Dataset Information

Causality between major depressive disorder and functional dyspepsia: a two-sample Mendelian randomization study.

ABSTRACT:

Background

To investigate the causal relationship between major depression and functional dyspepsia using two-sample Mendelian randomization.

Methods

Data for major depression and functional dyspepsia were obtained from genome-wide association studies. We selected Single Nucleotide Polymorphisms (SNPs) strongly associated with severe depression. Mendelian randomization analysis was conducted using methods such as Inverse-Variance Weighted (IVW), MR-Egger, and Weighted Median Estimator (WME). Sensitivity analysis was performed to assess the robustness of the results.

Results

A total of 31 eligible SNPs were identified as instrumental variables for major depression. IVW analysis indicated a positive causal relationship between the two conditions (β = 0.328; SE = 0.137; p = 0.017), suggesting that severe depression increases the risk of functional dyspepsia (OR = 1.389; 95% CI: 1.062-1.816). Sensitivity tests showed no evidence of heterogeneity or horizontal pleiotropy (p > 0.05).

Conclusion

MR analysis had shown that major depressive disorder is associated with an increased risk of functional dyspepsia.

SUBMITTER: Du Y

PROVIDER: S-EPMC11298389 | biostudies-literature | 2024

REPOSITORIES: biostudies-literature

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Publications

Causality between major depressive disorder and functional dyspepsia: a two-sample Mendelian randomization study.

Du Yaming Y Wang Rui R Xu Xinzi X Wang Junli J Shao Wei W Chen Guohua G

Frontiers in neurology 20240722

<h4>Background</h4>To investigate the causal relationship between major depression and functional dyspepsia using two-sample Mendelian randomization.<h4>Methods</h4>Data for major depression and functional dyspepsia were obtained from genome-wide association studies. We selected Single Nucleotide Polymorphisms (SNPs) strongly associated with severe depression. Mendelian randomization analysis was conducted using methods such as Inverse-Variance Weighted (IVW), MR-Egger, and Weighted Median Estim ...[more]

PMID: 39105061

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Project description:BackgroundMajor depressive disorder (MDD) is a highly heterogeneous mental illness and a major public health problem worldwide. A large number of observational studies have demonstrated a clear association between MDD and coronary heart disease (CHD), and some studies have even suggested that the relationship is bidirectional. However, it was unknown whether any causal relationship existed between them and whether causality was bidirectional in such an instance. Thus, we aimed to determine whether there is a bidirectional causal relationship between major depressive disorders and coronary heart disease.MethodsOur two-sample Bidirectional Mendelian Randomization Study consisted of two parts: forward MR analysis regarded MDD as exposure and CHD as the outcome, and reverse MR analysis considered CHD as exposure and MDD as the outcome. Summary data on MDD and CHD were obtained from the IEU Open GWAS database. After screening criteria(P < [Formula: see text]), 47 MDD-associated SNPs and 39 CHD-associated SNPs were identified. The inverse-variance weighted (IVW) method, ME-Egger regression, and weighted median method were used to estimate causality. In addition, sensitivity methods, including the heterogeneity test, horizontal pleiotropy test, and leave-one-out method, were applied to ensure the robustness of causal estimation.ResultsBased on the MR-Egger regression intercept test results, there did not appear to be any horizontal pleiotropy in this study (MDD: intercept = -0.0000376, P = 0.9996; CHD: intercept = -0.0002698, P = 0.920). Accordingly, IVW results suggested consistent estimates of causal effect values. The results showed that people with MDD increased the risk of CHD by 14.7% compared with those without MDD (OR = 1.147, 95%CI: 1.045-1.249, P = 0.009). But there was no direct evidence that CHD would increase the risk of MDD(OR = 1.008, 95%CI: 0.985-1.031, P = 0.490). The heterogeneity test and funnel plot showed no heterogeneity in 47 SNPs of MDD (Q = 42.28, [Formula: see text]=0, P = 0.629), but there was heterogeneity in 39 SNPs of CHD (Q = 62.48, [Formula: see text]=39.18%, P = 0.007). The leave-one-out method failed to identify instances where a single SNP was either biased toward or dependent on the causation.ConclusionOur study supports a one-way causal relationship between MDD and CHD, but there is no bidirectional causal relationship. MDD increases the risk of CHD, but there is no evidence that CHD increases the risk of MDD. Therefore, the influence of psychological factors should also be considered in the prevention and treatment of CHD. For MDD patients, it is necessary to prevent cardiovascular diseases.

Project description:BackgroundMental disorders, characterized as products of biopsychosocial interactions, have emerged as a leading contributor to the worldwide rise in overall morbidity and disability rates. Life's essentials can affect nearly every aspect of our lives, from physical to mental health. In this study, we try to identify the associations between life's essentials and mental disorders.MethodThree assumptions of Mendelian randomization (MR) were applied to obtain the genetic instruments associated with smoking, sleep, and body mass index (BMI) in genome-wide association studies. Then, we conducted univariable MR (UVMR) and multivariable MR (MVMR) two-sample analyses to estimate the causal effects of these life's essentials on two mental disorders namely, major depressive disorder (MDD) and bipolar disorder (BD). Additionally, multiple sensitivity analyses were performed to evaluate the reliability and stability of the study results.ResultsIn the MR analysis of the association of smoking, sleep, and BMI with MDD, we obtained 78, 39, and 302 genetic instruments, respectively. Smoking [odds ratio (OR), 1.03; 95% confidence interval (CI), 1.01-1.06; p = 0.004], sleep (OR, 1.04; 95% CI, 1.02-1.06; p < 0.001), and BMI (OR, 1.01; 95% CI, 1.01-1.02; p < 0.001) were all considered as risk factors for MDD and were independent of each other (smoking: OR, 1.03, 95% CI, 1.01-1.06, p = 0.008; sleep: OR, 1.03, 95% CI, 1.01-1.05, p = 0.001; and BMI: OR, 1.01, 95% CI, 1.01-1.02, p < 0.001). Additionally, 78, 38, and 297 genetic instruments were obtained in the MR analysis of smoking, sleep, and BMI with BD, respectively. Causal associations were observed between smoking (OR, 2.46; 95% CI, 1.17-5.15; p = 0.017), sleep (OR, 2.73; 95% CI, 1.52-4.92; p < 0.001), and BD, and smoking (OR, 2.43; 95% CI, 1.69-3.16; p = 0.018) might be a mediator in the causal effects of sleep on BD. Finally, there was no inconsistency between sensitivity and causality analysis, proving that our results are convincing.ConclusionThe study results provide strong evidence that smoking, sleep, and BMI are causally related to MDD and BD, which need further research to clarify the underlying mechanism.

Dataset Information

Causality between major depressive disorder and functional dyspepsia: a two-sample Mendelian randomization study.

Background

Methods

Results

Conclusion

Publications

Causality between major depressive disorder and functional dyspepsia: a two-sample Mendelian randomization study.

Similar Datasets

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