Vitamin D, Selenium and Vitamin E all now appear hit or miss for preventing prostate cancer.
Vitamin D and prostate Cancer
Jacob Schor, ND, FABNO
June 22, 2009
A paper published June 18, 2009 [last week] tells us that African American men living in Philadelphia have abysmally low levels of vitamin D. The mean vitamin D level was 13.7 ng/ml. A full 61% of the men tested had levels less than 15. This is impressively low. It’s even lower than the previous numbers reported for Boston (17-25 ng/ml) or Washington, DC (18ng/ml). For the last couple of years most researchers have considered 30 ng/ml as the bottom line between ok and too low.
African American men in the United States have a higher than average risk of dying of prostate cancer. Among black men, 19% will be diagnosed with prostate cancer, and 5% of those will die from this disease. Prostate cancer is the fourth most common reason overall for death in African-American men.
Could it be their lower vitamin D levels? The idea that vitamin D levels were inversely correlated with prostate cancer risk was proposed as a hypothesis in 1990. Hanchette and Schwartz’s 1992 paper showed a correlation between geographic areas with higher ultraviolet light exposure and lower risk of prostate cancer. This added support to the hypothesis.
Yet recent evidence has been inconsistent. A study published a year ago, in June 2008, by researchers from the National Cancer Institute found no evidence to support this connection. The researchers compared blood drawn years before from 749 men with prostate cancer and compared it with blood from men without prostate cancer. No correlation was seen between vitamin D and risk for prostate cancer. Quite disconcertingly though the men with any but the lowest levels of vitamin D were at higher risk of having a more aggressive form of cancer.
A May 2009 study published in the American Journal of Epidemiology did not find the link between vitamin D and tumor aggressiveness nor did they see any correlation between vitamin D levels and prostate cancer risk. The data for this study was collected in multiple European countries, looked at vitamin D levels in 652 men with prostate cancer and compared the numbers against 752 matched controls without cancer.
A March 2009 paper in the International Journal of Cancer did lend weak support to the idea. The researchers compared life time sun exposure in 1,020 cases of prostate cancer against 5044 controls. Men with darker skin, who burnt easily and men with the least sun exposure had slightly increased risk of prostate cancer. They wrote, “Our data and meta-analyses provide limited support for the hypothesis that increased exposure to sunlight may reduce prostate cancer risk.”
There’s a 2009 study from the guys in Roswell Park, a cancer research institute in western New York state, near Buffalo. This was a small study, 170 men with prostate cancer controlled with 100 controls. It looks like everyone was equally deficient in Vitamin D: the mean vitamin D level was below 30 in those with cancer and also for the control group. No big difference stood out between the guys with prostate cancer and those without.
A very large Harvard study appears to contradict many of these other studies. Over an 18-year period the researchers tracked data on 14,916 male physicians. Of these men, 1,066 were diagnosed with prostate cancer and of those, 496 had more aggressive disease. Median vitamin D levels were 25 ng/ml in the winter and spring and 32 ng/ml during the summer and fall. It looks like the average participant was deficient almost year round.
Men whose levels for both vitamin D-3 and for active D were both below the median had double the risk of aggressive prostate cancer. This study also calculated the risks associated with various genetic variations of the vitamin D receptors on the cells. Less functional forms of the receptor in combination with low vitamin D levels increased risk of cancer. High vitamin D levels appear to cancel out the risk caused by weaker receptors.
A new review article by Graland is set to be published next month in the Annals of Epidemiology. Extrapolating from current data, Graland calculates that,
“… raising the minimum year-around serum 25(OH)D level to 40 to 60 ng/mL ….would prevent approximately 58,000 new cases of breast cancer and 49,000 new cases of colorectal cancer each year, and three fourths of deaths from these diseases in the United States and Canada….Such intakes also are expected to reduce case-fatality rates of patients who have breast, colorectal, or prostate cancer by half.”
If our target level for vitamin D is between 40-60 ng/ml, there is little wonder that many of these studies have not shown benefit. Few if any participants had levels adequate to protect against cancer.
