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Natural Therapies for Prostate Support (LUTS and BPH)

By Ronald Steriti, ND, PhD

Prostate health becomes more important as men become older. Approximately 50 percent of men over age 60 have prostate issues. The following is a brief summary of recent research on natural therapies that may be useful in treating benign prostatic hyperplasia (BPH) and lower urinary tract symptoms (LUTS).

Lower Urinary Tract Symptoms

The symptoms commonly associated with BPH are collectively called lower urinary tract symptoms, although BPH is not always the cause. LUTS can be categorized into two broad categories:

  • Filling or irritative symptoms: Frequency, urgency, dysuria (painful urination) and nocturia (the need to urinate at night).
  • Voiding or obstructive symptoms: Poor stream, hesitancy, terminal dribbling, incomplete voiding and overflow incontinence (occurs in chronic retention).

There are several causes of LUTS, so it is important to get an accurate diagnosis of the cause.

  • BPH with obstruction
  • Detrusor muscle weakness and/or instability
  • Urinary tract infection (UTI)
  • Chronic prostatitis
  • Calculi
  • Malignancy: prostate or bladder
  • Neurological disease, e.g. multiple sclerosis, spinal cord injury, cauda equina syndrome

Benign Prostatic Hyperplasia

BPH is an age-related, non-malignant enlargement of the prostate gland. Hyperplasia is an increase in the numbers of cells, as opposed to a hypertrophy (an increase in cell size). BPH is very common, affecting almost 10 percent of men in their 40s and increasing every decade thereafter. According to the National Institute on Aging, more than half of men in their 60s have BPH. Among men in their 70s and 80s, the figure may be as high as 90 percent.

As the prostate enlarges, it causes compression of the urethra, preventing the bladder from adequately releasing urine. Decreased caliber and force of urination are classic signs. Residual urine, distention of the bladder, more frequent urination (especially at night) and UTI are common.

Etiologies

Testosterone and DHT: Prostate growth is stimulated primarily by the hormones testosterone and dihydrotestosterone (DHT). The following is a summary of the mechanism of BPH:

  • Serum levels of testosterone fall while levels of estrogens and prolactin increase as men age.
  • Testosterone converts into DHT via 5-alpha reductase.
  • DHT binds to androgen receptors five times stronger than testosterone.
  • Androgen receptor stimulation is increased by the action of sex-hormone-binding globulin (SHBG).
  • When estrogen attaches to SHBG, it sensitizes (amplifies) the androgen signal.

Inflammation: Inflammation (prostatis) is a common finding in BPH and several herbs have anti-inflammatory effects.1 Prostatatitis from bacterial infections is often related to BPH since the frequencies of UTI increase as retention of urine in the bladder increases. Chronic nonbacterial prostatitis is also common and may be related to an autoimmune response.

Oxidative stress: Several studies have shown that BPH is associated with increased oxidative stress, which increases with age.2,3

Nitric oxide: Several studies have proposed that nitric oxide may be the causal link between BPH and sexual dysfunction Nitric oxide is involved in the physiologic regulation of smooth muscle relaxation in the prostate. Nitric oxide (NO)-synthase-containing nerves in the prostate, urethra and bladder neck cause relaxation upon activation.4-6

Melatonin: Several researchers propose that melatonin, secreted by the pineal gland at night, may inhibit prostate growth.7 One study showed that circadian patterns of melatonin were depressed in patients with prostate cancer as compared to young men and elderly patients with BPH.8

Lab Tests and Assessments

Conventional medicine relies on digital rectal exams and transrectal ultrasonography to assess the prostate. This is followed by serum measurements of prostate specific antigen (PSA) to rule out prostate cancer. Urinalysis shows pyuria and pH changes due to chronic residual urine. Urine culture is often positive (sometimes due to chronic residual urine). Post-void residual (> 100 cc) is increased. Elevated serum creatinine may be present if there is obstructive uropathy.

