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  • 1
    Keywords: CANCER ; OBESITY ; body mass index ; nutrition ; ENERGY-INTAKE ; PHYSICAL-ACTIVITY ; BODY-MASS INDEX ; weight gain ; 10 EUROPEAN COUNTRIES ; eating at restaurants ; eating at work ; EPIC-PANACEA ; FAST-FOOD CONSUMPTION ; OUT-OF-HOME ; RESTAURANT USE
    Abstract: Objective: The aim of this study was to examine the association of body mass index (BMI) and weight gain with eating at restaurants and similar establishments or eating at work among 10 European countries of the European Prospective Investigation into Cancer and Nutrition (EPIC) study. Subjects: This study included a representative sample of 24 310 randomly selected EPIC participants. Methods: Single 24-h dietary recalls with information on the place of consumption were collected using standardized procedures between 1995 and 2000. Eating at restaurants was defined to include all eating and drinking occasions at restaurants, cafeterias, bars and fast food outlets. Eating at work included all eating and drinking occasions at the workplace. Associations between eating at restaurants or eating at work and BMI or annual weight changes were assessed using sex-specific linear mixed-effects models, controlling for potential confounders. Results: In southern Europe energy intake at restaurants was higher than intake at work, whereas in northern Europe eating at work appeared to contribute more to the mean daily intake than eating at restaurants. Cross-sectionally, eating at restaurants was found to be positively associated with BMI only among men (beta = +0.24, P = 0.003). Essentially no association was found between BMI and eating at work among both genders. In a prospective analysis among men, eating at restaurants was found to be positively, albeit nonsignificantly, associated with weight gain (beta = +0.05, P = 0.368). No association was detected between energy intake at restaurants and weight changes, controlling for total energy intake. Conclusion: Among men, eating at restaurants and similar establishments was associated with higher BMI and possibly weight gain.
    Type of Publication: Journal article published
    PubMed ID: 20661252
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  • 2
    Keywords: CANCER ; lung cancer ; SUPPORT ; COHORT ; EPIDEMIOLOGY ; MORTALITY ; RISK ; HETEROCYCLIC AMINES ; ASSOCIATION ; WOMEN ; FISH ; DIET ; FAT ; CONSUMPTION ; EPIC ; meat ; CALIBRATION ; DIETARY HABITS ; RECALLS ; HEME IRON ; MUTAGENS
    Abstract: Evidence from case-control studies, but less so from cohort studies, suggests a positive association between meat intake and risk of lung cancer. Therefore, this association was evaluated in the frame of the European Prospective Investigation into Cancer and Nutrition, EPIC. Data from 478,021 participants, recruited from 10 European countries, who completed a dietary questionnaire in 1992-2000 were evaluated; 1,822 incident primary lung cancer cases were included in the present evaluation. Relative risk estimates were calculated for categories of meat intake using multi-variably adjusted Cox proportional hazard models. In addition, the continuous intake variables were calibrated by means of 24-h diet recall data to account for part of the measurement error. There were no consistent associations between meat consumption and the risk of lung cancer. Neither red meat (RR = 1.06, 95% CI 0.89-1.27 per 50 g intake/day; calibrated model) nor processed meat (RR = 1.13, 95% CI 0.95-1.34 per 50 g/day; calibrated model) was significantly related to an increased risk of lung cancer. Also, consumption of white meat and fish was not associated with the risk of lung cancer. These findings do not support the hypothesis that a high intake of red and processed meat is a risk factor for lung cancer
    Type of Publication: Journal article published
    PubMed ID: 21479828
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  • 3
    Keywords: CANCER ; EXPOSURE ; validation ; MEASUREMENT ERROR ; nutrition ; CALIBRATION ; MULTICENTER ; FOOD ; HEMOGLOBIN ADDUCTS ; glycidamide
    Abstract: BACKGROUND: Acrylamide is a chemical compound present in tobacco smoke and food, classified as a probable human carcinogen and a known human neurotoxin. Acrylamide is formed in foods, typically carbohydrate-rich and protein-poor plant foods, during high-temperature cooking or other thermal processing. The objectives of this study were to compare dietary estimates of acrylamide from questionnaires (DQ) and 24-h recalls (R) with levels of acrylamide adduct (AA) in haemoglobin. METHODS: In the European Prospective Investigation into Cancer and Nutrition (EPIC) study, acrylamide exposure was assessed in 510 participants from 9 European countries, randomly selected and stratified by age, sex, with equal numbers of never and current smokers. After adjusting for country, alcohol intake, smoking status, number of cigarettes and energy intake, correlation coefficients between various acrylamide measurements were computed, both at the individual and at the aggregate (centre) level. RESULTS: Individual level correlation coefficient between DQ and R measurements (r DQ,R) was 0.17, while r DQ,AA and r R,AA were 0.08 and 0.06, respectively. In never smokers, r DQ,R, r DQ,AA and r R,AA were 0.19, 0.09 and 0.02, respectively. The correlation coefficients between means of DQ, R and AA measurements at the centre level were larger (r 〉 0.4). CONCLUSIONS: These findings suggest that estimates of total acrylamide intake based on self-reported diet correlate weakly with biomarker AA Hb levels. Possible explanations are the lack of AA levels to capture dietary acrylamide due to individual differences in the absorption and metabolism of acrylamide, and/or measurement errors in acrylamide from self-reported dietary assessments, thus limiting the possibility to validate acrylamide DQ measurements.
