Prostate cancer can cause any of the following symptoms:
• A need to urinate frequently, especially at night
• Difficulty starting urination or holding back urine
• Inability to urinate
• Weak or interrupted flow of urine
• Painful or burning urination
• Difficulty in having an erection
• Painful ejaculation
• Blood in urine or semen
• Frequent pain or stiffness in the lower back, hips, or upper thighs
Prostate cancer is a form of cancer that develops in the prostate, a doughnut-shaped gland about the size of a walnut that lies below the bladder and surrounds the urethra (the tube that connects the bladder to the tip of the penis). Prostate cancer is the most-diagnosed form of cancer in American men. Each year roughly 200,000 men are diagnosed with prostate cancer and more than 30,000 will die from it. In many respects, prostate cancer is the mirror of breast cancer in women: it is a hormone-sensitive cancer that will affect at least one out of every six men now living in the United States.
Most prostate cancers are slow-growing; however, there are cases of aggressive prostate cancer. The cancer cells may metastasize (spread) from the prostate to other parts of the body, particularly the bones and lymph nodes. Next to lung cancer, in men prostate cancer is the second-leading cause of death due to cancer.
The symptoms listed above are not specific for prostate cancer, especially the first four, which are usually a sign of benign prostatic hyperplasia (BPH), a noncancerous enlargement of the prostate (see the chapter “Prostate Enlargement [BPH]”). The symptoms listed can also indicate a prostate infection. If you are experiencing any of these symptoms, it is important to see a doctor immediately.
Researchers are studying factors that may increase the risk of this disease. Studies have found that the following risk factors are associated with prostate cancer:
• Family history of prostate (or breast) cancer. A man’s risk for developing prostate cancer is two times higher if his father has had the disease, five times higher if a brother has had it, and two times higher if his mother or sister has had breast cancer.
• Age. In the United States, prostate cancer is found mainly in men over age 55, and more than 8 out of 10 cases are in men over 65. The average age of patients at the time of diagnosis is 70.
• Race. Prostate cancer is roughly twice as common in African-American men as in white men. It is less common in Asian and Native American men.
• Hormonal factors. Testosterone is thought to stimulate hormone-dependent prostate cancer in much the same way that estrogen stimulates breast cancer. Other hormones implicated are estrogen and prolactin.
• Diet and dietary factors. Current research indicates that diets high in red meat, dairy, and saturated fat are associated with an increased risk of developing prostate cancer. Risks are also increased for those who have diets low in fruits, vegetables, phytoestrogens, selenium, vitamin E, lycopene, and other dietary antioxidants.
The most important aspect of detecting prostate cancer for men over the age of 50 years is seeing a physician for an annual physical exam that includes:
• Digital rectal exam. The doctor inserts a lubricated, gloved finger into the rectum and feels the prostate through the rectal wall to check for hard or lumpy areas.
• Blood test for prostate-specific antigen (PSA). PSA is usually elevated in men with prostate cancer. A normal PSA level ranges from 0 to 4 ng/ml. A PSA level of 4 to 10 ng/ml is considered slightly elevated, levels between 10 and 20 ng/ml are considered moderately elevated, and anything above that is considered highly elevated. The higher the PSA level, the more likely it is that cancer is present. However, approximately 35% of men with diagnosed prostate cancer will have a PSA of less than 4 ng/ml. The level of PSA in the blood tends to rise with prostate cancer, but minor elevations may be due to less serious conditions such as prostatitis (inflammation of the prostate) and BPH. PSA levels alone do not give doctors enough information to distinguish between benign prostate conditions and cancer; the doctor will take the result of this test into account in deciding whether to check further for signs of prostate cancer. In addition to being used as a screening test, PSA is also used to monitor patients with a history of prostate cancer to see if the cancer has come back. Researchers are looking for ways to distinguish between cancerous and benign conditions, and between slow-growing cancers and fast-growing, potentially lethal cancers. Some of the methods being studied are:
PSA velocity. PSA velocity is based on changes in PSA levels over time. A sharp rise in the PSA level raises the suspicion of cancer.
