Benign Prostatic Hyperplasia

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 about 8% in the third decade of life to greater than 90% in the ninth decade.[1] The etiology is multifactorial and not well understood. Family history, age, and hormone concentrations appear to play a role in BPH development. Testosterone and dihydrotestosterone, while necessary for BPH to occur, are not alone adequate to cause the condition. The role of estrogen in BPH remains unclear. Symptoms are related to obstruction of the urethra and include hesitancy, reduced urine flow rate, dribbling, urgency, frequency, and nocturia.

Risk Factors

The following factors are associated with increased risk of BPH:

Aging. BPH occurs more commonly with advancing age.

Family history. Data suggest an autosomal dominant genetic pattern.[2]

Androgen. Higher dihydrotestosterone concentrations are associated with BPH.

Obesity. Excessive adiposity 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.[3] ,[4] 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.[5] ,[6]

Diet. Red meat and elevated fat intake have been shown to increase risk for BPH, while increased vegetable consumption has been shown to decrease risk.[7]

Diagnosis

Diagnosis begins with a good history, noting relevant signs and symptoms, as well as medications and any medical conditions that may contribute to urinary dysfunction. It can be helpful to administer a scoring test to gauge symptom severity; some examples are American Urologic Association Symptom Score and International Prostate Symptom Score. Urinanalysis should always be performed to check for blood, crystals, or infection. DRE will typically detect prostate enlargement. The surface of the prostate should be smooth and is usually symmetrical; asymmetry or induration suggests malignancy. Some men with large prostates have no obstructive symptoms, while men with small prostates may have obstructive symptoms.

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, such as urine flow rate and post-void residual volume. Urination frequency and volume measurements can be helpful, especially if symptoms occur primarily at night. By keeping track of intake and output, it is possible to determine if excessive fluid intake may be contributing to urinary frequency and nocturia.

Treatment

The purpose of BPH treatment is to improve the patient’s quality of life. Restriction of fluids for 1-2 hours prior to bedtime may help improve nocturnal frequency. Sitting while urinating can increase bladder emptying for men with BPH.[8]

Observation alone (“watchful waiting”) is appropriate if symptoms are mild or not bothersome.

Medical treatment includes use of alpha-1-adrenergic antagonists, such as prazosin, terazosin, doxazosin, tamsulosin, and alfuzosin, which relax smooth muscle and allow for increased urinary flow rate. These medications are the most common first-line pharmaceutical treatment for BPH. The various drugs in this class appear to have similar efficacy. Choice of drug may be based on side effect profile as well as cost.[9] The most common side effect is orthostatic hypotension; therefore the medication should be taken just prior to bedtime.[10]

In cases of moderate or greater prostate enlargement, 5-alpha-reductase inhibitors, such as finasteride and dutasteride, can be administered to block the conversion of testosterone to dihydrotestosterone. A combination of an alpha-adrenergic antagonist and finasteride appears to improve long-term outcomes.[11] This class of medication can take months to have a clinical effect on prostate size.[12] The most common side effect of this class of medications is sexual dysfunction.[13]

Anticholinergic medications such as oxybutynin, solifenacin, and tolterodine are a second line option for treatment but are associated with significant side effects such as dry mouth, constipation, and cognitive impairment. They should be used with caution.[14]

Phosphodiesterase-5 inhibitors such as tadalafil and vardenafil may be considered for treatment in patients who have concomittent erectile dysfunction.[15]

Plant extracts from saw palmetto ( Serenoa repens), Pygeum a fricanum, and Secale cereale, along with concentrated beta-sitosterol (a plant sterol), may play treatment roles, but need further investigation.

Surgical options for severe refractory symptoms include transurethral resection of the prostate (TURP), transurethral incision of the prostate, open prostatectomy, laser prostatectomy (or photovaporization), microwave therapy, and transurethral needle ablation, among others. There are varying levels of evidence to support each of the above procedures.

Nutritional Considerations

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.[16] -,[17] ,[18] ,[19] 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.[20] ,[21]

Including soy products. Asian men have a lower risk for prostate disease, compared with their Western counterparts; some have suggested that the difference may be partly attributable to a higher intake of isoflavones and related compounds in their plant-rich diets.[22] ,[23] Isoflavones in soy foods may inhibit 5-alpha reductase and aromatase, which, in turn, reduces the age-related increase in estrogen’s effect on prostate stromal cell proliferation.[22]

Reducing 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 those in the lowest decile, as well as a 70% higher risk for moderate-to-severe lower urinary tract symptoms in men consuming the most calories.[20]

Increasing fruit and vegetable intake. The Health Professionals Follow-up Study found that consumption of fruits and vegetables overall, particularly those rich in beta-carotene, lutein, zeaxanthin, and vitamin C, was inversely related to BPH incidence.[24] Examples of these foods are carrots, spinach, sweet potatoes, broccoli, collard greens, corn, oranges, melon, and kiwi. Limited evidence suggests that allium vegetable consumption (e.g., onions, garlic) are also inversely related to BPH incidence.[25]

Orders

See Basic Diet Orders Chapter

Low-fat diet.

Exercise prescription.

