Mendelian randomization—a powerful tool to study the causal effects of atrial fibrillation on loss of brain volume

Andreasen, Laura

doi:10.1186/s12916-021-01946-1

Cited by 2 publications

(2 citation statements)

References 5 publications

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“…Causality cannot be inferred directly from traditional observational studies [19] . However, a two-way Mendelian randomization (MR) design can support a causal relationship between an exposure and outcome based on the genetic variations associated with risk factors of interest [20] .…”

Section: Introductionmentioning

confidence: 99%

Causality between alcohol consumption and schizophrenia: A bidirectional Mendelian randomization study

Liu,

Han

et al. 2024

Preprint

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Background: Observational studies have revealed an association between alcohol consumption and schizophrenia (SZ), and have identified high alcohol consumption as an independent risk factor for SZ. However, due to the limitations of observational studies, the causal relationship between SZ and alcohol consumption is unknown. This study used two-way Mendelian randomization (MR) to determine the causal relationship between alcohol consumption phenotype (drinks consumed per week, DPW) and SZ risk. Methods: We conducted bidirectional MR analysis using the aggregate statistical data of a European individual genome-wide association study (GWAS). Causality was evaluated using the inverse variance weighting (IVW), MR-Egger, and weighted median methods. We also used the MR-Egger intercept to detect horizontal multiplicity, and conducted sensitivity analysis to evaluate the robustness of the results. Results: High DPW did not increase the risk of SZ according to IVW, MR-Egger, and weighted median methods using 78 single nucleotide polymorphisms (SNPs) from the GWAS database. Similarly, MR-Egger analysis with 123 SNPs revealed no causal effect of SZ on DPW (OR = 1.00, 95% Cl: 0.95–1.04, p = 0.92). However, both IVW and weighted median methods (n=123 SNPs) indicated that SZ increased DPW (OR = 1.01, 95% Cl: 1.00–1.02; p = 0.01 and p = 8.78 × 10-3, respectively). Further, MR-Egger regression showed that directional multiplicity did not bias the MR results (intercept = 9.70 × 10-4, p = 0.52), while leave-one-out sensitivity analysis indicated that no single SNP significantly influenced the association. Conclusions: This MR study suggests that the genetic factors associated with SZ also increase the risk of excessive alcohol consumption. Interventions for reducing or eliminating alcohol consumption may improve the clinical management of SZ.

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Section: Introductionmentioning

confidence: 99%

Causality between alcohol consumption and schizophrenia: A bidirectional Mendelian randomization study

Liu,

Han

et al. 2024

Preprint

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“…Nowadays, Mendelian randomization (MR) has emerged as a powerful method for identifying causal relationships between risk factors and diseases via genetic variants [22][23][24]. Unlike observational studies, MR uses genetic variants randomly assigned at conception as instrumental variables (IVs) to estimate the causal effect of exposure on outcome and can lessen the bias due to confounders or reverse causation [25,26].…”

Section: Introductionmentioning

confidence: 99%

Causal Relationship between Angina and Hepatic Failure as Revealed by Mendelian Randomization

Xu,

Dirsch,

Dahmen

2024

JCM

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Background: Patients with angina are often suffering from comorbidities such as varying degrees of hepatic dysfunction. However, the impact of angina on the incidence of hepatic failure (HF) remains unclear. Methods: The genetic data were retrieved from genome-wide association studies. Five Mendelian randomization methods were used to investigate the causal relationship between unstable angina (UA), stable angina (SA), and HF. The result of the Inverse variance weighted (IVW) method was deemed the principal result. In addition, we performed a comprehensive sensitivity analysis to verify the robustness of the results. Results: The IVW results showed that UA (Odds ratio (OR): 2.055, 95% confidence interval (CI): 1.171–3.606, p = 0.012) was causally associated with the incidence of HF. SA (OR: 1.122, 95% CI: 0.738–1.706, p = 0.591) was not causally associated with the incidence of HF. Sensitivity analysis did not identify any bias in the results. Conclusions: UA turned out to be a risk factor for HF. SA does not have a significant causal effect on HF. Therefore, it is highly recommended that patients with chronic liver disease seek prompt medical attention and undergo regular monitoring of liver function when experiencing UA. This may help them to reduce the risk of HF.

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Mendelian randomization—a powerful tool to study the causal effects of atrial fibrillation on loss of brain volume

Cited by 2 publications

References 5 publications

Causality between alcohol consumption and schizophrenia: A bidirectional Mendelian randomization study

Causality between alcohol consumption and schizophrenia: A bidirectional Mendelian randomization study

Causal Relationship between Angina and Hepatic Failure as Revealed by Mendelian Randomization

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