While reading through these papers, several other interesting papers related to prostate cancer crossed my screen.
We’ve mentioned in the past that risk for prostate cancer increases in men with metabolic syndrome. A May 2009 article in the journal Urology reported an increased risk for prostate cancer in African American Men with metabolic syndrome. This information probably begs a review of the articles that link vitamin D deficiency with metabolic syndrome but let’s put that off for another time.
A 2009 article in Nutrition and Cancer looked for differences in diet between African Americans and Caucasians to account for differences in prostate cancer risk. The compared diets of 478 men with prostate cancer against the diets of 382 men without cancer. The white guys ate a lot more vegetables (3.4 vs. 2.5) and fruits or fruit juices (1.6 vs. 1.3) compared to their African American counterparts. Certain nutrients were protective against getting cancer. A dietary constituent called cryptoxanthin reduced risk by almost half (Overall Risk [OR] = 0.51), fiber by almost as much (OR= 0.56) vitamin C (OR=0.60). Fruits and vegetable shad the largest effect (OR=0.46). Protein and grain consumption increased risk. Those in the highest tertile of protein or grain consumption almost doubled risk (OR=1.99).
Two other nutrients need mentioning. In years past there were strong suggestions that selenium and vitamin E offered protection against prostate cancer. These suggestions came from 2 randomized clinical trials plus epidemiological evidence. These indications were strong enough to set up a large clinical trial to test effect. The Selenium and Vitamin E Cancer Prevention Trial, known by the acronym SELECT, was a randomized, placebo-controlled trial that followed 35, 533 men at 427 sites for an average of five and a half years. The men were assigned to one of 4 groups; 400 mcg selenium, 400 IU vitamin E, selenium + vitamin E, or placebo. The researchers reported last January in the Journal of the American Medical Association that they couldn’t see any benefit from the various combinations over the placebo. So much for the idea that vitamin E or selenium will prevent prostate cancer.
There is a lot we don’t understand about prostate cancer. Incidence rates for prostate cancer have changed over the years. “Age-adjusted rates of prostate cancer incidence rose 69 percent in U.S. men from 1989 to 1992, compared with 20 percent from 1985 to 1988, and 3 percent from 1981 to 1984.4 For white men, the incidence rate peaked in 1992 at 185 new cases per 100,000 men before dropping 27 percent to 135 new cases per 100,000 in 1994. Incidence in African American men peaked in 1993 at 265 cases per 100,000 before declining 11 percent to 234 cases per 100,000 in 1994.” The explanation most commonly used to explain this is that doctors were starting to rely more on PSA levels instead of exams to detect prostate cancer at about the time of this surge in incidence.
Prevalence and correlates of vitamin D status in African American men.
Tseng M, Giri V, Bruner DW, Giovannucci E.
ABSTRACT: BACKGROUND: Few studies have examined vitamin D insufficiency in African American men although they are at very high risk. We examined the prevalence and correlates of vitamin D insufficiency among African American men in Philadelphia. METHODS: Participants in this cross-sectional analysis were 194 African American men in the Philadelphia region who were enrolled in a risk assessment program for prostate cancer from 10/96-10/07. All participants completed diet and health history questionnaires and provided plasma samples, which were assessed for 25-hydroxyvitamin D (25(OH)D) concentrations. We used linear regression models to examine associations with 25(OH)D concentrations and logistic regression to estimate odds ratios (OR) for having 25(OH)D >=15 ng/mL. RESULTS: Mean 25(OH)D was 13.7 ng/mL, and 61% of men were classified as having vitamin D insufficiency (25(OH)D <15 ng/mL). Even among men with vitamin D intake [greater than or equal to]400 IU/day, 55% had 25(OH)D concentrations <15 ng/mL. In multivariate models, 25(OH)D concentrations were significantly associated with supplemental vitamin D intake (OR 4.3, 95% confidence interval (CI) 1.5, 12.4) for >400 vs. 0 IU/day), milk consumption (OR 5.9, 95% CI 2.2, 16.0 for >=3.5 vs. <1 time per week), and blood collection in the summer. Additionally, 25(OH)D concentrations increased with more recreational physical activity (OR 1.3, 95% CI 1.1, 1.6 per hour). A significant inverse association of body mass index with 25(OH)D concentrations in bivariate analyses was attenuated with adjustment for season of blood collection. CONCLUSIONS: The problem of low vitamin D status in African American men may be more severe than previously reported. Future efforts to increase vitamin D recommendations and intake, such as through supplementation, are warranted to improve vitamin D status in this particularly vulnerable population.
