What are the main risk factors for prostate cancer in men?
Executive summary
The principal, well-established risk factors for prostate cancer are advancing age, race/ethnicity (notably higher risk in men of African descent), and a family history or inherited genetic mutations; these three are repeatedly identified by major reviews and public-health bodies as the core drivers of risk [1] [2] [3]. A second tier of modifiers—obesity/metabolic factors, certain occupational or environmental exposures, and lifestyle and dietary elements—have mixed or growing evidence and appear to affect incidence, aggressiveness, or progression rather than being uniformly causal [4] [5] [6].
1. Age: the dominant, unavoidable risk
Age is the single strongest predictor: prostate cancer incidence rises sharply after about age 55 and peaks in the seventh decade of life, with most diagnoses occurring in men over 65, making age an incontrovertible baseline risk that every man faces as he grows older [1] [7].
2. Race and ethnicity: disparities with biological and structural components
Men of African ancestry have a substantially higher risk of prostate cancer and of dying from it compared with white men; studies and public-health summaries note roughly 60% higher risk in African Americans in some cohorts and earlier onset and more advanced disease at diagnosis in these groups, while Asian and Hispanic men generally show lower rates—findings that reflect a mix of genetic susceptibility, tumor biology, and social determinants of health [1] [2] [8].
3. Family history and inherited genes: doubling or more of risk
Having a first‑degree relative with prostate cancer — especially a father or brother — roughly doubles to triples a man’s risk, and specific inherited syndromes (for example Lynch syndrome) and rare high-penetrance gene variants account for a minority but clinically significant share of cases; expert sources emphasize that most prostate cancers still occur in men without a family history, but heredity remains an important stratifier for screening decisions [3] [9] [10].
4. Obesity and metabolic/hormonal factors: modifiers of aggressive disease
Obesity and related metabolic changes — higher insulin, IGF‑1, leptin and adiposity‑related hormonal shifts — are associated not consistently with incidence but more reliably with higher risk of advanced or fatal prostate cancer in several cohort analyses, suggesting these factors influence progression or aggressiveness rather than initiation in all cases [4] [6] [5].
5. Diet, lifestyle and physical activity: inconclusive but plausible effects
Dietary elements (calcium supplements, high α‑linolenic acid in some studies), low consumption of certain vegetables or tomato products, alcohol and physical activity have produced inconsistent results across studies; major organizations note that while lifestyle may influence risk and progression, clear causal dietary prescriptions are not firmly established and require cautious interpretation [3] [6] [11].
6. Environmental and occupational exposures: signals that need confirmation
Some international research links high pesticide exposure and certain occupational hazards (eg, firefighters, veterans in some analyses) to increased prostate cancer risk, but the evidence varies by exposure level and study design; these remain important hypotheses for targeted research and workplace policy, not definitive universal causes [5] [9].
7. Infections, inflammation, hormones and other biological hypotheses
Reviews highlight inflammation, prior infections of the prostate, hormonal milieu (testosterone and estrogen balance), and early‑life growth factors (eg, adolescent IGF‑1 and adult height correlations) as plausible contributors to carcinogenesis or progression; however, mechanisms are heterogeneous and findings differ by tumor grade, so these remain active areas of research rather than settled risk factors [11] [6] [4].
8. What is not supported or remains uncertain
Some previously raised links—such as a causal link between vasectomy and prostate cancer—have not been confirmed in recent analyses, and many associations (dietary items, multivitamins, coffee) show inconsistent or small effects; major reviews therefore restrict “established” status to age, race/ethnicity and family history while treating others as modifiers or research leads [5] [1] [3].
Limitations of this synthesis include heterogeneous study designs and the longstanding latent period of prostate cancer, which complicates teasing out initiation versus progression effects; where source coverage is incomplete, definitive statements were avoided and gaps flagged for further study [6] [1].