Despite improvements in care, women with diabetes who become pregnant remain at high risk of adverse maternal and fetal outcomes including congenital malformations, perinatal mortality, spontaneous preterm delivery, and macrosomia. 1 3 It is now well accepted that exposure to maternal hyperglycemia, in pregnancy complicated by type 1 (T1D), type 2 (T2D), or gestational diabetes mellitus (GDM), is the primary cause of these potentially devastating complications. 4 6 Hyperglycemia is toxic from the earliest stages of embryo development with the risk of congenital malformations and fetal death rising dramatically with increasing maternal HbA1c. A recent U.K. population–based cohort study of over 400,000 singleton pregnancies indicated that every 1% increase in HbA1c was associated with a 30% increase in the risk of major congenital abnormality. 7 Maternal glucose levels equilibrate with the fetal circulation, and this elevated glucose drives insulin secretion leading to abnormal growth acceleration and increased risk of shoulder dystocia, labor induction, and cesarean section. The consequences of these intrauterine metabolic abnormalities may extend well beyond pregnancy as offspring are at increased risk for obesity, impaired glucose tolerance, and the development of T2D later in life. 4 , 5 , 8 , 9 The risks of maternal complications also increase and include worsening and/or development of nephropathy and retinopathy. 10 , 11 Efforts to avoid these devastating complications can be particularly challenging for women early in pregnancy as increased insulin sensitivity often results in a three- to fivefold increase in the rate of severe hypoglycemia, although the consequences on the developing fetus have not yet been determined. Severe hypoglycemia remains the leading cause of death in pregnant women with T1D.