Is vitamin D deficiency a risk factor for prostate cancer? (Hypothesis).
Schwartz GG, Hulka BS.
Department of Epidemiology, University of North Carolina, School of Public Health, Chapel Hill 27599.
Prostate cancer is a major cause of cancer death among males, yet little is known about its etiology. We hypothesize that Vitamin (Hormone) D deficiency may underlie the major risks for prostate cancer, including age, Black race, and northern latitudes. These factors all are associated with decreased synthesis of Vitamin D. Mortality rates from prostate cancer in the U.S. are inversely correlated with ultraviolet radiation, the principal source of Vitamin D. This hypothesis is consistent with known antitumor properties of Vitamin D, and may suggest new avenues for research in prostate cancer.
Geographic patterns of prostate cancer mortality. Evidence for a protective effect of ultraviolet radiation.
Hanchette CL, Schwartz GG.
Department of Geography, University of North Carolina, Chapel Hill.
BACKGROUND. Prostate cancer is the most prevalent nonskin cancer among men in the United States and is the second leading cause of cancer deaths in men. The cause of prostate cancer remains obscure. Recently it was hypothesized that low levels of vitamin D, a hormone with potent antitumor properties, may increase the risk for clinical prostate cancer. METHODS. Because the major source of vitamin D is casual exposure to ultraviolet (UV) radiation, the authors examined the geographic distributions of UV radiation and prostate cancer mortality in 3073 counties of the contiguous United States using linear regression and trend surface analyses. RESULTS. The geographic distributions of UV radiation and prostate cancer mortality are correlated inversely (P < 0.0001). Prostate cancer mortality exhibits a significant north-south trend, with lower rates in the South. These geographic patterns are not readily explicable by other known risk factors for prostate cancer. CONCLUSIONS. These data lend support to the hypothesis that UV radiation may protect against clinical prostate cancer. Viewed in conjunction with other recent data, including those demonstrating a differentiating effect of vitamin D on human prostate cancer cells, these findings suggest that vitamin D may have an important role in the natural history of prostate cancer.
J Natl Cancer Inst. 2008 Jun 4;100(11):759-61.
Serum vitamin D concentration and prostate cancer risk: a nested case-control study.
Ahn J, Peters U, Albanes D, Purdue MP, Abnet CC, Chatterjee N, Horst RL, Hollis BW, Huang WY, Shikany JM, Hayes RB; Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial Project Team.
Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, 6120 Executive Blvd, Bethesda, MD 20892, USA. Ahnj@mail.nih.gov
BACKGROUND: Epidemiological studies have yielded inconsistent associations between vitamin D status and prostate cancer risk, and few studies have evaluated whether the associations vary by disease aggressiveness. We investigated the association between vitamin D status, as determined by serum 25-hydroxyvitamin D [25(OH)D] level, and risk of prostate cancer in a case-control study nested within the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial. METHODS: The study included 749 case patients with incident prostate cancer who were diagnosed 1-8 years after blood draw and 781 control subjects who were frequency matched by age at cohort entry, time since initial screening, and calendar year of cohort entry. All study participants were selected from the trial screening arm (which includes annual standardized prostate cancer screening). Conditional logistic regression was used to estimate adjusted odds ratios (ORs) with 95% confidence intervals (CIs) by quintile of season-standardized serum 25(OH)D concentration. Statistical tests were two-sided. RESULTS: No statistically significant trend in overall prostate cancer risk was observed with increasing season-standardized serum 25(OH)D level. However, serum 25(OH)D concentrations greater than the lowest quintile (Q1) were associated with increased risk of aggressive (Gleason sum > or = 7 or clinical stage III or IV) disease (in a model adjusting for matching factors, study center, and history of diabetes, ORs for Q2 vs Q1 = 1.20, 95% CI = 0.80 to 1.81, for Q3 vs Q1 =1.96, 95% CI = 1.34 to 2.87, for Q4 vs Q1 = 1.61, 95% CI = 1.09 to 2.38, and for Q5 vs Q1 = 1.37, 95% CI = 0.92 to 2.05; P(trend) = .05). The rates of aggressive prostate cancer for increasing quintiles of serum 25(OH)D were 406, 479, 780, 633, and 544 per 100 000 person-years. In exploratory analyses, these associations with aggressive disease were consistent across subgroups defined by age, family history of prostate cancer, diabetes, body mass index, vigorous physical activity, calcium intake, study center, season of blood collection, and assay batch. CONCLUSION: The findings of this large prospective study do not support the hypothesis that vitamin D is associated with decreased risk of prostate cancer; indeed, higher circulating 25(OH)D concentrations may be associated with increased risk of aggressive disease.
Serum vitamin D and risk of prostate cancer in a case-control analysis nested within the European Prospective Investigation into Cancer and Nutrition (EPIC).
Travis RC, Crowe FL, Allen NE, Appleby PN, Roddam AW, Tjønneland A, Olsen A, Linseisen J, Kaaks R, Boeing H, Kröger J, Trichopoulou A, Dilis V, Trichopoulos D, Vineis P, Palli D, Tumino R, Sieri S, Bueno-de-Mesquita HB, van Duijnhoven FJ, Chirlaque MD, Barricarte A, Larrañaga N, González CA, Argüelles MV, Sánchez MJ, Stattin P, Hallmans G, Khaw KT, Bingham S, Rinaldi S, Slimani N, Jenab M, Riboli E, Key TJ.
Cancer Epidemiology Unit, University of Oxford, Oxford, UK.
Results from the majority of studies show little association between circulating concentrations of vitamin D and prostate cancer risk, a finding that has not been demonstrated in a wider European population, however. The authors examined whether vitamin D concentrations were associated with prostate cancer risk in a case-control study nested within the European Prospective Investigation into Cancer and Nutrition (1994-2000). Serum concentrations of 25-hydroxyvitamin D were measured in 652 prostate cancer cases matched to 752 controls from 7 European countries after a median follow-up time of 4.1 years. Conditional logistic regression models were used to calculate odds ratios for prostate cancer risk in relation to serum 25-hydroxyvitamin D after standardizing for month of blood collection and adjusting for covariates. No significant association was found between 25-hydroxyvitamin D and risk of prostate cancer (highest vs. lowest quintile: odds ratio = 1.28, 95% confidence interval: 0.88, 1.88; P for trend = 0.188). Subgroup analyses showed no significant heterogeneity by cancer stage or grade, age at diagnosis, body mass index, time from blood collection to diagnosis, or calcium intake. In summary, the results of this large nested case-control study provide no evidence in support of a protective effect of circulating concentrations of vitamin D on the risk of prostate cancer.
Life course sun exposure and risk of prostate cancer: Population-based nested case-control study and meta-analysis.
Gilbert R, Metcalfe C, Oliver SE, Whiteman DC, Bain C, Ness A, Donovan J, Hamdy F, Neal DE, Lane JA, Martin RM.
Department of Social Medicine, University of Bristol, Bristol, United Kingdom.
