Background <p>Observational studies have suggested strong correlations between obesity (as measured by body mass index [BMI]), lifestyle factors such as smoking, alcohol consumption, coffee intake, and insomnia, and dilated cardiomyopathy (DCM). However, the causal relationship between these factors and DCM remains unclear.</p> Methods <p>A two-sample Mendelian randomization analysis was performed to evaluate these associations. Genetic instruments significantly associated exposures (including BMI, smoking, alcohol consumption, coffee intake, and insomnia) at the genome-wide significance threshold (<i>p</i> &lt; 5 × 10⁻⁸) were selected from relevant genome-wide association studies. Summary-level data for DCM were obtained from the IEU Open GWAS project, comprising 1,444 cases and 353,937 controls.</p> Results <p>Genetically predicted BMI was positively associated with DCM (odds ratio [OR] per one standard deviation (SD) increase, 1.68; 95% confidence interval [CI], 1.4–2.1; <i>p</i> = 6.44 × 10<sup>− 7</sup>). The OR for DCM was 31.86 (95% CI, 3.95–257.27; <i>p</i> = 0.001) for one SD increase in smoking. However, genetically predicted alcohol consumption, coffee intake, and insomnia were not significantly associated with the risk of DCM in our primary analysis.</p> Conclusion <p>Our findings suggest the potential causal links among BMI, smoking, and DCM, underscoring the importance of lifestyle interventions in managing DCM. This study also provides a foundation for future research aimed at identifying individuals highly at risk for DCM.</p>

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Adiposity, Lifestyle Factors, and Dilated Cardiomyopathy: A Two-Sample Mendelian Randomization Study

  • Zonghan Zhao,
  • Mianxian Li,
  • Juan Li,
  • Fuhua Lei

摘要

Background

Observational studies have suggested strong correlations between obesity (as measured by body mass index [BMI]), lifestyle factors such as smoking, alcohol consumption, coffee intake, and insomnia, and dilated cardiomyopathy (DCM). However, the causal relationship between these factors and DCM remains unclear.

Methods

A two-sample Mendelian randomization analysis was performed to evaluate these associations. Genetic instruments significantly associated exposures (including BMI, smoking, alcohol consumption, coffee intake, and insomnia) at the genome-wide significance threshold (p < 5 × 10⁻⁸) were selected from relevant genome-wide association studies. Summary-level data for DCM were obtained from the IEU Open GWAS project, comprising 1,444 cases and 353,937 controls.

Results

Genetically predicted BMI was positively associated with DCM (odds ratio [OR] per one standard deviation (SD) increase, 1.68; 95% confidence interval [CI], 1.4–2.1; p = 6.44 × 10− 7). The OR for DCM was 31.86 (95% CI, 3.95–257.27; p = 0.001) for one SD increase in smoking. However, genetically predicted alcohol consumption, coffee intake, and insomnia were not significantly associated with the risk of DCM in our primary analysis.

Conclusion

Our findings suggest the potential causal links among BMI, smoking, and DCM, underscoring the importance of lifestyle interventions in managing DCM. This study also provides a foundation for future research aimed at identifying individuals highly at risk for DCM.