Age-adjusted PSA. Age is an important factor in increasing PSA levels. For this reason, some doctors use age-adjusted PSA levels to determine when diagnostic tests are needed. When age-adjusted PSA levels are used, a different PSA level is defined as normal for each 10-year age group. Doctors who use this method suggest that men younger than age 50 should have a PSA level below 2.5 ng/ml, while a PSA level up to 6.5 ng/ml would be considered normal for men in their 70s.
PSA density. PSA density considers the relationship of the PSA level to the size and weight of the prostate. In other words, an elevated PSA might not arouse suspicion in a man with a very enlarged prostate. The use of PSA density to interpret PSA results is controversial because cancer might be overlooked in a man with an enlarged prostate.
Free vs. attached PSA. PSA circulates in the blood in two forms: free or attached to a protein molecule. With benign prostate conditions, there is more free PSA, while cancer produces more of the attached form. If the PSA is between 4 and 10 mg/ml, a free PSA of less than 10% suggests a high risk of cancer, while a free PSA of more than 25% suggests a low risk of cancer.
• Biopsy. A biopsy of the prostate involves taking tissue samples from the prostate via the rectum with the use of a biopsy gun that inserts and removes special hollow-core needles (usually three to six on each side of the prostate) in less than a second. Prostate biopsies are routinely done on an outpatient basis. The tissue samples are then examined under a microscope to determine whether cancer cells are present and to evaluate the microscopic features (or Gleason score) of any cancer found. In general, the higher the Gleason score, the more aggressive the cancer.
TO SCREEN OR NOT TO SCREEN?
The rationale for early detection of cancer is that it leads to more effective treatment. Unfortunately, the data on PSA screening for prostate cancer do not support this notion. Several reviews on the impact of PSA screening showed no statistically significant difference in death due to prostate cancer between men randomly assigned to screening and those who were not screened.1,2 In fact, the Centers for Disease Control and Prevention and the U.S. Preventive Services Task Force believe that PSA screening produces more harm than good based upon very extensive analyses. Harms of screening included high rates of false-positive results for the PSA test and the adverse events associated with biopsies (such as infection, bleeding, and pain) and with the treatment of prostate cancer with chemotherapy and radiation. It is believed that in most cases the prostate cancer would not have seriously affected the patient’s life expectancy if it had simply been left alone. Most prostate cancers are extremely slow-growing, meaning that men can live with prostate cancer, rather than die from it. In fact, autopsy studies report that more than 30% of all men over the age 50 have evidence of prostate cancer, but only 3% will die from it.
Our feeling is that the problem with early screening is not the screening but what happens after the screening. In the case of PSA screening, the approach should be “watchful waiting” vs. immediate biopsy unless accompanied by significant PSA velocity or family history or unless the patient is African-American. And if the biopsy is positive, even then a conservative approach should be taken with the majority of men. Now, that does not mean that we advocate idleness with watchful waiting. In fact, we recommend just the opposite: an aggressive focus on the measures detailed in this chapter, which can help prevent or even reverse the disease.
The therapeutic goal is to reduce as many risk factors as possible while simultaneously implementing dietary and lifestyle factors associated with prostate cancer prevention. Most of the lifestyle factors linked to preventing cancer in general, such as avoiding cigarette smoke or excessive intake of alcohol, also apply to prostate cancer. The same is true for dietary factors. Therefore, we recommend strengthening the “four cornerstones of good health” detailed in Section II of this book:
• A positive mental attitude
• A health-promoting lifestyle
• A health-promoting diet
• Supplementary measures
Focusing on these key foundations provides the strongest general protection against cancer of any type.
