Population studies suggest that atopic dermatitis (AD) is associated with an increased risk of obesity, however a causal relationship between these two conditions remains to be established. We therefore use Mendelian randomization (MR) to evaluate whether obesity and AD are causally interlinked. We used summary statistics extracted from genome wide association studies of Body Mass Index (BMI) and AD. MR analysis was performed in both directions to establish the direction of causality between BMI and AD. We find that genetically determined increase in adiposity is associated with increased risk of AD (odds ratio of AD 1.08 [95% CI 1.01 to 1.14; p = 0.015] per unit increase in BMI). Conversely, genetically determined increased risk of AD is not associated with a higher BMI (change in BMI attributable to AD based on genetic information: 0.00; 95% CI − 0.02 to 0.02; p = 0.862). There was no evidence for confounding of these genetic analyses by horizontal pleiotropy. Our results indicate that the association of AD with obesity is likely to reflect a causal role for adiposity in the development of AD. Our findings enhance understanding of the etiology of AD, and the basis for experimental studies to evaluate the mechanistic pathways by which adiposity promotes AD.

人口研究表明，特应性皮炎 (AD) 与肥胖风险增加有关，但这两种情况之间的因果关系仍有待确定。因此，我们使用孟德尔随机化 (MR) 来评估肥胖和 AD 是否存在因果关系。我们使用从体重指数 (BMI) 和 AD 的全基因组关联研究中提取的汇总统计数据。在两个方向上进行 MR 分析以确定 BMI 和 AD 之间的因果关系方向。我们发现遗传决定的肥胖增加与 AD 风险增加有关（每单位 BMI 增加，AD 的比值比为 1.08 [95% CI 1.01 至 1.14；p = 0.015]）。相反，由基因决定的 AD 风险增加与较高的 BMI 无关（基于遗传信息的 AD 导致的 BMI 变化：0.00；95% CI - 0.02 至 0.02；p = 0.862）。没有证据表明水平多效性会混淆这些遗传分析。我们的结果表明 AD 与肥胖的关联可能反映了肥胖在 AD 发展中的因果作用。我们的研究结果增强了对 AD 病因的理解，并为评估肥胖促进 AD 的机制途径的实验研究奠定了基础。