Dataset Information

Modifiable factors for migraine prophylaxis: A mendelian randomization analysis.

ABSTRACT: Objective: To examine the causal effect of potentially modifiable risk factors contributing to migraine pathogenesis. Methods: We performed Mendelian randomization analyses and acquired data from United Kingdom Biobank, FinnGen Biobank, and the MRC IEU OpenGWAS data infrastructure. An inverse-variance weighted (IVW) model was used to examine the relationship between 51 potentially modifiable risk factors and migraine in 3215 participants with migraine without aura (MwoA), 3541 participants with migraine with aura (MwA), and 176,107 controls. We adopted a Bonferroni-corrected threshold of p = 9.8 × 10-4 (.05 divided by 51 exposures) as a sign of significant effect, and a p < .05 was considered as the sign of a suggestive association. Results: More years of schooling significantly correlated with lower odds of MwoA pathogenesis (OR .57 [95%CI .44 to .75], p < .0001). More vitamin B12 intake (OR .49 [95%CI .24 to .99], p = .046) and lower level of stress [OR 8.17 (95%CI 1.5 to 44.36), p = .015] or anxiety disorder (OR 1.92 × 109 [95%CI 8.76 to 4.23*1017], p = .029) were suggestive to be correlated lower odds of MwoA pathogenesis. More coffee intake (OR .39 [95%CI .22 to .7], p = .001), lower level of eicosapentaenoic acid status (OR 2.54 [95%CI 1.03 to 6.26], p = .043), and more light physical activity (OR .09 [95%CI .01 to .94], p = .046) were suggestive to be associated with lower odds of MwA. Conclusion: The years of schooling, light physical activity, vitamin B12 intake, and coffee intake were the protective factors for migraine; stress, anxiety, and eicosapentaenoic acid status were harmful factors. Interventions could be developed based on modifying these factors for migraine prophylaxis.

SUBMITTER: Zheng H

PROVIDER: S-EPMC9878312 | biostudies-literature | 2023

REPOSITORIES: biostudies-literature

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Modifiable factors for migraine prophylaxis: A mendelian randomization analysis.

Zheng Hui H Shi Yun-Zhou YZ Liang Jing-Tao JT Lu Liang-Liang LL Chen Min M

Frontiers in pharmacology 20230112

<b>Objective:</b> To examine the causal effect of potentially modifiable risk factors contributing to migraine pathogenesis. <b>Methods:</b> We performed Mendelian randomization analyses and acquired data from United Kingdom Biobank, FinnGen Biobank, and the MRC IEU OpenGWAS data infrastructure. An inverse-variance weighted (IVW) model was used to examine the relationship between 51 potentially modifiable risk factors and migraine in 3215 participants with migraine without aura (MwoA), 3541 part ...[more]

PMID: 36713835

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Project description:BackgroundLung cancer is the major cause of mortality in tumor patients. While its incidence rate has recently declined, it is still far from satisfactory and its potential modifiable risk factors should be explored.MethodsWe performed a two-sample Mendelian randomization (MR) study to investigate the causal relationship between potentially modifiable risk factors (namely smoking behavior, alcohol intake, anthropometric traits, blood pressure, lipidemic traits, glycemic traits, and fasting insulin) and lung cancer. Besides, a bi-directional MR analysis was carried out to disentangle the complex relationship between different risk factors. Inverse-variance weighted (IVW) was utilized to combine the estimation for each SNP. Cochrane's Q value was used to evaluate heterogeneity and two methods, including MR-Egger intercept and MR-PRESSO, were adopted to detect horizontal pleiotropy.ResultsThree kinds of smoking behavior were all causally associated with lung cancer. Overall, smokers were more likely to suffer from lung cancer compared with non-smokers (OR = 2.58 [1.95, 3.40], p-value = 2.07 x 10-11), and quitting smoking could reduce the risk (OR = 4.29[2.60, 7.07], p-value = 1.23 x 10-8). Furthermore, we found a dose-response relationship between the number of cigarettes and lung cancer (OR = 6.10 [5.35, 6.96], p-value = 4.43x10-161). Lower HDL cholesterol could marginally increase the risk of lung cancer, but become insignificant after Bonferroni correction (OR = 0.82 [0.68, 1.00], p-value = 0.045). In addition, we noted no direct causal relationship between other risk factors and lung cancer. Neither heterogeneity nor pleiotropy was observed in this study. However, when treating the smoking behavior as the outcome, we found the increased BMI could elevate the number of cigarettes per day (beta = 0.139[0.104, 0.175], p-value = 1.99x10-14) and a similar effect was observed for the waist circumference and hip circumference. Additionally, the elevation of SBP could also marginally increase the number of cigarettes per day (beta = 0.001 [0.0002, 0.002], p-value = 0.018).ConclusionSmoking behavior might be the most direct and effective modifiable way to reduce the risk of lung cancer. Meanwhile, smoking behavior can be affected by other risk factors, especially obesity.

