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Article
Collection: Nutrition and Prostate Cancer Dr. James Meschino, D.C.,
M.S. Nutrition and
Prostate Health A Research Report by Dr. James Meschino, D.C., M.S. ~ Research and Clinical Director of the RenaiSanté Institute of Integrative Medicine ~ Prostate cancer is the most common
cancer in North American men and as well as in other Western countries. As
reported in the Journal of the National Cancer Institute, as much as 75% of
prostate cancer may be avoidable if men followed more prudent nutritional
practices.(1) In Japan the
incidence of prostate cancer is 80% lower than in North America and much of the
Western world. Low rates are also found in Africa and Eastern Europe. Migration
studies reveal that when men relocate from a low- to high-risk region of the
world and abandon their traditional dietary patterns, their incidence of
prostate cancer rises to approach that of North American men.(2,3) In recent years a number of specific
nutrients have been identified that are linked to prostate cancer and the
age-related changes that lead to prostate enlargement (benign prostatic
hyperplasia); which affects 50-60% of men by age 40-59 and 80% of men by the age 80. Thus, nutritional support for
the prostate gland is an extremely important aspect of preserving the health
and function of this gland and in the prevention and treatment of prostate
disease. (4,5) Age–Related Changes To The Prostate As men age (by age 40), the prostate
gland tends to accelerate the rate at which it converts testosterone to dihydrotestosterone
(DHT). The build up of DHT in prostate cells stimulates them to divide and
multiply at a faster rate. This results in more prostate cells (more prostate
mass) leading to prostate enlargement and other problems. As the prostate
enlarges under the direction of DHT, men often notice symptoms such as reduced
strength of their urine stream, more frequent urination, repeated night time
urination, bladder urgency and related symptoms.(5) More rapid cell division rates also
increase the chances of forming cancerous DNA
mutations in the genetic blueprints of the cell. In fact DHT is known to
promote the spread of existing prostate cancer. Amazingly, males born without
the genetic ability to synthesize DHT are virtually immune from ever developing
prostate cancer in their lifetime. There is no question that DHT is linked to
prostate cancer and prostate enlargement in a number of ways. (6,7) The exciting news for men is that
there are specific nutrients and natural bioactive compounds that are available
in foods and in certain supplement products that have been shown to block the
conversion of testosterone to DHT and exert other protective effects within the
prostate gland. As such, the consumption of these products at the correct
dosage and standardized grade have been shown to be effective in the treatment
of enlarged prostate problems and some of these natural agents mentioned below
are associated with the prevention of prostate cancer (and more recently with
prostate cancer treatment support).(8) Nutrients That Block The Build Up Of DHT There are several known natural
agents that can effectively block the build up of DHT within the prostate
gland. The primary ones include the standardized grade of Saw Palmetto, Pygeum
Africanum, Beta-sitosterol, Soy isoflavones and Stinging Nettle (urtica
dioica). Numerous studies have shown that
the fatty acids and sterols present in Saw Palmetto block the build up of DHT
and exert other favourable effects on prostate health. Saw Palmetto extract is
a proven therapy for enlarged prostate problems and has recently been used in
trials with prostate cancer patients, yielding impressive results in helping to
contain the disease. Pygeum Africanum contains active
compounds known as triterpenes, which have also been shown to be effective in
the treatment of enlarged prostate problems in numerous human studies. In recent years, prestigious
medical journals such as the Lancet and the British Journal of Urology have
published research papers demonstrating that Beta-sitosterol (found in saw
palmetto, soy products and other in plant foods) is also extremely effective in
reversing benign prostatic hyperplasia (prostate enlargement) Soy products and soy extract contain several
important isoflavones; the most important of which include genistein and
diadzein. These isoflavones directly inhibit the build up of DHT and exhibit
many other biological properties that are related to the prevention of prostate
disease. As previously stated, in Japan, where soy isoflavone intake is high (avg.
50 mg per day), prostate cancer incidence is 80% lower than in North America. The herbal agent Stinging Nettle
also enjoys a reputation in Europe as natural agent that has consistently been
shown to reverse trends of prostate enlargement. (9-29) Prostate Antioxidants Studies indicate that prostate
cancer may result from free radical damage to healthy prostate cells,
converting them into cancer cells. Evidence is very strong to suggest that the
antioxidant lycopene (derived from tomatoes) plays an essential role in
protecting prostate cells from free radical damage. Human studies such as the
Physicians’ Health Study and the Health Professionals’ Follow Up Study have
shown a striking correlation between higher lycopene blood levels and/or intake
levels, and a marked reduction in prostate cancer development (as much as a 40%
reduction). Experimental evidence also supports this protective effect of
lycopene. Soy isoflavones (mentioned earlier
in this review) are also known to provide antioxidant protection to the
prostate gland and soy intake is highly correlated with reduced prostate cancer
development in epidemiological and experimental studies. More
recently, there has been the suggestion that vitamin E and selenium
supplementation may provide antioxidant support to the prostate, further
helping to reduce prostate cancer risk. (30-36,3,6) Protecting Your Prostate To help combat the age-related
changes to the prostate gland that lead to problems of enlargement and the
multi-step processes involved in prostate cancer development, all men should
practice prudent nutritional practices throughout their lifetime. Due to the
changes that occur at around age 40, men this age and older should consider
taking a supplement that contains the correct dosage and standardized grade of
Saw Palmetto, Pygeum Africanum, Beta-sitosterol, Soy isoflavones, Stinging
Nettle, Lycopene and other prostate support ingredients. I suggest that you
speak to your health practitioner about taking Prostate 40 PLUS (by
Nutra Therapeutics) or a product yielding the same or very similar ingredients.
