Editorial: In Utero Exposure to Maternal Affective Symptoms: Prenatal Programming of Child Psychopathology Is Independent of Shared Genes of Risk

The womb is an influential first home. This felicitous phrase is attributed to David Barker, often called the father of the late 20th century developmental origins of health and disease hypothesis, which asserts that maternal experiences during pregnancy are biologically transmitted to, and embedded in, the fetus, shaping child development.1 Specifically, Barker focused on maternal inadequate nutrition as a key in utero exposure to which the fetus biologically adapts, leading to biologically programmed changes, meaning long-lasting, that potentially put the offspring at risk for future metabolic diseases.1 In more recent developmental origins of health and disease publications, the impact of affective symptoms in pregnant women—defined broadly to include perceived stress, depression, and anxiety—on fetal and infant brain and behavior development has been identified. There is a third pathway for the familial inheritance of risk for psychiatric illness beyond shared genes and compromised parental postnatal mental health and caregiving: prenatal programming of risk for psychopathology originating in mental health symptoms of mothers.1 However, despite decades of experimental preclinical studies demonstrating maternal prenatal stress predicting altered offspring outcomes,2 the alternative interpretation—that shared genes of risk account for the outcomes—has remained challenging to disprove for human studies, perhaps particularly when the mother reports on her own and her child’s mental health (a common study design further addressed below). In this context, the article by Chen et al.3 using polygenic risk scores to provide a single measure of genomic risk for complex phenotypes reports rigorous and original results demonstrating effects of maternal affective symptoms on child psychiatric outcomes while controlling for genomic risk.