From the Department of Epidemiology, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC.
Norwegian Institute of Public Health, Physical and Mental health, Oslo, Norway.
Epidemiology. 2019 Jan;30(1):130-144. doi: 10.1097/EDE.0000000000000937.
Attention deficit hyperactivity disorder (ADHD) is the most common neurobehavioral disorder in children, yet its etiology is poorly understood. Early thyroid hormone disruption may contribute to the development of ADHD. Disrupted maternal thyroid hormone function has been associated with adverse neurodevelopmental outcomes in children. Among newborns, early-treated congenital hypothyroidism has been consistently associated with later cognitive deficits.
We systematically reviewed literature on the association between maternal or neonatal thyroid hormones and ADHD diagnosis or symptoms. We searched Embase, Pubmed, Cinahl, PsycInfo, ERIC, Medline, Scopus, and Web of Science for articles published or available ahead of print as of April 2018.
We identified 28 eligible articles: 16 studies of maternal thyroid hormones, seven studies of early-treated congenital hypothyroidism, and five studies of neonatal thyroid hormones. The studies provide moderate evidence for an association between maternal thyroid hormone levels and offspring ADHD, some evidence for an association between early-treated congenital hypothyroidism and ADHD, and little evidence for an association between neonatal thyroid hormone levels and later ADHD.
The reviewed articles suggest an association between maternal thyroid function and ADHD, and possibly between early-treated congenital hypothyroidism and ADHD. Study limitations, however, weaken the conclusions in our systematic review, underlining the need for more research. Importantly, there was much variation in the measurement of thyroid hormone function and of ADHD symptoms. Recommendations for future research include using population-based designs, attending to measurement issues for thyroid hormones and ADHD, considering biologically relevant covariates (e.g., iodine intake), and assessing nonlinear dose-responses.
注意力缺陷多动障碍(ADHD)是儿童中最常见的神经行为障碍,但病因知之甚少。早期甲状腺激素紊乱可能导致 ADHD 的发生。母体甲状腺激素功能障碍与儿童神经发育不良结局有关。在新生儿中,早期治疗的先天性甲状腺功能减退症与以后的认知缺陷一直有关。
我们系统地回顾了关于母体或新生儿甲状腺激素与 ADHD 诊断或症状之间关联的文献。我们搜索了 Embase、Pubmed、Cinahl、PsycInfo、ERIC、Medline、Scopus 和 Web of Science,以获取截至 2018 年 4 月发表或预印本可用的文章。
我们确定了 28 篇合格的文章:16 项关于母体甲状腺激素的研究,7 项关于早期治疗的先天性甲状腺功能减退症的研究,和 5 项关于新生儿甲状腺激素的研究。这些研究为母体甲状腺激素水平与后代 ADHD 之间的关联提供了中等证据,为早期治疗的先天性甲状腺功能减退症与 ADHD 之间的关联提供了一些证据,为新生儿甲状腺激素水平与以后的 ADHD 之间的关联提供了很少的证据。
综述文章表明母体甲状腺功能与 ADHD 之间存在关联,并且早期治疗的先天性甲状腺功能减退症与 ADHD 之间可能存在关联。然而,研究的局限性削弱了我们系统综述中的结论,强调需要更多的研究。重要的是,甲状腺激素功能和 ADHD 症状的测量存在很大差异。未来研究的建议包括使用基于人群的设计,关注甲状腺激素和 ADHD 的测量问题,考虑生物学相关的协变量(如碘摄入量),并评估非线性剂量反应。