There is currently no means of primary prevention for prostate cancer. Increased exposure to ultraviolet-radiation may be protective, but the literature is inconclusive. We investigated associations of life course exposure to sunlight with prostate cancer. The study design was a UK-wide nested case-control study, based on 1,020 prostate specific antigen-detected cases and 5,044 matched population controls and a systematic review with meta-analysis. Men with olive/brown skin (OR = 1.47; 95% CI: 1.00 to 2.17), men who burnt rarely/never (OR = 1.11; 0.95 to 1.29) and men with the lowest levels of intense sun exposure in the 2 years prior to diagnosis (OR = 1.24; 1.03 to 1.50) had an increased prostate cancer risk. However, amongst men with prostate cancer, spending less time outside was associated with a reduced risk of advanced cancer (OR = 0.49; 0.27 to 0.89) and high Gleason grade (OR = 0.62; 0.43 to 0.91), and men who burnt rarely/never had a reduced risk of advanced cancer (OR = 0.71; 0.47 to 1.08). The meta-analysis provided weak evidence that men with the lowest (versus highest) sunlight exposure had an increased prostate cancer risk (4 studies, random-effects pooled relative risk = 1.13; 0.98 to 1.29) and higher advanced or fatal prostate cancer risk (6 studies, random-effects pooled relative risk = 1.14; 0.98 to 1.33). Our data and meta-analyses provide limited support for the hypothesis that increased exposure to sunlight may reduce prostate cancer risk. The findings warrant further investigation because of their implications for vitamin D chemoprevention trials. (c) 2009 UICC.
Vitamin D deficiency and insufficiency among patients with prostate cancer.
Trump DL, Chadha MK, Sunga AY, Fakih MG, Ashraf U, Silliman CG, Hollis BW, Nesline MK, Tian L, Tan W, Johnson CS.
Department of Medicine, Roswell Park Cancer Institute, Buffalo, NY, USA.
OBJECTIVE To assess the frequency of vitamin D deficiency among men with prostate cancer, as considerable epidemiological, in vitro, in vivo and clinical data support an association between vitamin D deficiency and prostate cancer outcome. PATIENTS, SUBJECTS AND METHODS The study included 120 ambulatory men with recurrent prostate cancer and 50 with clinically localized prostate cancer who were evaluated and serum samples assayed for 25-OH vitamin D levels. Then 100 controls (both sexes), matched for age and season of serum sample, were chosen from a prospective serum banking protocol. The relationship between age, body mass index, disease stage, Eastern Cooperative Oncology Group performance status, season and previous therapy on vitamin D status were evaluated using univariate and multivariate analyses. RESULTS The mean 25-OH vitamin D level was 25.9 ng/mL in those with recurrent disease, 27.5 ng/mL in men with clinically localized prostate cancer and 24.5 ng/mL in controls. The frequency of vitamin D deficiency (<20 ng/mL) and insufficiency (20-31 ng/mL) was 40% and 32% in men with recurrent prostate; 28% had vitamin D levels that were normal (32-100 ng/mL). Among men with localized prostate cancer, 18% were deficient, 50% were insufficient and 32% were normal. Among controls, 31% were deficient, 40% were insufficient and 29% were normal. Metastatic disease (P = 0.005) and season of blood sampling (winter/spring; P = 0.01) were associated with vitamin D deficiency in patients with prostate cancer, while age, race, performance status and body mass index were not. CONCLUSIONS Vitamin D deficiency and insufficiency were common among men with prostate cancer and apparently normal controls in the western New York region.
A prospective study of plasma vitamin D metabolites, vitamin D receptor polymorphisms, and prostate cancer.
Li H, Stampfer MJ, Hollis JB, Mucci LA, Gaziano JM, Hunter D, Giovannucci EL, Ma J.
Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America. firstname.lastname@example.org
BACKGROUND: Vitamin D insufficiency is a common public health problem nationwide. Circulating 25-hydroxyvitamin D3 (25[OH]D), the most commonly used index of vitamin D status, is converted to the active hormone 1,25 dihydroxyvitamin D3 (1,25[OH]2D), which, operating through the vitamin D receptor (VDR), inhibits in vitro cell proliferation, induces differentiation and apoptosis, and may protect against prostate cancer. Despite intriguing results from laboratory studies, previous epidemiological studies showed inconsistent associations of circulating levels of 25(OH)D, 1,25(OH)2D, and several VDR polymorphisms with prostate cancer risk. Few studies have explored the joint association of circulating vitamin D levels with VDR polymorphisms. METHODS AND FINDINGS: During 18 y of follow-up of 14,916 men initially free of diagnosed cancer, we identified 1,066 men with incident prostate cancer (including 496 with aggressive disease, defined as stage C or D, Gleason 7-10, metastatic, and fatal prostate cancer) and 1,618 cancer-free, age- and smoking-matched control participants in the Physicians' Health Study. We examined the associations of prediagnostic plasma levels of 25(OH)D and 1,25(OH)2D, individually and jointly, with total and aggressive disease, and explored whether relations between vitamin D metabolites and prostate cancer were modified by the functional VDR FokI polymorphism, using conditional logistic regression. Among these US physicians, the median plasma 25(OH)D levels were 25 ng/ml in the blood samples collected during the winter or spring and 32 ng/ml in samples collected during the summer or fall. Nearly 13% (summer/fall) to 36% (winter/spring) of the control participants were deficient in 25(OH)D (<20 ng/ml) and 51% (summer/fall) and 77% (winter/spring) had insufficient plasma 25(OH)D levels (<32 ng/ml). Plasma levels of 1,25(OH)2D did not vary by season. Men whose levels for both 25(OH)D and 1,25(OH)2D were below (versus above) the median had a significantly increased risk of aggressive prostate cancer (odds ratio [OR] = 2.1, 95% confidence interval [CI] 1.2-3.4), although the interaction between the two vitamin D metabolites was not statistically significant (pinteraction = 0.23). We observed a significant interaction between circulating 25(OH)D levels and the VDR FokI genotype (pinteraction < 0.05). Compared with those with plasma 25(OH)D levels above the median and with the FokI FF or Ff genotype, men who had low 25(OH)D levels and the less functional FokI ff genotype had increased risks of total (OR = 1.9, 95% CI 1.1-3.3) and aggressive prostate cancer (OR = 2.5, 95% CI 1.1-5.8). Among men with plasma 25(OH)D levels above the median, the ff genotype was no longer associated with risk. Conversely, among men with the ff genotype, high plasma 25(OH)D level (above versus below the median) was related to significant 60% approximately 70% lower risks of total and aggressive prostate cancer. CONCLUSIONS: Our data suggest that a large proportion of the US men had suboptimal vitamin D status (especially during the winter/spring season), and both 25(OH)D and 1,25(OH)2D may play an important role in preventing prostate cancer progression. Moreover, vitamin D status, measured by 25(OH)D in plasma, interacts with the VDR FokI polymorphism and modifies prostate cancer risk. Men with the less functional FokI ff genotype (14% in the European-descent population of this cohort) are more susceptible to this cancer in the presence of low 25(OH)D status.
Vitamin D for cancer prevention: global perspective.
Garland CF, Gorham ED, Mohr SB, Garland FC.
Department of Family and Preventive Medicine, University of California San Diego, La Jolla, CA, USA.
PURPOSE: Higher serum levels of the main circulating form of vitamin D, 25-hydroxyvitamin D (25(OH)D), are associated with substantially lower incidence rates of colon, breast, ovarian, renal, pancreatic, aggressive prostate and other cancers. METHODS: Epidemiological findings combined with newly discovered mechanisms suggest a new model of cancer etiology that accounts for these actions of 25(OH)D and calcium. Its seven phases are disjunction, initiation, natural selection, overgrowth, metastasis, involution, and transition (abbreviated DINOMIT). Vitamin D metabolites prevent disjunction of cells and are beneficial in other phases. RESULTS/CONCLUSIONS: It is projected that raising the minimum year-around serum 25(OH)D level to 40 to 60 ng/mL (100-150 nmol/L) would prevent approximately 58,000 new cases of breast cancer and 49,000 new cases of colorectal cancer each year, and three fourths of deaths from these diseases in the United States and Canada, based on observational studies combined with a randomized trial. Such intakes also are expected to reduce case-fatality rates of patients who have breast, colorectal, or prostate cancer by half. There are no unreasonable risks from intake of 2000 IU per day of vitamin D(3), or from a population serum 25(OH)D level of 40 to 60 ng/mL. The time has arrived for nationally coordinated action to substantially increase intake of vitamin D and calcium.
