ABSTRACT
BACKGROUND: Vitamin D deficiency is common among women of reproductive age (WRA) in Bangladesh, but the causes remain unclear. OBJECTIVE: To explain the high prevalence of vitamin D deficiency in WRA in Dhaka, Bangladesh, we compared the vitamin D status of pregnant women with that of their husbands and between pregnant and nonpregnant states. METHODS: This study was an observational substudy of the Maternal Vitamin D for Infant Growth trial conducted in Dhaka, Bangladesh. Women (n = 1300) were enrolled in the second trimester of pregnancy and randomly assigned to 1 of 5 arms consisting of different doses of vitamin D supplements or placebo, with 1 arm continuing supplementation until 6 mo postpartum. A subgroup of trial participants and their husbands with plasma 25-hydroxyvitamin D [25(OH)D] concentration measurements (n = 84), and placebo-group trial participants with serum 25(OH)D measured in the second trimester of pregnancy and 6 mo postpartum (n = 89) were studied using linear mixed-effects regression models. RESULTS: The mean ± SD plasma 25(OH)D in pregnant women in the second trimester was 23 ± 11 nmol/L. Adjusting for age and season, 25(OH)D of pregnant women was 30 nmol/L lower (95% CI: -36, -25 nmol/L) than that of men. Only 9% of total variance in 25(OH)D was explained by factors shared by spousal pairs. Selected nonshared factors (BMI, time spent outdoors, involvement in an outdoor job, sunscreen use) did not explain the association of sex with 25(OH)D. Adjusting for age, season, and BMI, 25(OH)D was similar during pregnancy and 6 mo postpartum (mean difference: -2.4 nmol/L; 95% CI: -5.3, 0.4 nmol/L). CONCLUSIONS: In Dhaka, WRA have substantially poorer vitamin D status than men. Variation in 25(OH)D is not greatly influenced by determinants shared by spouses. Measured nonshared characteristics or pregnancy did not account for the gender differential in 25(OH)D. This trial was registered at clinicaltrials.gov as NCT01924013.
ABSTRACT
Bisphenol A (BPA), a ubiquitous endocrine disruptor that is present in many household products, has been linked to obesity, cancer, and, most relevant here, childhood neurological disorders such as anxiety and hyperactivity. However, how BPA exposure translates into these neurodevelopmental disorders remains poorly understood. Here, we used zebrafish to link BPA mechanistically to disease etiology. Strikingly, treatment of embryonic zebrafish with very low-dose BPA (0.0068 µM, 1,000-fold lower than the accepted human daily exposure) and bisphenol S (BPS), a common analog used in BPA-free products, resulted in 180% and 240% increases, respectively, in neuronal birth (neurogenesis) within the hypothalamus, a highly conserved brain region involved in hyperactivity. Furthermore, restricted BPA/BPS exposure specifically during the neurogenic window caused later hyperactive behaviors in zebrafish larvae. Unexpectedly, we show that BPA-mediated precocious neurogenesis and the concomitant behavioral phenotype were not dependent on predicted estrogen receptors but relied on androgen receptor-mediated up-regulation of aromatase. Although human epidemiological results are still emerging, an association between high maternal urinary BPA during gestation and hyperactivity and other behavioral disturbances in the child has been suggested. Our studies here provide mechanistic support that the neurogenic period indeed may be a window of vulnerability and uncovers previously unexplored avenues of research into how endocrine disruptors might perturb early brain development. Furthermore, our results show that BPA-free products are not necessarily safer and support the removal of all bisphenols from consumer merchandise.
