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. 2024 Apr 20;24(1):91.
doi: 10.1186/s12894-024-01474-z.

Mendelian randomization study supports positive bidirectional causal relationships between genetically predicted insomnia symptom and liability to benign prostatic hyperplasia

Nannan Li  1   2 , Ke Yang  1   2 , Liang Deng  1   2 , Youjie Zeng  3 , Si Cao  4 , Dong Chen  5   6
Affiliations

Mendelian randomization study supports positive bidirectional causal relationships between genetically predicted insomnia symptom and liability to benign prostatic hyperplasia

Nannan Li et al. BMC Urol. .

Abstract

Background: Sleep quality may be related to benign prostatic hyperplasia (BPH), however causal associations have not been established. This study aimed to evaluate causal relationships between six sleep traits ([i] day time napping, [ii] daytime sleepiness, [iii] insomnia, [iv] long sleep duration, [v] short sleep duration, and [vi] sleep duration per hour) and BPH through a bidirectional Mendelian randomization (MR) study.

Methods: Genome-wide association summary statistics of sleep traits and BPH were downloaded from public databases. Inverse variance weighting (IVW) was used as the main approach for causal inference. For causal estimates identified by IVW, various sensitivity analyses were performed to assess the reliability of the results: (i) four additional MR methods to complement IVW; (ii) Cochran's Q test to assess heterogeneity; (iii) MR-Egger intercept test and MR-PRESSO global test to assess horizontal pleiotropy; and (iv) leave-one-out method to assess stability.

Results: Forward MR analyses indicated that genetically predicted insomnia symptom significantly increased BPH risk (OR = 1.267, 95% CI: 1.003-1.601, P = 0.048), while reverse MR analyses identified that genetically predicted liability to BPH significantly increased the incidence of insomnia (OR = 1.026, 95% CI: 1.000-1.052, P = 0.048). In a replicate MR analysis based on summary statistics including exclusively male participants, the finding of increased risk of BPH due to genetically predicted insomnia symptom was further validated (OR = 1.488, 95% CI: 1.096-2.022, P = 0.011). No further causal links were identified. In addition, sensitivity tests demonstrated the reliability of the MR results.

Conclusion: This study identified that a higher prevalence of genetically predicted insomnia symptoms may significantly increase the risk of BPH, while genetically predicted liability to BPH may in turn increase the incidence of insomnia symptom. Therefore, improving sleep quality and reducing the risk of insomnia could be a crucial approach for the prevention of BPH.

Keywords: Incidence risk; Insomnia; Mendelian randomization; Prostatic Hyperplasia; Risk factors.

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Conflict of interest statement

The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
General flowchart of this MR study
Fig. 2
Fig. 2
MR results identified by the IVW approach. (A) Forward MR analysis by IVW to assess the causal effects of six sleep traits on BPH. (B) Reverse MR analysis by IVW to assess the causal effects of BPH on six sleep traits
Fig. 3
Fig. 3
Assessment of the stability of MR results by leave-one-out sensitivity test. (A) MR leave − one − out sensitivity analysis for insomnia on BPH in forward MR analysis. (B) MR leave − one − out sensitivity analysis for BPH on insomnia in reverse MR analysis
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