We now know that gestational diabetes mellitus is a serious condition that, if not properly diagnosed and managed, can have cyclic, intergenerational consequences. Newborns exposed to maternal hyperglycemia during pregnancy have a high risk of being born overweight and of eventually becoming obese children and adults. These newborns also are at a high risk of developing diabetes themselves later in life.
The prevalence of gestational diabetes mellitus (GDM) is increasing in every ethnic group. In the Kaiser Permanente system in Colorado, a state which has traditionally had the lowest obesity rate of any state in the United States, the prevalence of GDM doubled from 1994 to 2002, with significant increases in all racial/ethnic groups (Diabetes Care 2005;28:579-84). Such increases in GDM prevalence are happening worldwide – one part of a worldwide epidemic of obesity and diabetes that is overtaking our youth.
We've learned that GDM is one sign post on the way to the development of overt type 2 diabetes. Indeed, a majority of women with GDM will acquire diabetes within 5 years.
In the last decade or so, our clinical research focus has centered on the in utero risks to the fetus. In a striking study of the potential impact of intrauterine hyperglycemia exposure on later development, Dr. D. Dabelea and coinvestigators compared siblings in the Pima Indian population who were born before and after their mothers were diagnosed with diabetes. The children who were born after their mothers had developed diabetes had almost double the rate of obesity as adolescents than their siblings who were born before their mother's diagnosis of diabetes. Even though these siblings ate the same diet and came from the same gene pools (with the same fathers), they experienced dramatically different health outcomes in adolescence as a result of the differing intrauterine environments (Diabetes 2000;49:2208-11).
This and other studies have given us a body of supplementary science showing that exposure to high blood glucose in utero causes accumulation of fat in the fetus. Even though that baby fat might be lost in early childhood, prenatal exposure nevertheless genetically programs the fetus for a higher risk of developing fatness as an adult.
As I detailed in the last Master Class in obstetrics (see Ob.Gyn News, July 2011, pp. 24–25), we now also have evidence from two randomized controlled trials that interventions to control blood glucose are effective in reducing rates of newborn obesity and therefore should improve adolescent and adult health downstream.
The two randomized trials – the Australian Carbohydrate Intolerance Study in Pregnant Women (N. Engl. J. Med. 2005;352:2477-86) and a study published several years later by Dr. Mark B. Landon and his colleagues (N. Engl. J. Med. 2009; 361:1339-48) – demonstrated the positive impact of treating even mild forms of GDM, with the largest effects being on reducing newborn obesity. Although the offspring of mothers who were treated and not treated in those studies have not yet been followed into adulthood, it seems fair to expect that the children of mothers who were treated for GDM will have significantly better health profiles downstream.
Treating GDM, and learning how to maximize glucose control, has thus moved to center stage in obstetric practice.
Trials of Dietary Change
In Dr. Landon's landmark study, more than 90% of the women randomized to the treatment group (versus usual prenatal care) needed only dietary counseling and education about blood glucose control for effective treatment of abnormal blood glucose levels. Surprisingly, fewer than 10% needed insulin as well.
That we can manage many of our patients with diet alone is welcome good news. To be successful with this approach, however, we must be vigilant in monitoring the effectiveness of dietary counseling and identifying early on those patients for whom dietary treatment is not enough.
We also must be more vigilant in detecting GDM, because the maximal time of fetal fat accretion is at about 32-34 weeks' gestation. GDM is typically diagnosed at about 28 weeks' gestation, and patients usually are not engaged in a regime of blood sugar testing and dietary change until about 30-31 weeks. If we wait until 34-35 weeks' gestation to change course with treatment – adding insulin or oral hypoglycemic agents – significant body fat accumulation by the fetus already will have occurred.
Screening for GDM even earlier than currently recommended, at 26 weeks' gestation if possible, and providing dietary counseling as early as possible are worthwhile goals. Our advice is that patients be moved on to a medication regimen if more than one-third of their blood glucose measurements are still abnormal after 2 weeks of dietary change. A more stringent standard may be more prudent, but for now we believe there is enough evidence to warrant this modest change in practice, and we find that it is a rule that most patients can understand.