ArticleSexual medicine2024
Association of serum uric acid with male sexual hormones and erectile dysfunction: a bidirectional 2-sample Mendelian randomization analysis.
Article in Sexual medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- The importance of ALPK1 kinase functionality as a potential biomarker for inflammatory diseases.Molecular biology reports · 2025Review
- Association between uric acid/high-density lipoprotein cholesterol ratio and testosterone deficiency in adult American men: findings from the national health and nutrition examination survey 2011-2016.BMC public health · 2025Article
- Sex differences in the association between the uric acid to high density lipoprotein cholesterol ratio and mild cognitive impairment in patients with type 2 diabetes mellitus.Frontiers in nutrition · 2025Article
- Commentary: Risk factors for mild cognitive impairment in type 2 diabetes: a systematic review and meta-analysis.Frontiers in endocrinology · 2025Article
- Comparison of different insulin resistance surrogates in predicting hyperuricemia in non-diabetic Yi residents in Yunnan Province.Frontiers in endocrinology · 2025Article
- Geneticsbiologiesingle cell and expression analysis for erectile dysfunction and cervical cancer targets.Discover oncology · 2024Article
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Authors and funding
6 authors.
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Abstract
Background: Observational studies indicated that serum uric acid (SUA) was associated with male sexual hormones and erectile dysfunction (ED). However, their relationship was still heterogeneous. Aim: This study conducted 2-sample univariate mendelian randomization (UVMR) and multivariate mendelian randomization (MVMR) to explore the causal relationship between SUA and sexual hormones as well as ED. Methods: Genetic variants associated with SUA were derived from the UK Biobank database (N = 437 354). Outcomes from the IEU Open GWAS and summary data sets were sexual hormones (sex hormone-binding globulin [SHBG], testosterone, estradiol [E2], follicle-stimulating hormone, luteinizing hormone) and ED, with 3301 to 625 650 participants. UVMR analysis primarily utilized the inverse variance weighted method, complemented by MVMR analysis. Thorough sensitivity analyses were carried out to ensure the reliability of results. Moreover, mediation analysis was conducted to estimate the mediated effect between SUA and outcomes. Outcomes: The primary outcomes included results of UVMR and MVMR analysis and mediation analysis, along with sensitivity analyses involving the Cochran Results: UVMR analysis revealed that an elevated SUA level could decrease levels of SHBG (β = -0.10, Clinical Implications: Given the causal relationship between SUA and sexual hormones, we must focus on SUA and E2 levels in men, especially patients with hypogonadism and ED. Strengths and Limitations: This study evaluated the causal effect of SUA on male sexual hormones and ED genetically for the first time, clarifying the common biases in observational studies and confirming the negative relationship between SUA and testosterone level. Limitations include a population based on European ancestry, some crossover of the samples, and unobserved confounding factors. Conclusion: Genetic studies provide evidence for the causal relationship between SUA and male sexual hormones (SHBG, testosterone, E2), while the relationship between SUA and ED should be further evaluated.
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