Larsson Susanna C, Roos Per M
Unit of Cardiovascular and Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden; Department of Surgical Sciences, Uppsala University, Uppsala, Sweden.
Unit of Cardiovascular and Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden; Department of Clinical Physiology, St.Goran Hospital, Stockholm, Sweden.
Neurobiol Aging. 2020 Mar;87:140.e1-140.e3. doi: 10.1016/j.neurobiolaging.2019.10.024. Epub 2019 Nov 6.
We conducted a mendelian randomization study to investigate the association between serum 25-hydroxyvitamin D (S-25OHD) concentrations and amyotrophic lateral sclerosis (ALS). Summary-level data for genetic predictors of S-25OHD concentrations were acquired from 2 genome-wide association studies, comprising up to 79,366 individuals. The corresponding data for ALS were collected from 12,577 ALS cases and 23,475 controls. None of 7 single-nucleotide polymorphisms predicting S-25OHD concentrations was associated with ALS, and there was no overall association of genetic predisposition to higher S-25OHD concentrations with ALS. The odds ratio of ALS per genetically predicted one standard deviation increase of S-25OHD concentrations was 0.96 (95% confidence interval: 0.86-1.08; p = 0.52). We conclude that increasing S-25OHD concentrations will unlikely reduce ALS incidence.
我们进行了一项孟德尔随机化研究,以调查血清25-羟基维生素D(S-25OHD)浓度与肌萎缩侧索硬化症(ALS)之间的关联。S-25OHD浓度的遗传预测因子的汇总数据来自2项全基因组关联研究,涉及多达79366名个体。ALS的相应数据收集自12577例ALS病例和23475名对照。预测S-25OHD浓度的7个单核苷酸多态性均与ALS无关,并且遗传易感性导致较高S-25OHD浓度与ALS之间没有总体关联。每遗传预测S-25OHD浓度增加一个标准差,ALS的优势比为0.96(95%置信区间:0.86-1.08;p=0.52)。我们得出结论,提高S-25OHD浓度不太可能降低ALS的发病率。