The Generation R Study Group, Erasmus University Medical Centre, Rotterdam, Netherlands.
Department of Internal Medicine, Academic Center For Thyroid Diseases, Erasmus University Medical Centre, Rotterdam, Netherlands.
J Nutr. 2020 Jun 1;150(6):1516-1528. doi: 10.1093/jn/nxaa051.
Severe iodine deficiency during pregnancy can cause intellectual disability, presumably through inadequate placental transfer of maternal thyroid hormone to the fetus. The association between mild-to-moderate iodine deficiency and child neurodevelopmental problems is not well understood.
We investigated the association of maternal iodine status during pregnancy with child attention-deficit hyperactivity disorder (ADHD) and autistic traits.
This was a collaborative study of 3 population-based birth cohorts: Generation R (n = 1634), INfancia y Medio Ambiente (n = 1293), and the Avon Longitudinal Study of Parents and Children (n = 2619). Exclusion criteria were multiple fetuses, fertility treatment, thyroid-interfering medication use, and pre-existing thyroid disease. The mean age of assessment in the cohorts was between 4.4 and 7.7 y for ADHD symptoms and 4.5 and 7.6 y for autistic traits. We studied the association of the urinary iodine-to-creatinine ratio (UI/Creat) <150 μg/g-in all mother-child pairs, and in those with a urinary-iodine measurement at ≤18 weeks and ≤14 weeks of gestation-with the risk of ADHD or a high autistic-trait score (≥93rd percentile cutoff), using logistic regression. The cohort-specific effect estimates were combined by random-effects meta-analyses. We also investigated whether UI/Creat modified the associations of maternal free thyroxine (FT4) or thyroid-stimulating hormone concentrations with ADHD or autistic traits.
UI/Creat <150 μg/g was not associated with ADHD (OR: 1.2; 95% CI: 0.7, 2.2; P = 0.56) or with a high autistic-trait score (OR: 0.8; 95% CI: 0.6, 1.1; P = 0.22). UI/Creat <150 μg/g in early pregnancy (i.e., ≤18 weeks or ≤14 weeks of gestation) was not associated with a higher risk of behavioral problems. The association between a higher FT4 and a greater risk of ADHD (OR: 1.3; 95% CI: 1.0, 1.6; P = 0.017) was not modified by iodine status.
There is no consistent evidence to support an association of mild-to-moderate iodine deficiency during pregnancy with child ADHD or autistic traits.
妊娠期间严重碘缺乏可导致智力障碍，这可能是由于母体甲状腺激素向胎儿的胎盘转运不足所致。轻度至中度碘缺乏与儿童神经发育问题之间的关系尚不清楚。
我们研究了妊娠期间母体碘状况与儿童注意缺陷多动障碍（ADHD）和自闭症特征之间的关系。
这是一项对 3 个人群为基础的出生队列的合作研究：生育队列研究（n=1634）、INfancia y Medio Ambiente（n=1293）和雅芳纵向父母与子女研究（n=2619）。排除标准为多胎妊娠、生育治疗、甲状腺干扰药物使用和预先存在的甲状腺疾病。这些队列的平均评估年龄为 ADHD 症状 4.4 至 7.7 岁和自闭症特征 4.5 至 7.6 岁。我们研究了所有母婴对子中尿碘/肌酐比值（UI/Creat）<150μg/g 以及妊娠 18 周和 14 周时尿碘测量值≤18 周和≤14 周时，与 ADHD 或高自闭症特征评分（≥93 百分位截止值）风险之间的关系，使用逻辑回归。通过随机效应荟萃分析合并队列特异性效应估计值。我们还研究了 UI/Creat 是否改变了母体游离甲状腺素（FT4）或促甲状腺激素浓度与 ADHD 或自闭症特征之间的关系。
UI/Creat <150μg/g 与 ADHD（OR：1.2；95%CI：0.7，2.2；P=0.56）或高自闭症特征评分（OR：0.8；95%CI：0.6，1.1；P=0.22）无关。妊娠早期（即≤18 周或≤14 周）UI/Creat <150μg/g 与行为问题风险增加无关。较高的 FT4 与 ADHD 风险增加之间的关联（OR：1.3；95%CI：1.0，1.6；P=0.017）不受碘状态的影响。
没有一致的证据支持妊娠期间轻度至中度碘缺乏与儿童 ADHD 或自闭症特征之间存在关联。
