Nutrition: What is it and why is it important?

Introduction

FGM/C and Its Health Consequences: Implications for Policy, Advocacy, and Investment
When this information becomes available from experimental data, it will be possible to replace the approximations presented here with calculations based on actual data. Growth of LNCaP cells was stimulated by noncytotoxic, low concentrations of sodium selenite; while growth inhibition occurred in PC-3 cells at these concentrations—prompting the authors to suggest that selenium may be beneficial in advanced prostate cancer—selenium supplementation may have adverse effects in hormone-sensitive prostate cancer. Only a few studies have been reported on the effects of MCP in animals bearing implanted cancers and only one involving prostate cancer. Likewise, a systematic review and meta-analysis evaluated lycopene dietary intake and circulating lycopene with prostate cancer risk. Will not stick to wounds, Cools and soothes on contact. Patients with high levels of VDR expression had lower PSA at diagnosis, less advanced tumor stage, and reduced risk of lethal prostate cancer compared with patients with lower levels of VDR expression in tumors.

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The Ketogenic Diet for Health

Experts at the University of Florida say that 16 key minerals are essential for human biochemical processes:. What it does - a systemic affects entire body electrolyte, essential in co-regulating ATP an important carrier of energy in cells in the body, also key in making RNA with sodium. What it does - key for producing stomach acid, important in the transport of molecules between cells, and vital for the proper functioning of nerves.

What it does - a systemic electrolyte, and essential in regulating ATP with potassium. Important for nerve function and regulating body fluid levels. Excess - hypernatremia - can also cause cells to malfunction, extremely high levels can be fatal. What it does - important for muscle, heart, and digestive health.

Builds bone, assists in the synthesis and function of blood cells. Deficiency - hypocalcaemia - muscle cramps, abdominal cramps, spasms, and hyperactive deep tendon reflexes. Excess - hypercalcemia - muscle weakness, constipation , undermined conduction of electrical impulses in the heart, calcium stones in the urinary tract, impaired kidney function, and impaired absorption of iron, leading to iron deficiency.

What it does - important for the structure of DNA, transporter of energy ATP , component of cellular membrane, helps strengthen bones.

Deficiency - hypophosphatemia, an example is rickets. What it does - processes ATP; required for good bones and management of proper muscle movement. Hundreds of enzymes rely on magnesium to work properly. Deficiency - hypomagnesemia - irritability of the nervous system with spasms of the hands and feet, muscular twitching and cramps, constipation, and larynx spasms.

Excess - hypermagnesemia - nausea, vomiting, impaired breathing, low blood pressure. Very rare, but may occur if patient has renal problems. What it does - required by many enzymes. Important for reproductive organ growth.

Also important in gene expression and regulating the nervous and immune systems. Deficiency - short stature , anemia , increased pigmentation of skin, enlarged liver and spleen, impaired reproductive function, impaired wound healing, and immune deficiency. Excess - suppresses copper and iron absorption. What it does - required for proteins and enzymes, especially hemoglobin, the oxygen-carrying compound in blood. Deficiency - wobbliness, fainting, hearing loss , weak tendons and ligaments.

Less commonly, can be a cause of diabetes. Deficiency - anemia or pancytopenia reduction in the number of red and white blood cells, as well as platelets and neurodegeneration. Excess - can interfere with body's formation of blood cellular components; in severe cases, convulsions, palsy, and eventually death similar to arsenic poisoning.

Deficiency - developmental delays, enlarged thyroid gland in the neck , and fatigue. What it does - essential cofactor for antioxidant enzymes. Deficiency - Keshan disease - myocardial necrosis tissue death in the heart leading to weakening of the heart; Kashin-Beck disease - break down of cartilage. Excess - garlic-smelling breath, gastrointestinal disorders, hair loss , sloughing of nails, fatigue, irritability, and neurological damage. What it does - vital part of three important enzyme systems, xanthine oxidase, aldehyde oxidase, and sulfite oxidase.

It has a vital role in uric acid formation, in carbohydrate metabolism, and sulfite detoxification. Deficiency - may affect metabolism and blood counts, but as this deficiency often occurs at the same time as other mineral deficiencies, it is hard to say which deficiency caused which health problem. It is called a vitamin when our bodies cannot synthesize produce enough or any of it, so we need to get it from our food. Vitamins are classified as water soluble they can be dissolved in water or fat soluble they can be dissolved in fat.

For humans, there are four fat-soluble vitamins A, D, E, and K and nine water-soluble vitamins eight B vitamins and vitamin C. Water-soluble vitamins need to be consumed more regularly because they are eliminated faster in urine and are not easily stored. Fat-soluble vitamins are absorbed through the intestines with the help of fats lipids. They are more likely to accumulate in the body because they are harder to get rid of quickly.

If too many vitamins build up, it is called hypervitaminosis. A very low-fat diet can affect the absorption of fat-soluble vitamins. We know that most vitamins have many different functions. Below is a list of vitamins, and some of their roles.

Note that most often vitamin overdose symptoms are related to supplementation or impaired metabolism or excretion, not vitamin intake from foods. Overdose disease - rare hypersensitive reactions resembling anaphylactic shock when an overdose is due to injection. Deficiency disease - ariboflavinosis mouth lesions, seborrhea, and vascularization of the cornea. Overdose disease - liver damage, skin problems, and gastrointestinal complaints, plus other problems. Deficiency disease - paresthesia tingling, pricking, or numbness of the skin with no apparent long-term physical effect.

Deficiency disease - anemia, peripheral neuropathy. Overdose disease - nerve damage, proprioception is impaired the ability to sense where parts of the body are in space. Chemical name - biotin. Deficiency disease - scurvy , which can lead to a large number of complications.

Overdose disease - vitamin C megadose - diarrhea , nausea, skin irritation, burning upon urination, depletion of copper in the body, and higher risk of kidney stones.

Deficiency disease - rickets, osteomalacia softening of bone , recent studies indicate higher risk of some cancers , autoimmune disorders, and chronic diseases. Overdose disease - hypervitaminosis D headache , weakness, disturbed digestion, increased blood pressure, and tissue calcification.