There is so much convincing evidence on the role of diet in prostate cancer that Dr. William Fair and colleagues from Memorial Sloan-Kettering Cancer Center went so far as to suggest that prostate cancer may be a nutritional disease.4 Key causative dietary factors include diets rich in animal foods (particularly grilled and broiled meats, saturated fat, and dairy products) and low in protective nutrients such as lycopene, selenium, vitamin E, soy isoflavones and other dietary phytoestrogens, omega-3 fatty acids (particularly those from fish), and isothiocyanates from vegetables in the brassica (cabbage) family. As is also the case in breast cancer, these dietary factors are known to affect sex hormone levels, detoxification mechanisms, and antioxidant status.5,6
MALE-PATTERN BALDNESS AND PROSTATE CANCER
Men with male-pattern baldness appear to have an increased risk for prostate cancer, according to a study of more than 4,000 men tracked since the 1970s by a research team from the National Institutes of Health. The results indicated that men with any degree of male-pattern baldness (characterized by gradual hair loss at the front and/or crown of the head) in their mid-twenties were 50% more likely to develop prostate cancer.3
It was hypothesized that there might be an association between male-pattern baldness and prostate cancer on the basis that both conditions are sensitive to testosterone levels. There are receptors for testosterone on the cells of both hair follicles and the prostate. Male-pattern baldness has also been linked to a higher risk for heart disease.
These findings mean not that balding men will definitely get prostate cancer, but only that they are at increased risk, meaning that they would be wise to be more aggressive with dietary and supplementation programs to reduce their risk of developing prostate cancer.
In fact, it would be worthwhile to read the chapter “Breast Cancer (Prevention)” to gain an even greater appreciation of how diet can affect hormone-sensitive tissues like the breast and prostate. One of the interesting dietary associations in breast cancer is the high risk that comes with eating well-done or charbroiled meat; frequent consumption of well-done meat, for example, was associated with a nearly 500% increase in breast cancer. With prostate cancer the risk is a little less but still very significant. Higher consumption of hamburgers, processed meats, grilled meats, and well-done meat was associated with an approximately 50 to 80% increase in aggressive forms of prostate cancer.7
Another food that has been strongly implicated in prostate cancer is milk. In a study conducted in Canada, researchers found a twofold increased risk of prostate cancer associated with an increased intake of milk. Interestingly, it was the only dairy product associated with an increased risk for prostate cancer.8 Initially researchers thought the risk might be due to the calcium, but it now appears that it is due to milk’s high phosphorus content.9
High intakes of certain foods are associated with a reduction in prostate cancer risk, while high intakes of other foods are associated with increased risk:5–10
• Fish: 44% reduced risk
• Tomatoes, tomato sauce, tomato juice: 35% reduced risk
• Green leafy vegetables: 34% reduced risk
• Soy: 30% reduced risk
• Vegetables high in carotenoids: 29% reduced risk
• High-glycemic-index foods: 64% increased risk
• Hamburgers: 79% increased risk
• Processed meat: 57% increased risk
• Grilled red meat: 63% increased risk
• Well-done red meat: 52% increased risk
• Milk: 111% increased risk
Without question the dietary recommendations in the chapter “A Health-Promoting Diet” are powerful in helping to protect against prostate cancer. It is also important to point out that the Mediterranean diet has been shown to help prevent prostate cancer. That would be expected given that it is high in vegetables, legumes, dried and fresh fruits, and fish; olive oil is its main fat source; it is low in animal fats, processed red meat, milk and dairy products; and it includes regular but low alcohol intake (wine with meals).11
The isoflavones of soy—genistein and daidzein—exert significant protection against prostate cancer, according to population-based studies.12 Test tube and animal studies have confirmed that soy isoflavones inhibit the growth of prostate cancer cells.13 Since both testosterone-dependent and testosterone-independent prostate cancer cells are inhibited, it appears that soy isoflavones possess several types of anticancer action. The high intake of soy may be one of the key protective factors accounting for the low rate of prostate cancer in Japan and China compared with other parts of the world: blood and urine concentrations of soy isoflavones (an indicator of intake) were found to be 7 to 10 times higher in Japanese men consuming a traditional Japanese diet compared with Finnish men consuming a typical Western diet.12 A study of 12,395 California Seventh-Day Adventist men found that men who drank soy milk had a 70% reduction in the risk of prostate cancer.14 A study of 42 countries found soy to have a higher protective value against prostate cancer than any other dietary factor.12 Higher blood levels of genistein are associated with a significantly reduced risk of developing prostate cancer.15 A daily dietary intake of 45 to 90 mg soy isoflavones is recommended for prevention of prostate cancer. Information on the isoflavone content of common soy foods can be found on page 788.
