Association Between Metabolic Syndrome and Prostate Cancer: A Systematic Review

Background/Objectives: Metabolic syndrome is a prevalent global health concern characterized by central obesity, insulin resistance, hypertension, and dyslipidemia. Growing evidence suggests that metabolic dysregulation may influence prostate cancer risk and disease behavior; however, findings across studies remain inconsistent. This systematic review aimed to evaluate the association between metabolic syndrome and prostate cancer risk, clinicopathologic characteristics, and disease outcomes. Methods: A systematic literature search was conducted in PubMed/MEDLINE from database inception through the final search update on 10 January 2026, with supplementary searches of Google Scholar, Wiley Online Library, the Clinical Oncology journal collection, and reference lists. Observational studies assessing the relationship between metabolic syndrome and prostate cancer outcomes were eligible for inclusion. Two reviewers independently screened titles and abstracts, followed by full text review to determine eligibility. Discrepancies were resolved through consensus. Risk of bias was assessed using design-specific tools, including the Newcastle–Ottawa Scale, Cochrane Risk of Bias 2 tool, and Joanna Briggs Institute checklist. Findings were synthesized narratively because of heterogeneity in study design, metabolic syndrome definitions, populations, outcomes, and effect estimates. Results: A total of 1304 records were identified across all databases. After duplicate assessment, records underwent title and abstract screening, followed by full text assessment. Twenty-four studies, ranging from small clinic-based cohorts to large population-based cohorts exceeding 5 million participants, met the inclusion criteria and were included in the qualitative synthesis. Most studies were cohort or case–control designs conducted in North America, Europe, and Asia. Overall, evidence for a uniform association between composite metabolic syndrome and prostate cancer incidence was inconsistent. Associations appeared more suggestive for clinically significant, high-grade, or adverse pathological features, although findings varied by study design, metabolic syndrome definition, detection context, and adjustment level. Several studies suggested that individual components of metabolic syndrome, particularly obesity and insulin resistance, may be key drivers of these associations. Conclusions: Available evidence suggests a heterogeneous relationship between metabolic syndrome, related metabolic abnormalities, and prostate cancer outcomes. Evidence for a uniform association with overall prostate cancer incidence was inconsistent, whereas signals were more frequently reported for clinically significant, high-grade, or adverse pathological features. However, these findings should be interpreted cautiously because of observational study designs, heterogeneous MetS definitions, detection context, and variable adjustment. Further well-designed prospective studies are needed to clarify temporality, causal pathways, and the contributions of individual metabolic components.