Overdose disease - dehydration, vomiting, irritability, constipation, build up of excess calcium. Most foods contain a combination of some or all of the seven nutrient classes. We require some nutrients regularly, and others less frequently. If you want to buy multivitamins, then there is an excellent selection online with thousands of customer reviews.

We picked linked items based on the quality of products, and list the pros and cons of each to help you determine which will work best for you. We partner with some of the companies that sell these products, which means Healthline UK and our partners may receive a portion of revenues if you make a purchase using a link s above.

Article last updated by Tim Newman on Fri 1 September All references are available in the References tab. Sustaining the elimination of iodine deficiency disorders IDD. What is it and why is it important?. MNT is the registered trade mark of Healthline Media. Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a healthcare professional. Privacy Terms Ad policy Careers.

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Sign in Log in with your Medical News Today account to create or edit your custom homepage, catch-up on your opinions notifications and set your newsletter preferences. Register for a free account Sign up for a free Medical News Today account to customize your medical and health news experiences. Register take the tour. Table of contents What is nutrition? These findings suggest that galectin-3 expression may play a role in prostate cancer cell chemoresistance and that the efficacy of cisplatin treatment in prostate cancer may be improved by inhibiting galectin Only a few studies have been reported on the effects of MCP in animals bearing implanted cancers and only one involving prostate cancer.

In the study, rats were given 0. The analysis revealed that treatment with 0. In a pilot study , patients with advanced solid tumors various types of cancers were represented, including prostate cancer received MCP 5 g MCP powder dissolved in water 3 times a day for at least 8 weeks. Following treatment, improvements were reported in some measures of quality of life , including physical functioning, global health status, fatigue , pain, and insomnia.

In one prospective pilot study , MCP was well tolerated by the majority of treated patients, with the most commonly reported side effects being pruritus , dyspepsia , and flatulence. The pomegranate tree Punica granatum L. The arils are mainly composed of water and also contain phenolics and flavonoids. Anthocyanins, which are flavonoids present in arils, are responsible for the red color of the fruit and its juice.

Research studies suggest that pomegranates have beneficial effects on a number of health conditions, including cardiovascular disease,[ 6 ] and may also have positive effects on oral or dental health. Research studies in the laboratory have examined the effects of pomegranate on many prostate cancer cell lines and in rodent models of the disease.

Ellagitannins the main polyphenols in pomegranate juice are hydrolyzed to ellagic acid , and then to urolithin A UA derivatives. According to a tissue distribution experiment in wild-type mice, the prostate gland rapidly takes up high concentrations of UA after oral or intraperitoneal administration 0.

Ellagic acid EA was detected in the prostate following intraperitoneal, but not oral, administration of pomegranate extract 0.

Treating human prostate cancer cells with individual components of the pomegranate fruit has been shown to inhibit cell growth. Treating cells with EGCG, kaempferol, and punicic acid further resulted in apoptosis, with punicic acid a major constituent of pomegranate seeds being the strongest inducer of apoptosis.

Additionally, findings from this study suggested that punicic acid may activate apoptosis by a caspase-dependent pathway. Pomegranate extracts have also been shown to inhibit the proliferation of human prostate cancer cells in vitro. All four treatments resulted in statistically significant increases in apoptosis and dose-dependent decreases in cell proliferation in the three cell lines. As a result, CYP1B1 inhibitors may be effective anticarcinogenic targets.

In a study reported in , the effects of pomegranate metabolites on CYP1B1 activation and expression in CWR22Rv1 prostate cancer cells were examined. In addition, the insulin-like growth factor IGF system has been implicated in prostate cancer. However, these substances may have induced apoptosis by different mechanisms. The results showed that treatment with PJ increased adhesion and decreased the migration of prostate cancer cells.

Molecular analyses revealed that PJ increased the expression of cell-adhesion related genes and inhibited the expression of genes involved in cytoskeletal function and cellular migration. These findings suggested that PJ may be beneficial in slowing down or preventing cancer cell metastasis. The effects of pomegranate on prostate cancer have been examined using a number of rodent models of the disease. In one study, athymic nude mice were injected with tumor-forming cells.

Following inoculation, animals were randomly assigned to receive normal drinking water or PJ 0. Small, solid tumors appeared earlier in mice drinking normal water only than in mice drinking PJ 8 days vs. Moreover, tumor growth rates were significantly reduced in mice drinking PJ compared with mice drinking normal water only.

Animals drinking PJ also exhibited significant reductions in serum PSA levels compared with animals drinking normal water only. In a study reported in , 6-week-old transgenic adenocarcinoma of the mouse prostate TRAMP mice received normal drinking water or PJ 0. The PJ-supplemented mice exhibited significantly increased life spans compared with the water-fed mice. Three clinical studies have examined the effect of interventions with pomegranate products on changes in PSADT in patients with biochemically recurrent prostate cancer who had a rising PSA after surgery or radiation therapy for presumed localized cancer.

The second phase II study was published in and randomly assigned 92 patients to either 1 g polyphenol gallic acid content equivalent to 8 ounces of pomegranate juice [47 patients] or 3 g 45 patients of pomegranate extract powder for up to 18 months. The third trial was a randomized, double-blinded , placebo controlled study published in Of the patients who enrolled, 64 patients were treated with placebo, 17 patients were treated with PJ, and patients were treated with pomegranate liquid extract, which contained the same compounds found in PJ, with the exception of a higher proportional content of pomegranate polyphenol and a lower anthocyanidin content.

The differences in results between the trials may be partly because of less aggressive disease in the patient population with lower starting PSA values, but may also be because the first two trials lacked a placebo arm. All three trials found that pomegranate extract was safe to consume.

In light of these findings, researchers wondered if there may be a sensitive subpopulation that might benefit from PJ. One potential genetic biomarker candidate is manganese superoxide dismutase MnSOD , which is the primary antioxidant enzyme in mitochondria.

The AA genotype has been associated with more aggressive prostate cancer and with more sensitivity to antioxidants than the VA or VV genotype. In summary, the finding that men with the AA genotype who received pomegranate extract had greater lengthening of PSADT than did men in the placebo arm, along with the safe profile of PJ and extract in three large studies, suggest that there may be benefit in further studies in the AA MnSOD subpopulation.

