171-OR: Diagnosing GDM in Pregnancy—Closing the Door after the Horse Has Bolted?

RCTs of GDM treatment reduces adverse pregnancy outcomes but not long-term offspring diabesity which is influenced by genetic and epigenetic programming. The vital window for programming is pre- and immediate post-conceptional, strongly influenced by maternal nutrition and metabolism. Diagnosing GDM later in the pregnancy systematically misses this window. Metabolic-endocrine abnormalities of ‘GDM’ are detectable years before pregnancy (Catalano 2013; Han 2016). There is little data to track the life course evolution of pregnancy hyperglycaemia. Pune Maternal Nutrition Study (1993) has serial glycemic and BMI data on girls born in the cohort at 6, 12 and 18 years, in pregnancy and post-delivery. By 2020, pregnancy data (28-wks gestation) was available on 170. They were 21-years old, BMI 22 kg/m2, twenty had GDM (IADPSG). We compared serial data of Q4 of fasting plasma glucose (FPG, N=44, ‘hyperglycemic’) with 126 ‘normoglycemic’. Figure shows that hyperglycemic girls had higher FPG and BMI at 6, 12 and 18-years and continued to remain so post-delivery. Our data shows that pregnancy glycemia reflects life course glycemia. Diagnosing ‘GDM’ in pregnancy ignores exposure of ova and young conceptus to an abnormal metabolic milieu, failing to prevent periconceptional programming of diabesity. There is an urgent need to reconsider strategies about GDM diagnosis and treatment to curtail the escalating epidemic of diabesity in the young.