ABSTRACT
The risk of obesity is cumulative for each individual, and exposure begins at conception. Women who are obese, still growing, or diabetic provide an intrauterine environment for their fetus that differs from women who do not have these characteristics. The intrauterine environment appears to influence later risk for obesity through various mechanisms, often referred to as “fetal programming,” which include changes in the central nervous system, in ratio of fat to lean body mass, in insulin metabolism, and in other hormonal factors. High birth weight (HBW) and exposure to diabetes in utero are both consistently associated with higher BMI later in life (attained BMI). However, when adjusted for confounders such as parental BMI, gestational age, and socioeconomic status, the relationship between birth weight and attained BMI is less robust, and recent studies suggest that the greater attained BMI may reflect greater lean body mass rather than fat mass. Low birth weight (LBW) is more consistently associated with attained BMI and has been implicated as a risk factor for central adiposity and risk of chronic disease. LBW followed by rapid “catch-up” growth in childhood appears to pose an additional risk for adult obesity. Furthermore, rates of LBW have risen while rates of HBW have fallen between 1980 and 2001. Taken as a whole, these finding suggest that the intrauterine environment plays an important, albeit complex, role in the etiology of obesity.