In a study of prostate cancer patients reported in , the PJ intervention was well tolerated and no serious adverse effects were observed. In a pilot study reported in , the safety of PJ in patients with erectile dysfunction was examined. No serious adverse effects were observed during this study, and no participant dropped out due to adverse side effects. In the analysis of the results, no statistical comparisons were made of the adverse side effects observed in the intervention arm and the placebo arm.

Selenium is an essential trace mineral involved in a number of biological processes, including enzyme regulation, gene expression, and immune function. Selenium was discovered in and named after the Greek goddess of the moon, Selene.

Food sources of selenium include meat, vegetables, and nuts. The selenium content of the soil where food is raised determines the amount of selenium found in plants and animals. Selenium is a component of the enzyme glutathione peroxidase, an enzyme that functions as an antioxidant. Selenium is implicated in a number of disease states. Selenium deficiency may result in Keshan disease, a form of childhood cardiomyopathy, and Kaskin-Beck disease, a bone disorder. Selenium may also play a role in cancer.

Animal and epidemiological studies have suggested there may be an inverse relationship between selenium supplementation and cancer risk. The results indicated that selenium supplementation did not affect risk of skin cancer, although incidences of lung , colorectal , and prostate cancer were significantly reduced. There is evidence that selenoproteins may be associated with carcinogenesis.

For example, reduced expression of glutathione peroxidase 3 and SEPP have been observed in some tumors , while increased expression of glutathione peroxidase 2 occurs in colorectal and lung tumors. Different selenium-containing compounds have variable effects on prostate cancer cells as well as normal cells and tissues. Both naturally occurring and synthetic organic forms of selenium have been shown to decrease the growth and function of prostate cancer cells.

Studies have suggested that selenium nanoparticles may be less toxic to normal tissues than are other selenium compounds. One study investigated the effects of selenium nanoparticles on prostate cancer cells. The treated cells had decreased activity of the androgen receptor , which led to apoptosis and growth inhibition. In a study, prostate cancer cells treated with sodium selenite a natural form of selenium exhibited increased levels of p53 a tumor suppressor.

Findings also revealed that p53 may play a key role in selenium-induced apoptosis. In a second study, the prostate cancer cell line LNCaP was modified to separately overexpress each of four antioxidant enzymes. Cells from the modified cell line were then treated with sodium selenite.

The cells overexpressing manganese superoxide dismutase MnSOD were the only ones able to suppress selenite-induced apoptosis. These findings suggest that superoxide production in mitochondria may be important in selenium-induced apoptosis occurring in prostate cancer cells and that levels of MnSOD in cancer cells may determine the effectiveness of selenium in inhibiting those cells. One study treated prostate cancer cells and benign prostatic hyperplasia BPH cells with sodium selenite.

Growth of LNCaP cells was stimulated by noncytotoxic, low concentrations of sodium selenite; while growth inhibition occurred in PC-3 cells at these concentrations—prompting the authors to suggest that selenium may be beneficial in advanced prostate cancer—selenium supplementation may have adverse effects in hormone-sensitive prostate cancer. A study investigated whether various forms of selenium i. Elderly dogs received nutritionally adequate or supranutritional levels of selenium in the form of SeMet or Se-yeast.

Both types of selenium supplementation increased selenium levels in toenails and prostate tissue to a similar degree. The different forms of selenium supplementation showed no significant differences in DNA damage, proliferation, or apoptosis in the prostate. At least one study has compared these three forms of selenium in athymic nude mice injected with human prostate cancer cells and found that MSeA was more effective in inhibiting tumor growth than was SeMet or selenite.

Mice were fed selenium-depleted or selenium-containing at nutritional or supranutritional levels diets for 6 months or 4 weeks and were then injected with PC-3 prostate cancer cells. Adult mice that were fed selenium-containing diets exhibited fewer tumors than did adult mice fed selenium-depleted diets. In adult mice, selenium-depleted diets resulted in tumors with more necrosis and inflammation compared with selenium-containing diets.

However, in young mice, tumor development and histopathology were not affected by dietary selenium. TRAMP mice that received MSeA treatment starting at age 10 weeks exhibited less aggressive prostate cancer than did mice that started treatment at 16 weeks, suggesting early intervention with MSeA may be more effective than later treatment. The same research group later investigated some of the cellular mechanisms responsible for the different effects of MSeA and MSeC.

MSeA mainly affected proteins related to prostate differentiation , androgen receptor signaling, protein folding, and endoplasmic reticulum-stress responses, whereas MSeC affected enzymes involved in phase II detoxification or cytoprotection. The results of epidemiological studies suggest some complexity in the association between the blood levels of selenium and the risk of acquiring prostate cancer.

As part of the European Prospective Investigation into Cancer and Nutrition EPIC -Heidelberg study, men completed dietary questionnaires, had blood samples taken, and were monitored every 2 to 3 years for up to 10 years.

The findings revealed a significantly decreased risk of prostate cancer for individuals with higher blood selenium concentrations. Various molecular pathways have been explored to better understand the association between blood selenium levels and the development of prostate cancer.

A retrospective analysis of prostate cancer patients and healthy controls showed an association between aggressive prostate cancer and decreased selenium and SEPP status. Two SNPs were significantly associated with prostate cancer incidence: For men with the alanine-alanine AA genotype , higher selenium levels were associated with a reduced risk of presenting with aggressive disease, whereas the opposite was seen among men with a valine V allele.

The authors recommended caution in the use of selenium supplements among men with prostate cancer. Risk of prostate cancer mortality rose at all levels of selenium consumption. The authors reported no statistically significant association between selenium supplement use and biochemical recurrence , cardiovascular disease mortality, or overall mortality.

Blood samples were collected at the start and end of the study. Compared with the placebo group, men who received selenium supplements exhibited significantly increased activity of two blood selenium enzymes and significantly decreased levels of prostate-specific antigen PSA at the end of the study.

A meta-analysis published in reviewed human studies that investigated links between selenium intake, selenium status, and prostate cancer risk. While there was no change in PSA levels between the groups after 6 months, the participants receiving supplements reported improved quality of life and showed decreases in low-density lipoprotein cholesterol and total cholesterol.