    Type of Publication: Journal article published
    PubMed ID: 23114503
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  • 4
    Keywords: CANCER ; COHORT ; RISK ; IMPACT ; CARCINOGENESIS ; BIOMARKERS ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; VARIANTS ; HEALTH ; PLASMA ; AGE ; colorectal cancer ; smoking ; COLORECTAL-CANCER ; FIBER ; COLON-CANCER ; MASS-SPECTROMETRY ; EPIC ; nutrition ; education ; NESTED CASE-CONTROL ; physical activity ; ONCOLOGY ; case-control study ; REGRESSION ; ASSOCIATIONS ; VARIANT ; PHYSICAL-ACTIVITY ; biomarker ; methods ; dietary patterns ; GENOTYPE ; LOCUS ; prospective ; CANCER-RISK ; nested case-control study ; COMMON MUTATION ; MTHFR POLYMORPHISMS ; FOLIC-ACID ; Genetic ; FOLATE STATUS ; METHYLENETETRAHYDROFOLATE REDUCTASE POLYMORPHISM ; nested case control study ; C677T MTHFR POLYMORPHISM ; CARBON METABOLIC PATHWAY ; HUMAN METHIONINE SYNTHASE
    Abstract: Background: A potential dual role of folate in colorectal cancer (CRC) is currently subject to debate. We investigate the associations between plasma folate, several relevant folate-related polymorphisms, and CRC risk within the large European Prospective Investigation into Cancer and Nutrition cohort. Methods: In this nested case-control study, 1,367 incident CRC cases were matched to 2,325 controls for study center, age, and sex. Risk ratios (RR) were estimated with conditional logistic regression and adjusted for smoking, education, physical activity, and intake of alcohol and fiber. Results: Overall analyses did not reveal associations of plasma folate with CRC. The RR (95% confidence interval; P-trend) for the fifth versus the first quintile of folate status was 0.94 (0.74-1.20; 0.44). The polymorphisms MTHFR677C -〉 T, MTHFR1298A -〉 C, MTR2756A -〉 G, MTRR66A -〉 G, and MTHFD11958G -〉 A were not associated with CRC risk. However, in individuals with the lowest plasma folate concentrations, the MTHFR 677TT genotype showed a statistically nonsignificant increased CRC risk [RR (95% CI; P-trend) TT versus CC = 1.39 (0.87-2.21); 0.12], whereas those with the highest folate concentrations showed a nonsignificant decreased CRC risk [RR TT versus CC = 0.74 (0.39-1.37); 0.34]. The SLC19A180G -〉 A showed a positive association with CRC risk [RR AA versus GG 1.30 (1.06-1.59); 〈0.01]. Conclusions: This large European prospective multicenter study did not show an association of CRC risk with plasma folate status nor with MTHFR polymorphisms. Impact: Findings of the present study tend to weaken the evidence that folate plays an important role in CRC carcinogenesis. However, larger sample sizes are needed to adequately address potential gene-environment interactions. Cancer Epidemiol Biomarkers Prev; 19(5); 1328-40. (C)2010 AACR
    Type of Publication: Journal article published
    PubMed ID: 20447924
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