Endocrine Abstracts

Background: Animal studies have indicated that maternal androgen levels influence the intrauterine environment and development of the offspring. As human data are missing, we investigated the possible association between maternal androgens and offspring size at birth in humans.

Methods: Randomly collected parous Caucasian women (n=147) were followed prospectively through pregnancy. Maternal serum levels of dehydroepiandrosterone sulphate (DHEAS), androstenedione, testosterone and sex hormone binding globulin (SHBG) were measured at gestational weeks 17 and 33. The main outcome measures were weight and length at birth. Associations between maternal androgen levels and offspring birth weight and length were investigated using multiple linear regression modelling adjusted for potential confounding by maternal height, pre-pregnancy body mass index, smoking, parity, offspring gender, and gestational age at birth.

Results: Increasing maternal testosterone levels at week 17 and week 33 were both associated with lower birth weights and lengths. Accordingly, at week 17 an increase in maternal testosterone levels from the 25^th to the 75^th percentile was associated with a decrease in birth weight by 160 grams (95% CI; 29 to 290 grams), while at week 33 that estimate was 115 grams (95% CI; 21 to 207 grams). No similar associations were observed for DHEAS, androstenedione or SHBG.

Discussion: Increasing maternal testosterone levels during human pregnancy are associated with growth reduction in utero, and the weight difference compares with the impact that traditional factors, such as foetal gender or maternal smoking, have on birth weight. Newborn size characteristics are important predictors of a multitude of disorders in adult life. Hence, our identification of elevated maternal testosterone levels as a new indicator of intrauterine growth restriction in humans is important as it opens up the possibility to better understand the mechanisms involved in intrauterine growth. This in turn, may help to elucidate the mechanism(s) behind the ‘foetal origins hypothesis’.