Selenium was given in the form of Se-yeast. Men receiving the high-dose selenium, and who had the highest baseline plasma selenium levels, had a higher PSA velocity than did men in the placebo group.

There was not a significant effect of selenium supplements on PSA velocity in men who had lower baseline levels of selenium. In , results of a phase III randomized, placebo-controlled trial investigating the effect of selenium supplementation on prostate cancer incidence in men at high risk for the disease were reported.

They were monitored every 6 months, up to 5 years. Compared with placebo, selenium supplementation had no effect on prostate cancer incidence or PSA velocity. The results suggested that selenium supplementation had no effect on prostate cancer risk. The primary endpoint of the clinical trial was incidence of prostate cancer. There were no statistically significant differences in rates of prostate cancer in the four groups.

On the basis of those findings, the data and safety monitoring committee recommended that participants stop taking the study supplements. Updated results were published in There was also greater incidence of prostate cancer in men who had taken selenium than in men who took placebo, but those differences were not statistically significant.

A number of explanations have been suggested, including the dose and form of vitamin E that was used in the trial as well as the specific form of selenium chosen for the study. SELECT researchers chose selenomethionine because it was the major component of Se-yeast and because selenite was not absorbed well by the body, resulting in lower selenium stores.

Total selenium concentration in the absence of supplementation was not associated with prostate cancer risk. The authors concluded that men should avoid selenium supplementation at doses exceeding recommended dietary intakes. Toenail selenium concentration was inversely associated with risk of total prostate cancer odds ratio , 0. Selenium supplementation was well tolerated in many clinical trials. In two published trials, there were no differences reported in adverse effects between placebo or treatment groups.

Although records of soy use in China date back to the 11th century BC, it was not until the 18th century that the plant reached Europe and the United States. The soybean is an incredibly versatile plant: Soy foods contain a number of phytochemicals that may have health benefits but isoflavones have garnered the most attention.

Among the isoflavones found in soybeans, genistein is the most abundant and may have the most biological activity. Isoflavones are quickly taken up by the gut and can be detected in plasma as soon as 30 minutes after the consumption of soy products.

Studies suggest that maximum levels of isoflavone plasma concentration may be achieved by 6 hours after soy product consumption.

Some studies suggest that soy may have health benefits, including decreasing risk of cardiovascular disease and cancer. A link between isoflavones and cancer was discovered in when it was shown that genistein inhibited a protein tyrosine kinase that is often overexpressed in cancer cells.

A number of laboratory studies have examined ways in which soy components affect prostate cancer cells. In one study, human prostate cancer cells and normal prostate epithelial cells were treated with either an ethanol vehicle carrier or isoflavones.

Treatment with genistein decreased COX-2 mRNA and protein levels in cancer cells and normal epithelial cells more than did treatment with the vehicle. In addition, cells treated with genistein exhibited reduced secretion of prostaglandin E2 PGE2 and reduced mRNA levels of the prostaglandin receptors EP4 and FP, suggesting that genistein may exert chemopreventive effects by inhibiting the synthesis of prostaglandins, which promote inflammation. The isoflavones were shown to down regulate growth factors involved in angiogenesis e.

These findings suggest that genistein and daidzein may have chemopreventive properties. However, during the 72 hours of incubation , only genistein provoked effects on the dynamic phenotype and decreased invasiveness in PC-3 cells.

These results imply that invasive activity is at least partially dependent on membrane fluidity and that genistein may exert its antimetastatic effects by changing the mechanical properties of prostate cancer cells. No such effects were observed for daidzein at the same dose. Some experiments have compared the effects of individual isoflavones with isoflavone combinations on prostate cancer cells.

In one study, human prostate cancer cells were treated with a soy extract containing genistin, daidzin, and glycitin , genistein, or daidzein.

The soy extract induced cell cycle arrest and apoptosis in prostate cancer cells to a greater degree than did treatment with the individual isoflavones. Genistein and daidzein activated apoptosis in noncancerous benign prostatic hyperplasia BPH cells, but the soy extract had no effect on those cells. These findings suggested that products containing a combination of active compounds e. All of the treatments resulted in decreased cell proliferation, but the greatest reductions occurred using the combination of genistein, biochanin A, and quercetin.

The triple combination treatment induced more apoptosis in prostate cancer cells than did individual or doublet compound treatments.

These results indicate that combining phytoestrogens may increase the effectiveness of the individual compounds. At least one study has examined the combined effect of soy isoflavones and curcumin. Human prostate cancer cells were treated with isoflavones, curcumin, or a combination of the two. Curcumin and isoflavones in combination were more effective in lowering PSA levels and expression of the androgen receptor than were curcumin or the isoflavones individually. Animal models of prostate cancer have been used in studies investigating the effects of soy and isoflavones on the disease.

Mice fed low-dose genistein exhibited more cancer cell metastasis and greater osteopontin expression than mice fed the control or the high-dose genistein diet. These results indicate that timing and dose of genistein treatment may affect prostate cancer outcomes and that genistein may exert biphasic control over prostate cancer.

Mice that were fed genistein exhibited less cancer cell metastasis, but no change in primary tumor volume, than did mice fed a control diet. Furthermore, other data suggested that genistein inhibits metastasis by impairing cancer cell detachment. In addition, there was a reduction in tumor cell apoptosis in the genistein-treated mice compared with the vehicle-treated mice. These findings suggest that genistein may stimulate metastasis in an animal model of advanced prostate cancer.

Radiation therapy is commonly used in prostate cancer, but, despite this treatment, disease recurrence is common. Therefore, combining radiation with additional therapies may provide longer-lasting results.

Cells that were treated with both isoflavones and radiation exhibited greater decreases in cell survival and greater expression of proapoptotic molecules than cells treated with isoflavones or radiation only.

Nude mice were implanted with prostate cancer cells and treated by gavage with genistein Mixed isoflavones were more effective than genistein in inhibiting prostate tumor growth, and combining isoflavones with radiation resulted in the largest inhibition of tumor growth. In addition, mice given soy isoflavones in combination with radiation did not exhibit lymph node metastasis, which was seen previously in other experiments combining genistein with radiation.