There are several other tests that may be useful for a complete evaluation and to aid therapeutic choice, including:

  • Testosterone and DHT
  • Estrogen status, primarily via estradiol measurement
  • Melatonin
  • C-Reactive Protein (CRP) to assess inflammation

Several labs offer salivary male hormone assessments that measure several of those mentioned above. Testosterone and melatonin may be measured four times in a 24-hour period to assess circadian rhythm. Comprehensive panels often include measurements of DHEA and cortisol to assess the role of adrenal function.

Conventional Treatments

Surgery: Several forms of surgery are available to remove portions of the prostate. Although successful, unpleasant side effects include decreased sexual function and bladder incontinence.

5-alpha reductase inhibitors: Finasteride (Proscar) is the most common 5-alpha reductase inhibitor, which decreases the conversion of testosterone to DHT. It often requires six months to a year before significant results are evident.

Alpha blockers: Alpha blockers such as terazosin (Hytrin) and prazosin (Minipress) relax the muscles around the prostate, which relieves many of the symptoms of BPH. Alpha-blocker drugs are also anti-hypertensives.

Natural Therapies

Diet: One study showed that a diet low in fat and red meat and high in protein and vegetables may reduce the risk of symptomatic BPH.9 Another study found that a diet rich in vegetables may reduce the occurrence of BPH.10 A case-control study found that the risk of BPH significantly decreased with increasing intake of carotene, alpha-carotene, beta-carotene, and cis-beta-carotene and also decreased with vitamin C and iron intake.11

Saw palmetto: Saw palmetto (Serenoa repens) is the leading herb for men’s health and prostate support. Saw palmetto is an ancient herbal remedy for urinary symptoms that has been used for enlarged prostate and BPH.1,12,13 Recent reviews and meta-analysis have been negative, and recent studies have mixed results.14 One study found that LUTS/BPH patients who used phytotherapy had markedly lower utility scores than those patients not using phytotherapy despite comparable clinical parameters.15 The TRIUMPH study recorded the treatment and outcomes of 2,351 newly presenting patients in six European countries over a one-year follow-up period. Significant improvements were seen in 43 percent of patients on phytotherapy with Serenoa repens or Pygeum africanum, compared to 57 percent of those on Finasteride and 68 percent on alpha-blockers.16 Another study found positive effects with a particular saw palmetto gel capsule (two per day for 12 weeks). The maximum urinary flow rate was significantly higher and relative urinary resistance was significantly lower, but there was no significant difference in mean prostate volume or International Prostate Symptom Score.17 A recent study published found Serenoa repens (320 mg per day) to be equivalent to Tamsulosin, an alpha-1a-selective alpha-blocker used in the symptomatic treatment of BPH.18 Another study found no positive benefit with BPH after one year of treatment with saw palmetto extract (160 mg twice a day).19

Permixon: A hexane extract, is the most studied form of saw palmetto. A meta-analysis pooled the results of 17 clinical trials on Permixon involving 4,280 patients and lasting from three weeks to two years. It found that Permixon was associated with a mean reduction in the International Prostate Symptom Score and other measured symptoms of BPH compared to placebo.20

Pygeum africanum: Traditional African healers use Pygeum africanum (African plum) bark to treat bladder and urination disorders. It is particularly helpful for symptoms associated with BPH. Positive research led to its common use in Europe. It is less commonly used in the United States where prescription drugs or saw palmetto are more commonly used.21,22 A study found Pygeum to be effective both in vivo (PC-3 and LNCaP cells) and in vitro (TRAMP mouse model) against prostate cancer.23

Cactus: One article has proposed that cactus flower extracts exerts an effect on BPH by inhibiting lipid peroxidation, androgen aromatization and testosterone reduction.24

Beta sitosterol: Phytosterols or plant sterols are structurally similar to cholesterol. The most common phytosterols are beta-sitosterol, campesterol and stigmasterol. Several studies have shown that beta-sitosterol improves prostate function.25,26 A meta-analysis concluded that nonglucosidic beta-sitosterols improve urinary symptoms and flow measures.27 Another article found that beta-sitosterol and resveratrol shared similar mechanisms against prostate cancer and the combination was more potent than either alone.28 The results of the Beta-Sitosterol Study Group showed that beta-sitosterol treatment resulted in significant improvement in symptoms and urinary flow parameters in the treatment of BPH.29 Another randomized, double-blind, placebo-controlled clinical trial showed that beta-sitosterol (130 mg per day for six months) resulted in significant improvements in BPH symptoms.30

