People who have been exposed to many stressful events across the life course may enter pregnancy at a greater biologic age, with ongoing vascular, neuroendocrine, and metabolic dysfunction that increases risk for poor maternal and infant outcomes.1, 2, 3 Early life stress, including deprivation and maltreatment, may have particularly negative effects on health prior to and during pregnancy. In order to develop prevention strategies, we need a clear understanding of the pathways through which preconception stressful experiences lead to poor perinatal outcomes.

In the United States, 5.8% of pregnant people are diagnosed with gestational diabetes.4, 5, 6 Gestational diabetes (GDM) is associated with elevated risk of maternal and infant complications.7 Following pregnancy, GDM is associated with cardiometabolic dysfunction for the birthing person (e.g., diabetes, dyslipidemia, hypertension) and, possibly, for the child (obesity).8, 9, 10, 11, 12 Preconception cardiometabolic and mental health may drive GDM risk with risk factors including adiposity, dysglycemia (i.e., prediabetes), hyperinsulinemia, and depression.13, 14, 15

Stressful experiences, particularly those occurring in early life, may also increase risk of GDM. Childhood adversity, including trauma and other stressful experiences, results in long-term physiologic changes, including metabolic dysfunction and obesity.16, 17 In turn, these may result in worse outcomes during pregnancy, including GDM. Few studies have explored the relationship between childhood adversity and GDM; and evidence to date is inconsistent.18, 19, 20 Further, studies to date have not explored whether preconception health may account for all or some of the observed association between childhood adversity and GDM.

The goal of this study was to estimate the association of childhood family environment with gestational diabetes among female participants in the Coronary Artery Risk Development in Young Adults study (CARDIA) who had a pregnancy ≥ 20 weeks gestation over the study period (1985-2016) and to test whether the association is explained by effect modification or mediation by preconception abdominal adiposity.