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Surtees P.G.,University of Cambridge | Wainwright N.W.J.,University of Cambridge | Luben R.N.,University of Cambridge | Khaw K.-T.,University of Cambridge | Bingham S.A.,Medical Research Council Center for Nutritional Epidemiology in Cancer Prevention and Survival
Breast Cancer Research and Treatment | Year: 2010

Women commonly attribute the experience of stress as a contributory cause of breast cancer. The purpose of this study is to investigate the associations between a history of social stress and breast cancer risk. A total of 11,467 women with no prior history of breast cancer, participants in the European Prospective Investigation into Cancer (EPIC)-Norfolk population-based prospective cohort study, completed a comprehensive assessment of lifetime social adversity exposure. Summary measures of social adversity were defined according to difficult circumstances in childhood, stressful life events and longer-term difficulties in adulthood, derived measures representing the subjective 'impact' of life events and associated 'stress adaptive capacity', and perceived stress over a 10-year period. Incident breast cancers were identified through linkage with cancer registry data. During 102,514 (median 9) person-years of follow-up, 313 incident breast cancers were identified. No associations were observed between any of the summary social adversity measures and subsequent breast cancer risk, with or without adjustment for age, menopausal status, parity, use of menopausal hormones, age at menarche, age at first birth, family history of breast cancer, physical activity, social class, body mass index, height, and alcohol intake. This study found no evidence that social stress exposure or individual differences in its experience are associated with the development of breast cancer. These findings may aid strategies designed to meet the psychosocial and emotional needs of breast cancer survivors and may be interpreted in a positive way in the context of commonly voiced beliefs that the experience of stress is a contributory cause of their disease. © 2009 Springer Science+Business Media, LLC. Source


Spencer E.A.,University of Oxford | Key T.J.,University of Oxford | Appleby P.N.,University of Oxford | Dahm C.C.,Medical Research Council Center for Nutritional Epidemiology in Cancer Prevention and Survival | And 15 more authors.
Cancer Causes and Control | Year: 2010

Objective: Some but not all epidemiological studies have reported that high intakes of red and processed meat are associated with an increased risk of colorectal cancer. In the UK Dietary Cohort Consortium, we examined associations of meat, poultry and fish intakes with colorectal cancer risk using standardised individual dietary data pooled from seven UK prospective studies. Methods: Four- to seven-day food diaries were analysed, disaggregating the weights of meat, poultry and fish from composite foods to investigate dose-response relationships. We identified 579 cases of colorectal cancer and matched with 1,996 controls on age, sex and recruitment date. Conditional logistic regression models were used to estimate odds ratios for colorectal cancer associated with meat, poultry and fish intakes, adjusting for relevant covariables. Results: Disaggregated intakes were moderately low, e.g. mean red meat intakes were 38.2 g/day among male and 28.7 g/day among female controls. There was little evidence of association between the food groups examined and risk for colorectal cancer: Odds ratios (95% confidence intervals) for a 50 g/day increase were 1.01 (0.84-1.22) for red meat, 0.88 (0.68-1.15) for processed meat, 0.97 (0.84-1.12) for red and processed meat combined, 0.80 (0.65-1.00) for poultry, 0.92 (0.70-1.21) for white fish and 0.89 (0.70-1.13) for fatty fish. Conclusions: This study using pooled data from prospective food diaries, among cohorts with low to moderate meat intakes, shows little evidence of association between consumption of red and processed meat and colorectal cancer risk. © 2010 Springer Science+Business Media B.V. Source


Waterworth D.M.,Glaxosmithkline | Ricketts S.L.,University of Cambridge | Song K.,Glaxosmithkline | Chen L.,University of Ottawa | And 72 more authors.
Arteriosclerosis, Thrombosis, and Vascular Biology | Year: 2010

OBJECTIVE-: Genetic studies might provide new insights into the biological mechanisms underlying lipid metabolism and risk of CAD. We therefore conducted a genome-wide association study to identify novel genetic determinants of low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides. METHODS AND RESULTS-: We combined genome-wide association data from 8 studies, comprising up to 17 723 participants with information on circulating lipid concentrations. We did independent replication studies in up to 37 774 participants from 8 populations and also in a population of Indian Asian descent. We also assessed the association between single-nucleotide polymorphisms (SNPs) at lipid loci and risk of CAD in up to 9 633 cases and 38 684 controls. We identified 4 novel genetic loci that showed reproducible associations with lipids (probability values, 1.6×10-8 to 3.1×10-10). These include a potentially functional SNP in the SLC39A8 gene for HDL-C, an SNP near the MYLIP/GMPR and PPP1R3B genes for LDL-C, and at the AFF1 gene for triglycerides. SNPs showing strong statistical association with 1 or more lipid traits at the CELSR2, APOB, APOE-C1-C4-C2 cluster, LPL, ZNF259-APOA5-A4-C3-A1 cluster and TRIB1 loci were also associated with CAD risk (probability values, 1.1×10-3 to 1.2×10-9). CONCLUSION-: We have identified 4 novel loci associated with circulating lipids. We also show that in addition to those that are largely associated with LDL-C, genetic loci mainly associated with circulating triglycerides and HDL-C are also associated with risk of CAD. These findings potentially provide new insights into the biological mechanisms underlying lipid metabolism and CAD risk. © 2010 American Heart Association, Inc. Source


Key T.J.,University of Oxford | Appleby P.N.,University of Oxford | Cairns B.J.,University of Oxford | Luben R.,University of Cambridge | And 23 more authors.
American Journal of Clinical Nutrition | Year: 2011

Background: Epidemiologic studies of dietary fat and breast cancer risk are inconsistent, and it has been suggested that a true relation may have been obscured by the imprecise measurement of fat intake. Objective: We examined associations of fat with breast cancer risk by using estimates of fat intake from food diaries and food-frequency questionnaires (FFQs) pooled from 4 prospective studies in the United Kingdom. Design: A total of 657 cases of breast cancer in premenopausal and postmenopausal women were matched on study, age, and recruitment date with 1911 control subjects. Nutrient intakes were estimated from food diaries and FFQs. Conditional logistic regression was used to estimate ORs for breast cancer associated with total, saturated, monounsaturated, and polyunsaturated fat intakes with adjustment for relevant covariates. Results: Neither the food diaries nor the FFQs showed any positive associations between fat intake and overall breast cancer risk. ORs (95% CIs) for the highest compared with lowest quintiles of percentage of energy from total fat were 0.90 (0.66, 1.23) for food diaries and 0.80 (0.59, 1.09) for FFQs. Conclusion: In this study, breast cancer risk was not associated with fat intake in middle-aged women in the United Kingdom, irrespective of whether diet was measured by food diaries or by FFQs. © 2011 American Society for Nutrition. Source

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