Grapes: One study found that a grape suspension significantly reduced the severity of obstructed bladder dysfunction in rabbits. The authors proposed that these results are consistent with the hypothesis that ischemia is a major etiological factor in obstructive dysfunction, and that treatment with antioxidants and membrane stabilization compounds such as those in the grape suspension can be effective in the treatment of obstructive bladder pathology.31

Lycopene: Lycopene, an extract from tomatoes, is one of the major carotenoids in the diet of North Americans and Europeans. It has been shown to reduce the risk of prostate cancer and BPH. In a study of 40 patients with BPH, subjects used lycopene (15 mg/day) or placebo for six months. Lycopene supplementation resulted in decreased PSA levels, whereas there was no change in the placebo group. The placebo group also experienced a progression of prostate enlargement. The prostate did not enlarge in the lycopene group. Symptoms of the disease, as assessed via the International Prostate Symptom Score questionnaire, were improved in both groups, with a significantly greater effect in men taking lycopene supplements.32

Anti-cancer supplements: Several vitamins and herbs may be beneficial for BPH, as they reduce the incidence of prostate cancer. These include:

  • Garlic and onions33,34
  • Curcumin (turmeric)35
  • EGCG in green tea36
  • Milk thistle37
  • Vitamin D38,39
  • Vitamins C and E40-42
  • Vitamin K43,44
  • Resveratrol45-47
  • Zinc48-50
  • Selenium51,52
  • Glutathione53-56

Although they may be relevant to BPH/LUTS, a full review of these vitamins and herbs is reserved for an article specifically on prostate cancer.