Omega-3 Fatty Acids
The risk of prostate cancer is reduced with a higher intake of fish rich in the omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). In a population-based study, reduced prostate cancer risk was associated with a high red blood cell content of EPA and DHA.16 This study provided further support to previous population-based studies as well as test tube and animal experiments showing that these omega-3 fatty acids inhibit prostate cancer cells.
Just as in breast cancer again, the benefits of these long-chain omega-3 fatty acids are magnified when the level of animal fat (saturated fat, and arachidonic acid in particular) is also reduced. A high ratio of dietary omega-6 to omega-3 fatty acids is major risk factor for prostate cancer.17
While the data are clear that increased consumption of long-chain omega-3 fatty acids from fish offers protection against prostate cancer, there has been some controversy about recommending flaxseed oil, which contains the omega-3 fatty acid alpha-linolenic acid (ALA), to men; we believe this is based upon the misunderstanding of some research results. While ALA shows benefit against breast cancer, some initial studies indicated that ALA may actually increase the risk of prostate cancer.18–20 However, in some of these studies ALA intake was used simply as a marker for meat intake. In the absence of consuming vegetable sources of ALA, such as flaxseed or canola oil, the primary dietary source is from meat. It is also possible that deficiencies of zinc or other nutrients involved in the conversion of the shorter-chain ALA to the longer-chain EPA and DHA are ultimately responsible for the elevations in ALA noted in men with prostate cancer. About 50% of all men with prostate cancer are deficient in zinc. More recent analysis shows that there is no concern with ALA as a risk factor in prostate cancer.21
Nonetheless, studies also seem to indicate that if diets are high in ALA and low in antioxidants (especially lycopene, discussed below) it could be a problem. Unfortunately, no one has actually looked at the effect of flaxseed oil in prostate cancer. It is very likely that the lignan content overrides any problem with ALA. At this time it appears that men in general may be better off avoiding flaxseed oil supplements and focusing on ground flaxseed (for the lignans) and fish (for the omega-3 fatty acids).
Ground flaxseed appears to be quite helpful not only in preventing prostate cancer but also in men with existing prostate cancer. In addition to its phytoestrogenic effect, flaxseed lignans also bind to male hormone receptors and promote the elimination of testosterone. In a study of men with prostate cancer, a low-fat diet (with fat providing 20% or less of total calories) supplemented with 30 g ground flaxseed (roughly 2 tbsp) reduced serum testosterone by 15%, slowed the growth rate of cancer cells, and increased the death rate of cancer cells after only 34 days.23
AFRICAN-AMERICAN MEN, FAT INTAKE, AND PROSTATE CANCER
African-American men develop prostate cancer twice as frequently as white men. Although genetics could play a role, a more likely explanation is dietary differences. In a study conducted by the National Cancer Institute of men who had been newly diagnosed with biopsy-proved prostate cancer and matched controls without prostate cancer, it was shown that increased consumption of foods high in animal fat was linked to prostate cancer (independent of intake of other calories) among black men compared with whites. The higher the intake of animal fat, the greater the risk for advanced prostate cancer. These results indicate that diet plays a major role in why black men have a higher rate of prostate cancer and show that a reduction of fat from animal sources in the diet could lead to decreased incidence and mortality rates for prostate cancer, particularly among African-Americans.22
Several population-based studies suggested that vitamin E supplementation prevents prostate cancer.5,6 The same sort of protection has been demonstrated in some clinical studies as well. In one, a total of 29,133 male smokers ages 50 to 69 from southwestern Finland were randomly assigned to receive vitamin E (50 mg), beta-carotene (20 mg), both nutrients, or a placebo for 5 to 8 years (median 6.1 years). A 32% decrease in the incidence of prostate cancer was observed among the 14,564 subjects receiving vitamin E compared with the 14,569 not receiving it. Mortality from prostate cancer was 41% lower among men receiving vitamin E. However, in the 14,560 subjects receiving beta-carotene, prostate cancer incidence was actually 23% higher and mortality was 15% higher compared with the 14,573 not receiving it.24 Once again these results emphasize the importance of broad-spectrum antioxidant support.
