Overview and Risk Factors
Benign prostatic hyperplasia (BPH) is the most common benign neoplasm of men. The stromal and, to a lesser degree, epithelial cells of the prostate become hyperplastic, causing the prostate to enlarge. The prevalence of BPH increases with age, rising from 8% in the third decade of life, to 40% to 50% in the fifth decade, to greater than 90% in the ninth decade. The etiology is multifactorial and not well understood. Testosterone and dihydrotestosterone, while necessary for BPH to occur, are not alone adequate to cause the condition. Research findings are unclear as to a possible pathogenic role of estrogen. Symptoms are related to obstruction of the urethra and include hesitancy, reduced urine flow rate, dribbling, urgency, frequency, and nocturia.
The following factors are associated with increased risk of BPH:
Aging. BPH occurs more commonly with advancing age.
Family history. Data suggest a genetic link with an autosomal dominant pattern.1
Androgen. Higher androgen levels are associated with BPH.
Obesity. Excessive overweight may make detection more difficult via digital rectal examination (DRE). In addition, obesity, particularly abdominal obesity, may increase risk for BPH, presumably due to resultant hyperinsulinemia.2,3 Elevated levels of estrogens secondary to conversion from testosterone in adipose tissues may also play a role.
Physical inactivity. The Health Professionals Study and Massachusetts Male Aging Study found lower levels of physical activity to be associated with increased risk for BPH.4,5
Diagnosis and Treatment
A DRE will typically detect prostate enlargement. The surface of the prostate should be smooth and is usually symmetrical; induration suggests malignancy. Prostate biopsy, ultrasound, and/or the prostate-specific antigen (PSA) blood test help rule out malignancy and confirm a diagnosis of BPH. Other tests are available to evaluate bladder and urethral function.
The purpose of BPH treatment is to improve the patient’s quality of life.
Observation alone(“watchful waiting”) is appropriate if symptoms are mild.
Medical treatment includes use of alpha-adrenergic antagonists, such as, prazosin, terazosin, doxazosin, tamsulosin, and alfuzosin, which relax smooth muscle. Tamsulosin and alfuzosin cause fewer adverse side effects than other medications.6 When moderate or greater prostate enlargement exists, administration of 5-alpha-reductase inhibitors, such as finasteride, blocks the conversion of testosterone to dihydrotestosterone. A combination of an alpha-adrenergic antagonist and finasteride appears to improve long-term outcomes.7
Plant extracts from saw palmetto (Serenoa repens), the American dwarf palm, and Pygeum africanum (an African plum tree) have shown efficacy in treating symptoms, although their mechanism(s) of action is not yet clear.8,9
Surgical options for severe symptoms include transurethral resection of the prostate (TURP), transurethral incision of the prostate, “open” prostatectomy, laser photoselective vaporization, interstitial laser therapy, microwave therapy, radiofrequency therapy, and intraurethral stenting, among others.
Research studies have examined the relationship between dietary factors and the risk of BPH. The following factors are associated with reduced risk in epidemiologic studies:
Limiting or avoiding animal products and vegetable oils. Several studies have implicated high total meat and animal product intake in BPH, particularly beef and dairy products.10-13 The Health Professionals Follow-Up Study found that higher intakes of total protein, animal protein, and polyunsaturated fatty acids including eicosapentanoic acid (EPA), docosahexanoic acid (DHA), and vegetable oils were all associated with BPH.14
Soy product intake. Epidemiologic evidence shows that Asian men have a lower risk for prostate disease than their Western counterparts; the difference appears to be associated in part with higher intake of isoflavones in Asian diets.15,16 Isoflavones in soy foods may help prevent BPH through several mechanisms, most notably by inhibition of 5-alpha reductase and aromatase, which, in turn, reduces the age-related increase in estrogen’s effect on prostate stromal cell proliferation.15
Lower energy intake. Some studies have shown an association between higher caloric intake and a greater risk for BPH. The Health Professionals Follow-Up Study reported a 50% increase in risk for BPH in men in the highest decile of calorie intake compared with the lowest decile, as well as a 70% higher risk for moderate-to-severe lower urinary tract symptoms in men consuming the most calories (OR=1.70).14
What to Tell the Family
BPH is not a symptom of old age. Rather, it is a problem that has dietary and lifestyle components. Patients should consider following a reduced-fat diet that is low in or free from animal products and includes regular consumption of soy foods. Family members who also follow this therapeutic diet are likely to benefit themselves and improve the patient’s adherence to this regimen.
1. Sanda MG, Beaty TH, Stutzman RE, et al. Genetic susceptibility of benign prostatic hyperplasia. J Urol. 1994;152:115-119.
2. Dahle SE, Chokkalingam AP, Gao YT, Deng J, Stanczyk FZ, Hsing AW. J Urol. 2002;168:599-604.
3. Hammarsten J, Hogstedt B, Holthuis N, Mellstrom D. Prostate Cancer Prostatic Dis. 1998;1:157-162.
4. Meigs JB, Mohr B, Barry MJ, Collins MM, McKinlay JB. Risk factors for clinical benign prostatic hyperplasia in a community-based population of healthy aging men. J Clin Epidemiol. 2001;54:935-944.
5. Platz EA, Kawachi I, Rimm EB, et al. Physical activity and benign prostatic hyperplasia. Arch Intern Med. 1998;158:2349-2356.
6. Wilt TJ, Mac Donald R, Rutks I. Tamsulosin for benign prostatic hyperplasia. Cochrane Database Syst Rev. 2003;(1):CD002081.
7. McConnell JD, Roehrborn CG, Bautista OM, et al. The long-term effect of doxazosin, finasteride, and combination therapy on the clinical progression of benign prostatic hyperplasia. N Engl J Med. 2003;349:2387-2398.
8. Buck AC. Is there a scientific basis for the therapeutic effects of serenoa repens in benign prostatic hyperplasia? Mechanisms of action. J Urol. 2004;172:1792-1799.
9. Wilt T, Ishani A, Mac Donald R, et al. Pygeum africanum for benign prostatic hyperplasia. Cochrane Database Syst Rev. 2002;(1):CD001044.
10. Koskimaki J, Hakama M, Huhtala H, Tammela TL. Association of dietary elements and lower urinary tract symptoms. Scand J Urol Nephrol. 2000;34:46-50.
11. Lagiou P, Wuu J, Trichopoulou A, Hsieh C-C, Adami H-O, Trichopoulos D. Diet and benign prostatic hyperplasia: a study in Greece. Urology. 1999;54:284-290.
12. Chyou PH, Nomura AM, Stemmermann GN, Hankin JH. A prospective study of alcohol, diet, and other lifestyle factors in relation to obstructive uropathy. Prostate. 1993;22:253-264.
13. Araki H, Watanabe H, Mishina T, Nakao M. High-risk group for benign prostatic hypertrophy. Prostate. 1983;4:253-264.
14. Suzuki S, Platz EA, Kawachi I, Willett WC, Giovannucci E. Intakes of energy and macronutrients and the risk of benign prostatic hyperplasia. Am J Clin Nutr. 2002;75:689-697.
15. Gaynor ML. Isoflavones and the prevention and treatment of prostate disease: Is there a role? Cleveland Clinic J Med. 2003;70:203-216.
16. Denis L, Morton MS, Griffiths K. Diet and its preventive role in prostatic disease. Eur Urol. 1999;35:377-387.