Considerations in the Management of Gestational Diabetes Mellitus: “You Are What Your Mother Ate!”

It is clear that there remains a global crisis in the development and consequences of chronic diseases such as obesity and type 2 diabetes. These conditions lead to complications that increase morbidity and mortality, such as heart disease, stroke, amputations, and kidney disease. We have learned a great deal about the pathogenesis of these disorders and also about both treatment and preventive interventions. Clearly, there remains considerable progress to be made specifically in addressing these conditions and, more importantly, in preventing these conditions in resourcepoor areas. Over the recent past, there has been a startling new set of observations on the genesis of these conditions. There are data that certain processes observed in utero and in early childhood can certainly affect the risk of developing chronic diseases at a later age (1–3). This clearly provides a great opportunity to interdict on these pathophysiological processes when they may have the greatest effect. As such, there is a growing interest in learning more about epigenetic phenomena and how these events that can be observed in prenatal and early postnatal life can modulate the risk for the development of chronic diseases (i.e., obesity and type 2 diabetes) in adolescence and early adulthood. In this regard, it is of great interest to study a metabolic environment that may play a great role in later issues affecting human health. Specifically, given the importance of the maternal environment and the potential impact that gestational diabetes mellitus (GDM) may have, we devote a special section in this issue of Diabetes Care to articles related to GDM. The topics covered in this special section include evaluation of dietary factors, intervention strategies to prevent and treat GDM, and appropriate screening and diagnostic testing. As is the case with most topics, new data are presented that address specific areas, while at the same time, data are presented that set the stage for the next logical step in addressing scientific and clinical questions. In the late 1950s and early 1960s, glucose levels in pregnancy that predicted the development of type 2 diabetes in the mother and the incidental observation of an increased perinatal mortality rate focused attention on this occasionally observed but hitherto little considered problem (4,5). Since then, knowledge has increased dramatically, and differences of opinion and controversy have increased exponentially. The link between maternal glucose levels and adverse pregnancy outcomes exhibits a continuumof risk (6). This continuum also applies to the progression of women with hyperglycemia in pregnancy to postpartum type 2 diabetes (7). Although an increased perinatal mortality rate is nownot consideredamajor problem for women in the developed world, it still exists and fetal morbidity is still present.Much recent concern and research have focused on the adverse effects of intrauterine programming and the expression of epigenetic changes in adult life (2,3,8), which has generated the interest in providing a special section in Diabetes Care. Given that there is no apparent threshold level but a continuum of risk for all adverse events related to the maternal glucose levels, how diagnostic levels and treatment targets have been derived is a matter of consensus. For evidence related to the diagnostic levels, we are indebted to the Hyperglycemia and Adverse Pregnancy Outcome (HAPO) study (9), and for consensus, to the recommendations of the International Association of the Diabetes and Pregnancy Study Groups (10), subsequently endorsed by theWorld HealthOrganization (WHO) (11). WHO, in addition to the diagnostic criteria, has also changed the terminology. Allwomenwith anabnormal result at any stage of pregnancywill be classified as having hyperglycemia in pregnancy and then subdivided into having either diabetes in pregnancy or GDM. Few clinicians would dispute that dietary factors are crucial to the development