Causal Associations Between Lifestyle Habits and Risk of Benign Prostatic Hyperplasia: A Two-Sample Mendelian Randomization Study

J Gerontol A Biol Sci Med Sci. 2024 Jan 1;79(1):glad187. doi: 10.1093/gerona/glad187.

Abstract

Background: Benign prostatic hyperplasia (BPH) most often occurs in older men; previous studies and clinical experience suggest a potential link between lifestyle habits such as sleep habits, sedentary behavior, exercise levels, and BPH, but whether they have a clear causal relationship and the direction of that causality is unclear. We aimed to investigate the causal relationship between lifestyle habits and BPH using 2-sample Mendelian randomization (MR) analysis.

Methods: Instrumental genetic independent variables strongly associated with the selected exposure factors were filtered from published genome-wide association studies (GWAS) consisting primarily of European ancestry samples. GWAS from BPH was analyzed as an MR outcome with the inverse-variance weighted method, maximum likelihood, weighted median method, MR-Egger regression, and several sensitivity analyses, including Cochran's Q test, intercept of MR-Egger, and MR pleiotropy residual sum and outlier test.

Results: MR analysis showed a significant causal risk relationship between sleep duration and BPH, with an odds ratio of 0.42 (95% confidence interval, 0.25-0.69, p = .001) for BPH when sleep duration was increased by 1 standard deviation, but we did not find a causal relationship between the 2 when we performed a reverse analysis. However, sedentary behavior and different levels of exercise did not significantly affect the risk of BPH.

Conclusions: This study showed a strong causal relationship between sleep levels and BPH, with adequate sleep duration being a protective factor for BPH.

Keywords: Benign prostatic hyperplasia; Exercise; Mendelian randomization; Sedentary; Sleep.

MeSH terms

  • Aged
  • Genome-Wide Association Study
  • Habits
  • Humans
  • Life Style
  • Male
  • Mendelian Randomization Analysis
  • Prostatic Hyperplasia* / genetics