Nutritional influences on benign prostatic hyperplasia

Townsend Letter for Doctors and Patients, Dec, 2004 by Melvyn R. Werbach

Amino Acids

Double-blind studies have found the combination of L-glutamic acid 530 mg, L-alanine 200 mg and glycine 90 mg, taken 3 times daily, to have some therapeutic efficacy. Subjective improvement, reduction in residual urine and shrinkage of the prostate have been reported. (1) In fact, the efficacy of this combination has become so well accepted that has been used as the 'control drug' against which to test the efficacy of other possibly therapeutic agents.

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Essential Fatty Acids

When testosterone enters the prostate cell, it both converts to dihydrotestosterone and stimulates the synthesis and release of prostaglandins. Released prostaglandins, in turn, inhibit further testosterone binding to the prostate. It has been suggested that, with aging, declining prostaglandin synthesis causes testosterone binding to increase, causing unrestrained cell growth leading to prostatic hypertrophy. (2)

While randomized trials have yet to explore the efficacy of giving specific essential fatty acids, an early open trial gave 19 patients a combination of linoleic, linolenic and arachidonic acids. After several weeks, all showed a reduction in the size of the prostate, an increase in the force of the urinary stream and a diminution of residual urine. Twelve no longer had any residual urine and 13 no longer had nocturia. (3)

Phytosterols

Phytosterols are cholesterol analogs found in vegetables which decrease cholesterol absorption by displacing cholesterol from bile salt (taurocholate) micelles. (4) Various extracts of one phytosterol, beta-sitosterol, have been studied for the treatment of BPH under double-blind conditions, and in most studies have shown efficacy. (5)

Selenium

A research team found prostatic cadmium concentrations in benign prostatic hyperplasia (BPH) to be considerably higher than in normal tissue, with the dihydrotestosterone level directly proportional to cadmium concentrations. (6) Although another investigator failed to confirm these findings, (7) prostatic hyperplasia has been produced in animals by injecting cadmium into the prostate. (8) Furthermore, in vitro, cadmium stimulates the growth of human prostatic epithelium.

Also in vitro, the proper concentration of selenium inhibited cadmium-stimulated prostatic growth. (9) Animal work has also demonstrated that selenium supplementation, at least when given concurrent with cadmium exposure, protects against cadmium toxicity. (10) As selenium intake is frequently inadequate in Western-type diets, insurance against inadequate selenium nutriture may therefore be protective.

Zinc

The prostate contains a higher concentration of zinc than any other organ in the body, (11) perhaps because of the important relationship between zinc and prostatic androgens. For example, the secretion of prolactin, a hormone that increases testosterone uptake by the prostate, is inhibited by zinc. (12) Zinc also inhibits the activity of 5-alpha-reductase, the enzyme that converts testosterone to dihydrotestosterone, (13) and inhibits the specific binding of androgens to the prostatic cytosol and nuclear androgen receptors. (14)

Patients with BPH may have higher plasma zinc levels, (15) suggesting that zinc is interacting with the enlarged gland on a systemic basis. Prostatic zinc levels may also rise, although the increase is in the prostatic fluid rather than within cells (16) as tissue binding is reduced. (17)

Since benign prostatic hyperplasia is an androgen-dependent metabolic disorder marked by increased intraprostatic concentration of dihydrotestosterone (which stimulates tissue growth), zinc supplementation could theoretically be beneficial. Back in 1974, an unpublished open trial of zinc supplementation reported that zinc (150 mg zinc sulfate daily for 2 months, followed by 50 to 100 mg daily) successfully reduced both symptoms and prostatic size in the majority of a group of 19 patients. (18) Unfortunately, these early findings have yet to be confirmed.

Modified from Werbach MR with Moss J. Textbook of Nutritional Medicine. Tarzana, California, Third Line Press, Inc., 1999.

References

1. Dumrau F. Benign prostatic hyperplasia: Amino acid therapy for symptomatic relief. Am J Geriatr 10:426-30, 1962

2. Klein LA, Staff JS. Prostaglandins and the prostate. An hypothesis on the etiology of benign prostatic hyperplasia. Prostate 4(3):247-51, 1983

3. Hart JP, Cooper WL. Vitamin F in the treatment of prostatic hyperplasia. Report Number 1, Lee Foundation for Nutritional Research, Milwaukee, WI, 1941

4. Ikeda I et al. Inhibition of cholesterol absorption in rats by plant sterols. J Lipid Res 29(12):1573-82, 1988

5. Klippel KF et al. A multicentric, placebo-controlled, double-blind clinical trial of sitosterol (phytosterol) for the treatment of benign prostatic hyperplasia. Br J Urol 80(3):427-32, 1997

6. Habib FK et al. Metal-androgen interrelationships in carcinoma and hyperplasia of the human prostate. J Endocrinol 71(1):133-41, 1976