Dataset Information

No bidirectional relationship between depression and periodontitis: A genetic correlation and Mendelian randomization study.

ABSTRACT:

Background

Observational and in-vivo research suggested a bidirectional relationship between depression and periodontitis. We estimated the genetic correlation and examined directionality of causation.

Methods

The study used summary statistics from published genome wide association studies, with sample sizes ranging from 45,563 to 797,563 individuals of European ancestry. We performed linkage disequilibrium score regression (LDSC) to estimate global correlation and used Heritability Estimation from Summary Statistics (ρ-HESS) to further examine local genetic correlation. Latent Heritable Confounder Mendelian randomization (LHC-MR), Causal Analysis using Summary Effect estimates (CAUSE), and conventional MR approaches assessed bidirectional causation.

Results

LDSC observed only weak genetic correlation (r_g = 0.06, P-Value = 0.619) between depression and periodontitis. Analysis of local genetic correlation using ρ-HESS did not reveal loci of significant local genetic covariance. LHC-MR, CAUSE and conventional MR models provided no support for bidirectional causation between depression and periodontitis, with odds ratios ranging from 1.00 to 1.06 in either direction.

Conclusions

Results do not support shared heritability or a causal connection between depression and periodontitis.

SUBMITTER: Nolde M

PROVIDER: S-EPMC9355660 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature

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Publications

No bidirectional relationship between depression and periodontitis: A genetic correlation and Mendelian randomization study.

Nolde Michael M Holtfreter Birte B Kocher Thomas T Alayash Zoheir Z Reckelkamm Stefan Lars SL Ehmke Benjamin B Baurecht Hansjörg H Baumeister Sebastian-Edgar SE

Frontiers in immunology 20220722

<h4>Background</h4>Observational and <i>in-vivo</i> research suggested a bidirectional relationship between depression and periodontitis. We estimated the genetic correlation and examined directionality of causation.<h4>Methods</h4>The study used summary statistics from published genome wide association studies, with sample sizes ranging from 45,563 to 797,563 individuals of European ancestry. We performed linkage disequilibrium score regression (LDSC) to estimate global correlation and used Her ...[more]

PMID: 35935963

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Project description:Background: Previous studies demonstrated a controversial relationship between sarcopenia (SP) and osteoarthritis (OA) and their genetic causality is unclear. Thus, we conducted a Mendelian randomization (MR) analysis to evaluate the possible causal association between sarcopenia-related traits (appendicular lean mass (ALM), grip strength, usual walking pace) and OA. Method: We used pooled genetic data from the UK Biobank for ALM(n = 450,243), left-hand grip strength (n = 461,026), right-hand grip strength (n = 461,089) and usual walking pace (n = 459,915). Moreover, summary statistics for OA were obtained from the latest study conducted by the Genetics of Osteoarthritis Consortium, including all OA (n = 826,690), hand OA (n = 303,7782), hip OA (n = 353,388) and knee OA (n = 396,054). The primary method for estimating causal effects was the inverse-variance weighted (IVW) method, with the utilizing of false discovery rate adjusted p values (P FDR). Additional MR methods such as MR-Egger regression, MR pleiotropy residual sum and outlier (MR-PRESSO), weighted median were employed as supplementary analyses. Results: We discovered ALM (odds ratio (OR) = 1.103, 95% confidence interval (CI) = 1.052-1.156, P FDR = 2.87E-04), hand grip strength (left, IVW OR = 0.823, 95% CI = 0.712 to 0.952, P FDR = 0.020; right, OR = 0.826, 95% CI = 0.718 to 0.950, P FDR = 0.020), and usual walking pace (OR = 0.339, 95% CI = 0.204 to 0.564, P FDR = 2.38E-04) were causally associated with OA risk. In the reverse MR analysis, we identified a causal effect of OA on ALM (β = -0.258, 95% CI = -0.369 to 0.146, P FDR = 0.6.07E-06), grip strength (left, β = -0.064, 95% CI = -0.104 to 0.024, P FDR = 0.002; right, β = -0.055, 95% CI = -0.095 to 0.014, P FDR = 0.008), and usual walking pace (β = -0.104, 95% CI = -0.147 to 0.061, P FDR = 1.61E-05). Conclusion: This present study suggests an obvious causality of SP on OA, with condition exhibiting site-specific effects, while evidence was also provided for the causal effect of OA on SP.

Dataset Information

No bidirectional relationship between depression and periodontitis: A genetic correlation and Mendelian randomization study.

Background

Methods

Results

Conclusions

Publications

No bidirectional relationship between depression and periodontitis: A genetic correlation and Mendelian randomization study.

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