In summary the current scientific evidence suggests that the following
nutrition factors can favorably affect prostate health and should be strongly
considered by all men throughout their lifetime: 1.
Consume
a diet that is low in saturated fat. 2.
Remain
at or near your ideal body weight. 3.
Consume
alcohol in moderation or not at all. 4.
Consume
tomato and tomato products on a daily basis. 5.
Use
more soy products, such as tofu, veggie burgers, miso soup, soy nuts and soy
milk. 6.
By
age 40, consider taking a prostate support supplement such as Prostate 40
PLUS (by Nutra Therapeutics); containing all the important prostate factors
reviewed in this report. It is vital that the herbal and accessory compounds
are present at the correct dosage and standardized grade, in order to yield
sufficient amounts of their bioactive agents. 7. Consider taking a high potency multi-vitamin and mineral that is enriched with other antioxidants, including Vitamin E (400 I.U.), selenium (100-200 mcg), Vitamin C (1000 mg) etc., (eg. Nutra Therapeutics Multi Vitamin and Mineral or a comparable supplement). References
Can Prostate
Cancer Be Prevented with the Help of Vitamins? by Dr. James
Meschino D.C., M.S. Reporting in the Journal of the National Cancer Institute Dr. Walter Willett of Harvard University provided data to suggest that as much as 75% of prostate cancer is avoidable by dietary influences. Considering that prostate cancer is the most frequently diagnosed cancer among U.S. and Canadian men and the second leading cause of cancer death, researchers are actively investigating nutritional agents that can minimize risk of this common degenerative disease. Within the category of vitamins and vitamin-like compounds that may reduce risk of prostate cancer according to recent evidence, are vitamin D, vitamin E, lycopene (a compound related to beta-carotene and vitamin A) and selenium. For instance, a recent report demonstrated that men with low blood levels of vitamin D had a significantly higher risk of prostate cancer development. Important advances in understanding how to suppress prostate cancer development appears to involve the role of vitamin D and its effects on regulating prostate cell maturation and cell division rate (differentiation and proliferation). Prostate cancer cells are known to have vitamin D receptors and vitamin D has been shown to significantly inhibit the growth of prostate cancer under clinical and experimental conditions. The same is true in rat studies using a synthetic vitamin A analogue (N-4-hydroxyphenyl-retinamide). The importance of controlling and regulating the growth and replication rate of prostate cells is the most likely mechanism that vitamin D may reduce prostate cancer development. Further research is underway to better understand this relationship. In the meantime I suggest that healthy adult men ensure that they are ingesting 400 I.U. to 1,000 I.U. of vitamin D per day as part of a vitamin and mineral support. Another proposed mechanism for the development of prostate cancer involves free radicals. A number of studies suggest a link between free radicals (oxidative stress) and tumor development in various tissues. In several studies higher intake and/or blood levels of the antioxidants vitamin E and Lycopene have been associated with a decrease in prostate cancer incidence. Vitamin E and Lycopene are capable of quenching free radicals thereby minimizing their ability to damage genetic material (DNA), enzymes and other cellular components. As pointed out by Olson and Pienta, vitamin E has the potential to decrease DNA damage and inhibit malignant transformation through its antioxidant function. Additionally, Vitamin E affects the immune system; decreased vitamin E is associated with decreased immune response while high levels exert a stimulatory effect on immune function. In the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study, long-term supplementation with vitamin E was associated with a 32% decrease in the incidence of prostate cancer compared with those not receiving vitamin E supplementation. Moreover, death from prostate cancer was 41% lower among men receiving the vitamin E supplement. The length of this supplementation study was 5-8 years and the dosage of vitamin E was 50 mg (alpha-tocopherol). Previous studies have observed that low blood levels of vitamin E in smokers are associated with an increased risk of prostate cancer. Many researchers believe that antioxidant function is an important means to prevent prostate cancer initiation and promotion. This contention is further supported by the work of Clark et al. who demonstrated that supplementation with the mineral selenium (mean time period 4.5 years) was associated with a 63% lower incidence of prostate cancer. Selenium has indirect antioxidant properties of its own. The Health Professionals Follow-up Study also supports the hypothesis that antioxidant function can prevent prostate cancer. In this study of nearly 48,000 subjects Giovannucci et al. reported that a significant decrease in risk of developing prostate cancer was associated with of lycopene. Lycopene is found in tomatoes and certain tomato products and is known for its potent antioxidant properties. Lycopene is the most effective quencher of singlet oxygen (a very aggressive and harmful free radical) of the major carotenoids (beta-carotene-like compounds) and is the primary carotenoid in the blood and various tissues, including the prostate gland. An intake level of at least 6 mg per day or more of lycopene was associated