Another form of vitamin E, known as gamma-tocopherol, may prove to be more important against prostate cancer than the alpha-tocopherol form, which has been used in virtually all the vitamin E research. Eight different compounds—four tocopherols and four tocotrienols—make up the vitamin E family. They have some functions that are similar and other functions that are completely different. Alpha-tocopherol became synonymous with vitamin E for two main reasons: (1) of the eight, it is the most abundant in the human body, and (2) it is by far the most effective of the eight for what was originally thought of as vitamin E’s main function—to support reproduction.
Our blood and tissue contain much more alpha-tocopherol than gamma-tocopherol despite the fact that in the typical American diet we consume twice as much gamma-tocopherol as alpha. The reason is that the liver is able to identify the alpha-tocopherol as it is absorbed from the gut and bind it to a special protein, called the alpha-tocopherol transfer protein. It recognizes the alpha-tocopherol and preferentially puts more of it in lipoproteins—proteins that carry fat and cholesterol (e.g., LDL, VLDL, and HDL).
So why is gamma-tocopherol important? It has some actions of its own, but more likely it is metabolized to a more active compound known as LLU-alpha-tocopherol. This compound and other metabolites may act to better protect the prostate from oxidative damage as well as promote apoptosis (programmed cell death), which helps prevent cells from becoming cancerous.
In one study, 117 men who developed prostate cancer and 233 matched control subjects had toenail and plasma samples assayed for selenium, alpha-tocopherol, and gamma-tocopherol.25 The risk of prostate cancer declined (but not linearly) with increasing concentrations of alpha-tocopherol. For gamma-tocopherol, men with the highest levels had a fivefold reduction in the risk of developing prostate cancer compared with men with the lowest levels. The association between selenium and prostate cancer risk was in the protective direction. Statistically significant protective associations for high levels of selenium and alpha-tocopherol were observed only when gamma-tocopherol concentrations were high as well. These results indicate that in order to achieve the greatest degree of protection, natural mixed tocopherols that include both alpha- and gamma-tocopherol should be used, rather than only alpha-tocopherol.
Remember that vitamin E is available in many different forms. First of all, there is natural vs. synthetic. Natural forms of vitamin E are designated d-, as in d-alpha-tocopherol, while synthetic forms are dl-, as in dl-alpha-tocopherol. The prefixes d- and l- refer to two versions of the vitamin E molecule that are, in effect, mirror images of each other, the way your right hand is a mirror image of your left. In the human body, only the natural form is recognized. Although the synthetic form has antioxidant activity, it may actually inhibit the natural form from entering cell membranes. Therefore, natural vitamin E (d-alpha-tocopherol) has greater benefit than the synthetic form (dl-alpha-tocopherol). We strongly recommend avoiding synthetic vitamin E.
Like vitamin E, selenium has also shown benefit in preventing prostate cancer in some studies. A 10-year cancer prevention trial found that selenium supplementation appears to significantly lower the incidence of not only prostate cancer but also lung and colon cancers in people with a history of skin cancer.26 The primary purpose of the study was to see if dietary supplements of selenium could lower the incidence of basal cell or squamous cell skin cancers, but seven years into the study several secondary end points (including the incidence of three commonly occurring cancers: lung, colorectal, and prostate) were added.