Racial Differences in Risk of Prostate Cancer Associated With Metabolic Syndrome.
Beebe-Dimmer JL, Nock NL, Neslund-Dudas C, Rundle A, Bock CH, Tang D, Jankowski M, Rybicki BA.
Barbara Ann Karmanos Cancer Institute, Wayne State University, Detroit, Michigan, USA; Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan.
OBJECTIVES: To perform a case-control study to test the association between metabolic syndrome features and prostate cancer. The metabolic syndrome refers to a cluster of conditions serving as risk factors for cardiovascular disease. The metabolic syndrome is prevalent in the United States, and the spectrum of specific features has been shown to differ by race and ethnicity. A number of recent reports have linked metabolic syndrome to prostate cancer; however, most studies have not had racially diverse populations to explore differences in risk. METHODS: A case-control study was conducted to test the association between metabolic syndrome features and prostate cancer among 637 patients and 244 controls, with African-American men constituting 43% of the study population. RESULTS: Metabolic syndrome, defined using a modified version of the Adult Treatment Panel III criteria, was marginally associated with an increased risk of prostate cancer in African-American men (odds ratio [OR] 1.71, 95% confidence interval [CI] 0.97-3.01), but not in white men (OR 1.02, 95% CI 0.64-1.62). After stratifying the patients by stage at diagnosis, African-American men with organ-confined disease were more likely to have a history of metabolic syndrome than were the controls (OR 1.82; 95% CI 1.02-3.23), but no association was observed among those with advanced-stage disease (OR 0.93; 95% CI 0.31-2.77). When evaluating the specific features of the metabolic syndrome, obesity was inversely related to prostate cancer among white men (OR 0.51, 95% CI 0.33-0.80) but unrelated to risk among African-American men (OR 1.15, 95% CI 0.70-1.89). CONCLUSIONS: In the present investigation, the metabolic syndrome was associated with prostate cancer risk in African-American men, but not in white men. The prevalence of this syndrome, coupled with the racial disparity in prostate cancer incidence and outcomes after diagnosis, warrant additional investigation.
Intake of plant foods and associated nutrients in prostate cancer risk.
Lewis JE, Soler-Vilá H, Clark PE, Kresty LA, Allen GO, Hu JJ.
Department of Psychiatry and Behavioral Sciences, University of Miami Miller School of Medicine, 1120 NW 14th Street, Miami, FL 33136, USA.
Plant foods and associated nutrients may impact prostate cancer (PC) risk and survival. Therefore, we compared dietary intake, mainly plant food groups among 382 controls and 478 PC cases (373 incident and 105 prevalent cases). Caucasian controls had significantly higher daily servings of vegetables (3.4 vs. 2.5, P= 0.002) and fruits and/or fruit juices (1.6 vs. 1.3, P = 0.02) compared to African American controls. In Caucasians, incident cases reported lower intake of fiber, vitamin C, vitamin A, alpha -carotene, beta -carotene, cryptoxanthin, folate, genistein, daidzein, and fruits and/or fruit juice than controls and/or prevalent cases. In African Americans, incident cases had lower intake of alpha -carotene compared to controls and prevalent cases. Reduced PC risk was associated with the highest tertile of cryptoxanthin (OR = 0.51; 95% CI = 0.35-0.75), fiber (OR = 0.56; 95% CI = 0.35-0.89), vitamin C (OR = 0.60; 95% CI = 0.41-0.88), and fruits and/or fruit juices (OR = 0.46; 95% CI = 0.31-0.68), with significant linear trends. Increased risk of PC was associated with the highest tertile of protein (OR = 1.99; 95% CI = 1.05-3.79) and daily servings of grains (OR = 1.99; 95% CI = 1.23-3.22) with significant linear trends. In summary, we demonstrate racial/ethnic differences in dietary intake of plant foods. The significantly higher consumption of protective dietary constituents among prevalent cases compared to incident cases suggests that PC survivors may be amenable to dietary change.