with approximately a 21% reduction in prostate cancer incidence in The Health Professionals Follow-up Study, compared with men consuming less than 2.3 mg per day. Taken together the emerging research appears to suggest that vitamin D and the antioxidants vitamin E, selenium and lycopene may significantly reduce the risk of prostate cancer and premature death. Dietary interventions including these nutrients may well hold part of the answer to reducing the risk of this common disease. Prostate cancer is the most common cancer in males in North America. As part of a good chemo-preventive program to reduce the risk of developing this disease, healthy male adults should consider a multiple vitamin that contains 400 I.U.of vitamin D, 400 I.U. of vitamin E, 200 mcg. of selenium and 6 mg. of lycopene extract. Be advised that other nutritional factors may also help to prevent prostate cancer and are discussed in other review papers within this site. Copyright 1998 Dr. James Mescino D.C., M.S. References: 1. Liehr J.G. Androgen – Induced redox changes in prostate cancer cells: what are causes and effects? J Natl Cancer Inst. 1997; 1:3-6 2. Ripple MO et al. Prooxident-antioxidant shift induced by Androgen treatment of human prostate carcinoma cells. J Natl Cancer Inst. 1997; 89; 1:40-48 3. Grovannucci et al. Intake of carotenoids and retinol in relation to risk of prostate cancer. J Natl Cancer Inst. 1995; 87; 23:1767-76 4. Heinonen OP et al. Prostate cancer and supplementation with Alpha-Tocopheral and Beta-Carotene : Incidence and mortality in a controlled trial. J Natl Cancer Inst. 1998; 90; 6:440-446 5. Olson KB et al. Vitamins A and E: Further clues for prostate cancer prevention. J Natl Cancer Inst. 1998; 90; 6: 414-415 6. Ross RK et al. Do diet and androgens alter prostate cancer risk via a common etiologic pathway? J Natl Cancer Inst. 1994; 86; 4:252-54 7. Gann PH et al. Prospective study of plasma fatty acids and risk of prostate cancer. J Natl Cancer Inst. 1994; 86; 4:281-86 8. Linehan WM. Inhibition of prostate cancer metastasis: a critical challenge ahead. J Natl Cancer Inst. 1995; 87; 5: 331-32 Prostate Cancer
and Dietary Fat by Dr. James
Meschino D.C., M.S. Worldwide evidence strongly suggests that a high fat diet is a significant risk factor for the development of invasive prostate cancer. Autopsy studies from around the world have demonstrated that 15-30% of men over the age of 50 have cancer cells within the prostate gland regardless of their country of origin or race. However, the tendency for prostate cancer to grow and metastasize is far more prevalent in Western Europe, the United States and Canada, where the fat content of the diet is higher than in Japan and developing countries. The American male obtains approximately 36% of his daily energy intake from dietary fat, the majority of which is saturated and monounsaturated fats. Studies, especially those comparing prostate cancer rates between countries, have revealed differences between the fat content of diets in high and low-risk areas. Armstrong and Doll found that prostate cancer mortality in 32 countries was highly associated with total fat consumption, a finding similar to that for breast cancer. Rose et al. subsequently confirmed these data and determined that this association was limited to animal fat intake and did not include vegetable fat intake. Studies of migrant populations have also implicated environmental factors, such as diet in the development of prostate cancer. Furthermore, migrants who move from low-risk areas to the United States gradually assume the high risk of the U.S. population for prostate cancer. A number of observational (epidemiological) and prospective studies have found a strong association between high saturated fat intake and prostate cancer. High fat meat and dairy products have been specifically identified as foods strongly related to increased prostate cancer development. A large cohort study of Seventh-day Adventists found that overweight men had a relative risk of 2.5 for the development of prostate cancer, compared with men of normal weight. In addition this study found that men who consumed large amounts of milk, cheese, eggs and meat had a relative risk of 3.6 for the development of prostate cancer. Data from the Health Professionals Follow-up Study recently supported the contention that a high fat diet substantially increases risk of developing clinically significant prostate cancer. This study involved a prospective cohort of 51,529 U.S. men, aged 40 through 75, who work in the health professions. Total fat consumption was directly related to risk of advanced prostate cancer (age-and energy-adjusted relative risk =1.79) for high versus low quintile (20%) of intake. This association was due primarily to animal fat, but not vegetable fat. Red meat represented the food group with the strongest positive association with advanced cancer. Armstrong and Doll hypothesized that dietary fat may be a major cause of prostate cancer and could account in part for the 120-fold variation in incidence rates among countries. Investigation continues to help determine the mechanism through which high intakes of animal fats may promote prostate cancer development. Dietary fat may increase serum sex hormones, which can encourage cancer formation or progression. Cooked meats are known to contain carcinogens such as cholesterol epoxides, which may accumulate in the prostate gland and promote cancerous changes. There is scientific support for these mechanisms as well as other postulated mechanisms. Without