Table_1_Association between dietary zinc intake and epilepsy: findings from NHANES 2013–2018 and a Mendelian randomization study.DOCX
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BackgroundThe association between dietary zinc intake and epilepsy remains unclear. This study aimed to investigate the relationship between zinc intake from the diet and epilepsy, employing Mendelian randomization (MR) to explore potential causal links between zinc and epilepsy.MethodsThe cross-sectional study utilized data from the National Health and Nutrition Examination Survey (NHANES) conducted between 2013 and 2018. Among the 4,434 participants included, 1.5% (67/4,434) reported having epilepsy. Restricted cubic spline models and logistic regression models were employed to examine the relationships between dietary zinc intakes and epilepsy. Subsequently, a 2-sample Mendelian randomization (MR) analysis was conducted using the inverse variance weighted (IVW) approach as the primary analysis.ResultsIn the restricted cubic spline (RCS) analysis, the relationship between dietary zinc consumption and epilepsy displayed an L-shaped curve (nonlinear, p = 0.049). After multivariate adjustments, the adjusted odds ratios for epilepsy in T2 (5.0–11.0 mg/day) and T3 (≥11.0 mg/day) were 0.49 (95% confidence interval [CI]: 0.26–0.92, p = 0.026) and 0.60 (95% CI: 0.31–1.17, p = 0.132), respectively, compared to the lowest dietary zinc consumption tertile (T1, ≤5.0 mg/day). The IVW method indicated that genetically predicted zinc intake per standard-deviation increase was inversely associated with three types of epilepsy, including all types of epilepsy (OR = 1.06, 95% CI: 1.02–1.11, p = 0.008), generalized epilepsy (OR = 1.13, 95% CI: 1.01–1.25, p = 0.030), and focal epilepsy (documented hippocampal sclerosis) (OR = 1.01, 95% CI: 1.00–1.02, p = 0.025).ConclusionOur findings suggest that a daily zinc intake ranging from 5.0 to 11.0 mg is associated with the lowest risk of epilepsy. Furthermore, Mendelian randomization (MR) studies provide additional support for the existence of a causal relationship between zinc and epilepsy.
背景:膳食锌摄入与癫痫之间的关联尚不明确。本研究旨在探讨膳食锌摄入与癫痫之间的关系,采用孟德尔随机化(MR)方法,以探究锌与癫痫之间潜在的因果联系。
方法:一项横断面研究利用了2013年至2018年间进行的全国健康与营养调查(NHANES)数据。在4,434名参与者中,1.5%(67/4,434)报告患有癫痫。采用限制性三次样条模型和逻辑回归模型,分析了膳食锌摄入与癫痫之间的关系。随后,采用逆方差加权(IVW)方法进行了两样本孟德尔随机化(MR)分析,作为主要分析方法。
结果:在限制性三次样条(RCS)分析中,膳食锌消耗与癫痫之间的关系呈现出L型曲线(非线性,p=0.049)。在多变量调整后,与最低膳食锌摄入的三分位数(T1,≤5.0mg/天)相比,T2(5.0–11.0mg/天)和T3(≥11.0mg/天)的癫痫调整比值比分别为0.49(95%置信区间[CI]:0.26–0.92,p=0.026)和0.60(95% CI:0.31–1.17,p=0.132)。IVW方法表明,每标准差增加的遗传预测锌摄入量与三种类型的癫痫呈负相关,包括所有类型的癫痫(OR=1.06,95% CI:1.02–1.11,p=0.008)、全身性癫痫(OR=1.13,95% CI:1.01–1.25,p=0.030)和局灶性癫痫(记录的海马硬化)(OR=1.01,95% CI:1.00–1.02,p=0.025)。
结论:我们的研究结果表明,每日锌摄入量在5.0至11.0mg之间与最低的癫痫风险相关。此外,孟德尔随机化(MR)研究为锌与癫痫之间因果关系的存在提供了额外的支持。
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