The Parker Institute, Research Unit for Dietary Studies, Bispebjerg and Frederiksberg Hospital, Frederiksberg, Denmark.
Department of Public Health and Department of Clinical Medicine, Aarhus University, Aarhus, Denmark.
Epilepsia. 2020 Jun;61(6):1282-1290. doi: 10.1111/epi.16520. Epub 2020 May 4.
Epilepsy is a nervous system abnormality that may be caused by unknown exposures during fetal development. Studies have shown neuroprotective effects of early exposure to vitamin D in other neurological disorders, and seasonal variation in birth of children with epilepsy. We aimed to investigate if neonatal 25(OH)D was associated with risk of childhood epilepsy.
This case-cohort study compared neonatal 25(OH)D levels from children with epilepsy (n = 403) and a random selected cohort of controls (n = 1163), assessing the hazard of first epilepsy diagnosis between 1 and 4 years of age from a weighted Cox proportional hazard model. Analyses were adjusted for parental education, maternal age, maternal epilepsy, maternal ethnicity, and gestational age, and additionally for season of birth and smoking during pregnancy.
The mean (standard deviation [SD]) of neonatal 25(OH)D levels were 30.8(19.6) nmol/L among cases and 28.5(19.4) nmol/L among the cohort. The hazard ratio (HR) of epilepsy was in a dose-response pattern higher among children from the highest neonatal 25(OH)D quintiles (P-trend = .004). Results were unchanged after including season of birth in the analysis, where a significantly higher HR of epilepsy was observed among children in the two highest quintiles compared to children in the lowest quintile (Q4: HR 1.62, 95% CI 1.07-2.47 and Q5: HR 1.86, 95% CI 1.21-2.86).
In this study, the risk of childhood epilepsy increased with neonatal 25(OH)D categories in a dose-response pattern, suggesting an association between a high neonatal 25(OH)D and the risk of childhood epilepsy. Considering that adjusting for season of birth strengthened the results, we conclude that maternal intake of vitamin D, and not vitamin D from sun exposure, was the vitamin D source associated with epilepsy. Although we cannot, in the present study, control for compounds in the diet like pollutants or heavy metals, which may correlate with dietary vitamin D, future studies investigating fetal origin of epilepsy should focus on compounds correlating with vitamin D.
癫痫是一种神经系统异常，可能由胎儿发育过程中未知的暴露引起。研究表明，维生素 D 早期暴露对其他神经紊乱具有神经保护作用，而且儿童癫痫的出生季节存在季节性变化。我们旨在研究新生儿 25（OH）D 是否与儿童癫痫的发病风险有关。
本病例-队列研究比较了癫痫患儿（n=403）和随机选择的对照组（n=1163）的新生儿 25（OH）D 水平，使用加权 Cox 比例风险模型评估 1 至 4 岁时首次癫痫诊断的风险。分析调整了父母教育程度、母亲年龄、母亲癫痫、母亲种族和胎龄，并进一步调整了出生季节和怀孕期间吸烟情况。
病例组新生儿 25（OH）D 水平的平均值（标准差）为 30.8（19.6）nmol/L，队列组为 28.5（19.4）nmol/L。25（OH）D 水平最高五分位数的儿童癫痫风险呈剂量-反应模式升高（P 趋势=0.004）。在分析中纳入出生季节后，结果保持不变，与最低五分位数的儿童相比，两个最高五分位数的儿童癫痫风险显著升高（Q4：HR 1.62，95%CI 1.07-2.47 和 Q5：HR 1.86，95%CI 1.21-2.86）。
在这项研究中，儿童癫痫的风险随着新生儿 25（OH）D 水平呈剂量-反应模式增加，提示新生儿 25（OH）D 水平与儿童癫痫的发病风险之间存在关联。考虑到调整出生季节可以增强结果，我们得出结论，与癫痫相关的是母体维生素 D 摄入，而不是来自阳光暴露的维生素 D。虽然在本研究中，我们无法控制饮食中与污染物或重金属等化合物有关的情况，这些化合物可能与饮食中的维生素 D 有关，但未来研究胎儿癫痫病因时，应重点关注与维生素 D 相关的化合物。
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