The prevalence of benign prostatic hyperplasia is intrinsically linked with the aging process, establishing it as one of the most common clinical conditions in older men. The histological evidence of BPH is remarkably common in autopsy studies, with a prevalence of 50% to 60% for men in their 60s, which escalates to as high as 80% to 90% in men older than 70 years [1]. The clinical manifestation of BPH, often presenting as lower urinary tract symptoms (LUTS), also shows a clear age-dependent increase. Epidemiological data indicates a prevalence of approximately 8% to 10% in men aged 40 and older. This figure rises substantially with age, affecting about 50% of men between the ages of 51 and 60, 70% of men aged 60 to 69, and around 80% of men over the age of 70 [5, 6].
The etiology of BPH is multifactorial, involving a complex interplay of non-modifiable and modifiable risk factors that contribute to its development and progression. Understanding these factors is essential for both patient counseling and the development of potential preventive strategies.
Risk Factors for BPH
The risk factors for BPH can be broadly categorized as non-modifiable and modifiable, as detailed in the table below.
| Category | Risk Factor | Description |
|---|---|---|
| Non-Modifiable | Age | The most significant and well-established risk factor. The incidence and prevalence of BPH increase markedly with advancing age. |
| Genetics | A strong familial predisposition has been demonstrated. Studies have shown that first-degree relatives of men with BPH have a four-fold increased risk of developing the condition [7]. | |
| Geography/Ethnicity | Geographic and ethnic variations in BPH prevalence have been reported, suggesting a role for genetic and environmental influences. | |
| Modifiable | Obesity & Metabolic Syndrome | Observational studies have consistently linked obesity and components of the metabolic syndrome with an increased risk of BPH. Proposed mechanisms include increased systemic inflammation and higher levels of circulating estrogens [8]. |
| Diabetes Mellitus | Diabetes, particularly when requiring insulin, appears to increase the risk of developing BPH, LUTS, and the likelihood of needing surgical intervention [9]. | |
| Dietary Factors | Certain dietary habits may influence BPH risk. High intake of alcohol, caffeine, and supplemental vitamin C has been associated with an increased risk, whereas diets rich in beta-carotene, carotenoids, and vitamin A may be protective [10]. | |
| Inflammation | Chronic inflammation within the prostate is often found in histological specimens of BPH. While the exact cause is unclear, it is thought to contribute to the proliferative process. The use of non-steroidal anti-inflammatory drugs (NSAIDs) has shown a modest benefit in improving BPH symptoms [11]. | |
| Physical Activity | A sedentary lifestyle is associated with a higher risk of BPH, while regular physical activity may have a protective effect. |
References
[5] Mathey, L. I. P. (2022). Benign Prostatic Hyperplasia: Epidemiology, Pathophysiology and Clinical Manifestations. IntechOpen. Available from: https://www.intechopen.com/chapters/81872
[6] Enlarged Prostate (Benign Prostatic Hyperplasia). (n.d.). Yale Medicine. Retrieved from: https://www.yalemedicine.org/conditions/enlarged-prostate-benign-prostatic-hyperplasia-bph
[7] Sanda, M. G., Beaty, T. H., Stutzman, R. E., Childs, B., & Walsh, P. C. (1994). Genetic susceptibility of benign prostatic hyperplasia. The Journal of urology, 152(1), 115–119.
[8] Parsons, J. K. (2007). Benign Prostatic Hyperplasia and Male Lower Urinary Tract Symptoms: Epidemiology and Risk Factors. Current Bladder Dysfunction Reports. Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC3989819/
[9] Ng, M., Leslie, S. W., & Baradhi, K. M. (2024). Benign Prostatic Hyperplasia. In StatPearls. StatPearls Publishing. Available from: https://www.ncbi.nlm.nih.gov/books/NBK558920/
[10] Maserejian, N. N., Giovannucci, E. L., & McKinlay, J. B. (2011). Dietary, but not supplemental, vitamin C is associated with decreased risk of benign prostatic hyperplasia. The Journal of urology, 185(4), 1387–1393.
[11] Kahokehr, A., & Gilling, P. J. (2011). The role of inflammation in benign prostatic hyperplasia. Therapeutic advances in urology, 3(4), 181–186.