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Environmental rather than genetic fetal overgrowth: defining the difference and hints for diagnosis and management

Excessive fetal birth weight or macrosomia can be associated with traumatic delivery and both short-term and long-term neonatal complications. Moreover, evidence is accumulating that macrosomia/being large-for-gestational age (LGA) as a result of excessive and unbalanced intrauterine growth places the individual at increased risk for metabolic short-term complications and more importantly can influence metabolic disorders in adulthood1. Traditionally, maternal diabetes was considered as the main environmental (rather than genetic) cause of macrosomia, along with maternal obesity and accelerated maternal weight gain during pregnancy. In 1952, Pedersen2 was the first to postulate that maternal hyperglycemia was transmitted to the fetus, which, in turn, produced and released large amounts of insulin, resulting in fetal hyperinsulinemia. This would cause various aspects of diabetic fetopathy, including deposition of large amounts of body fat, giving the infant its characteristic appearance. Barker et al.3 later suggested that events during fetal life have implications for adult disease. This theory has effectively shifted focus from managing and preventing short-term complications at delivery to changing and modulating the uterine milieu in order to prevent excessive intrauterine growth and long-term complications such as obesity, Type 2 diabetes and the metabolic syndrome. It would seem logical to assume that the shorter the time a fetus is exposed to an unfavorable and metabolically ‘hostile’ environment, the lower its risk of later unfavorable consequences. Clinically, this approach implies a need to improve prenatal diagnostic capabilities as well as a need for intensive therapy during pregnancy. In this Editorial, we aim to define precisely: metabolic macrosomia, its causes, the prenatal metabolic (maternal) and sonographic (fetal) diagnosis and its relationship to maternal carbohydrate metabolism. Specifically, we link sonographic evidence reported in the recent literature, including in this issue of the Journal, to the extensive recently published evidence, collected and evaluated over an 8-year period from a huge cohort of mothers and offspring, of the multicentric, multinational Hyperglycemia and Adverse Pregnancy Outcome (HAPO) study4–6, and evaluate the effect of treatment on the mildest forms of carbohydrate intolerance presented recently in a randomized controlled trial performed by the Maternal Fetal Medicine Unit (MFMU) network in the USA7.