There is little debate that obesity has reached epidemic proportions. At last count, at least one-third of adults in the United States were obese, and all states, except Colorado, have experienced a doubling in obesity rates from 1980-2007. Should this upward spiral continue, projections for 2030 suggest 40% and 80% of the worldwide population will be obese or overweight, respectively. Several methods define obesity (skin fold, % of ideal body weight, waist:hip ratios, body mass index [BMI]); however, BMI (weight [kg]/height [m ) is the most often used method, which defines a BMI of >24.6 kg/m ² as overweight and of ≥30 kg/m ² as obese. To place this in perspective, a weight of 124-154 lbs is a normal BMI for a woman who is 5 feet 6 inches tall. Remarkably, 30% of adult women are unable to maintain their weight within the range of a normal BMI.

The prevalence of obesity during pregnancy has prompted the Institute of Medicine (IOM) to recommend new guidelines for gestational weight gain (GWG) during pregnancy. Nonetheless, obesity that is independent of GWG has been associated with adverse outcomes for both mother (miscarriage, thromboembolism, diabetes mellitus, preeclampsia, hemorrhage, cesarean section delivery, wound infection) and infant (congenital anomalies, stillbirth, neonatal death). Adherence to the IOM GWG guidelines, however, is difficult for many women. In a population-based study that assessed GWG, Chu et al demonstrated that approximately 40% of normal weight women and 60% of overweight women gained more weight during pregnancy than recommended. Obese women gained less weight as a group compared with the normal and overweight groups; however, approximately 25% still exceeded IOM recommendations. In addition, GWG was increased in women who were <19 years old, white, or >12 years of education.

If pregnancy can be considered a window to future health, excessive GWG is a first glimpse at unhealthy trends that lead to adverse outcomes that are associated with obesity. An examination of the Danish National Birth Cohort by Nohr et al identified GWG as a determinant of long-term obesity. Obese women with GWG of <10 kg were below their prepregnancy weight at 6 months after delivery and were able to reduce their BMI; by contrast, 12% of overweight and 14% of obese women with excessive GWG, respectively, moved up a BMI category. Each successive pregnancy potentially allows for successive weight gain that perpetuates the obesity cycle and increases risks for cardiovascular disease, metabolic syndrome, and diabetes mellitus in later life.

If the window during pregnancy provides a picture of adverse health consequences for mothers, what vision is revealed for the offspring? The increase in obesity of children mirrors the epidemic rise that is seen in adults. In adults, obesity is defined using a BMI cutoff of ≥30 kg/m ² ; the more acceptable definition of obesity for children is a BMI of ≥95th percentile, specific for age and gender. Overweight is defined as a BMI between the 85th and 95th percentiles. Data suggest that 37.1% of infants are overweight and that 16.9% of children and adolescents are obese. In addition, evidence suggests that the trend toward obesity starts as early as 6 weeks. Using a nested case control design, McCormick et al demonstrated a 16% prevalence of infant obesity and also noted children who were obese at age 24 months were more likely to have been obese at age 6 months (odds ratio, 13.3; 95% confidence interval, 4.50–39.53). Although additional evidence will be needed, this study suggests that interventions for obesity may need to be initiated early in infancy. The Bogalusa Heart Study included >12,000 children. Eighty-four percent of obese children became obese as adults, and as adults, 65% of these had a BMI of ≥35 kg/m ² . During childhood, they were likely to have cardiovascular risk factors, such as elevated lipid levels, insulin levels, or increased blood pressure. Skinfold-thickness measurements also confirmed evidence of excess adiposity. The prevalence of the aforementioned risks and measurements increased exponentially as the cutoff for BMI increased further from >95th to >99th percentile.

Epidemiologic studies suggest a U-shaped relation between birthweight and adult manifestations of obesity, hypertension, and insulin resistence. Barker identified a portion of this U-shaped relationship when he investigated the effects of maternal malnutrition during the Dutch famine of 1944-45. Fetal growth restriction and low birthweight were associated with an increased incidence of diabetes mellitus, cardiovascular disease, and increased BMI in adult life. The other portion of the U-shaped relationship or “fetal over nutrition” is supported by several studies. In a retrospective cohort study of >8400 children, Whitaker et al reported that children who were born to obese mothers (based on BMI in the first trimester) had double the rate of obeseity at age 2 years. In women with BMI ≥30 kg/m ² , the prevalence of childhood obesity (BMI, >95th percentile) at ages 2, 3, and 4 years was 15.1%, 20.6%, and 24.1%, respectively. The infants who were overweight at 3-5 years of age were 4.1-7.9 times more likely to be obese in young adulthood. Oken et al in the prospective study, Project Viva, studied 1000 predominantly non–low-income mothers and infants. The mothers had a rate of excessive GWG of 51%, which, after adjustment for covariates, was associated with an odds ratio of 4.35 (95% confidence interval, 1.69–11.24) for obesity at 3 years of age (BMI, >95th vs <50th percentile). In addition, increased GWG was associated with higher offspring BMI z-score, triceps and subscapular skinfold thicknesses, and systolic blood pressure. In the Growing Up Today study that included nearly 12,000 participants, Oken found a strong, nearly linear, association between total maternal GWG and childhood obesity (BMI, >95th vs <85th percentile) at the ages of 9-14 years.

There is some evidence to suggest that maternal obesity influences the in utero environment by altering the regulation of appetite, satiety, and adipocyte maturation. Fetal neuronal pathways that regulate appetite and satiety are functioning by the third trimester. Leptin, which is synthesized by adipose tissue and the placenta, promotes development of satiety pathways in the fetus, although appetite dysregulation may result in both deficient or high fatty nutrient environments, thus contributing to the obese phenotype in humans. In animal models, adipose tissue has been identified as a principal target of programming, although different mechanisms for hypertrophy and hyperplasia may be activiated under conditions of undernutrition vs overnutrition. Additional animal studies demonstrated that early postnatal alterations in feeding may be associated with alterations in the function of hypothalamic nuclei, which are influencial in appetite regulation. Also, postnatal hyperphagia has been noted in offspring of rats that were fed high-fat diets during pregnancy. These offspring also continued to consume more and maintain higher body weights than controls.

Paradoxically, both growth restriction and macrosomia are associated with obesity and its complications later in life. Answers to this paradox will become evident only when we have studied all components of the puzzle: maternal contribution, in utero environmnent, fetal programming, and early postnatal development. Studies that will address the maternal component can take advantage of pregnancy as a teachable time-frame and involve education and lifestyle intervention, nutrition, and exercise. These are all components of first-line therapy for obesity. The characteristics of teachable moments include times when personal risk and the potential for adverse outcome are perceived as increased, when there is a strong emotional response, and when the environment promotes redefining self-concepts and social roles. Pregnancy provides a time-frame that incorporates all these characteristics and is therefore an excellent teachable moment in the lives of our patients. Only a few randomized trials that have focused on lifestyle intervention have been conducted, with varying results. A recent review and metaanalysis of available intervention trials suggested that dietary intervention, specifically targeted for the overweight and obese pregnant groups, resulted in GWG within the IOM recommended limits. This same analysis did not find an association with GWG and infant birthweight, which differs from other trials.

Clearly well-designed trials are needed. Changing the course of the current obesity epidemic will have long-range implications for the health status of current and future generations.