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  • AGE  (4)
  • 1
    Keywords: CANCER ; MODEL ; MODELS ; FOLLOW-UP ; COHORT ; POPULATION ; INTERVENTION ; ASSOCIATION ; PATTERNS ; DESIGN ; ENERGY ; AGE ; WOMEN ; MEN ; OBESITY ; smoking ; COUNTRIES ; DIET ; FAT ; BLOOD-PRESSURE ; ALCOHOL ; PROJECT ; CONSUMPTION ; nutrition ; SMOKERS ; CALIBRATION ; MANAGEMENT ; physical activity ; ASSOCIATIONS ; PATTERN ; WEIGHT ; ENERGY-INTAKE ; LOW-CARBOHYDRATE ; PHYSICAL-ACTIVITY ; dietary patterns ; BODY-MASS INDEX ; prospective ; EUROPEAN COUNTRIES ; WAIST CIRCUMFERENCE ; WEIGHT CHANGE ; RANDOMIZED CLINICAL-TRIAL ; Lead ; Follow up ; weight gain ; OBESE ADULTS ; PLASMA LEPTIN ; PROTEIN DIET
    Abstract: Background: Meat intake may be related to weight gain because of its high energy and fat content. Some observational studies have shown that meat consumption is positively associated with weight gain, but intervention studies have shown mixed results. Objective: Our objective was to assess the association between consumption of total meat, red meat, poultry, and processed meat and weight gain after 5 y of follow-up, on average, in the large European population who participated in the European Prospective Investigation into Cancer and Nutrition-Physical Activity, Nutrition, Alcohol, Cessation of Smoking, Eating Out of Home and Obesity (EPIC-PANACEA) project. Design: A total of 103,455 men and 270,348 women aged 25-70 y were recruited between 1992 and 2000 in 10 European countries. Diet was assessed at baseline with the use of country-specific validated questionnaires. A dietary calibration study was conducted in a representative subsample of the cohort. Weight and height were measured at baseline and self-reported at follow-up in most centers. Associations between energy from meat (kcal/d) and annual weight change (g/y) were assessed with the use of linear mixed models, controlled for age, sex, total energy intake, physical activity, dietary patterns, and other potential confounders. Results: Total meat consumption was positively associated with weight gain in men and women, in normal-weight and overweight subjects, and in smokers and nonsmokers. With adjustment for estimated energy intake, an increase in meat intake of 250 g/d (eg, one steak at approximate to 450 kcal) would lead to a 2-kg higher weight gain after 5 y (95% CI: 1.5, 2.7 kg). Positive associations were observed for red meat, poultry, and processed meat. Conclusion: Our results suggest that a decrease in meat consumption may improve weight management. Am J Clin Nutr 2010; 92: 398-407
    Type of Publication: Journal article published
    PubMed ID: 20592131
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  • 2
    Keywords: RISK ; AGE ; WOMEN ; POLYPHENOLS ; GREECE ; CALIBRATION ; HEART-DISEASE ; POSTMENOPAUSAL WOMEN ; ADULTS ; ESOPHAGEAL CANCER ; intake ; nonsmokers ; Anthocyanidins ; DIETARY FLAVONOID INTAKE ; EPIC-Europe ; Food sources ; LONG-ISLAND
    Abstract: Anthocyanidins are bioactive flavonoids with potential health-promoting effects. These may vary among single anthocyanidins considering differences in their bioavailability and some of the mechanisms involved. The aim of the present study was to estimate the dietary intake of anthocyanidins, their food sources and the lifestyle factors (sex, age, BMI, smoking status, educational level and physisical activity) involved among twenty-seven centres in ten European countries participating in the European Prospective Investigation into Cancer and Nutrition (EPIC) study. Anthocyanidin intake and their food sources for 36 037 subjects, aged between 35 and 74 years, in twenty-seven redefined centres were obtained using standardised 24 h dietary recall software (EPIC-SOFT). An ad hoc food composition database on anthocyanidins (cyanidin, delphinidin, malvidin, pelargonidin, peonidin, petunidin) was compiled using data from the US Department of Agriculture and Phenol-Explorer databases and was expanded by adding recipes, estimated values and cooking factors. For men, the total anthocyanidin mean intake ranged from 19.83 (SE 1.53) mg/d (Bilthoven, The Netherlands) to 64.88 (SE 1.86) mg/d (Turin, Italy), whereas for women the range was 18.73 (SE 2.80) mg/d (Granada, Spain) to 44.08 (SE 2.45) mg/d (Turin, Italy). A clear south to north gradient intake was observed. Cyanidins and malvidins were the main anthocynidin contributors depending on the region and sex. Anthocyanidin intake was higher in non-obese older females, non-smokers, and increased with educational level and physical activity. The major food sources were fruits, wine, non-alcoholic beverages and some vegetables. The present study shows differences in both total and individual anthocyanidin intakes and various lifestyle factors throughout Europe, with some geographical variability in their food sources
    Type of Publication: Journal article published
    PubMed ID: 21481290
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  • 3
    Keywords: CANCER ; Germany ; LUNG ; MODEL ; FOLLOW-UP ; lung cancer ; LUNG-CANCER ; COHORT ; incidence ; MORTALITY ; NEW-YORK ; POPULATION ; RISK ; RISK-FACTORS ; ASSOCIATION ; AGE ; MEN ; smoking ; COUNTRIES ; cancer risk ; POPULATIONS ; DIET ; DIETARY ; NETHERLANDS ; case-control studies ; CONSUMPTION ; EPIC ; EPIC study ; European Prospective Investigation into Cancer and Nutrition ; FRUIT ; nutrition ; QUESTIONNAIRE ; SMOKERS ; VEGETABLES ; EUROPE ; FOOD ; RELATIVE RISK ; cancer,diet,epidemiology,fruits,vegetables,lung cancer,smoking ; FLAVONOIDS ; NONSMOKING WOMEN
