Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Keywords: ENERGIES ; CANCER ; MODEL ; FOLLOW-UP ; POPULATION ; RISK ; ASSOCIATION ; hormone ; ENERGY ; AGE ; WOMEN ; colorectal cancer ; MEN ; PROSPECTIVE COHORT ; smoking ; COLORECTAL-CANCER ; cancer risk ; FISH ; FIBER ; COLON-CANCER ; DOSE-RESPONSE ; Jun ; DIET ; DIETARY ; UNITED-STATES ; ALCOHOL-CONSUMPTION ; nutrition ; ASSOCIATIONS ; RE ; ENERGY-INTAKE ; EPIC CALIBRATION ; PHYSICAL-ACTIVITY ; INTERVAL ; TESTS ; alcohol consumption ; MEAT INTAKE ; DIETARY CARCINOGENS ; GENETIC SUSCEPTIBILITY ; N-NITROSATION ; RED MEAT
    Abstract: Background. Current evidence suggests that high red meat intake is associated with increased colorectal cancer risk. High fish intake may be associated with a decreased risk, but the existing evidence is less convincing. Methods: We prospectively followed 478040 men and women from 10 European countries who were free of cancer at enrollment between 1992 and 1998. Information on diet and lifestyle was collected at baseline. After a mean follow-up of 4.8 years, 1329 incident colorectal cancers were documented. We examined the relationship between intakes of red and processed meat, poultry, and fish and colorectal cancer risk using a proportional hazards model adjusted for age, sex, energy (nonfat and fat sources), height, weight, work-related physical activity, smoking status, dietary fiber and folate, and alcohol consumption, stratified by center. A calibration substudy based on 36994 subjects was used to correct hazard ratios (HRs) and 95% confidence intervals (CIs) for diet measurement errors. All statistical tests were two-sided. Results: Colorectal cancer risk was positively associated with intake of red and processed meat (highest [〉 160 g/day] versus lowest [〈 20 g/day] intake, HR = 1.35, 95% CI = 0.96 to 1.88; P-trend = .03) and inversely associated with intake of fish (〉 80 g/day versus 〈 10 g/day, HR = 0.69, 95% CI = 0.54 to 0.88; P-trend 〈 .001), but was not related to poultry intake. Correcting for measurement error strengthened the associations between colorectal cancer and red and processed meat intake (per 100-g increase HR = 1.25, 95% CI = 1.09 to 1.41, P-trend = .001 and HR = 1.55, 95% CI = 1.19 to 2.02, P-trend = .001 before and after calibration, respectively) and for fish (per 100 g increase HR = 0.70, 95% CI = 0.57 to 0.87, P-trend 〈 .001 and HR = 0.46, 95% CI = 0.27 to 0.77, P-trend = .003; before and after correction, respectively). In this study population, the absolute risk of development of colorectal cancer within 10 years for a study subject aged 50 years was 1.71% for the highest category of red and processed meat intake and 1.28% for the lowest category of intake and was 1.86% for subjects in the lowest category of fish intake and 1.28% for subjects in the highest category of fish intake. Conclusions: Our data confirm that colorectal cancer risk is positively associated with high consumption of red and processed meat and support an inverse association with fish intake
    Type of Publication: Journal article published
    PubMed ID: 15956652
    Signatur Availability
    BibTip Others were also interested in ...