reductions in incidence or improvements in treatment, by the year 2000, about 40,000 U.S. men will die annually from prostate cancer. Although an exact mechanism is yet not understood, reducing intake of animal fat (high fat meat and dairy) is a prudent step in the prevention of prostate cancer. Findings from the Health Professional Follow-up Study are consistent with this recommendation. In Japan, where prostate cancer deaths are 80% less frequent than in the United States, fat intake is only 15-20% of total energy per day, this appears to be a good target level of fat intake in regards to the prevention of many cancers, cardiovascular disease and other degenerative conditions. Copyright 1998 Dr. James Meschino D.C., M.S. References: 1. Pienta K and Esper P. Is dietary fat a risk factor for prostate cancer? J Natl Cancer Inst. 1993; 85;19:1538-40 2. Giovannucci E. et al. A prospective study of dietary fat and risk of prostate cancer. J Natl Cancer Inst. 1993; 85; 19:1571-79 3. Haenszel W, Kurihara M: Studies of Japanese migrants. I. Mortality from cancer and other diseases among Japanese in the United States. J. Natl Cancer Inst. 40:43-68, 1968 4. Staszewski W, Haenszel W: Cancer mortality among the Polish-born in the United States. J Natl Cancer Inst 35:291-297, 1965 5. Armstrong B, Doll R: Environmental factors and cancer incidence and mortality in different countries, with special references to dietary practices. Int J Cancer 15:617-631, 1975 6. Waterhouse J, Muir C, Shanmurgaratnam K, et al, eds: Cancer in five continents, vol IV. IARC Sci Publ No. 42. Lyon: IARC, 1982 7. Graham S, Haughey B, Marshall J, et al. Diet in the epidemiology of carcinoma of the prostate glad. J Natl Cancer Inst 70:687-692, 1983 8. Snowdon DA, Phillips RL, Choi W: Diet, obesity, and risk of fatal prostate cancer. Am J Epidemiol 120:244-250, 1984 9. Mills PK, Beeson WL, Phillips RL, et al.: Cohort study of diet, lifestyle, and prostate cancer in Adventist men. Cancer 64:598-604, 1989 Soybean
Phytoestrogens and the Prevention of Prostate Cancer by Dr. James
Meschino D.C., M.S. The geographic distribution of clinical prostate cancer in men is relatively low in the Far East and high in the industrialized West. Progeny of migrants from the East to the West are increasingly vulnerable to the disease. One change that accompanies migration is diet, and, in this instance, soybeans contribute much more to the diets in the East than in the West. It has been speculated that isoflavones (phytoestrogens) found in soybeans may contribute to the prevention of hormone-related cancers, including prostate cancer in men. Genistein, a prominent phytoestrogen component of soybeans, has been identified with multiple functions related to cancer prevention. Scientific investigation suggests that genistein can slow down the rate of cell division, block the growth of new blood vessels around cancer cells (anti-angiogenesis), suppress the "in vitro" growth of human breast and prostate cancer cell lines and inhibit the enzyme (5-alpha-reductase) which converts testosterone to dihydrotestosterone. All of these metabolic effects are associated with reduced risk of prostate cancer growth and progression. Further, genistein may suppress prostate cancer by binding to receptors on the prostate gland, blocking the entrance of testosterone into the gland. This anti-androgenic effect is made possible because genistein is a phytoestrogen, which means it can bind to the receptors on reproductive organs and exert a mild estrogen-like effect A number of animal studies have recently demonstrated the potential for soy phytoestrogens to inhibit prostate cancer. Pollard and Luckert used rats that are inherently susceptible to spontaneous and induced metastasizing cancer (adenocarcinomas) in the prostate gland and seminal vesicles. Before being treated with a cancer causing agent (methylnitrosourea) some of the rats were fed a high soy diet, rich in genistein and other isoflavones. In rats fed the high soy diet the incidence of prostate-related cancer was reduced and the disease-free period was prolonged by 27% compared with rats fed the same diet but low in isoflavones. The authors speculate that the suppressive effect of a high soy (isoflavone) diet on the development of spontaneous cancers in the prostate complex will have more relevance to the disease in humans. This is due to the fact that human prostate cancer has a longer latency period (time between initiation of the disease and the point at which it starts to grow and spread and become clinically relevant). Also, human tumors have a slower growth rate and a longer testosterone dependency period than the chemically induced prostrate cancers developed in rats. There is a consensus that if a chemo-preventive (chemical or nutritional) strategy could be developed that would be effective and also simple, nutritionally beneficial, inexpensive, and readily administered, indeed it would be a significant accomplishment. The regular consumption of soy products may provide such a benefit. Prostate cancer is 80% less frequent in Japan, than the United States. In Japan the average daily consumption of soybeans is approximately 30 grams per day. In the United States the average daily consumption is less than 4 grams per day. (Soyatech Inc., Based FAO/WHO consumption data). At this point in time it seems prudent to include soy products into the diet on a daily basis. This can take the form of roasted soybeans, soy milk, tofu, miso soup, tempeh, low fat soy cheese or textured vegetable protein burgers, hot dogs, sausages, etc. Soy extract supplementation may also be of benefit to elevate circulating levels of isoflavones. The above-mentioned foods are widely available today. As incredible as it seems, soy isoflavones may be one of the most important medicinal substances in the prevention of prostate cancer, which is the second leading cause of cancer death in men after lung cancer. Copyright 1998 Dr. James Meschino D.C., M.S. References: 1. Pollard M. and Luckert PH. Influence of Isoflavones in Soy Protein Isolates on development of induced prostate-related cancers in L-W rats. Nutr. And Cancer 1997; 28; 1:41-45 2. Wynder, EL, Mabuchi, K, and Whitmore, WF, Jr: Epidemiology of cancer of the prostate. Cancer 28, 344-360, 1971. 