Project description:BackgroundPotentially modifiable risk factors including obesity, diabetes, hypertension, and smoking are associated with Alzheimer disease (AD) and represent promising targets for intervention. However, the causality of these associations is unclear. We sought to assess the causal nature of these associations using Mendelian randomization (MR).Methods and findingsWe used SNPs associated with each risk factor as instrumental variables in MR analyses. We considered type 2 diabetes (T2D, NSNPs = 49), fasting glucose (NSNPs = 36), insulin resistance (NSNPs = 10), body mass index (BMI, NSNPs = 32), total cholesterol (NSNPs = 73), HDL-cholesterol (NSNPs = 71), LDL-cholesterol (NSNPs = 57), triglycerides (NSNPs = 39), systolic blood pressure (SBP, NSNPs = 24), smoking initiation (NSNPs = 1), smoking quantity (NSNPs = 3), university completion (NSNPs = 2), and years of education (NSNPs = 1). We calculated MR estimates of associations between each exposure and AD risk using an inverse-variance weighted approach, with summary statistics of SNP-AD associations from the International Genomics of Alzheimer's Project, comprising a total of 17,008 individuals with AD and 37,154 cognitively normal elderly controls. We found that genetically predicted higher SBP was associated with lower AD risk (odds ratio [OR] per standard deviation [15.4 mm Hg] of SBP [95% CI]: 0.75 [0.62-0.91]; p = 3.4 × 10(-3)). Genetically predicted higher SBP was also associated with a higher probability of taking antihypertensive medication (p = 6.7 × 10(-8)). Genetically predicted smoking quantity was associated with lower AD risk (OR per ten cigarettes per day [95% CI]: 0.67 [0.51-0.89]; p = 6.5 × 10(-3)), although we were unable to stratify by smoking history; genetically predicted smoking initiation was not associated with AD risk (OR = 0.70 [0.37, 1.33]; p = 0.28). We saw no evidence of causal associations between glycemic traits, T2D, BMI, or educational attainment and risk of AD (all p > 0.1). Potential limitations of this study include the small proportion of intermediate trait variance explained by genetic variants and other implicit limitations of MR analyses.ConclusionsInherited lifetime exposure to higher SBP is associated with lower AD risk. These findings suggest that higher blood pressure--or some environmental exposure associated with higher blood pressure, such as use of antihypertensive medications--may reduce AD risk.

Project description:BackgroundWhile several risk factors for knee osteoarthritis (KOA) have been recognized, the pathogenesis of KOA and the causal relationship between modifiable risk factors and KOA in genetic epidemiology remain unclear. This study aimed to determine the causal relationship between KOA and its risk factors.MethodsData were obtained from published Genome-Wide Association study (GWAS) databases. A two-sample Mendelian randomization (MR) analysis was performed with genetic variants associated with risk factors as instrumental variables and KOA as outcome. First, inverse variance weighting was used as the main MR analysis method, and then a series of sensitivity analyses were conducted to comprehensively evaluate the causal relationship between them.ResultsUnivariate forward MR analysis revealed that genetically predicted hypothyroidism, hyperthyroidism/thyrotoxicosis, educational level, income level, metabolic syndrome (MS), essential hypertension, height, hot drink temperature, diet (abstaining from sugar-sweetened or wheat products), and psychological and psychiatric disorders (stress, depression, and anxiety) were causally associated with KOA. Reverse MR exhibits a causal association between KOA and educational attainment. Multivariate MR analysis adjusted for the inclusion of potential mediators, such as body mass index (BMI), smoking, alcohol consumption, and sex, exhibited some variation in causal effects. However, hyperthyroidism/thyrotoxicosis had a significant causal effect on KOA, and there was good evidence that height, hypothyroidism, educational level, psychological and psychiatric disorders (stress, depression, and anxiety), and abstaining from wheat products had an independent causal relationship. The mediating effect of BMI as a mediator was also identified.ConclusionThis study used MR to validate the causal relationship between KOA and its risk factors, providing new insights for preventing and treating KOA in clinical practice and for developing public health policies.

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Modifiable factors for migraine prophylaxis: A mendelian randomization analysis.

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Modifiable factors for migraine prophylaxis: A mendelian randomization analysis.

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