These preclinical findings suggest that mixed isoflavones may increase the efficacy of radiation therapy for prostate cancer. Numerous clinical studies have been conducted examining the impact of soy use on indicators of the effectiveness of prostate cancer prevention or treatment approaches. These studies have included a wide range of participants from healthy control subjects to prostate cancer patients at various stages of the disease and have used a number of different interventions such as soy supplements, beverages, and breads.

In , a meta-analysis of studies that investigated soy food consumption and risk of prostate cancer was reported. The results of this meta-analysis suggested that high consumption of nonfermented soy foods e. No association was found between high consumption of fermented soy foods e. There were no differences in urinary concentrations of the isoflavones genistein and daidzein between healthy men and prostate cancer patients. Men who produced equol a metabolite of daidzein were at a lower risk of prostate cancer than men who were nonproducers.

Overall, there were no differences in PSA levels between the placebo and the treatment groups. Although soy is a standard part of many Asian diets, it is less common in Western diets. Therefore, feasibility studies were undertaken to investigate whether Western participants would adhere to soy-supplementation interventions.

In one study, healthy men were randomly assigned to consume a low-soy usual diet or high-soy soy servings bid diet for 3 months. Following a 1-month washout period, the men crossed over to the other treatment. Reductions approaching statistical significance were seen in PSA levels following the high-soy diet.

These findings suggest that this type of soy intervention study is feasible i. In one study, men at risk of prostate cancer or with low-grade prostate cancer received one of three types of protein isolate soy protein, alcohol-washed soy protein [a common method of producing soy protein concentrate that results in some loss of isoflavones], or milk protein for 6 months.

Soy protein consumption did not alter prostate tissue biomarkers , alcohol-washed soy protein exerted mixed effects, and less prostate cancer was detected after 6 months in men who had consumed soy proteins compared with men who consumed milk protein. Japanese men who had serum PSA levels between 2. There were no differences in PSA values or in incidence of biopsy-detectable prostate cancer before and after treatment in the isoflavone or placebo groups.

Other plants also contain some of the same isoflavones found in soy. In addition, the isoflavone intervention was well tolerated by the patients and did not cause side effects. In a study reported in , patients with rising PSA levels who had been treated with radiation as the primary treatment for prostate cancer drank a soy beverage daily providing approximately mg isoflavones for 6 months.

The results showed that the soy beverage was well-tolerated and was associated with an increase in PSA doubling time. These findings suggested that drinking the soy beverage may have helped to slow the progression of prostate cancer. Then, for an additional 6 months, all participants received the isoflavone supplement. Although treatment with the supplements raised serum concentration levels of genistein and daidzein, there was no effect on PSA levels.

In a study reported in , prostate cancer patients scheduled for radical prostatectomy were randomly assigned to receive a placebo or 30 mg genistein daily for 3 to 6 weeks before surgery. Among the patients who received genistein, serum PSA levels decreased by 7. The investigators noted that the 12 genes involved in cell cycle control and the 9 genes involved in apoptosis were down regulated in the tumor tissues of the isoflavone-treated men, compared with the controls.

In a second phase II, multidose, randomized placebo-controlled trial,[ 34 , 36 ] 45 men with localized prostate cancer received supplements with either 40, 60, or 80 mg of purified isoflavones or no supplement from the time of biopsy to prostatectomy. Significant increases in plasma isoflavones were observed with all isoflavone doses, compared with placebo, and significant increases in serum total estradiol were observed in the 40 mg and 60 mg isoflavone-treated arms.

However, significant increases in serum-free testosterone were observed in the 60 mg isoflavone-treated arm. Compared with the control group and other treatment arms, the 40 mg isoflavone-treated arm had the lowest percentage of cells expressing Ki, although this was not statistically significant for this sample size and duration of intervention. This study concluded that 40 mg of isoflavones may be the best dose to use in a future definitive, larger phase II clinical trial to evaluate purified isoflavones in prostate carcinogenesis.

Patients who received the soy protein supplement exhibited larger decreases in total serum PSA and free testosterone than did patients who received the placebo, but these differences were not statistically significant. Clinical studies have been conducted in prostate cancer patients to test soy as a possible treatment for prostate cancer.

In one study, prostate cancer patients scheduled to undergo radical prostatectomy were randomly assigned to receive soy supplements three The isoflavone concentration in prostatic tissue was sixfold higher than in serum following treatment with the soy supplements, suggesting that the prostate may accumulate potentially anticarcinogenic levels of isoflavones.

Patients who ate the high-phytoestrogen bread saw more favorable changes in PSA levels than did patients who ate the wheat bread, indicating that diets rich in phytoestrogens may help to reduce risk of prostate cancer development and progression.

In a small study, ten men with prostate cancer recurrence were advised to consume three 8-ounce glasses of soy milk every day for 2 years. Androgen deprivation therapy is commonly used for locally advanced and metastatic prostate cancer.

However, this treatment is associated with a number of adverse side effects including sexual dysfunction, decreased quality of life , and changes in cognition. Neither study found an improvement in side effects following isoflavone treatment, compared with placebo treatment. The results showed no difference between the two groups in PSA levels or in levels of metabolic and inflammatory parameters e.

Prostaglandins promote inflammation and may contribute to cancer by increasing cell proliferation and inhibiting apoptosis. The findings of a study reported in suggest that soy isoflavones may have chemopreventive effects via inhibition of the prostaglandin pathway. In the study, prostate cancer patients scheduled to undergo prostatectomy were randomly assigned to receive a placebo or a soy isoflavone supplement providing isoflavones, Overall, soy was well tolerated in clinical studies of prostate cancer patients.

Vitamin D, also called calciferol, cholecalciferol D3 , or ergocalciferol D2 , is a fat-soluble vitamin found in fatty fish, fish liver oil, eggs, and fortified dairy products.

Vitamin D is made naturally by the body when exposed to sunlight. In , researchers discovered that heated, oxidized cod-liver oil, called fat-soluble factor A and later known as vitamin D, played an important role in curing rickets in rats. Vitamin D is needed for bone growth and protects against osteoporosis in adults.

