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Published on: November 2, 2013
Clinical biomarker-based biological aging and risk of benign prostatic hyperplasia: A large prospective cohort study
Qiao Huang1,2, Bing-Hui Li1,2, Yong-Bo Wang1,2
1Center for Evidence-Based and Translational Medicine Zhongnan Hospital of Wuhan University Wuhan China.
Insights
Biological aging, not just chronological age, is a significant risk factor for benign prostatic hyperplasia (BPH). Interventions to slow biological aging may reduce BPH risk and progression.
Area of Science:
- Gerontology and Urology
- Biomarker Discovery
- Epidemiology
Background:
- Chronological age (CAge) is a known risk factor for benign prostatic hyperplasia (BPH).
- Evidence linking biological age (BAge) and accelerated aging (AAge) to BPH is limited.
- Understanding aging's impact on BPH is crucial for disease management.
Purpose of the Study:
- To investigate the association of CAge, BAge, and AAge with incident BPH risk.
- To evaluate multiple BAge and AAge measures in a large prospective cohort.
- To determine if accelerated aging is an independent risk factor for BPH.
Main Methods:
- Utilized UK Biobank data from 135,933 males without BPH at baseline.
- Calculated three BAge measures (KDM, PhenoAge, HD) and two AAge measures (KDM-AAge, PhenoAge-AAge).
- Employed Cox proportional hazard models to analyze associations with incident BPH over a median follow-up of 13.15 years.
Main Results:
- Both advanced CAge and BAge measures were associated with increased BPH risk, exhibiting threshold effects.
- Nonlinear relationships were observed between AAge measures and BPH risk.
- Accelerated aging (AAge > 2 SD) significantly elevated BPH risk (HR 1.115-1.180), particularly in younger males (<50 years) and those with lower testosterone levels.
Conclusions:
- Biological aging is an independent and modifiable risk factor for BPH.
- Slowing biological aging through health interventions could mitigate prostate aging and reduce BPH burden.
- This study highlights the importance of assessing biological aging in BPH risk stratification.
Objective:
Chronological age (CAge), biological age (BAge), and accelerated age (AAge) are all important for aging-related diseases. CAge is a known risk factor for benign prostatic hyperplasia (BPH); However, the evidence of association of BAge and AAge with BPH is limited. This study aimed to evaluate the association of CAge, Bage, and AAge with BPH in a large prospective cohort.
Method:
A total of 135,933 males without BPH at enrolment were extracted from the UK biobank. We calculated three BAge measures (Klemera-Doubal method, KDM; PhenoAge; homeostatic dysregulation, HD) based on 16 biomarkers. Additionally, we calculated KDM-BAge and PhenoAge-BAge measures based on the Levine method. The KDM-AAge and PhenoAge-AAge were assessed by the difference between CAge and BAge and were standardized (mean = 0 and standard deviation [SD] = 1). Cox proportional hazard models were applied to assess the associations of CAge, Bage, and AAge with incident BPH risk.
Results:
During a median follow-up of 13.150 years, 11,811 (8.690%) incident BPH were identified. Advanced CAge and BAge measures were associated with an increased risk of BPH, showing threshold effects at a later age (all P for nonlinearity <0.001). Nonlinear relationships between AAge measures and risk of BPH were also found for KDM-AAge (P = 0.041) and PhenoAge-AAge (P = 0.020). Compared to the balance comparison group (-1 SD < AAge < 1 SD), the accelerated aging group (AAge > 2 SD) had a significantly elevated BPH risk with hazard ratio (HR) of 1.115 (95% CI, 1.000-1.223) for KDM-AAge and 1.180 (95% CI, 1.068-1.303) for PhenoAge-AAge, respectively. For PhenoAge-AAge, subgroup analysis of the accelerated aging group showed an increased HR of 1.904 (95% CI, 1.374-2.639) in males with CAge <50 years and 1.233 (95% CI, 1.088-1.397) in those having testosterone levels <12 nmol/L. Moreover, AAge-associated risk of BPH was independent of and additive to genetic risk.
Conclusions:
Biological aging is an independent and modifiable risk factor for BPH. We suggest performing active health interventions to slow biological aging, which will help mitigate the progression of prostate aging and further reduce the burden of BPH.
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