References

  1. 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(5 Pt 1):1792-9.
  2. Aryal M, et al. Oxidative stress in benign prostate hyperplasia. Nepal Med Coll J 2007;9(4):222-4.
  3. Aydin A, et al. Oxidative stress and antioxidant status in non-metastatic prostate cancer and benign prostatic hyperplasia. Clin Biochem 2006;39(2):176-9.
  4. McVary K. Lower urinary tract symptoms and sexual dysfunction: epidemiology and pathophysiology. BJU Int, 2006;97(Suppl 2):23-8; discussion 44-5.
  5. Hedlund P. Nitric oxide/cGMP-mediated effects in the outflow region of the lower urinary tract--is there a basis for pharmacological targeting of cGMP? World J Urol 2005;23(6):362-7.
  6. Klotz T, et al. Nitric oxide based influence of nitrates on micturition in patients with benign prostatic hyperplasia. Int Urol Nephrol 1999;31(3):335-41.
  7. Laudon M, et al. Putative melatonin receptors in benign human prostate tissue. J Clin Endocrinol Metab 1996;81(4):1336-42.
  8. Bartsch C, et al. Melatonin and 6-sulfatoxymelatonin circadian rhythms in serum and urine of primary prostate cancer patients: evidence for reduced pineal activity and relevance of urinary determinations. Clin Chim Acta 1992;209(3):153-67.
  9. 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 2008;167(8):925-34.
  10. Rohrmann S, et al. Fruit and vegetable consumption, intake of micronutrients, and benign prostatic hyperplasia in US men. Am J Clin Nutr 2007;85(2):523-9.
  11. Tavani A, et al. Intake of selected micronutrients and the risk of surgically treated benign prostatic hyperplasia: a case-control study from Italy. Eur Urol 2006;50(3):549-54.
  12. Serenoa repens. Altern Med Rev 1998;3(3):227-9.
  13. Gordon AE, Shaughnessy AF. Saw palmetto for prostate disorders. Am Fam Physician 2003;67(6):1281-3.
  14. Dedhia RC, McVary KT. Phytotherapy for lower urinary tract symptoms secondary to benign prostatic hyperplasia. J Urol 2008;179(6):2119-25.
  15. Dedhia RC, et al. Impact of phytotherapy on utility scores for 5 benign prostatic hyperplasia/lower urinary tract symptoms health states. J Urol 2008;179(1):220-5.
  16. Hutchison A, et al. The efficacy of drugs for the treatment of LUTS/BPH, a study in 6 European countries. Eur Urol 2007;51(1):207-15, discussion 215-6.
  17. Shi R, et al. Effect of saw palmetto soft gel capsule on lower urinary tract symptoms associated with benign prostatic hyperplasia: a randomized trial in Shanghai, China. J Urol 2008;179(2):610-5.
  18. Hizli F, Uygur MC. A prospective study of the efficacy of Serenoa repens, tamsulosin, and Serenoa repens plus tamsulosin treatment for patients with benign prostate hyperplasia. Int Urol Nephrol 2007;39(3):879-86.
  19. Bent S, et al. Saw palmetto for benign prostatic hyperplasia. N Engl J Med 2006;354(6):557-66.
  20. Boyle P, et al. Updated meta-analysis of clinical trials of Serenoa repens extract in the treatment of symptomatic benign prostatic hyperplasia. BJU Int 2004;93(6):751-6.
  21. Edgar AD, et al. A critical review of the pharmacology of the plant extract of Pygeum africanum in the treatment of LUTS. Neurourol Urodyn 2007;26(4):458-63, discussion 464.
  22. Katz AE. Flavonoid and botanical approaches to prostate health. J Altern Complement Med 2002;8(6):813-21.
  23. Shenouda NS, et al. Phytosterol Pygeum africanum regulates prostate cancer in vitro and in vivo. Endocrine 2007;31(1):72-81.
  24. Jonas A, et al. Cactus flower extracts may prove beneficial in benign prostatic hyperplasia due to inhibition of 5alpha reductase activity, aromatase activity and lipid peroxidation. Urol Res 1998;26(4):265-70.
  25. Awad AB, Fink CS. Phytosterols as anticancer dietary components: evidence and mechanism of action. J Nutr 2000;130(9):2127-30.
  26. Bradford PG, Awad AB. Phytosterols as anticancer compounds. Mol Nutr Food Res 2007;51(2):161-70.
  27. Wilt T, et al. Beta-sitosterols for benign prostatic hyperplasia. Cochrane Database Syst Rev 2000(2):CD001043.
  28. Awad AB, et al. Effect of resveratrol and beta-sitosterol in combination on reactive oxygen species and prostaglandin release by PC-3 cells. Prostaglandins Leukot Essent Fatty Acids 2005;72(3):219-26.
  29. Berges RR, et al. Randomised, placebo-controlled, double-blind clinical trial of beta-sitosterol in patients with benign prostatic hyperplasia. Beta-sitosterol Study Group. Lancet 1995;345(8964):1529-32.