What to Tell the Family

BPH is not necessarily 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. Effective medications are available with minimal side effects. Severe obstructive symptoms (e.g., urinary retention and bladder stones) should be treated with surgery to avoid permanent bladder failure or kidney damage.

References

  1. Berry SJ et al: The development of human benign prostatic hyperplasia with age. J Urol 132:474, 1984  [PMID:6206240]
  2. Sanda MG et al: Genetic susceptibility of benign prostatic hyperplasia. J Urol 152:115, 1994  [PMID:7515446]
  3. Dahle SE et al: Body size and serum levels of insulin and leptin in relation to the risk of benign prostatic hyperplasia. J Urol 168:599, 2002  [PMID:12131317]
  4. Hammarsten J et al: Components of the metabolic syndrome-risk factors for the development of benign prostatic hyperplasia. Prostate Cancer Prostatic Dis 1:157, 1998  [PMID:12496910]
  5. Meigs JB et al: Risk factors for clinical benign prostatic hyperplasia in a community-based population of healthy aging men. J Clin Epidemiol 54:935, 2001  [PMID:11520654]
  6. Platz EA et al: Physical activity and benign prostatic hyperplasia. Arch Intern Med 158:2349, 1998  [PMID:9827786]
  7. Kristal AR et al: Dietary patterns, supplement use, and the risk of symptomatic benign prostatic hyperplasia: results from the prostate cancer prevention trial. Am J Epidemiol 167:925, 2008  [PMID:18263602]
  8. de Jong Y et al: Urinating Standing versus Sitting: Position Is of Influence in Men with Prostate Enlargement. A Systematic Review and Meta-Analysis. PLoS ONE 9:, 2014  [PMID:25051345]
  9. Djavan B, Marberger M: A meta-analysis on the efficacy and tolerability of alpha1-adrenoceptor antagonists in patients with lower urinary tract symptoms suggestive of benign prostatic obstruction. Eur Urol 36:1, 1999  [PMID:10364649]
  10. Wilt TJ, Mac Donald R, Rutks I: Tamsulosin for benign prostatic hyperplasia. Cochrane Database Syst Rev  [PMID:12535426]
  11. McConnell JD et al: The long-term effect of doxazosin, finasteride, and combination therapy on the clinical progression of benign prostatic hyperplasia. N Engl J Med 349:2387, 2003  [PMID:14681504]
  12. Tacklind J et al: Finasteride for benign prostatic hyperplasia. Cochrane Database Syst Rev Oct 06  [PMID:20927745]
  13. Gacci M et al: Impact of medical treatments for male lower urinary tract symptoms due to benign prostatic hyperplasia on ejaculatory function: a systematic review and meta-analysis. J Sex Med 11:1554, 2014  [PMID:24708055]
  14. McVary KT et al: Update on AUA guideline on the management of benign prostatic hyperplasia. J Urol 185:1793, 2011  [PMID:21420124]
  15. Liu L et al: Phosphodiesterase-5 inhibitors for lower urinary tract symptoms secondary to benign prostatic hyperplasia: a systematic review and meta-analysis. Urology 77:123, 2011  [PMID:21195830]
  16. Koskimäki J et al: Association of dietary elements and lower urinary tract symptoms. Scand J Urol Nephrol 34:46, 2000  [PMID:10757270]
  17. Lagiou P et al: Diet and benign prostatic hyperplasia: a study in Greece. Urology 54:284, 1999  [PMID:10443726]
  18. Chyou PH et al: A prospective study of alcohol, diet, and other lifestyle factors in relation to obstructive uropathy. Prostate 22:253, 1993  [PMID:7683816]
  19. Araki H et al: High-risk group for benign prostatic hypertrophy. Prostate 4:253, 1983  [PMID:6189108]
  20. Suzuki S et al: Intakes of energy and macronutrients and the risk of benign prostatic hyperplasia. Am J Clin Nutr 75:689, 2002  [PMID:11916755]
  21. Nandeesha H: Benign prostatic hyperplasia: dietary and metabolic risk factors. Int Urol Nephrol 40:649, 2008  [PMID:18246440]
  22. Gaynor ML: Isoflavones and the prevention and treatment of prostate disease: is there a role? Cleve Clin J Med 70:203, 2003  [PMID:12678210]
  23. Denis L, Morton MS, Griffiths K: Diet and its preventive role in prostatic disease. Eur Urol 35:377, 1999  [PMID:10325492]
  24. Rohrmann S et al: Fruit and vegetable consumption, intake of micronutrients, and benign prostatic hyperplasia in US men. Am J Clin Nutr 85:523, 2007  [PMID:17284753]
  25. Galeone C et al: Onion and garlic intake and the odds of benign prostatic hyperplasia. Urology 70:672, 2007  [PMID:17991535]

Last updated: January 10, 2018

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TY - ELEC T1 - Benign Prostatic Hyperplasia ID - 1342049 Y1 - 2018/01/10/ PB - Nutrition Guide for Clinicians UR - https://nutritionguide.pcrm.org/nutritionguide/view/Nutrition_Guide_for_Clinicians/1342049/all/Benign_Prostatic_Hyperplasia ER -