    Abstract: Intake of fruits and vegetables is thought to protect against the development of lung cancer. However, some recent cohort and case-control studies have shown no protective effect. We have assessed the relation between fruit and vegetable intake and lung cancer incidence in the large prospective investigation on diet and cancer, the European Prospective Investigation Into Cancer and Nutrition (EPIC). We studied data from 478,021 individuals that took part in the EPIC study, who were recruited from 10 European countries and who completed a dietary questionnaire during 1992-1998. Follow-up was to December 1998 or 1999, but for some centres with active follow-up to June 2002. During follow-up, 1,074 participants were reported to have developed lung cancer, of whom 860 were eligible for our analysis. We used the Cox proportional hazard model to determine the effect of fruit and vegetable intake on the incidence of lung cancer. We paid particular attention to adjustment for smoking. Relative risk estimates were obtained using fruit and vegetable intake categorised by sex-specific, cohort-wide quintiles. After adjustment for age, smoking, height, weight and gender, there was a significant inverse association between fruit consumption and lung cancer risk: the hazard ratio for the highest quintile of consumption relative to the lowest being 0.60 (95% Confidence Interval 0.46-0.78), p for trend 0.0099. The association was strongest in the Northern Europe centres, and among current smokers at baseline, and was strengthened when the 293 lung cancers diagnosed in the first 2 years of follow-up were excluded from the analysis. There was no association between vegetable consumption or vegetable subtypes and lung cancer risk. The findings from this analysis can be regarded as re-enforcing recommendations with regard to enhanced fruit consumption for populations. However, the effect is likely to be small compared to smoking cessation. (C) 2003 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 14639614
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  • 4
    Keywords: RECEPTOR ; APOPTOSIS ; CANCER ; EXPRESSION ; proliferation ; CELL ; CELL-PROLIFERATION ; MODEL ; MODELS ; PROSTATE ; COMMON ; COHORT ; HISTORY ; RISK ; GENE ; GENES ; FAMILY ; INDEX ; SEQUENCE ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; VARIANTS ; BREAST ; NO ; STAGE ; HEALTH ; AGE ; family history ; SNP ; MEN ; prostate cancer ; PROSTATE-CANCER ; cancer risk ; HUMAN GENOME ; BETA ; POPULATIONS ; case-control studies ; BODY ; ESTROGEN-RECEPTOR ; REGRESSION-MODELS ; MASS INDEX ; MASSES ; BODIES ; SINGLE ; ONCOLOGY ; case control study ; case-control study ; REGRESSION ; FAMILIES ; VARIANT ; SINGLE NUCLEOTIDE POLYMORPHISMS ; SNPs ; GRADE ; regulation ; cell proliferation ; GROWTH-FACTOR-I ; ESTROGEN ; biomarker ; case control studies ; INTERVAL ; analysis ; methods ; HAPLOTYPE ; HAPLOTYPES ; LOCUS ; single-nucleotide ; estrogen receptor ; FAMILY-HISTORY ; USA ; INCREASED RISK ; cancer research ; CANCER-RISK ; MULTIETHNIC COHORT ; SET ; nested case-control study ; case control ; LOGISTIC-REGRESSION ; BODY-MASS ; BODY-MASS-INDEX ; ER-BETA ; EXONS ; GENETIC-VARIATION ; TAG SNPS
    Abstract: Background: Estrogen receptor beta (ESR2) may play a role in modulating prostate carcirtogenesis through the regulation of genes related to cell proliferation and apoptosis. Methods: We conducted nested case-control studies in the Breast and Prostate Cancer Cohort Consortium (BPC3) that pooled 8,323 prostate cancer cases and 9,412 controls from seven cohorts. Whites were the predominant ethnic group. We characterized genetic variation in ESR2 by resequencing exons in 190 breast and prostate cancer cases and genotyping a dense set of single nucleotide polymorphisms (SNP) spanning the locus in a multiethnic panel of 349 cancer-free subjects. We selected four haplotype-tagging SNPs (htSNP) to capture common ESR2 variation in Whites; these htSNPs were then genotyped in all cohorts. Conditional logistic regression models were used to assess the association between sequence variants of ESR2 and the risk of prostate cancer. We also investigated the effect modification by age, body mass index, and family history, as well as the association between sequence variants of ESR2 and advanced-stage (〉= T3b, N-1, or M-1) and high-grade (Gleason sum 〉= 8) prostate cancer, respectively. Results: The four tag SNPs in ESR2 were not significantly associated with prostate cancer risk, individually. The global test for the influence of any haplotype on the risk of prostate cancer was not significant (P = 0.31). However, we observed that men carrying two copies of one of the variant haplotypes (TACC) had a 1.46-fold increased risk of prostate cancer (99% confidence interval, 1.06-2.01) compared with men carrying zero copies of this variant haplotype. No SNPs or haplotypes were associated with advanced stage or high grade of prostate cancer. Conclusion: In our analysis focused on genetic variation common in Whites, we observed little evidence for any substantial association of inherited variation in ESR2 with risk of prostate cancer. A nominally significant (P 〈 0.01) association between the TACC haplotype and prostate cancer risk under the recessive model could be a chance finding and, in any event, would seem to contribute only slightly to the overall burden of prostate cancer
    Type of Publication: Journal article published
    PubMed ID: 17932344
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