3. Dhom, G: Epidemiologic aspects of latent and clinically manifest carcinoma of the prostate. J Cancer Res Clin Oncol 106, 210-218, 1983. 4. Yatani, R, Shiraishi, K, Nakakuki, I, Kusano, H, and Takanari T: Trends in frequency of latent prostate carcinoma in Japan from 1965-1979 and 1982-1986." JNCI 80, 683-687, 1988. 5. Breslow, N, Chan, CW, Dhom, G, Drury, RAB, Franks, LM, et al.: Latent carcinoma of prostate at autopsy in seven arears. Int J Cancer 20, 680-688, 1977. 6. Haenszel, W, and Kurihara, M: Studies of Japanese migrants. I. Mortality from cancer and other diseases among Japanese in the United States. JNCI 40, 43-68, 1968. 7. Adlercreutz, H, Markkanen H, and Watanable, S: Plasma concentrations of phyto-estrogens in Japanese men. Lancet 342, 1209-1210, 1993. 8. Reinli, K, and Block, G: Phytoestrogen content of foods – a compendium of literature values. Nutr Cancer 26, 123-148, 1996. 9. Adlercreutz, H, Honjo, H, Higashi, A, Fotsis, T, Hamalainen, E, et al.: Urinary excretion of lignans and isoflavonoid phytoestrogens in Japanese men and women consuming a traditional Japanese diet. Am J Clin Nutr 54, 1093-1100, 1991. 10. Bickoff, EM, Livingston, AL, Hendrickson, AP, and Booth, AN: Relative potencies of several estrogen-like compounds found in forages. J Agric Food Chem 10, 410-412, 1962. 11. Pollard, M, Luckert, PH, and Snyder, D: Prevention and treatment of experimental prostate cancer in Lobund-Wistar rats. I. Effects of estradiol, dihydrotestosterone, and castration. Prostate 15, 95-103, 1989. 12. Akiyama, T, Ishida, J. Nakagawa, S. Ogaware, H, Watanabe, S-I, et al.: Genistein, a specific inhibitor of tyrosine-specific protein kinases. J Biol Chem 262, 5592-5595, 1987 13. Fotsis, T, Pepper M Adlercreutz, H, Fleischmann, G, Hase, T, et al.: Genistein, a dietary-derived inhibitor of in vitro angiogenesis.: Proc Natl Acad Sci USA 90, 2690-2694, 1993. 14. Steele, VE, Pereira, MA, Sigman, CC, and Kelloff, GJ: Cancer chemoprevention agent development strategies for genistein. J Nutr 125, 7135-7165, 1995. 15. Adlecreutz, H, Markkanen, H, and Watanabe, S: Plasma concentrations of phytoestrogens in Japanese men.: Lancet 342, 1209-1210, 1993. 16. Messina M, and Erdman, JW, Jr (eds): First International Symposium on the Role of Soy in Preventing and Treating Chronic Disease. J Nutr 125, Suppl 5675-8085, 1995. Treating Prostate
Enlargement With Saw Palmetto by Dr. James
Meschino D.C., M.S. In recent years numerous scientific and clinical research studies have revealed that the standardized extract of saw palmetto can effectively treat the common disorder of the prostate gland – benign prostatic hyperplasia (BPH). Approximately 50 to 60% of men between age 40 and 59 years of age develop an enlarged prostate gland (benign prostatic hyperplasia). This disorder is characterized by increased frequency of urination, nighttime awakening to empty the bladder, reduced urine stream and caliber of urination. Benign prostatic hyperplasia is thought to be caused by an accumulation of testosterone in the prostate. Within the prostate gland, testosterone is converted to the more potent form of the hormone known as dihydrotestosterone (DHT). DHT stimulates the cells of the prostate to divide and multiply excessively, leading to an enlarged prostate. The enlarged prostate applies pressure to the urethra impairing urine flow to varying degrees. One of the paradoxes of aging is that although the male body makes less total testosterone, the prostate gland more aggressively converts available testosterone into DHT. This is due to an increased activity of an enzyme known as 5-alpha-reductase, which converts testosterone to DHT within the prostate gland. The other undesirable effect of faster cell division is the increasing accumulation of genetic errors that can lead to prostate cancer; which is the most common cancer in men in this part of the world. Interestingly, males born with a genetic defect that impairs their ability to make the 5-alpha-reductase enzyme (hence, no DHT formation is possible) are virtually immune to prostate cancer development as it rarely occurs in these individuals or in eunuchs. The prescription drug Finasteride (Proscar) used to treat benign prostatic hyperplasia, works by inhibiting the activity of the 5-alpha-reductase enzyme, blocking DHT formation to some degree. Although Proscar has received much attention clinical studies have demonstrated that a natural herbal product known as saw palmetto can outperform its therapeutic effects as a treatment for enlarged prostate problems and produce fewer side effects (eg., erectile dysfunction). The original clue that saw palmetto could be effective in this regard dates back to the American Indians who used saw palmetto berries in the treatment of genitourinary tract disturbances. Since the early 1980s intensive