Ann Intern Med. 2009 Mar 17;150(6):JC3-10, JC3-11.
JAMA. 2009 Jan 7;301(1):102-3.
JAMA. 2009 May 13;301(18):1876-7; author reply 1877.
JAMA. 2009 May 13;301(18):1876; author reply 1877.
Effect of selenium and vitamin E on risk of prostate cancer and other cancers: the Selenium and Vitamin E Cancer Prevention Trial (SELECT).
Lippman SM, Klein EA, Goodman PJ, Lucia MS, Thompson IM, Ford LG, Parnes HL, Minasian LM, Gaziano JM, Hartline JA, Parsons JK, Bearden JD 3rd, Crawford ED, Goodman GE, Claudio J, Winquist E, Cook ED, Karp DD, Walther P, Lieber MM, Kristal AR, Darke AK, Arnold KB, Ganz PA, Santella RM, Albanes D, Taylor PR, Probstfield JL, Jagpal TJ, Crowley JJ, Meyskens FL Jr, Baker LH, Coltman CA Jr.
Division of Cancer Medicine, University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Blvd, Houston, TX 77030, USA. email@example.com
CONTEXT: Secondary analyses of 2 randomized controlled trials and supportive epidemiologic and preclinical data indicated the potential of selenium and vitamin E for preventing prostate cancer. OBJECTIVE: To determine whether selenium, vitamin E, or both could prevent prostate cancer and other diseases with little or no toxicity in relatively healthy men. DESIGN, SETTING, AND PARTICIPANTS: A randomized, placebo-controlled trial (Selenium and Vitamin E Cancer Prevention Trial [SELECT]) of 35,533 men from 427 participating sites in the United States, Canada, and Puerto Rico randomly assigned to 4 groups (selenium, vitamin E, selenium + vitamin E, and placebo) in a double-blind fashion between August 22, 2001, and June 24, 2004. Baseline eligibility included age 50 years or older (African American men) or 55 years or older (all other men), a serum prostate-specific antigen level of 4 ng/mL or less, and a digital rectal examination not suspicious for prostate cancer. INTERVENTIONS: Oral selenium (200 microg/d from L-selenomethionine) and matched vitamin E placebo, vitamin E (400 IU/d of all rac-alpha-tocopheryl acetate) and matched selenium placebo, selenium + vitamin E, or placebo + placebo for a planned follow-up of minimum of 7 years and a maximum of 12 years. MAIN OUTCOME MEASURES: Prostate cancer and prespecified secondary outcomes, including lung, colorectal, and overall primary cancer. RESULTS: As of October 23, 2008, median overall follow-up was 5.46 years (range, 4.17-7.33 years). Hazard ratios (99% confidence intervals [CIs]) for prostate cancer were 1.13 (99% CI, 0.95-1.35; n = 473) for vitamin E, 1.04 (99% CI, 0.87-1.24; n = 432) for selenium, and 1.05 (99% CI, 0.88-1.25; n = 437) for selenium + vitamin E vs 1.00 (n = 416) for placebo. There were no significant differences (all P>.15) in any other prespecified cancer end points. There were statistically nonsignificant increased risks of prostate cancer in the vitamin E group (P = .06) and type 2 diabetes mellitus in the selenium group (relative risk, 1.07; 99% CI, 0.94-1.22; P = .16) but not in the selenium + vitamin E group. CONCLUSION: Selenium or vitamin E, alone or in combination at the doses and formulations used, did not prevent prostate cancer in this population of relatively healthy men. TRIAL REGISTRATION: clinicaltrials.gov identifier: NCT00006392.