Maternal lipids in pregnancy are associated with increased offspring cortisol reactivity in childhood

- We show that the maternal prenatal metabolic milieu predicts a child's cortisol response to a stressor at 3-5 years of age.
- Increased maternal prenatal obesity, triglycerides and total cholesterol were associated with increased offspring cortisol reactivity.
- Maternal metabolism may be a novel programming factor for the offspring's HPA axis.

Prenatal programming of hypothalamic-pituitary-adrenal (HPA) axis activity has long term implications for offspring health. Biological mechanisms underlying programming of the offspring HPA axis are poorly understood. We hypothesised that altered maternal metabolism including higher maternal obesity, glucose and lipids are novel programming factors for altered offspring HPA axis activity. Salivary cortisol levels were measured in 54 children aged 3-5 years under experimental conditions (before and after a delay of self-gratification test). Associations of child cortisol responses with maternal obesity in early pregnancy and with fasting glucose, triglycerides, HDL and total cholesterol measured in each pregnancy trimester were tested. Higher levels of maternal triglycerides and total cholesterol throughout pregnancy were associated with increased offspring cortisol reactivity. The associations were independent of maternal obesity and other confounders, suggesting that exposure to maternal lipids could be a biological mechanism of in utero programming of the offspring's HPA axis.