To study the role of vitamin D in cancer cell adhesion to endothelium, one study developed a microtube system that simulates the microvasculature of bone marrow. The study reported that 1,alpha-dihydroxyvitamin D3 1,D3 suppressed adhesion of prostate cancer cells in the microtube system.

In addition, it was shown that 1,D3 increased E-cadherin expression, which may prevent prostate cancer cell adhesion to endothelium by promoting cancer cell aggregation. One study examined the effects of VDBP-maf on prostate cancer cells. Treating prostate cancer cells with VDBP-maf resulted in inhibited cellular migration, proliferation, and reduced levels of urokinase plasminogen activator receptor uPAR; activity of this receptor correlates with tumor metastasis.

These findings suggest that VDBP-maf has a direct effect on prostate cancer cells. Studies have reported that 1,D3 may play an important role in prostate cancer biology. Studies have suggested that a newly discovered protein, protein disulfide isomerase family A, member 3 PDIA3 , may function as a membrane receptor binding to 1,D3. In addition, their findings suggest that 1,D3 may act on prostate cancer cells via multiple signaling pathways, indicating there may be a number of potential therapeutic targets.

Tumor progression was compared in two murine models of prostate cancer. In vitamin D receptor- knockout animals, rate of tumor progression and cellular proliferation were greater than in wild type animals. However, in mice that were supplemented with testosterone , these differences did not occur, suggesting that there may be significant interaction between androgen signaling and vitamin D signaling.

In a study, nude mice were fed a control diet or a diet deficient in vitamin D and were then injected with prostate cancer cells into bone marrow or into soft tissues. Osteolytic lesions were larger and progressed at a faster rate in vitamin D—deficient mice that had bone marrow injected with cancer cells than in mice that had adequate levels of vitamin D. However, there was no difference in soft tissue tumors among mice with different vitamin D levels.

Results of this study show that vitamin D deficiency is associated with growth of prostate cancer cells in bone but not in soft tissue.

A study evaluated calcitriol and a less-calcemic vitamin D analog in an aggressive transgenic adenocarcinoma of the mouse prostate TRAMP model. Neither vitamin D analog impacted the rate of development of castration -resistant prostate cancer in mice, whether they were treated before or after castration. However, both vitamin D analogs slowed progression of primary tumors in hormone-intact mice but enhanced distant organ metastases after prolonged treatment.

Cryotherapy may be used for treating prostate cancer. Studies have been conducted to identify potential agents that may help improve efficacy of the freezing procedure.

In a study, mice were injected with prostate cancer cells and treated with calcitriol, cryoablation , or both. The combination treatment group experienced larger necrotic areas, more apoptosis , and less cell proliferation than did the other experimental groups.

Vitamin D may help enhance other types of cancer treatments, such as radiation. The greatest reduction in cell proliferation occurred in cells treated with VPA, 1,D3, and radiation. The relationship between vitamin D and prostate cancer has been examined in numerous epidemiological studies. Vitamin D levels were analyzed annually for 5 years in patients with nonmetastatic prostate cancer.

Results showed that throughout the course of the study, vitamin D insufficiency was prevalent among these cancer patients. Analysis revealed that patients with the lowest concentrations of prediagnostic plasma hydroxy vitamin D [25 OH D] levels had a higher risk of developing metastatic prostate cancer than did patients with higher levels of 25 OH D. However, there was no association between metastatic prostate cancer and circulating levels of 1,25 OH D.

Results suggest that medium or high levels of serum 25 OH D may be associated with better prognoses than lower levels of serum 25 OH D. These findings indicate that 25 OH D may play a role in disease progression and may be a marker of prognosis in prostate cancer patients. Results suggested that men with a higher vitamin D status assessed via serum 25 OH D concentrations had a greater risk of developing prostate cancer than did men with lower vitamin D status.

In one case-control study of men who had undergone prostate biopsies , men who had lower vitamin D levels before biopsy were more likely to have cancer detected at biopsy than did men whose prebiopsy vitamin D levels were not lower. One hundred ninety men who participated in a large epidemiologic study underwent radical prostatectomy for clinically localized prostate cancer.

Men with adverse pathology had lower median serum 25 OH D An important means of obtaining vitamin D is via sunlight. Studies have investigated the potential link between sunlight exposure and prostate cancer. According to a study, PSA levels rise at a slower rate during spring and summer than at other times of the year; this may be related to higher vitamin D levels obtained during those months. Results of a meta-analysis, published in the same report, showed that men with low sun exposure had an increased risk of incident and advanced prostate cancer.

In addition, this relationship is more evident in areas north of 40 degrees N latitude. A number of studies have explored a possible connection between the vitamin D receptor VDR and risk of prostate cancer.

A prospective study examined VDR expression in prostate tumors. Patients with high levels of VDR expression had lower PSA at diagnosis, less advanced tumor stage, and reduced risk of lethal prostate cancer compared with patients with lower levels of VDR expression in tumors.

Five polymorphisms of VDR were identified in the participants. A meta-analysis, published in the same report, revealed no association between specific variants and prostate cancer stage TNM staging system , but found that three genotypes BSML , APAL , and TAQL may be associated with cancer grade Gleason score , suggesting there may be a link between specific VDR polymorphisms and advanced prostate cancer at diagnosis.

Variations in the three genes investigated were associated with changes in risk of recurrence and progression of prostate cancer as well as prostate cancer mortality. A meta-analysis of 45 observational studies found no association between intake of vitamin D and prostate cancer risk. Analysis of those studies found no association between dietary vitamin D or circulating concentrations of vitamin D and risk of prostate cancer. Calcitriol, the hormonally active form of vitamin D, has been the focus of some studies in prostate cancer patients.

In an open-label , phase II study, patients with recurrent prostate cancer were treated with calcitriol and naproxen for 1 year. The combination of calcitriol and naproxen was effective in decreasing the rate of rising PSA levels in study participants, suggesting it may slow disease progression.

The results indicated that while the treatments were well tolerated, they did not have an effect on participants' PSA levels. In most cases, symptoms of vitamin D toxicity are caused by hypercalcemia , but limited evidence suggests high concentrations of vitamin D may also be expressed in various organs, including the kidneys , bones, central nervous system , and cardiovascular system.

