The first 1,000 days of life is a critical window of development, determining susceptibility to adult obesity and cardiometabolic health [1,2]. Environmental insults during this rapid development phase may result in irreversible adverse outcomes. Animal and human studies provide evidence for the fetal origins of adult noncommunicable disease hypothesis [3–5]. This hypothesis suggests that intrauterine exposures affect the fetus’s development during sensitive periods, and increases the risk of noncommunicable diseases in adult life [3–5]. Systematic reviews confirm evidence of inverse epidemiological associations between birth weight and later development of hypertension [2] and coronary heart disease [6]. The fetal origins of disease hypothesis has 356been challenged as a possible statistical artifact [7], but has been confirmed by later studies with high follow-up rates and adjustment for confounders [8,9].