research has revealed that saw palmetto berries contain active ingredients that naturally inhibit the 5-alpha-reductase enzyme in the prostate gland. These active ingredients are comprised of fatty acids and sterols. Subsequent studies have demonstrated that in order to be effective saw palmetto extracts must be standardized to contain 85-95% fatty acids and sterols, which should be clearly stated on the label. The recommended dosage is 160 mg twice daily (or a 45-50% std grade of the solid powdered extract; dosage - 320 mg, twice daily). Saw palmetto berries by themselves are not effective as individual berries are comprised of only 1.5 % fatty acids and sterols. This is why a standardized extract yielding sufficient levels of fatty acids and sterols is vital to the herb's effective application. In this form saw palmetto also acts as an anti-estrogen. Estrogen contributes to prostate enlargement because it inhibits the breakdown and elimination of DHT. At least 12 human studies have shown that it is effective in nearly 90% of patients, usually within a period of 4-6 weeks. No significant side effects have been reported and toxicity studies demonstrate that it is an extremely safe natural substance. In my experience saw palmetto is extremely effective in the treatment of enlarged prostate problems. Furthermore, I believe that by age 40 all men should consider using saw palmetto and other synergistic natural agents (eg., pygeium africanum, beta-sitosterol, soy isoflavones, stinging nettle) to slow down the replication rate of prostate cells. By slowing down cell division there is a less likely chance that genetic errors and cancerous mutations will occur. The biological plausibility is strong that saw palmetto and related natural compounds can not only reverse benign prostatic hyperplasia, but also prevent its onset and defend against genetic errors and cancerous mutations. Also be aware that genistein, an isoflavonoid found in soy products can also inhibit the 5-alpha-reductase enzyme and possesses anti-estrogen activity. Other protective nutrients involved in prostate health and cancer prevention include lycopene, vitamin E, pygeum and vitamin D. A discussion of their influence on the prostate gland appears in other related articles under the heading of prostate disease. Copyright 1998 Dr. James Meschino D.C., M.S. References: 1. Tanagho EA et al. (eds): Smith's general urology. Norwalf (CT): Appleton and Lange, 1995 2. Thompson JM et al: Chemoprevention of prostate cancer. Semin Urol 1995; 13:122-9 3. Carrila E et al.: Binding of permixon, a new treatment for prostatic benign hyperplasia, to the cytosolic androgen receptor in the rat prostate. J Steroid Biochem 20, 521-523, 1984. 4. Sultan C, et al.: Inhibition of androgen metabolism and binding by a liposterolic extract of Serenoa repens B in human foreskin fibroblasts. . J Steroid Biochem 20, 515-519, 1984. 5. Di Silverio E et al.: Evidence that Serenoa repens extract displays antiestrogenic activity in prostatic tissue of benign prostatic hypertrophy. Eur Urol 21, 309-314, 1992. 6. Boccafoschi and Annoscia S: Comparison of Serenoa repens extract with placebo by controlled clinical trial in patients with prostatic adenomatosis. Urologia, 50, 1257-1268, 1983. 7. Cirillo-Marucco E et al.: Extract of Serenoa repens (Permixon) in the early treatment of prostatic hypertrophy. Urologia 5, 1269-1277, 1983. 8. Tripodi V et al.: Treatment of prostatic hypertrophy with Serenoa repens extract. Med Praxis 4, 41-46, 1983. 9. Emili E, Lo Cigno M, and Petrone U: Clinical trial of a new drug for treating hypertrophy of the prostate (Permixon). Urologia, 50, 1042-1048, 1983. 10. Greca P and Volpi R: Experience with a new drug in the medical treatment of prostatic adenoma. Urologia 52, 532-535, 1985. 11. Duvia R, Radice GP, and Galdini R: Advances in the phytotherapy of prostatic hypertrophy. Med Praxis 4, 143-148, 1983. 12. Tasca A et al.: Treatment of obstructive symptomatology caused by prostatic adenoma with an extract of Serenoa repens. Double-blind clinical study vs. placebo. Minerva Urol Nefrol 37, 87-91, 1985. 13. Cukier et al.: Permixon versus placebo. C R Ther Pharmacol Clin 4(25), 15-21, 1985. 14. Crimi A and Russo A: Extract of Serenoa repens for the treatment of the functional disturbances of prostate hypertrophy. Med Praxis 4, 47-51, 1983. 15. Champlault G. Patel JC and Bonnard AM: A double-blind trial of an extract of the plant Serenoa repens in benign prostatic hyperplasia. Br J Clin Pharmacol 18, 461-462, 1984; Champault G et al.: Medical treatment of prostatic adenoma. Controlled trial: PA 109 vs placebo in 110 patients. Ann Urol 18, 407-410, 1984. 16. Mattei FM, Capone M and Acconcia A: Serenoa repens extract in the medical treatment of benign prostatic hypertrophy. Urologia 55, 547-552, 1988. 17. Braeckman J: The extract of Serenoa repens in the treatment of benign prostatic hyperplasia: A multi-center open study. Curr Ther Res 55, 776-785, 1984. Soy Isoflavones
May Hold Key to the Prevention of Prostate Cancer by Dr. James
