Context Secondary analyses of two randomized controlled trials (RCTs) and supportive epidemiologic and preclinical indicated the potential of selenium and vitamin E for preventing prostate cancer. Objective To determine whether selenium or vitamin E or both could prevent prostate cancer with little or no toxicity in relatively healthy men. Design, Setting, and Participants Randomization of a planned 32,400 men to selenium, vitamin E, selenium plus vitamin E, and placebo in a double-blinded fashion. Participants were recruited and followed in community practices, local hospitals and HMOs, and tertiary cancer centers in the United States, Canada and Puerto Rico. Baseline eligibility included 50 years or older (African American) or 55 years or older (all others), a serum prostate-specific antigen (PSA) ≤ 4 ng/mL, and a digital rectal examination (DRE) not suspicious for prostate cancer. Between 2001 and 2004, 35,533 men (10% more than planned because of a faster-than-expected accrual rate) were randomly assigned to the four study arms, which were well balanced with respect to all potentially important risk factors. Interventions Oral selenium (200 µg/day from L-selenomethionine) and matched vitamin E placebo, vitamin E (400 IU/day of all rac-α-tocopheryl acetate) and matched selenium placebo, or the two combined or placebo plus placebo for a planned minimum of 7 and maximum of 12 years. Main Outcome Measures Prostate cancer (as determined by routine community diagnostic standards) and prespecified secondary outcomes including lung, colorectal and overall cancer. Results Study supplements were discontinued at the recommendation of the Data and Safety Monitoring Committee at a planned 7-year interim analysis because the evidence convincingly demonstrated no benefit from either study agent (p < 0.0001) and no possibility of a benefit to the planned degree with additional follow-up. As of October 23, 2008, median overall follow-up was 5.46 years (range, 4.17 and 7.33). Hazard ratios (number of prostate cancers, 99% confidence intervals [CIs]) for prostate cancer were 1.13 for vitamin E (n=473; CI, 0.91–1.41), 1.04 for selenium (n=432; CI, 0.83–1.30), and 1.05 for the combination (n=437; CI, 0.83–1.31) compared with placebo (n=416). There were no significant differences (all p-values > 0.15) in any prespecified cancer endpoints. There were nonsignificant increased risks of prostate cancer in the vitamin E arm (p=0.06; relative risk [RR]=1.13; 99% CI, 0l95–1.35) and of Type 2 diabetes mellitus in the selenium arm (p=0.16; RR=1.07; 99% CI, 0.94–1.22), but they were not observed in the combination arm. Conclusion Selenium or vitamin E, alone or in combination, did not prevent prostate cancer in this population at the doses and formulations used.

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A lifestyle intervention reducing dietary fat intake, with modest influence on body weight, may improve relapse-free survival of breast cancer patients receiving conventional cancer management. Longer, ongoing nonintervention follow-up will address original protocol design plans, which called for 3 years of follow-up after completion of recruitment.

These results suggest that high consumption of vegetables, particularly cruciferous vegetables, is associated with a reduced risk of prostate cancer.

Abstract"Mindful eating" describes a non-judgmental awareness of physical and emotional sensations associated with eating. This manuscript reports the development of a mindful eating questionnaire (MEQ) to support rigorous scientific inquiry into this concept. An item pool was developed based on hypothesized domains of mindful eating. A cross-sectional survey examined associations of MEQ scores with demographic and health-related characteristics. The MEQ was distributed to seven convenience samples between January-May, 2007, with an overall response rate of 62% (n=303). Participants were mostly female (81%) and white (90%), and had a mean age of 42±14.4 years (range 18-80 years). Exploratory factor analysis was used to identify factors, which were defined as the mean of items scored 1 to 4, where 4 indicated higher mindfulness; the mean of all factors was the summary MEQ score. Multiple regression analysis was used to measure associations of demographic characteristics, obesity, yoga practice and physical activity with MEQ scores. Domains of the final 28-item questionnaire were: Disinhibition, Awareness, External Cues, Emotional Response, and Distraction. The mean MEQ score was 2.92 ± 0.37, with a reliability (Chronbach's alpha) of 0.64. The covariate-adjusted MEQ score was inversely associated with BMI (3.02 for BMI <25 vs. 2.54 for BMI >30, p <0.001). Yoga practice, but neither walking nor moderate/intense physical activity, was associated with higher MEQ score. In this study sample, the MEQ had good measurement characteristics. Its negative association with BMI and positive association with yoga provide evidence of construct validity. Further evaluation in more diverse populations is warranted.

Studies on the relationship between obesity and prostate cancer incidence are inconsistent. In part, this inconsistency may be due to a differential effect of obesity on low-grade and high-grade cancer or confounding of the association of obesity with prostate cancer risk by diabetes. We investigated the associations of obesity and diabetes with low-grade and highgrade prostate cancer risk.

Although painful to admit, it is possible that epidemiologists have been deluded in their acceptance of food frequency questionnaires (FFQ) as the standard tool for dietary assessment in large studies of diet and cancer. The substantial limitations of FFQs have been known for some time (1) and published studies based on FFQ-derived data have long included in their discussion sections a litany of weaknesses due to suboptimal dietary assessment. However, few of us expected the astonishingly poor measurement characteristics of FFQs when compared with doubly labeled water (a gold standard for energy intake; ref.2), nor had we expected to learn that diet and cancer associations detected when dietary assessment is based on dietary biomarkers (e.g., ref.3) or food records (4) are undetectable when based on FFQs. We are facing a crisis: hundreds of millions of dollars and many scientists' careers have been invested in studies using only FFQs to measure diet, but it is possible that these studies have not been, and will not be, able to answer many if not most questions about diet and cancer risk.This commentary has two broad functions. First, it describes how FFQs were developed and why they became the standard measure of diet for epidemiologic research. Second, it suggests several directions for future research and practice to improve dietary assessment in studies of diet and cancer.

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