to the known pathways for the familial transmission of risk for mental illness, genetics, environment, and gene X environment interactions, there is another possibility: that some of the risk is conferred prenatally via changes in women’s mood–based physiology affecting fetal neurobehavioral development.
If pregnant women’s distress, similar to their nutrition, is influencing child