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The association between basal metabolic rate and osteoarthritis: a Mendelian randomization study

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Abstract Background The role of the basal metabolic rate (BMR) in osteoarthritis (OA) remains unclear, as previous retrospective studies have produced inconsistent results. Therefore, we performed a Mendelian randomization (MR) study to systematically investigate the causal relationship between the BMR and OA. Methods Single-nucleotide polymorphism (SNP) data related to BMR and OA were collected in a genome-wide association study. Using OA as the outcome variable and BMR as the exposure factor, SNPs with strong correlation with the BMR as the tool variable were screened. The correlation between the BMR and OA risk was evaluated using the inverse-variance weighted method, and heterogeneity and pleiotropy were evaluated using a sensitivity analysis. Results There was a potential causal relationship between the BMR and OA risk (odds ratio [OR], 1.014; 95% confidence interval [CI], 1.008–1.020; P = 2.29e − 6). A causal relationship was also revealed between the BMR and knee OA (OR, 1.876; 95% CI, 1.677–2.098; P = 2.98e − 28) and hip OA (OR, 1.475; 95% CI, 1.290–1.686; P = 1.26e − 8). Sensitivity analysis confirmed the robustness of these results. Conclusion Here, we identified a latent causal relationship between the BMR and the risk of OA. These results suggest that the risk of OA in the hip or knee joint may be reduced by controlling the BMR.
Title: The association between basal metabolic rate and osteoarthritis: a Mendelian randomization study
Description:
Abstract Background The role of the basal metabolic rate (BMR) in osteoarthritis (OA) remains unclear, as previous retrospective studies have produced inconsistent results.
Therefore, we performed a Mendelian randomization (MR) study to systematically investigate the causal relationship between the BMR and OA.
Methods Single-nucleotide polymorphism (SNP) data related to BMR and OA were collected in a genome-wide association study.
Using OA as the outcome variable and BMR as the exposure factor, SNPs with strong correlation with the BMR as the tool variable were screened.
The correlation between the BMR and OA risk was evaluated using the inverse-variance weighted method, and heterogeneity and pleiotropy were evaluated using a sensitivity analysis.
Results There was a potential causal relationship between the BMR and OA risk (odds ratio [OR], 1.
014; 95% confidence interval [CI], 1.
008–1.
020; P = 2.
29e − 6).
A causal relationship was also revealed between the BMR and knee OA (OR, 1.
876; 95% CI, 1.
677–2.
098; P = 2.
98e − 28) and hip OA (OR, 1.
475; 95% CI, 1.
290–1.
686; P = 1.
26e − 8).
Sensitivity analysis confirmed the robustness of these results.
Conclusion Here, we identified a latent causal relationship between the BMR and the risk of OA.
These results suggest that the risk of OA in the hip or knee joint may be reduced by controlling the BMR.

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