The results of the study were exciting to researchers because they showed the cancer prevention potential of simply adding a nutritional supplement to a normal diet. Participants in the randomized, double-blind study took either 200 mcg of selenium per day or a placebo for four and a half years and were followed for more than six additional years. Three-quarters of the participants were men. Total cancer incidence was significantly lower in the selenium group than in the placebo group (77 cases vs. 119), as was the incidence of some specific cancers: the selenium group had fewer lung cancers (17 vs. 31), fewer colorectal cancers (8 vs. 19), and fewer prostate cancers (13 vs. 35, a 63% reduction).
THE SELECT PROSTATE CANCER PREVENTION TRIAL
Because the evidence from preliminary studies with vitamin E and selenium was so convincing, the SELECT Prostate Cancer Prevention Trial, the largest prostate cancer prevention trial to date, sought to determine whether these two dietary supplements can protect against prostate cancer. The study randomly assigned 35,533 men to four groups: selenium (200 mcg per day) plus a placebo, vitamin E (400 IU per day) plus a placebo, selenium plus vitamin E, or placebo and placebo. Eligibility criteria were age 50 years or older for African-Americans, 55 years or older for Caucasians, a serum PSA level of 4 ng/ml or less, a digital rectal examination not suspicious for cancer, and normal blood pressure. While the study was planned to last 12 years, it was terminated after 7 years because no effect on the risk of prostate cancer in these relatively healthy men could be demonstrated by selenium, vitamin E, or the combination at the doses and formulations used in the study. Concerns of the SELECT trial were a modest increase in the risk of prostate cancer with vitamin E (6% increased risk) and in the risk of type 2 diabetes in the selenium group (7% increased risk).27
Reasons why selenium and vitamin E, alone or in combination, failed to prevent prostate cancer in the SELECT trial are not clear. However, our feeling is that the researchers may have been looking at the wrong form of tocopherol (see the discussion above about gamma-tocopherol). Also, other trials studying high-dose vitamin E for disease prevention have shown no benefit either. It may be that when taken at such high dosages, vitamin E loses its preventive effects. In the absence of companion antioxidants vitamin E may become a free radical itself or be unable to perform its function (see the discussion of lycopene below). The earlier positive studies used a dosage of 50 IU, not the 400 IU used in the SELECT Study. Next, several studies suggested that vitamin E is more protective against prostate cancer in smokers, and less than 60% of SELECT men were current or former smokers, whereas in some of the other studies with vitamin E all men were smokers. The fact that selenium was ineffective in preventing prostate cancer could be due to the subjects’ having sufficient levels of selenium before the trial started.28
The results also showed that overall mortality was 17% less in the selenium group than in the control group (108 deaths vs. 129), with this difference largely due to a 50% reduction in cancer deaths (29 vs. 57).
One of the most important anticancer nutrients, especially for the prostate, is lycopene—a carotene that provides the red color in tomato products. Lycopene is one of the major carotenes in the diet of North Americans and Europeans. More than 80% of lycopene consumed in the United States is derived from tomato products, although apricots, papaya, pink grapefruit, guava, and watermelon also contribute to dietary intake. Lycopene content of tomatoes can vary significantly, depending on type of tomato and stage of ripening. In the reddest strains of tomatoes, lycopene concentration is close to 50 mg/kg, compared with only 5 mg/kg in the yellow strains. Lycopene appears to be relatively stable during cooking and food processing. In fact, the absorption and utilization of lycopene from tomato paste or juice are up to five times greater compared with the absorption from raw tomatoes because it has been better liberated from the plant cell. Eating a lycopene source with some oil (e.g., olive oil) can also improve its absorption.
