Multiple Sclerosis Center, Sheba Medical Center, Ramat-Gann, Israel.
Preventive Neurology Unit, Wolfson Institute of Population Health, Queen Mary University London, Charterhouse Square, London, EC1M 6BQ, UK.
Sci Rep. 2022 Dec 22;12(1):22158. doi: 10.1038/s41598-022-26409-2.
Multiple Sclerosis (MS) has been linked to a variety of environmental risk factors, including smoking, Epstein-Barr Virus infection, and childhood obesity. There is some evidence to support a relationship between alcohol consumption and MS risk, but this finding has been inconsistent across cohorts. A protective link between alcohol consumption and MS risk is seen in Swedish and Danish cohorts, however evidence from other cohorts and mendelian randomisation studies have failed to support this relationship. We assessed the relationship between alcohol consumption (never vs. ever drinking) and MS in 409,228 individuals (2100 with MS) from UK Biobank (UKB). We used multivariable logistic regression models adjusted for age and sex. To determine whether there was evidence of statistical interaction between alcohol consumption and HLA-DRB115:01 genotype, we calculated interaction on the additive and multiplicative scales. We analysed data from 2100 individuals with MS (72.3% female, median age at recruitment 56) and 407,128 controls (53.9% female, median age at recruitment 58). We found no evidence for an association between alcohol consumption and MS risk (OR = 1.12, 95% CI 0.61-2.08, p = 0.314). As expected, the HLA-DRB115:01 allele was strongly associated with MS risk (OR = 2.72, 95% CI 2.72-2.72, p < 2 × 10). We found no evidence of statistical interaction between non-drinking and MS risk on either the multiplicative scale (p = 0.8) or on the additive scale (Attributable Proportion = 0.03, 95% CI - 0.43-0.29, P = 0.45). Empirical power calculations indicated reasonable statistical power (85%) to detect a protective effect of alcohol consumption of Relative Risk ≤ 0.7. We were thus unable to replicate findings from other cohorts within UK Biobank. The inconsistent association seen between studies may reflect limited statistical power to detect a weak effect, differences in population characteristics, or the lack of a true causal association.
多发性硬化症（MS）与多种环境风险因素有关，包括吸烟、爱泼斯坦-巴尔病毒感染和儿童肥胖。有一些证据表明饮酒与 MS 风险之间存在关联，但这一发现在不同队列中并不一致。在瑞典和丹麦队列中观察到饮酒与 MS 风险之间存在保护关联，但来自其他队列和孟德尔随机化研究的证据未能支持这种关联。我们评估了在英国生物库（UKB）的 409,228 个人（2100 名 MS 患者）中饮酒（从不饮酒与饮酒）与 MS 之间的关系。我们使用多变量逻辑回归模型调整了年龄和性别。为了确定饮酒与 HLA-DRB115:01 基因型之间是否存在统计学交互作用的证据，我们按加性和乘法尺度计算了交互作用。我们分析了来自 2100 名 MS 患者（72.3%为女性，招募时的中位年龄为 56 岁）和 407,128 名对照者（53.9%为女性，招募时的中位年龄为 58 岁）的数据。我们没有发现饮酒与 MS 风险之间存在关联的证据（OR=1.12，95%CI 0.61-2.08，p=0.314）。正如预期的那样，HLA-DRB115:01 等位基因与 MS 风险强烈相关（OR=2.72，95%CI 2.72-2.72，p<2×10）。我们在乘法尺度（p=0.8）或加性尺度（归因比例=0.03，95%CI-0.43-0.29，P=0.45）上均未发现非饮酒与 MS 风险之间存在统计学交互作用的证据。经验性功效计算表明，检测饮酒的保护作用（相对风险≤0.7）具有合理的统计功效（85%）。因此，我们无法复制 UK Biobank 中其他队列的发现。研究之间不一致的关联可能反映了检测弱效应的统计功效有限、人群特征的差异或缺乏真正的因果关联。