Symptoms of toxicity may be observed at an intake of 10, to 50, IU per day over a period of many years. Hypercalcemia results from the vitamin D—dependent increase in intestinal absorption of calcium, leading to rapid increases in blood calcium levels. Side effects include loss of the urinary concentrating mechanism of the kidney tubule resulting in polyuria and polydipsia , decrease in growth factor receptor, hypercalciuria, and the metastatic calcification of soft tissues.

The central nervous system may also be affected, resulting in severe depression and anorexia. A systematic review of the interactions and pharmacokinetics of vitamin D and drugs used for the treatment of cancer was published. Calcitriol was the most commonly administered form of vitamin D, and adults with prostate cancer and solid tumors were the most well-represented populations in this systematic review.

Hypophosphatemia was also observed in two studies [ 37 , 38 ] that administered vitamin D in conjunction with docetaxel in men with prostate cancer. The authors concluded that no adverse effects were experienced beyond what was expected from high-dose calcitriol supplementation and was denoted as having a low risk of interaction.

A number of studies evaluated the safety and efficacy of high-dose calcitriol in conjunction with chemotherapy drugs in men with androgen-independent prostate cancer, hormone-refractory prostate cancer, and metastatic castration-resistant prostate cancer. Most of the side effects were expected toxicities related to the chemotherapy. Grade 2 hypercalcemia was observed in one patient.

Administration of calcitriol was discontinued until hypercalcemia resolved. Supplementation was restarted after two weeks. In another patient, persistent grade 3 fatigue was observed, and treatment of calcitriol was discontinued as docetaxel was reduced. Phase I studies have looked at the maximum tolerated dose MTD of weekly intravenous and oral calcitriol in conjunction with various chemotherapy drugs for cancer treatment.

No significant bone marrow suppression was observed at any dose. The study suggests no major interaction between calcitriol and gefitinib. A second phase I study examined the MTD and pharmacokinetics of calcitriol when administered with paclitaxel over the course of 6 weeks.

Results demonstrate that very high doses of calcitriol can be safely administered with paclitaxel. However, it is important to note that participants were administered from 8 to 76 capsules of calcitriol with no report of adherence to the prescribed dose of calcitriol.

Vitamin E was discovered in as a factor essential for reproduction. Vitamin E occurs in eight different forms: Most dietary vitamin E comes from gamma-tocopherol. Food sources of vitamin E include vegetable oil, nuts, and egg yolks. The bioavailability of vitamin E depends on a number of factors, such as the food matrix containing vitamin E e. Research suggests that vitamin E may protect against a number of chronic diseases, such as cardiovascular disease. Participants in the study completed food-frequency questionnaires and were monitored for 5 years.

No association between vitamin E supplements and prostate cancer risk was found. However, a reduction in the risk of advanced prostate cancer was observed with high intakes of gamma-tocopherol. In a study, levels of trace elements and vitamin E were measured in prostate cancer patients. Prostate cancer patients had significantly lower levels of plasma vitamin E than did healthy controls. In addition, there was an inverse association between prostate-specific antigen levels and plasma vitamin E.

Studies suggest that alpha-tocopherol—associated protein TAP may have capabilities as a tumor suppressor in prostate cancer. In a study, prostate cancer specimens, which had been obtained from radical prostatectomy , were examined for TAP expression. Results showed reduced TAP expression in prostate cancer tissue and lower levels of TAP were associated with higher clinical stage and larger tumor size. Results showed an inverse association between serum alpha-tocopherol levels and sex steroid hormones, but only in smokers.

An inverse relationship was observed between alpha-tocopherol levels and prostate cancer, but only in current and recently former smokers. The North Carolina-Louisiana Prostate Cancer Project investigated racial and geographic differences in prostate cancer aggressiveness.

In 1, African American men and 1, white men studied with incident prostate cancer, inverse associations were observed between dietary sources of tocopherol and prostate cancer aggressiveness that were statistically significant in white men but not in African American men. The overall rates of prostate cancer were very similar in the vitamin E supplement and placebo groups, suggesting that vitamin E may not prevent prostate cancer.

Furthermore, vitamin E did not have an effect on total cancer or mortality in these participants. Baseline serum alpha-tocopherol levels and dietary intake of vitamin E had been assessed and participants were monitored for up to 19 years. Findings revealed that while there was no association between dietary vitamin E levels and prostate cancer risk, higher serum alpha-tocopherol levels may be associated with a decreased risk for developing advanced prostate cancer.

Results showed that genetic variations in the TTPA and SEC14L2 genes were associated with serum alpha-tocopherol but did not directly affect prostate cancer risk. However, results suggested that polymorphisms in SEC14L2 may influence the effect of alpha-tocopherol supplementation on prostate cancer risk. Serum alpha-tocopherol levels were assessed at baseline and 3 years later. Higher serum alpha-tocopherol levels, at both baseline and the 3-year point, were associated with improved prostate cancer survival.

CARET was a randomized, placebo-controlled study that investigated whether daily supplementation of beta-carotene and retinyl palmitate would reduce the risk of lung cancer in heavy smokers and asbestos -exposed workers. Results indicated that among current smokers, higher levels of serum alpha- and gamma-tocopherols were associated with reduced risk of aggressive prostate cancer. In addition, findings suggested there may be an interaction between myeloperoxidase MGO GA genotype , serum alpha-tocopherol level, and prostate cancer risk.

Specific genotypes were associated with increased prostate cancer risk in subjects with low levels of serum alpha-tocopherol, while those same genotypes along with higher levels of alpha-tocopherol were associated with reduced risk of prostate cancer.

There was also greater incidence of prostate cancer in men who had taken selenium than in men who had taken placebo, but those differences were not statistically significant. The authors concluded that men older than 55 years should avoid supplementation with either vitamin E or selenium at doses exceeding dietary recommendations. Alpha-tocopherols have been deemed Generally Recognized as Safe by the U. Food and Drug Administration. However, participants who took vitamin E alpha-tocopherol, IU qod experienced a greater number of hemorrhagic strokes than did participants who took placebo.

