ArticleAmerican journal of epidemiology2017
Causal Effect of Genetic Variants Associated With Body Mass Index on Multiple Sclerosis Susceptibility.
Article in American journal of epidemiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 2 syntheses or guidelines pooled it, 63 citations in OpenAlex.
- Uncovering the Causal Link Between Obesity-Associated Genes and Multiple Sclerosis: A Systematic Literature Review.Brain and behavior · 2025Pooled it
- Evidence for a causal relationship between low vitamin D, high BMI, and pediatric-onset MS.Neurology · 2017Pooled it
- Immune Cells as Mediators Between Gut Microbiota and Multiple Sclerosis: Insights From Mendelian Randomization.Immunity, inflammation and disease · 2026Article
- Integrating Genetics and Environment to Find Causal Mechanisms for Multiple Sclerosis.European journal of immunology · 2026Review
- Cross sectional analyses indicated that body fat distribution was not associated with performance-based and self-reported outcomes among ambulatory people with multiple sclerosis.Multiple sclerosis and related disorders · 2026Article
- Advances in Mendelian Randomization Studies of Obesity Over the Past Decade: Uncovering Key Genetic Mechanisms.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Review
- Metabolic reprogramming as a therapeutic target for modulating the Th17/Treg balance in autoimmune diseases: a comprehensive review.Frontiers in immunology · 2025Review
- Article
- Applying a genetic risk score model to enhance prediction of future multiple sclerosis diagnosis at first presentation with optic neuritis.Nature communications · 2024Article
- The role of mGenes & diseases · 2024Review
- Article
- Characterizing causal relationships of visceral fat and body shape on multiple sclerosis risk.Multiple sclerosis and related disorders · 2023Article
- Multiple Sclerosis Pathogenesis and Updates in Targeted Therapeutic Approaches.Current allergy and asthma reports · 2023Review
- Initial BMI effects on clinical presentation and prognosis in neuromyelitis optica spectrum disorder.Annals of clinical and translational neurology · 2023Article
- Article
- MicroRNAs as a possible biomarker in the treatment of multiple sclerosis.IBRO neuroscience reports · 2022Review
- Quantifying the phenome-wide disease burden of obesity using electronic health records and genomics.Obesity (Silver Spring, Md.) · 2022Article
- Environmental risk factors in multiple sclerosis: bridging Mendelian randomization and observational studies.Journal of neurology · 2022Review
- Risk Factors from Pregnancy to Adulthood in Multiple Sclerosis Outcome.International journal of molecular sciences · 2022Review
- Effects of Vitamin D and Body Mass Index on Disease Risk and Relapse Hazard in Multiple Sclerosis: A Mendelian Randomization Study.Neurology(R) neuroimmunology & neuroinflammation · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 10 institutions in 6 countries.
Funding
Abstract
Multiple sclerosis (MS) is an autoimmune disease with both genetic and environmental risk factors. Recent studies indicate that childhood and adolescent obesity double the risk of MS, but this association may reflect unmeasured confounders rather than causal effects of obesity. We used separate-sample Mendelian randomization to estimate the causal effect of body mass index (BMI) on susceptibility to MS. Using data from non-Hispanic white members of the Kaiser Permanente Medical Care Plan of Northern California (KPNC) (2006-2014; 1,104 cases of MS and 10,536 controls) and a replication data set from Sweden (the Epidemiological Investigation of MS (EIMS) and the Genes and Environment in MS (GEMS) studies, 2005-2013; 5,133 MS cases and 4,718 controls), we constructed a weighted genetic risk score using 97 variants previously established to predict BMI. Results were adjusted for birth year, sex, education, smoking status, ancestry, and genetic predictors of MS. Estimates in KPNC and Swedish data sets suggested that higher genetically induced BMI predicted greater susceptibility to MS (odds ratio = 1.13, 95% confidence interval: 1.04, 1.22 for the KPNC sample; odds ratio = 1.09, 95% confidence interval: 1.03, 1.15 for the Swedish sample). Although the mechanism remains unclear, to our knowledge, these findings support a causal effect of increased BMI on susceptibility to MS for the first time, and they suggest a role for inflammatory pathways that characterize both obesity and the MS disease process.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.