Collaborating Center for Food and Nutrition Policies
Collaborating Center for Food and Nutrition Policies
Trichopoulou A.,Collaborating Center for Food and Nutrition Policies |
Trichopoulou A.,Hellenic Health Foundation |
Bamia C.,Collaborating Center for Food and Nutrition Policies |
Lagiou P.,Collaborating Center for Food and Nutrition Policies |
And 4 more authors.
American Journal of Clinical Nutrition | Year: 2010
Background: Studies in the United States report inverse associations of the Mediterranean dietary pattern with breast cancer risk, and several studies in Mediterranean countries indicate inverse associations of breast cancer risk with intake of olive oil, a constitutional component of this diet. No study, however, has evaluated the association of the traditional Mediterranean diet with breast cancer in a Mediterranean country. Objective: We studied the relation of conformity to the Mediterranean diet with breast cancer risk in the context of the European Prospective Investigation into Cancer and Nutrition cohort in Greece. Design: We followed up 14,807 women for an average of 9.8 y and identified 240 incident breast cancer cases. Diet was assessed through a validated food-frequency questionnaire, and conformity to the Mediterranean diet was evaluated through a score (range = 0-9 points) incorporating the characteristics of this diet. Results: Increasing conformity to the Mediterranean diet was not associated with lower breast cancer risk in the entire cohort [hazard ratio (HR) = 0.88 for every 2 points; 95% CI: 0.75, 1.03] or in premenopausal women (HR = 1.01 for every 2 points; 95% CI: 0.80, 1.28), but there was a marginally significant inverse association among postmenopausal women (HR = 0.78 for every 2 points; 95% CI: 0.62, 0.98; P for interaction by menopausal status = 0.05). Conclusions: Conformity to the traditional Mediterranean diet may be associated with lower breast cancer risk among postmenopausal women and could explain, in part, the lower incidence of this disease in Mediterranean countries. © 2010 American Society for Nutrition.
Jakobsen M.U.,University of Aarhus |
Dethlefsen C.,Aarhus University Hospital |
Due K.M.,Aarhus University Hospital |
May A.M.,University Utrecht |
And 57 more authors.
British Journal of Nutrition | Year: 2013
Fish consumption is the major dietary source of EPA and DHA, which according to rodent experiments may reduce body fat mass and prevent obesity. Only a few human studies have investigated the association between fish consumption and body-weight gain. We investigated the association between fish consumption and subsequent change in body weight. Women and men (n 344Â 757) participating in the European Prospective Investigation into Cancer and Nutrition were followed for a median of 5·0 years. Linear and logistic regression were used to investigate the associations between fish consumption and subsequent change in body weight. Among women, the annual weight change was 5·70 (95Â % CI 4·35, 7·06), 2·23 (95Â % CI 0·16, 4·31) and 11·12 (95Â % CI 8·17, 14·08)Â g/10Â g higher total, lean and fatty fish consumption per d, respectively. The OR of becoming overweight in 5 years among women who were normal weight at enrolment was 1·02 (95Â % CI 1·01, 1·02), 1·01 (95Â % CI 1·00, 1·02) and 1·02 (95Â % CI 1·01, 1·04)Â g/10Â g higher total, lean and fatty consumption per d, respectively. Among men, fish consumption was not statistically significantly associated with weight change. Adjustment for potential over- or underestimation of fish consumption did not systematically change the observed associations, but the 95Â % CI became wider. The results in subgroups from analyses stratified by age or BMI at enrolment were not systematically different. In conclusion, the present study suggests that fish consumption has no appreciable association with body-weight gain. Copyright © The Authors 2012.
Michaud D.S.,Imperial College London |
Michaud D.S.,Brown University |
Gallo V.,Imperial College London |
Schlehofer B.,German Cancer Research Center |
And 47 more authors.
Cancer Epidemiology Biomarkers and Prevention | Year: 2010
Background: The etiologies of glioma and meningioma tumors are largely unknown. Although reproductive hormones are thought to influence the risk of these tumors, epidemiologic data are not supportive of this hypothesis; however, few cohort studies have published on this topic. We examined the relation between reproductive factors and the risk of glioma and meningioma among women in the European Prospective Investigation into Cancer and Nutrition (EPIC). Methods: After amean of 8.4 years of follow-up, 193 glioma and 194meningioma cases were identified among 276,212 women. Information on reproductive factors and hormone use was collected at baseline. Cox proportional hazard regression was used to determine hazard ratios (HR) and 95% confidence intervals (95% CI). Results: No associations were observed between glioma or meningioma risk and reproductive factors, including age at menarche, parity, age at first birth, menopausal status, and age at menopause. A higher risk of meningioma was observed among postmenopausal women who were current users of hormone replacement therapy (HR, 1.79; 95% CI, 1.18-2.71) compared with never users. Similarly, current users of oral contraceptives were at higher risk of meningioma than never users (HR, 3.61; 95% CI, 1.75-7.46). Conclusion: Our results do not support a role for estrogens and glioma risk. Use of exogenous hormones, especially current use, seems to increase meningioma risk. However, these findings could be due to diagnostic bias and require confirmation. Impact: Elucidating the role of hormones in brain tumor development has important implications and needs to be further examined using biological measurements. ©2010AACR.
Chan S.S.M.,University of East Anglia |
Chan S.S.M.,Norwich University |
Luben R.,University of Cambridge |
Van Schaik F.,University Utrecht |
And 30 more authors.
Inflammatory Bowel Diseases | Year: 2014
Background: Diet may have a role in the etiology of inflammatory bowel disease. In previous studies, the associations between increased intakes of carbohydrates, sugar, starch, and inflammatory bowel disease are inconsistent. However, few prospective studies have investigated the associations between these macronutrients and incident Crohn's disease (CD) or ulcerative colitis (UC). Methods: A total of 401,326 men and women were recruited between 1991 and 1998. At recruitment, dietary intakes of carbohydrate, sugar, and starch were measured using validated food frequency questionnaires. The cohort was monitored identifying participants who developed incident CD or UC. Cases were matched with 4 controls, and odds ratios were calculated for quintiles of total carbohydrate, sugar, and starch intakes adjusted for total energy intake, body mass index, and smoking. Results: One hundred ten participants developed CD, and 244 participants developed UC during follow-up. The adjusted odds ratio for the highest versus the lowest quintiles of total carbohydrate intake for CD was 0.87, 95% CI = 0.24 to 3.12 and for UC 1.46, 95% CI = 0.62 to 3.46, with no significant trends across quintiles for either (CD, Ptrend = 0.70; UC, Ptrend = 0.41). Similarly, no associations were observed with intakes of total sugar (CD, Ptrend = 0.50; UC, Ptrend = 0.71) or starch (CD, Ptrend = 0.69; UC, Ptrend = 0.17). Conclusions: The lack of associations with these nutrients is in agreement with many case-control studies that have not identified associations with CD or UC. As there is biological plausibility for how specific carbohydrates could have an etiological role in inflammatory bowel disease, future epidemiological work should assess individual carbohydrates, although there does not seem to be a macronutrient effect. Copyright © 2014 Crohn's & Colitis Foundation of America, Inc.