CONTEXT: The prenatal antecedents of polycystic ovary syndrome (PCOS) are not known, but prenatal androgen exposure is thought to contribute. This has not previously been investigated in large prospective studies of normal human pregnancy. OBJECTIVE: The aim of the study was to establish the prospective relationship between early life androgen exposure and PCOS in adolescence. DESIGN AND SETTING: A prospective cohort study was conducted in the general community. PATIENTS OR OTHER PARTICIPANTS: A total of 2900 pregnant women were recruited at 18 wk gestation. Prenatal androgen exposure was measured from maternal blood samples (at 18 and 34-36 wk) and umbilical cord blood. Timed (d 2-5 menstrual cycle) blood samples were collected, clinical hyperandrogenism was assessed, and transabdominal ultrasound examination of ovarian morphology was performed in 244 unselected girls from the Raine cohort aged 14-17 yr. MAIN OUTCOME MEASURE(S): We examined the relationship between early life androgen exposure and PCOS in adolescence. RESULTS: We did not observe a statistically significant relationship between early life androgen exposure and PCOS in adolescence. CONCLUSIONS: This is the first prospective study to evaluate the relationship between prenatal androgen exposure and PCOS in adolescence in normal pregnancy. Our findings do not support the hypothesis that maternal androgens, within the normal range for pregnancy, directly program PCOS in the offspring.
CONTEXT: The prenatal antecedents of polycystic ovary syndrome (PCOS) are not known, but prenatal androgen exposure is thought to contribute. This has not previously been investigated in large prospective studies of normal human pregnancy. OBJECTIVE: The aim of the study was to establish the prospective relationship between early life androgen exposure and PCOS in adolescence. DESIGN AND SETTING: A prospective cohort study was conducted in the general community. PATIENTS OR OTHER PARTICIPANTS: A total of 2900 pregnant women were recruited at 18 wk gestation. Prenatal androgen exposure was measured from maternal blood samples (at 18 and 34-36 wk) and umbilical cord blood. Timed (d 2-5 menstrual cycle) blood samples were collected, clinical hyperandrogenism was assessed, and transabdominal ultrasound examination of ovarian morphology was performed in 244 unselected girls from the Raine cohort aged 14-17 yr. MAIN OUTCOME MEASURE(S): We examined the relationship between early life androgen exposure and PCOS in adolescence. RESULTS: We did not observe a statistically significant relationship between early life androgen exposure and PCOS in adolescence. CONCLUSIONS: This is the first prospective study to evaluate the relationship between prenatal androgen exposure and PCOS in adolescence in normal pregnancy. Our findings do not support the hypothesis that maternal androgens, within the normal range for pregnancy, directly program PCOS in the offspring.
Authors: Grace Huang; Sara Cherkerzian; Eric B Loucks; Stephen L Buka; Robert J Handa; Bill L Lasley; Shalender Bhasin; Jill M Goldstein Journal: J Clin Endocrinol Metab Date: 2018-11-01 Impact factor: 5.958
Authors: Daniel A Dumesic; Luis R Hoyos; Gregorio D Chazenbalk; Rajanigandha Naik; Vasantha Padmanabhan; David H Abbott Journal: Reproduction Date: 2020-01 Impact factor: 3.906