Bennett David S, Birnkrant Jennifer M, Carmody Dennis P, Lewis Michael
Drexel University College of Medicine, GLAD Program, 4700 Wissahickon Avenue, Philadelphia, PA, 19144, United States.
Rutgers Robert Wood Johnson Medical School, Institute for the Study of Child Development, 89 French Street, New Brunswick, NJ 08901, United States.
Neurotoxicol Teratol. 2015 Jan-Feb;47:146-53. doi: 10.1016/j.ntt.2014.11.005. Epub 2014 Nov 18.
The purpose of the current study was to examine the relationship between prenatal cocaine exposure (PCE) and pubertal development. Children (n=192; 41% with PCE) completed the Pubertal Development Scale (Petersen et al. 1988) and provided salivary dehydroepiandrosterone (DHEA) samples at 6month intervals from 11 to 13years. PCE was examined as a predictor of pubertal status, pubertal tempo, and DHEA levels in mixed models analyses controlling for age, sex, environmental risk, neonatal medical problems, other prenatal exposures, and BMI. PCE interacted with age such that PCE predicted slower pubertal tempo during early adolescence. PCE also interacted with age to predict slower increases in DHEA levels during early adolescence. These findings suggest that PCE may affect pubertal development and, if slower pubertal tempo continues, could lead to delayed pubertal status in mid-adolescence.
本研究的目的是探讨产前可卡因暴露(PCE)与青春期发育之间的关系。儿童(n = 192;41%有产前可卡因暴露)完成了青春期发育量表(彼得森等人,1988年),并在11至13岁期间每隔6个月提供唾液脱氢表雄酮(DHEA)样本。在控制年龄、性别、环境风险、新生儿医疗问题、其他产前暴露和体重指数的混合模型分析中,将产前可卡因暴露作为青春期状态、青春期节奏和脱氢表雄酮水平的预测指标进行研究。产前可卡因暴露与年龄存在交互作用,即产前可卡因暴露预示着青春期早期的发育节奏较慢。产前可卡因暴露还与年龄相互作用,预测青春期早期脱氢表雄酮水平的增长较慢。这些发现表明,产前可卡因暴露可能会影响青春期发育,如果青春期节奏持续较慢,可能会导致青春期中期的青春期状态延迟。