Recent systematic reviews and meta-analyses, along with literature evaluations, report an inverse association indicating that higher ejaculation frequency is significantly correlated with a reduced risk of prostate cancer.
Prostate cancer (PCa) accounts for roughly 15% of diagnosed cancers among men, with disease incidence increasing worldwide. Age, family history and ethnicity, diet, physical activity, and chemoprevention all play a role in reducing PCa risk. The prostate is an exocrine gland that is characterized by its multi-functionality, being involved in reproductive aspects such as male ejaculation and orgasmic ecstasy, as well as playing key roles in the regulation of local and systemic concentrations of 5α-dihydrotestosterone. The increase in androgen receptors at the ventral prostate is the first elevated response induced by copulation. The regulation of prostate growth and function is mediated by an androgen-dependent mechanism. Binding 5-DHT to androgen receptors (AR) results in the formation of a 5α-DHT:AR complex. The interaction of the 5α-DHT:AR complex with the specific DNA enhancer element of androgen-regulated genes leads to the regulation of androgen-specific target genes to maintain prostate homeostasis. Consequently, ejaculation may play a significant role in the reduction of PCa risk. Thus, frequent ejaculation in the absence of risky sexual behavior is a possible approach for the prevention of PCa. In this review, we provide an insight into possible mechanisms regulating the impact of frequent ejaculation on reducing PCa risk.
Prostate cancer, constituting a substantial portion of global cancer incidence and mortality, prompts a critical examination of potential modifiers, notably ejaculation frequency. This narrative review explores the complex relationship between ejaculation frequency and prostate cancer risk, addressing the paucity of consensus and the intricate interplay of factors. The evidence drawn from eleven studies with diverse methodologies reveals a complex understanding of this association. While some studies suggest an inverse correlation between ejaculation frequency and prostate cancer risk, signifying a potential protective effect, others present conflicting findings, necessitating a comprehensive exploration. Evidence synthesis underscores the importance of considering age, urinary health, and lifestyle factors in elucidating the ejaculation frequency-prostate cancer relationship. Notably, technological advancements, including machine learning models and genetic markers, enhance the precision of patient counselling and individualized care. In a clinical context, the findings emphasize the clinical relevance of incorporating sexual behavior into preventive strategies. Public health campaigns emerge as influential tools, breaking taboos, raising awareness, and empowering men to prioritize their well-being. The paradigm shift in prostate cancer understanding, fueled by technology and personalized medicine, holds promise for more accurate risk assessments. Liquid biopsies, multiparametric MRI, and considerations of the gut microbiome present avenues for tailored preventive strategies. However, methodological challenges and study variations necessitate further research, emphasizing consistency, exploring underlying mechanisms, and a life course perspective.
This systematic review and meta-analysis aimed to update the evidence on how sexual activity factors, including frequency of intercourse, number of female sexual partners, age at first intercourse, and number of ejaculations and masturbations relate to prostate cancer. We conducted a comprehensive search across PubMed, Web of Science, and Scopus up to October 19, 2025. We also reviewed existing study references for additional relevant research. To assess study consistency, we used I2 statistics. Publication bias was evaluated using Begg and Egger tests. Our analysis reported pooled odds ratios (OR) with 95% confidence intervals using a random-effects model. The research protocol was approved by PROSPERO, ID CRD42024549018. From 5,311 identified studies, 29 (315,193 participants) met the inclusion criteria. Positive but non-significant associations were observed between prostate cancer and more frequent sexual intercourse (OR = 1.02; 95% CI: 0.88, 1.18), a higher number of female partners (OR = 1.01; 95% CI: 0.90, 1.12), and masturbation frequency (OR = 1.12; 95% CI: 0.82, 1.54). Older age at first intercourse showed a negative but non-significant association (OR = 0.99; 95% CI: 0.90, 1.08), whereas higher ejaculation frequency demonstrated a significant protective effect (OR = 0.83; 95% CI: 0.77, 0.90). These findings suggest that most sexual behaviors are not significantly associated with prostate cancer risk. However, higher ejaculation frequency appears to have a protective effect. The results highlight the multifactorial nature of prostate cancer and emphasize the need for further research to clarify the role of sexual activity in disease prevention.
prostate epithelial cell division [ 310 , 339 ]. Of note, if the ejaculation frequency impacts gene expression in the prostate tissue, then gene expression can influence tissue susceptibility to tumorigenesis and provide insight into the mechanisms whereby ejaculation affects PCa risk.
Due to the difficulty in establishing a connection between frequent ejaculation and gene expression patterns of prostate tissues in the context of health status and other lifestyle factors [ 354 , 355 , 356 ], more research is needed to uncover why frequent ejaculation may protect men from PCa. While a differential gene expression analysis in prostate tissue in the context of frequent ejaculation demonstrated some limitations [ 357 , 358 ], the analysis of differential gene expression profile and pathways in prostate tumor areas and in the adjacent normal tissues in the context of frequent ejaculation revealed that the identified genes and pathways serve as potential biological links between the frequency of ejaculation and prostate tumorigenesis [ 355 ]. Thus, the investigation of the biological basis of frequent ejaculations leading to the reduction of PCa risk may help develop a management protocol for the prevention or the reduction of PCa occurrence in men [ 354 , 355 ].
In addition to the prostate stagnation hypothesis [ 359 , 360 ], several mechanisms have been proposed to explain an inverse association between ejaculation frequency and PCa. The greater the frequency of ejaculation, the more the function of epithelial cells in the peripheral zone is impaired, thereby hindering the metabolic switch from citrate secretion to citrate oxidation, thus leading to the delay of tumor initiation in the prostate [ 354 , 358 ]. Alternatively, frequent ejaculation may reduce the development of intraluminal crystalloids in the prostate, which are associated with a higher risk of PCa tumorigenesis [ 354 , 355 ]. A higher ejaculation frequency may be associated with a reduction in psychologi
There is considerable evidence to suggest that frequent ejaculation reduces the risk of prostate cancer. The more frequently ejaculation occurs without risky sexual behavior, the lower the risk of prostate cancer. The mechanisms regulating the reduction in PCa risk associated with frequent ejaculations are attributed to the suppression of the sympathetic nervous system, resulting in a relief of tension and a slowing of the division of prostate epithelial cells. It is suggested that ejaculation frequency affects gene expression in prostate tissue and subsequently influences the susceptibility o
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