#LAUREN BEEM NASHVILLE CODE#

#LAUREN BEEM NASHVILLE CODE#

1(SAS Code included in Supplemental Material). Current literature consistently shows a relationship between maternal pre-pregnancy obesity, GWG, and later child obesity, as depicted in Fig. However, there is little research on quantifying the direct and indirect mechanism of maternal obesity on child obesity, mediated through GWG. These studies showed evidence of a synergistic effect of adverse maternal and child outcomes when the mother has both a high BMI and gains excessive weight during pregnancy. When studying the relationship between maternal and child obesity, previous literature has considered GWG to be a confounder to be adjusted for or interaction term. For example, a high pre-pregnancy BMI along with excessive GWG increases the risk of having a baby that is large for gestational age, and overweight or obese in childhood. In addition, these studies suggest that intrauterine exposure to maternal obesity may induce child obesity risk via dysregulated-appetite, metabolism, and activity levels. Evidence from cohort studies show that exceeding the IOM weight gain recommendation is associated with higher BMI percentiles and increased risk of overweight or obesity in offspring. In addition to a higher birth weight and GDM, pregnant overweight and obese women tend to exceed the Institute of Medicine (IOM) gestational weight gain (GWG) recommendations compared to normal-weight women. Even without preexisting diabetes, obese women are still more likely to develop GDM. GDM is associated with an increased risk of overweight or obesity in offspring. During gestation, insulin resistance in overweight and obese women is further exaggerated which results in maternal hyperinsulinemia, hyperglycemia and GDM. Also, obese and morbidly obese women, have higher odds of developing GDM. Elevated birth weight negatively affects the offspring weight status trajectory into childhood and adolescence, where children with higher birth weights have a higher likelihood of becoming overweight or obese. For example, obese and morbidly obese mothers are at increased risk of delivering a large-for-gestational age infant. Excess body weight has been associated with genetic variation and epigenetic response to environmental cues during intrauterine and early development, including, gestational diabetes mellitus (GDM), high maternal adiposity, birth weight, and poor diet and exercise behaviors. Obesity has a complex etiology, which extends beyond energy imbalances. Therefore, it is imperative to identify modifiable risk factors to reduce childhood obesity and its future consequences. Without increased attention to this epidemic, health care expenditures attributable to obesity are projected to increase by at least $48 billion per year by 2030, with obesity accounting for a loss of approximately 2 million productive person-years in working US adults. Children that are overweight or obese are also more likely to become obese adults, which introduces additional risks for various chronic diseases like cancer, heart disease, type 2 diabetes, and premature death. In addition to the social stigma, childhood obesity causes insulin resistance, hypertension, fatty liver disease, and other cardiovascular related diseases in adulthood. Approximately 17% of children aged 2–19 years in the United States are obese, and the rate of growth of the number of obese children has been considered an epidemic.

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