Article Text

  1. J. Huang,
  2. T. Lee,
  3. B. Chen,
  4. M. C. Lu
  1. Los Angeles, CA.


Background Current public health interventions to address the epidemic of childhood and adolescent obesity have focused on current risk factors such as school lunches or physical activities. Emerging research suggests that susceptibility to obesity may have a fetal origin.

Objective To 1) examine prenatal influences of obesity during childhood or adolescence, and 2) propose biological mechanisms for prenatal programming of obesity.

Methods A systematic review of the literature was performed using PubMed and MDConsult to search for animal models and epidemiological studies linking prenatal exposures to obesity. Overweight/obesity was defined by either Body Mass Index (BMI) or skinfold thickness over the age of five. Prenatal exposures included maternal smoking or undernutrition.

Results Eleven studies on maternal smoking and obesity in the offspring met inclusion and exclusion criteria. All 11 studies demonstrated a significant relationship; the odds of obesity increased by 24% to 120% after intrauterine exposure to maternal smoking. These findings persisted after adjustment for potential confounders in five studies. Three studies on maternal malnutrition and obesity in the offspring met inclusion and exclusion criteria. Two studies found prenatal exposure to undernutrition in the first and second trimesters, but not the third trimester, was associated with increased odds of obesity in the offspring. Potential pathophysiological mechanisms linking intrauterine malnutrition with obesity were considered, including prenatal programming of leptin and insulin resistance and glucose utilization.

Conclusion Clinicians, researchers, and public health professionals should focus on the prenatal period as a window of opportunity for obesity prevention.

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