In the initial report of results from SELECT, there were no significant differences between incidences of less severe adverse effects e. In a placebo-controlled , double-blind , randomized study, men with localized prostate cancer were randomly assigned to either a food supplement, Pomi-T, or placebo 2: The herbal ingredients in this supplement were raw, dry, powdered plant materials and one plant extract , none of which were chemically standardized.

Chemical standardization is widely performed with herbal extracts, as a means of enhancing the reproducibility of studies with herbal dietary supplements via qualitative and quantitative chemical analysis. There were no significant differences in age or Gleason score between the groups. The study found a median rise in PSA of The supplement was well tolerated with no significant increase in adverse events compared with placebo, although a trend was noted towards increased flatulence and loose bowels in the supplement group.

Important differences exist between pomegranate preparation and standardization. While dried fruit powder is commonly found in the marketplace, an equal amount of pomegranate fruit extract has a much higher content of polyphenols that are considered the bioactive constituents and can be used for the chemical standardization of preparations.

A high percentage of positive biopsies raises the concern for cancers missed on baseline biopsy , and thus, further study is warranted. However, a post hoc exploratory analysis found lower PSA values in men with intermediate-risk prostate cancer who consumed the tomato products and in men with the highest increases in lycopene levels. Zyflamend is a dietary supplement that contains supercritical fluid CO 2 and hydroalcoholic extracts of the following herbs, combined and suspended in olive oil:.

The individual components of Zyflamend have anti-inflammatory and possible anticarcinogenic properties. For example, results of a study suggest that Zyflamend may inhibit the growth of melanoma cells. The extracts in Zyflamend have been shown to have anti-inflammatory effects via inhibition of cyclooxygenase COX activity.

COXs are enzymes that convert arachidonic acid into prostaglandins , which are thought to play a role in tumor development and metastasis. The antitumorigenic mechanisms of action of Zyflamend are unknown, but according to one study, Zyflamend may suppress activation of nuclear factor-kappa B NF-kappa B a nuclear transcription factor involved in tumorigenesis and NF-kappa B—regulated gene products. In a study reported in , human prostate cancer cells were treated in vitro with Zyflamend.

Cells treated with the supplement at concentrations ranging from 0. Prostate cancer cells that were treated with a combination of Zyflamend 0. Although the individual components of Zyflamend have been shown to influence COX activity, one study examined the effects of the drug on COX-1 and COX-2 expression in prostate cancer cells.

The results revealed that Zyflamend, at a concentration of 0. At a concentration of 0. The findings indicated that 0. The supplement also inhibited cell proliferation and induced apoptosis. In addition, Zyflamend treatment resulted in a decrease in Rb phosphorylation Rb proteins control cell-cycle -related genes. These results indicate that Zyflamend may inhibit prostate cancer cell growth through a variety of mechanisms.

Cells treated with IGF-1 alone exhibited statistically significant, dose-dependent increases in cell proliferation, whereas cells treated with both IGF-1 and Zyflamend showed significant decreases in cell proliferation. Zyflamend was also shown to decrease cellular levels of the IGF-1 receptor and the androgen receptor in prostate cancer cells. Chinese goldthread and baikal skullcap appeared to be the most likely major contributors to the overall Zyflamend effect on HDAC expression.

Additional evidence that Zyflamend promotes apoptosis in cancer cells was obtained in laboratory and animal studies reported in Moreover, when nude mice with pancreatic cancer cell implants were randomly assigned to receive Zyflamend or a control treatment for 4 weeks, tumor cells from the Zyflamend-treated mice showed significant reductions in antiapoptotic proteins and significantly increased expression of DR5, compared with tumor cells from control-treated animals.

The combination treatment resulted in a significantly greater decrease in tumor growth than did treatment with gemcitabine or Zyflamend alone. Other findings from this study suggest that Zyflamend exerted its effects by sensitizing the pancreatic tumors to gemcitabine through suppression of multiple targets linked to tumorigenesis.

Zyflamend did not affect this patient's PSA level, but, after 18 months, repeat core biopsies of the prostate did not show PIN or cancer. In a phase I study designed to assess safety and toxicity, patients with HGPIN were assigned to take Zyflamend mg 3 times daily for 18 months, plus combinations of dietary supplements i. Zyflamend and the additional dietary supplements were well tolerated by the patients, and no serious adverse events occurred.

Zyflamend was well tolerated in the previously described clinical study. Mild heartburn was reported in 9 of 23 subjects, but it resolved when the study supplements were taken with food.

No serious toxicity or adverse events were reported in the study. Many widely available dietary supplements are marketed to support prostate health. African cherry Pygeum africanum and beta-sitosterol are two related supplements that have been studied as potential prostate cancer treatments. Bark from the P. Since , bark extracts from P. The extract is obtained by macerating and solubilizing the bark in an organic solvent. The extract is then purified from the solvent. Two components of P.

This activity is produced by each of these components at concentrations that are significantly lower than the clinically achieved concentration of the antiandrogen flutamide. Beta-sitosterol is a member of the phytosterol family of phytochemicals. As a type of phytosterol or plant sterol , beta-sitosterol has a similar structure to cholesterol. Phytosterols, including beta-sitosterol, reduce absorption of dietary cholesterol and their potential to protect against cardiovascular disease is under investigation.

Mean plasma beta-sitosterol concentration in a small group of healthy male volunteers in Vienna, Austria, was 2. Research has also suggested that phytosterols may have anticarcinogenic properties, but the exact mechanisms are unknown. Beta-sitosterol at very high concentrations i. The PDQ cancer information summaries are reviewed regularly and updated as new information becomes available.

This section describes the latest changes made to this summary as of the date above. This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about the use of nutrition and dietary supplements for reducing the risk of developing prostate cancer or for treating prostate cancer.

It is intended as a resource to inform and assist clinicians who care for cancer patients. It does not provide formal guidelines or recommendations for making health care decisions.

Board members review recently published articles each month to determine whether an article should:. Changes to the summaries are made through a consensus process in which Board members evaluate the strength of the evidence in the published articles and determine how the article should be included in the summary. Any comments or questions about the summary content should be submitted to Cancer.

Do not contact the individual Board Members with questions or comments about the summaries. Board members will not respond to individual inquiries.