Meschino, D.C., M.S. Prostate cancer is one of the most common cancers to affect men in Western countries (the leading cancer in U.S. and Canadian men), whereas in Africa, Eastern Europe, and Japan the risk of this disease remains low. Dietary and lifestyle factors appear to influence the development of this disease as migration studies indicate that a marked increase in prostate (and breast) cancer incidence occurs in persons that migrate from low- to high-risk geographical areas. Another intriguing fact is that postmortem evaluation indicates that the prevalence of latent (existing, but not manifest) prostate cancer is similar between high- and low-risk populations, with genetic and lifestyle factors implicated in the progression to the malignant form of the disease. Thus, by age 50, 15 to 30% of men have cancer cells present within the prostate gland regardless of where they reside. However, in low risk regions these cancer cells tend not to undergo promotion and progression to a clinically significant malignant state, but rather tend to remain dormant and non-life threatening. It is argued that certain dietary behaviors are directly involved in preventing the development of prostate cancer and/or prevent the further progression of latent prostate cancer. Intensive investigation has strongly suggested that soy isoflavones are one of the important dietary agents that appear to offer protection against prostate cancer. (1,2) In fact, a recent study using modern analytical technology to analyze dietary intakes of individual phytoestrogens in patients with prostate cancer or control subjects (cancer-free) indicated a significant protective effect of the soy isoflavones genistein and diadzein, as well as the phytoestrogen coumestrol. (3) Research in this area reveals that there are at least seven modes of action through which soy isoflavones (genistein and diadzein) may defend against prostate cancer: Anti-proliferative-soy isoflavones have been shown to inhibit two key enzymes within prostate cancer cells that trigger cell division and growth. These two enzymes include protein tyrosine kinase and topoismerase II. By blocking their activity soy isoflavones have demonstrated an impressive ability to greatly inhibit the growth and division of prostate cancer cells under experimental conditions. (4,5,6) Increase sex hormone-binding globulin-soy isoflavones stimulate the synthesis of sex hormone-binding globulin in vivo, thus reducing the plasma concentration of free, unbound sex hormones. As a result there is less available (unbound) testosterone and other steroid compounds that are free to bind to prostate receptors and exert their potentially hyperproliferative effects. It is well established that certain androgens and estrogens are linked to the progression and promotion of prostate cancer and higher serum levels of sex hormone-binding globulin is associated with a reduced risk of many hormone dependent cancers. (7,8) Decreased steroid hormone synthesis-soy isoflavones have demonstrated the ability to help block the over production of certain steroid hormones that influence the promotion and progression of prostate cancer. Specifically, soy isoflavones are known to inhibit 5 alpha-reductase, aromatase (estrogen synthase) and the 17 beta-hydroxysteroid dehydrogenase enzymes, which in turn block the synthesis (to an appreciable degree) of dihydrotestosterone, estrone and other steroid hormones, respectively. Dihydrotestosterone is known to enhance prostate cell division (including cancer cells) and is directly linked to the promotion and progression of prostate cancer in humans. The over production of estrogen hormone from adipose tissue is also associated with increased prostate cell proliferation and prostate cancer. (9,10,11) Antioxidant function-genistein, the most intensively researched soy isoflavonoid, also acts as a cellular antioxidant. As soy isoflavones are known to concentrate within prostatic fluids (at higher values than in plasma), they are considered to be an important defense against free radical damage and the cancerous mutations that are known to arise from free radical damage to prostate cells. (12,13,14) Apoptosis: Soy isoflavones have also been shown to selectively encourage prostate cancer cells to undergo programmed cell death (apoptosis). In particular genistein has been shown to inhibit cell growth and induce apoptosis by modulating transforming growth factor-beta signaling pathways. This effect has been clearly shown with both LNCaP and PC-3 human prostate cancer cell lines. (15,16) Anti-angiogenisis: Soy isoflavones demonstrate an ability to hinder the ability of cancer cells from growing the necessary capillaries that feed their growth as they attempt to spread (metastasize) to adjacent tissues. It appears that genistein, in particular, blocks the synthesis and/or release of growth factors required to form the extensive network of blood vessels necessary to aid the spread of the malignancy. (17,18) Androgen blockade: Soy isoflavones bind to androgen and estrogen receptors on the prostate gland, partially blocking access to the cell of testosterone, estrone and related hormone modulators of prostate cell (and prostate cancer cell) growth. The net effect appears to be a down-regulation influence whereby the growth and cell division rate of prostate cells is slowed and any existing prostate cancer cells are subjected to less of a stimulatory influence from various androgens and estrogens (due to lower intracellular concentrations). (19) This effect is readily apparent from studies that demonstrate that genistein inhibits the growth of benign prostate hypertrophy, prostate cancer tissue in histoculture (20) and growth of tumor cell implants in rats. (21) By all accounts sufficient evidence now exists to encourage the more frequent consumption of foods, supplements and nutraceuticals that are a rich source of soy isoflavones as a means to help prevent prostate cancer. Moreover, soy isoflavones may also be considered not only in a chemo preventive role, but possibly