Association of biological aging with prostate cancer: insights from the National Health and Nutrition Examination Survey

The link between biological aging and prostate cancer (PCa) risk, particularly as indicated by elevated prostate-specific antigen (PSA) levels, remains uncertain. This study utilized data from the National Health and Nutrition Examination Survey (2001-2010) to explore this association. Biological age was assessed using Klemera-Doubal method age (KDMAge) and phenotypic age (PhenoAge). PCa was identified through self-reported diagnoses, and highly probable PCa was determined by PSA levels. We analyzed the prevalence of PCa and PSA-defined highly probable PCa across quartiles of biological age measures using weighted chi-square and linear trend tests. Associations were evaluated using weighted multiple logistic regression models. Among 7,209 and 6,682 males analyzed, the overall weighted prevalence of PCa was 2.86%, increasing to 9.60% in those aged 65 and above. A significant rise in PCa prevalence was observed with higher quartiles of KDMAge or PhenoAge (P for trend < 0.001), particularly in those under 65. In this younger group, higher PhenoAge acceleration quartiles were linked to increased PCa prevalence and higher risk of PCa (OR = 1.50, P = 0.015) as well as highly probable PCa in those without a diagnosis (OR = 1.28, P = 0.031). These findings suggest that accelerated biological aging is associated with an increased risk of PCa and may indicate early risk as signaled by PSA levels, even in those without a PCa diagnosis.

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Publication Details

Journal
Aging Clinical and Experimental Research
Published
2024-10-24
DOI
https://doi.org/10.1007/s40520-024-02861-0
Citations
5
Primary Topic
Prostate Cancer Treatment and Research
Type
article
Field-Weighted Citation Impact
2.09

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Association of biological aging with prostate cancer: insights from the National Health and Nutrition Examination Survey

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Aging Clinical and Experimental Research
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article

Association of biological aging with prostate cancer: insights from the National Health and Nutrition Examination Survey

Chengxin Xie, Byeng-Chun Song, Chengling Yu, Zejun Yan, Junhui Jiang, Weiqi Yin
article en
5 citations

Abstract

The link between biological aging and prostate cancer (PCa) risk, particularly as indicated by elevated prostate-specific antigen (PSA) levels, remains uncertain. This study utilized data from the National Health and Nutrition Examination Survey (2001-2010) to explore this association. Biological age was assessed using Klemera-Doubal method age (KDMAge) and phenotypic age (PhenoAge). PCa was identified through self-reported diagnoses, and highly probable PCa was determined by PSA levels. We analyzed the prevalence of PCa and PSA-defined highly probable PCa across quartiles of biological age measures using weighted chi-square and linear trend tests. Associations were evaluated using weighted multiple logistic regression models. Among 7,209 and 6,682 males analyzed, the overall weighted prevalence of PCa was 2.86%, increasing to 9.60% in those aged 65 and above. A significant rise in PCa prevalence was observed with higher quartiles of KDMAge or PhenoAge (P for trend < 0.001), particularly in those under 65. In this younger group, higher PhenoAge acceleration quartiles were linked to increased PCa prevalence and higher risk of PCa (OR = 1.50, P = 0.015) as well as highly probable PCa in those without a diagnosis (OR = 1.28, P = 0.031). These findings suggest that accelerated biological aging is associated with an increased risk of PCa and may indicate early risk as signaled by PSA levels, even in those without a PCa diagnosis.

Aging Clinical and Experimental ResearchVol. 36(1)
Ningbo University (CN), Wenzhou Medical University (CN), Ningbo University of Finance & Economics (CN), Zhejiang Lab (CN), Ningbo University Affiliated Hospital (CN), Zhejiang Taizhou Hospital (CN), Ningbo First Hospital (CN), Taizhou University (CN)
Science and Technology Program of Zhejiang Province
Zero hunger
Openalex Percentile: Top 12%
Prostate Cancer Treatment and Research
2.09
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