  • 2
    Keywords: CANCER ; carcinoma ; INFORMATION ; COHORT ; DEATH ; incidence ; RISK ; SITE ; SITES ; GENE ; INFECTION ; DOWN-REGULATION ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; MOLECULE ; NO ; PROGRESSION ; DIFFERENCE ; PROMOTER ; MUTATION ; smoking ; RATES ; FRANCE ; MUTATIONS ; ADHESION ; case-control studies ; ADHESION MOLECULE ; EPIC ; HELICOBACTER-PYLORI ; nutrition ; SMOKERS ; METHYLATION ; E-cadherin ; ONCOLOGY ; case-control study ; RE ; INCREASE ; gastric cancer ; PROMOTER POLYMORPHISM ; HAPLOTYPE ; prospective ; Helicobacter pylori ; ENGLAND ; block ; GENE POLYMORPHISMS ; GENE POLYMORPHISM ; POSITION ; gastric adenocarcinoma ; CDH1 ; E-CADHERIN GENE
    Abstract: Despite declining incidence rates, gastric cancer (GC) is a major cause of death worldwide. E-Cadherin is an adhesion molecule that is thought to be involved in GC. Germline mutations in the E-Cadherin gene (CDH1) have been identified in hereditary diffuse GC. Also, a promoter polymorphism at position 160 C/A has been suggested to lead to transcriptional down regulation and has been shown to affect GC risk in some studies. However, very little information exists on the GC risk association of other CDH1 polymorphisms and it is unclear whether any associations may be different by GC anatomical sites or histological types. Thus, a case-control study (cases = 245/controls = 950) nested within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort was conducted to assess the GC risk association of eight CDH1 gene polymorphisms. None of the CDH1 polymorphisms or haplotypes analysed were associated with GC risk and no differences of effect were observed by Helicobacter pylori infection status. However, three CDH1 polymorphisms in the same haplotype block, including the CDH1-160C/A, interacted with smoking to increase GC risk in smokers but not in never smokers. These findings should be confirmed in larger independent studies. (c) 2008 Elsevier Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 18342503
    Signatur Availability
    BibTip Others were also interested in ...
  • 3
    Keywords: CANCER ; CELLS ; AGENTS ; CELL ; MODEL ; MODELS ; neoplasms ; FOLLOW-UP ; SYSTEM ; COHORT ; cohort study ; EPIDEMIOLOGY ; HISTORY ; incidence ; RISK ; INFECTION ; MECHANISM ; primary ; RISK-FACTORS ; mechanisms ; T cell ; T-CELL ; ASSOCIATION ; DISORDER ; SUSCEPTIBILITY ; NO ; LYMPHOMA ; CARE ; DESIGN ; PLASMA ; AGE ; WOMEN ; etiology ; MEN ; risk factors ; leukemia ; Jun ; diabetes ; ABNORMALITIES ; INFECTIONS ; EPIC ; nutrition ; immunosuppression ; non-hodgkin's lymphoma ; CHRONIC LYMPHOCYTIC-LEUKEMIA ; MULTIPLE-MYELOMA ; VIRAL-INFECTION ; insulin ; MELLITUS ; AGENT ; AUTOIMMUNITY ; multiple myeloma ; DISORDERS ; MEDICAL HISTORY ; INCREASE ; T-CELL LYMPHOMA ; prospective studies ; methods ; SUBTYPES ; metabolic syndrome ; BODY-MASS INDEX ; prospective ; prospective study ; RISK-FACTOR ; CANCERS ; B-CELL ; ENGLAND ; ENVIRONMENTAL-FACTORS ; host ; INCREASES ; viral ; European Prospective Investigation into Cancer ; non-Hodgkin ; neoplasm ; INTERLEUKIN-6 GENE
    Abstract: Background Non-Hodgkin's lymphomas are a heterogeneous group of neoplasms arising from the lymphopoietic system including a wide range of subtypes of either B-cell or T-cell lymphomas. The few established risk factors for the development of these neoplasms include viral infections and immunological abnormalities, but their etiology remains largely unknown. Evidence suggests that certain medical conditions may be linked, through immunosuppression, to the risk of non-Hodgkin's lymphoma. Multiple myeloma is a neoplasm of plasma cells that accounts for approximately 15% of lymphopoietic cancers. Increases in the incidence of non-Hodgkin's lymphoma and multiple myeloma in the past implicate environmental factors as potential causal agents. Design and Methods In the European Prospective Investigation into Cancer and Nutrition (EPIC), 1,213 histologically confirmed incident cases of non-Hodgkin's lymphoma and multiple myeloma (594 men; 619 women) were identified during a follow-up of 8.5 years. Cox proportional hazard models were used to explore the association between self-reported diabetes, diagnosed after 30 years of age, and the risk of non-Hodgkin's lymphoma overall and multiple myeloma and various lymphoma subtypes. Results We found no association between a personal history of diabetes and the risk of non-Hodgkin's lymphoma overall in men (HR: 1.28, 95% CI: 0.89-1.84), in women (HR: 0.71, 95% CI: 0.41-1.24), or in men and women combined (HR: 1.09, 95% CI: 0.80-1.47). Among the B-non-Hodgkin's lymphoma subtypes, we observed a statistically significant increased risk of B-cell chronic lymphocytic leukemia (HR: 2.0, 95% CI: 1.04-3.86) in men, but not in women (HR: 1.07, 95% CI: 0.33-3.43). Conclusions This prospective study did not provide evidence for a role of self-reported diabetes in the etiology of non-Hodgkin's lymphoma overall or multiple myeloma. We found an increased risk of B-cell chronic lymphocytic leukemia among men with diabetes, but not among women. We hypothesize that diabetes may not play a causal role in the etiology of B-cell chronic lymphocytic leukemia, though the underlying pathogenic mechanisms of both disorders may include shared genetic, host and/or environmental susceptibility factors
    Type of Publication: Journal article published
    PubMed ID: 18443270
    Signatur Availability
    BibTip Others were also interested in ...
