Maternal corticotropin-releasing hormone levels during pregnancy and offspring adiposity.

OBJECTIVE

Animal models suggest that fetal exposure to glucocorticoids can program adiposity, especially central adiposity, later in life. We examined associations of maternal corticotropin-releasing hormone (CRH) levels in the late 2nd trimester of pregnancy, a marker of fetal glucocorticoid exposure, with child adiposity at age 3 years.

RESEARCH METHODS AND PROCEDURES

We analyzed data from 199 participants in Project Viva, a prospective cohort study of pregnant women and their children, At age 3 years, the main outcomes were age-sex-specific BMI z score and the sum of subscapular (SS) and triceps (TR) skinfold thicknesses to represent overall adiposity, and ratio of SS to TR (SS:TR) to represent central adiposity.

RESULTS

Mean (standard deviation) maternal 2nd trimester log CRH was 4.94 (0.56) pg/mL. At age 3, mean (standard deviation) for BMI z score was 0.52 (1.02); for SS + TR, 16.51 (3.94) mm; and for SS:TR, 0.67 (0.17). Log CRH was mildly inversely correlated with birth weight (r = -0.08), chiefly because of its association with length of gestation (r = -0.21) rather than fetal growth (r = -0.004). After adjustment for sociodemographic factors, maternal smoking, BMI, and gestational weight gain, fetal growth, length of gestation, breastfeeding duration, and (for SS:TR only) child's 3-year BMI, each increment of 1 unit of log CRH was associated with a reduction in BMI z score [-0.43; 95% confidence interval (CI), -0.73, -0.14; p = 0.004] and possible reduction in SS + TR (-1.10; 95% CI, -2.33, 0.14; p = 0.08). In contrast, log CRH was associated with higher SS:TR (0.07; 95% CI, 0.02, 0.13; p = 0.007).

DISCUSSION

Fetal exposure to glucocorticoids, although associated with an overall decrease in body size, may cause an increase in central adiposity.