Dataset Information

The relationship between COVID-19, depressive disorder, and anxiety: a bidirectional Mendelian randomization study.

ABSTRACT:

Background

Previous clinical studies have found that negative mental states such as depression and anxiety are closely related to COVID-19 infection. We used Mendelian randomization (MR) to explore the relationship between depression, anxiety, and COVID-19 infection.

Methods

Our data were based on publicly available GWAS databases. The COVID-19 samples were obtained from the COVID-19 Host Genetics Initiative (HGI). The depression samples were obtained from the Psychiatric Genomics Consortium (PGC). The anxiety samples were derived from the Finngen database. We used inverse-variance weighting (IVW) as the primary analysis method, with weighted median, MR Egger, and multivariate MRI adjustment.

Results

There was no causal effect of different COVID-19 infection statuses on depression and anxiety as determined by MR analysis. In addition, in the reverse MR analysis, we found a significant causal effect of anxiety on severe symptoms after COVID-19 infection. The results of the MR Egger regression, weighted median, and weighted mode methods were consistent with the IVW method. Based on sensitivity analyses, horizontal pleiotropy was unlikely to influence the final results.

Conclusion

Our findings indicate that anxiety is a risk factor for severe symptoms following COVID-19 infection. However, the mechanism of interaction between the two needs further investigation.

SUBMITTER: Zihao L

PROVIDER: S-EPMC10622770 | biostudies-literature | 2023

REPOSITORIES: biostudies-literature

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Publications

The relationship between COVID-19, depressive disorder, and anxiety: a bidirectional Mendelian randomization study.

Zihao Liang L Jinyun Song S Shuanglin Gu G Xiuzhen Chen C Yonglin Li L Hongyu Zhao Z

Frontiers in psychiatry 20231019

<h4>Background</h4>Previous clinical studies have found that negative mental states such as depression and anxiety are closely related to COVID-19 infection. We used Mendelian randomization (MR) to explore the relationship between depression, anxiety, and COVID-19 infection.<h4>Methods</h4>Our data were based on publicly available GWAS databases. The COVID-19 samples were obtained from the COVID-19 Host Genetics Initiative (HGI). The depression samples were obtained from the Psychiatric Genomics ...[more]

PMID: 37928923

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Project description:Background & aimsCoronavirus disease 2019 (COVID-19) is strongly associated with myocarditis or pericarditis risk in observational studies, however, there are still studies that do not support the above conclusion. Whether the observed association reflects causation needs to be confirmed. We performed a bidirectional Mendelian randomization (MR) study to assess the causal relationship of COVID-19, which was divided into three groups, namely severe COVID-19, hospitalized COVID-19, and COVID-19 infection, measured by myocarditis or pericarditis.MethodsWe extracted summary genome-wide association statistics for the severe COVID-19 (case: 13,769, control: 1,072,442), hospitalized COVID-19 (case: 32,519, control: 2,062,805), COVID-19 infection (case: 122,616, control: 2,475,240), myocarditis (case 1,521, control 191,924), and pericarditis (case 979, control 286,109) among individuals of European ancestry. Independent genetic variants that exhibited a significant association with each phenotype at the genome-wide level of significance were utilized as instrumental variables. Estimation of the causal effect was mainly performed using the random effects inverse-variance weighted method (IVW). Additionally, other tests such as MR-Egger intercept, MR-PRESSO, Cochran's Q-test, "Leave-one-out", and funnel plots were conducted to assess the extent of pleiotropy and heterogeneity.ResultsNon-associations in the IVW and sensitivity analyses were observed for COVID-19 with myocarditis or pericarditis. Severe COVID-19 was not associated with myocarditis [odds ratio (OR), 1.00; 95% confidence interval (CI), 0.89-1.12; P = 0.99], pericarditis (OR = 0.90, 95% CI, 0.78-1.04, P = 0.17). Similar results can be observed in hospitalized COVID-19, and COVID-19 infection. At the same time, null associations were observed for myocarditis or pericarditis with COVID-19 traits in the reverse direction. The main results are kept stable in the sensitivity analysis.ConclusionThere is no evidence that COVID-19 is independently and causally associated with myocarditis or pericarditis.

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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.

Dataset Information

The relationship between COVID-19, depressive disorder, and anxiety: a bidirectional Mendelian randomization study.

Background

Methods

Results

Conclusion

Publications

The relationship between COVID-19, depressive disorder, and anxiety: a bidirectional Mendelian randomization study.

Similar Datasets

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