  30. Klippel KF, et al. A multicentric, placebo-controlled, double-blind clinical trial of beta-sitosterol (phytosterol) for the treatment of benign prostatic hyperplasia. German BPH-Phyto Study group. Br J Urol 1997;80(3):427-32.
  31. Agartan CA, et al. Protection of urinary bladder function by grape suspension. Phytother Res 200418(12):1013-8.
  32. Schwarz S, et al. Lycopene inhibits disease progression in patients with benign prostate hyperplasia. J Nutr 2008;138(1):49-53.
  33. Devrim E, Durak I. Is garlic a promising food for benign prostatic hyperplasia and prostate cancer? Mol Nutr Food Res 2007;51(11):1319-23.
  34. Galeone C, et al. Onion and garlic use and human cancer. Am J Clin Nutr 2006;84(5):1027-32.
  35. Nonn L, et al. Chemopreventive anti-inflammatory activities of curcumin and other phytochemicals mediated by MAP kinase phosphatase-5 in prostate cells. Carcinogenesis 2007;28(6):1188-96.
  36. Harper CE, et al. Epigallocatechin-3-Gallate suppresses early stage, but not late stage prostate cancer in TRAMP mice: mechanisms of action. Prostate 2007;67(14):1576-89.
  37. Singh RP, Agarwal R. Prostate cancer prevention by silibinin. Curr Cancer Drug Targets 2004;4(1):1-11.
  38. Bao BY, et al. Protective role of 1 alpha, 25-dihydroxyvitamin D3 against oxidative stress in nonmalignant human prostate epithelial cells. Int J Cancer 2008;122(12):2699-706.
  39. Flanagan JN, et al. Vitamin D metabolism in human prostate cells: implications for prostate cancer chemoprevention by vitamin D. Anticancer Res 2006;26(4A):2567-72.
  40. Peters U, et al. Vitamin E and selenium supplementation and risk of prostate cancer in the Vitamins and lifestyle (VITAL) study cohort. Cancer Causes Control 2008;19(1):75-87.
  41. Crispen PL, et al. Vitamin E succinate inhibits NF-kappa B and prevents the development of a metastatic phenotype in prostate cancer cells: implications for chemoprevention. Prostate 2007;67(6):582-90.
  42. Gunawardena K, et al. Combination therapy with vitamins C plus E inhibits surviving and human prostate cancer cell growth. Prostate 2004;59(3):319-27.
  43. Nimptsch K, et al. Dietary intake of vitamin K and risk of prostate cancer in the Heidelberg cohort of the European Prospective Investigation into Cancer and Nutrition (EPIC-Heidelberg). Am J Clin Nutr 2008;87(4):985-92.
  44. Tareen B, et al. A 12-week, open label, phase I/IIa study using apatone for the treatment of prostate cancer patients who have failed standard therapy. Int J Med Sci 2008;5(2):62-7.
  45. Stewart JR, et al. Resveratrol: a candidate nutritional substance for prostate cancer prevention. J Nutr 2003;133(7 Suppl):2440-3.
  46. Aggarwal BB, et al. Role of resveratrol in prevention and therapy of cancer: preclinical and clinical studies. Anticancer Res 2004;24(5A):2783-840.
  47. Gill C, et al. Resveratrol sensitizes androgen independent prostate cancer cells to death-receptor mediated apoptosis through multiple mechanisms. Prostate 2007;67(15):1641-53.
  48. Franklin RB, Costello LC. Zinc as an anti-tumor agent in prostate cancer and in other cancers. Arch Biochem Biophys 2007;463(2):211-7.
  49. Costello LC, Franklin RB. The clinical relevance of the metabolism of prostate cancer; zinc and tumor suppression: connecting the dots. Mol Cancer 2006;5:17.
  50. Costello LC, et al. Zinc and prostate cancer: a critical scientific, medical, and public interest issue (United States). Cancer Causes Control 2005;16(8):901-15.
  51. Pourmand G, et al. Serum selenium level and prostate cancer: a case-control study. Nutr Cancer 2008;60(2):171-6.
  52. Peters U, et al. Serum selenium and risk of prostate cancer-a nested case-control study. Am J Clin Nutr 2007;85(1):209-17.
  53. Hokaiwado N, et al. Glutathione S-transferase pi mediates proliferation of androgen independent prostate cancer cells. Carcinogenesis 2008; 29(6):1134-8.
  54. Katoh T, et al. Genetic polymorphisms of human cytosol glutathione S-transferases and prostate cancer. Pharmacogenomics 2008;9(1):93-104.
  55. Yu YP, et al. Glutathione peroxidase 3, deleted or methylated in prostate cancer, suppresses prostate cancer growth and metastasis. Cancer Res 2007;67(17):8043-50.
  56. Meiers I, et al. Glutathione S-transferase pi (GSTP1) hypermethylation in prostate cancer: review 2007. Pathology 2007.;9(3):299-304.

About the Author: Dr. Ronald Steriti graduated from Southwest College of Naturopathic Medicine and currently resides in Naples, Fla. He can be contacted via e-mail at .


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