Lycopene is a more potent scavenger of oxygen radicals than other major dietary carotenes, and it exerts additional anticancer effects. Lycopene’s role as a protector against prostate cancer was highlighted in a finding by Harvard researchers that of all the different types of carotenes, only lycopene was clearly linked to protection against prostate cancer.29 The men who had the greatest amounts of lycopene in their diet (6.5 mg per day) showed a 21% decreased risk of prostate cancer compared with those eating the least. When the researchers looked at only advanced prostate cancer, the high-lycopene group had an 86% decreased risk (although this did not reach statistical significance due to the small number of cases). In a study of patients with existing prostate cancer, lycopene supplementation (15 mg per day) was shown to slow tumor growth. In subjects consuming the lycopene supplement, prostate tumors shrank and produced reduced levels of prostate-specific antigen.30
Population-based studies also indicate that lycopene protects against cancers of the colon, cervix, lung, and breast. Researchers have also found a statistically significant association between high dietary lycopene and a lower risk of heart disease.31
Clearly, increasing the intake of lycopene is a key goal in preventing many cancers, including prostate cancer. Although lycopene supplements are available in pill form, there are excellent food sources of lycopene. For example, a 12-oz can of tomato paste contains 192 mg lycopene and costs around $1.59 (less than 1 cent per mg of lycopene). But a bottle of 30 lycopene capsules (15 mg each) totaling 450 mg costs $18.99 (nearly 6 cents per mg). While lycopene alone has clear benefit, it is important to point out that in a test tube study it was found that lycopene alone was not a potent inhibitor of prostate cancer cell proliferation. However, the simultaneous addition of lycopene together with alpha-tocopherol (vitamin E) resulted in a 90% decrease in cell proliferation.32
Population-based studies suggest that vitamin D protects against prostate cancer, although evidence is limited and inconsistent. In the most recent study, it was shown that men deficient in vitamin D were twice as likely to suffer from more aggressive prostate cancers, but there was no evidence of an association with overall prostate cancer risk.33
Berries and Other Sources of Proanthocyanidins
Blackberries, raspberries, blueberries, blackcurrants, cranberries, acai berries, and strawberries, as well as other fruits rich in similar flavonoids, such as pomegranates, cherries, and plums, appear to be extremely helpful in preventing prostate cancer, as test tube studies have shown impressive anticancer actions.34–37 In addition, a study showed that any use of grape seed extract was associated with a 41% reduced risk of prostate cancer.38 Studies in Italy showed similar protection with procyandin intake and a variety of cancers.39 It can be concluded that the same degree of protection would be found in other concentrated sources of procyanidolic oligomers (e.g., pine bark or extracts of cranberry, blueberry, pomegranate, or acai berry). Regular consumption of these foods and supplementation with a concentrated source of procyanidolic oligomers are recommended.
• Prostate cancer is the most-diagnosed form of cancer in American men.
• It is important to reduce as many risk factors as possible while simultaneously implementing dietary and lifestyle factors associated with prostate cancer prevention.
• There is so much convincing evidence on the role of diet in prostate cancer that some authorities have suggested that prostate cancer may be a nutritional disease.
• Higher consumption of hamburgers, processed meats, grilled meats, and well-done meat was associated with an approximately 50 to 80% increase in aggressive forms of prostate cancer.
• A Mediterranean-style diet has been shown to help prevent prostate cancer.
• Studies suggest that men who drink soy milk have a lower risk of prostate cancer.
• A high ratio of dietary omega-6 to omega-3 fatty acids is a major risk factor for prostate cancer.
• Diet plays a major role in why black men have a higher rate of prostate cancer.
• Selenium and vitamin E have not been proved to have any effect on the risk of prostate cancer.
• Gamma-tocopherol may prove to be more important against prostate cancer than alpha-tocopherol.
• Men who consume the greatest amounts of lycopene had a lower risk of prostate cancer.
• Use of grape seed extract was associated with a reduced risk of prostate cancer.
• Green tea polyphenols have shown considerable benefit in preventing prostate cancer.
Population-based studies have demonstrated that consumption of green tea (Camellia sinensis) may offer significant protection against many forms of cancer, including prostate cancer.40 In order to take advantage of this protection you would need to drink three to five cups per day, providing a minimum of 250 mg per day polyphenols (also referred to as catechins). However, emerging clinical data suggest that this dosage level may not be sufficient in high-risk individuals.