as chemotherapeutic agents as well. A recent report in the scientific literature indicated that in a case study, a 66-year old prostate cancer patient took a phytoestrogens supplement (160 mg per day) for one week before radical prostatectomy. On histological examination of the prostatectomy specimen, significant apoptosis in tumor cells suggestive of tumor regression was evident compared with the preoperative needle biopsy. (22) From the stand point of prostate cancer prevention the traditional Asian diet contains an average isoflavone content of 50mg per day. Epidemiological data indicate that the incidence of clinically important prostate cancer is 80% less in Japan than in Canada and the United States. (2,23,24) In summary, the body of evidence strongly suggests that men should consume sufficient soy products on a daily basis to yield a minimum of 50 mg of isoflavones as one means of prostate cancer chemoprevention. Soy isoflavones can be consumed from soy-based foods, supplements containing soy extract, and various soy-based functional foods (e.g. soy protein shake mix). References Yatani, R, Kusano, I, Shiraishi, T, Haysahi, T, and Stemmerman, GN: Latent prostate carcinoma: pathological and epidemiological aspects. Jpn J Clin Oncol 19, 319-326, 1989 Mitchell, J, et al. Effects of phytoestrogens on growth and DNA integrity in human prostate tumor cell lines: PC-3 and LNCaP. Nutr and Cancer, 2000: 38, 2: 223-228 Strom, SS, Yamamura, Y, Duporne, CM, Spitz, MR, Bahsain, RJ, et al: Phytoestrogen intake and prostate cancer: a case-control study using a new database. Nutr Cancer 33, 20-25, 1999 Akiyama, T, Ishida, J, Nakagawa, S, Ogawara, H, Watanabe, S, et al: Genistein, a specific inhibitor of tyrosine-specific protein kinases. J Biol Chem 262, 5592-5595, 1987 Kaufman, W: Human topoismerase II function, tyrosine phosphatydilation and cell cycle check points. Proc Soc Exp Biol med 289, 327-334, 1998 Constantinou, A, and Huberman, E: Genistein as an inducer of tumor cell differentiation: possible mechanisms of action. Proc Soc Exp Biol Med, 206, 109-115, 1995 Adlercreutz, H, Hockerstedt, K, Baanwart, C, Bloigu, S, Hamalainea, E, et al: Effect of dietary components, including lignans and phytoestrogens, on enterophepatic circulation and liver metabolism of estrogens, and on sex hormone-binding globulin (SHBG). J Steriod Biochem 27, 1135-1144, 1987 Adlercreutz, H, Hockerstedt, K, Baanwart, C, Hamalainea, E, Fotsis, T, et al: Association between dietary fibre, urinary excretion of lignans and isoflavosic phytoestrogens, and plasma non-protein bound sex hormones in relation to breast cancer. In Progress in Cancer Research and Therapy: Hormones and Cancer, P Bresciani, RJB King, ME Lippman, and JP Raynaud (eds.) New York: Raven, 1988, vol 3, chapt 35, pp. 409-412 Makela, S, Poutanes, M, Lehtimaki, J, Kostian, MI, Santi, R, et al: Estrogen-specific 176-hydroxysteroid oxidoreduotase type I (EC 1.1.1.62) as a possible target for the action of phytoestrogens. Proc Soc Exp Biol med 208, 51-59, 1995 Evans, BAJ, Griffiths, K, and Morton, MS: Inhibition of 5a-reductase in genital skin fibroblasts and prostate tissue by lignans and isoflavonoids. J Endocrinol 147, 295-302, 1995 Wang, C, Makela, T, Hase, T, Adlercreutz, H, and Mindy, MS: Lignans and flavonoids inhibit aromatase enzyme in human preadipocytes, Steroid Biochem Mol Biol 50, 205-212, 1994 Messina, M et al. First International Symposium on the role of soy in preventing and treating chronic disease. J Nutr 1995, 125 (suppl): 5675-8085 Wei, H, Bowen, R, Cai, Q, Barnes, S, and Wang, Y: P Antioxidant and antipromotional effects of the soybean isoflavone genistein. Proc Soc Exp Biol Med 206, 124-130, 1995 Mitchell, JH, Gardner, PT, McPhail, DB, Morrice, PC, Collins, AR, et al: Antioxidant efficacy of phytoestrogens in chemical and biological model systems. Arch Biochem Biophys 360, 142-148, 1998 Kime, H, Peterson, TG, and Barnes S: Mechanisms of action of the soy isoflavone genistein: emerging role for its effects via transforming growth factor-B-signaling pathways. Am J Clin Nutr, 68, S1418-1425, 1998 Sathymoorthy, N, Gilsdorf, JS, and Wang, TTY: Differential effects of genistein on transforming growth factor-B1 expression in normal and malignant mammary epithelial cells. Anticancer Res: 18, 2449-2453 1998 Fotsis, T, et al. Genistein, a dietary derived inhibitor of in vitro antiogenesis. Proc Natl Acad Sci USA, 1993, 90: 2690-2694 Steele, VE , et al., Cancer chemoprevention agent development strategies for genistein. J Nutr. 1995, 125: 7135-7165 Pollard, M, et al. Influence of isoflavones in soy protein isolates on development of induced prostate-related cancers in L-W rats. Nutr and Cancer. 1997: 28, 1: 41-45 Schleicher, T, Zheng, M, Shang, M and Lamartiniere, CA: Genistein inhibition of prostate cancer cell growth and metastasis in vivo (abstract) Am J Clin Nutr 68 Suppl, 15268, 1998 Geller, J, Sionit, L, Partido, C, Li, L, Tan, X, et al: Genistein inhibits the growth of human-patient BPH and prostate cancer in histoculture Prostate 34, 75-79, 1998 Stephens, FO: Phytoestrogens and prostate cancer: possible preventive role. Med J Aust 167, 138-140, 1997 Armstrong, B, et al. Environmental factors and cancer incidence and mortality in different countries, with special references to dietary practices. Int J Cancer, 1975; 15: 617-631 Haenszel, W, et al. Studies of Japanese migrants. Mortality from cancer and other diseases among Japanese in the United States. J Natl Cancer Inst., 1968; 40: 43-68 © Copyright: Dr. James Meschino, D.C., M.S.,2000 |