The best data on green tea’s anticancer effects may actually be on prostate cancer. Test tube and animal studies have shown that epigallocatechin gallate (EGCG)—a major polyphenol in green tea—inhibits both hormone-sensitive and hormone-insensitive prostate cancer cells. In one study, men with clinically localized prostate cancer were divided into groups and consumed either six cups of green tea per day or water for three to six weeks before undergoing surgery to remove the prostate (radical prostatectomy).41 With the use of highly sensitive lab analysis, metabolites of EGCG were detectable in both prostate tissue and urine in men consuming the green tea. This study also showed initial indications that EGCG metabolites in the prostate cancer cells helped induce apoptosis.
In another study, men who were about to undergo radical prostatectomy for prostate cancer were given either 1,300 mg per day of green tea polyphenols or a placebo until the time of the surgery. The results showed a significant reduction in serum levels of PSA in men with prostate cancer after brief treatment with green tea polyphenols.42
A proof-of-principle clinical trial was designed to assess the safety and efficacy of green tea polyphenols in preventing precancerous lesions from developing into prostate cancer within one year.43 The 60 men in the study were given either a placebo or 600 mg green tea polyphenol extract per day. After one year, only one tumor was diagnosed among the 30 extract-treated men, whereas nine cancers were found among the 30 placebo-treated men. Total PSA levels were consistently lower in the green tea group than in the placebo group. Men who had benign prostate hyperplasia (BPH) also significantly improved on the green tea polyphenol extract.
Pygeum (Pygeum africanum) is an evergreen tree native to Africa. An extract made from its bark has been well studied in promotion of a healthy prostate (see the chapter “Prostate Enlargement [BPH]”). Current treatment of prostate cancer often involves the use of antiandrogens, synthetic compounds that block the action of testosterone by inhibiting androgen receptors. These compounds have numerous side effects and typically are effective for only about 16 to 24 months, after which the prostate cancer cells cease being androgen-dependent. By contrast, pygeum has a different mechanism of action and efficiently represses the growth of both androgen-dependent prostate cancer cells and some types of androgen-independent prostate cancer cells. We recommend the use of pygeum extract in men with a high risk for prostate cancer.44,45
Focus on reducing risk factors for prostate cancer along with implementing dietary and lifestyle factors associated with prevention. In many cases, men with prostate cancer also have BPH, so if you have BPH, follow the recommendations in that chapter as well.
Diet and Lifestyle
• Follow the recommendations in the chapter “A Health-Promoting Lifestyle.”
• Follow the recommendations in the chapter “A Health-Promoting Diet.” In particular, employ the principles of the Mediterranean diet: eat more fish, whole grains, vegetables, and monounsaturated fats; consume soy foods and vegetables from the brassica (cabbage) family on a regular basis; add 1 tbsp ground flaxseed to the diet per day; avoid high-glycemic foods and unhealthful fats; and achieve and maintain ideal body weight.
• A high-potency multiple vitamin and mineral formula as described in the chapter “Supplementary Measures”
• Key individual nutrients:
Vitamin E (mixed tocopherols): 100 to 200 mg per day
Selenium: 100 to 200 mcg per day
Lycopene: 10 to 15 mg per day
Vitamin D3: 2,000 IU per day
• Fish oils: 1,000 mg EPA + DHA
• One of the following:
Grape seed extract (>95% procyanidolic oligomers): 100 to 300 mg per day
Pine bark extract (>95% procyanidolic oligomers): 100 to 300 mg per day
Some other flavonoid-rich extract with a similar flavonoid content, super greens formula, or another plant-based antioxidant that can provide an oxygen radical absorption capacity (ORAC) of 3,000 to 6,000 units or more per day
• Green tea extract (>80% total polyphenol content): 300 to 400 mg per day
• Pygeum extract (14% triterpene content): 50 to 100 mg per day for high-risk individuals