  • 4
    Keywords: ENERGIES ; CANCER ; Germany ; MODEL ; MODELS ; PROSTATE ; FOLLOW-UP ; INFORMATION ; COHORT ; RISK ; RISKS ; ASSOCIATION ; NO ; HEALTH ; PLASMA ; ENERGY ; AGE ; MEN ; PROSPECTIVE COHORT ; smoking ; prostate cancer ; PROSTATE-CANCER ; ethanol ; MULTIVARIATE ; RECRUITMENT ; ALCOHOL ; ALCOHOL-CONSUMPTION ; CONSUMPTION ; nutrition ; RELATIVE RISK ; ONCOLOGY ; WEIGHT ; ENERGY-INTAKE ; PHYSICAL-ACTIVITY ; HEIGHT ; biomarker ; USA ; cancer research ; RISK-FACTOR ; MIDDLE-AGED MEN ; energy intake ; WINE ; BEVERAGES
    Abstract: Alcohol is a risk factor for several types of cancer. However, the results for prostate cancer have been inconsistent, with most studies showing no association. Within the European Prospective Investigation into Cancer and Nutrition, detailed information were collected from 142,607 male participants on the intake of alcoholic beverages at recruitment (for 100% of the cohort) and over lifetime (for 76% of the cohort) between 1992 and 2000. During a median follow-up of 8.7 years, 2,655 prostate cancer cases were observed. Multivariate Cox proportional hazard models were used to examine the association of alcohol consumption at recruitment and average lifetime alcohol consumption with prostate cancer adjusted for age, center, smoking, height, weight, physical activity, and nonalcohol energy intake. Overall, neither alcohol consumption at baseline nor average lifetime alcohol consumption was associated with the risk for prostate cancer in this cohort of men. Men who consumed 〉= 60 g alcohol per day had a relative risk of 0.88 [95% confidence interval (95% CI) 0.72-1.081 compared with men with an intake of 0.1-4.9 g/d; the respective relative risk for average lifetime intake was 1.09 (95% CI, 0.86-1.39). For advanced prostate cancer (n=537), the relative risks for 〉= 60 and 0.1-4.9 g alcohol per day at baseline were 0.98 (95% CI, 0.66-1.44) and 1.28 (95% CI, 0.79-2-07), respectively, for average lifetime intake. No statistically significant association was observed for alcohol intake from specific alcoholic beverages. Our results indicate no association between the consumption of alcohol and prostate cancer in this cohort of European men
    Type of Publication: Journal article published
    PubMed ID: 18483352
    Signatur Availability
    BibTip Others were also interested in ...
  • 5
    Keywords: CANCER ; MODEL ; MODELS ; SUPPORT ; COHORT ; DEATH ; DISEASE ; EXPOSURE ; MORTALITY ; RISK ; TIME ; POLYMORPHISMS ; hippocampus ; CARE ; CIGARETTE-SMOKING ; smoking ; RATES ; DAMAGE ; RISK FACTOR ; PREVALENCE ; LIPID-PEROXIDATION ; CONSUMPTION ; EPIC ; nutrition ; CORTEX ; USA ; prospective ; INCREASED RISK ; RISK-FACTOR ; lipid ; amyotrophic lateral sclerosis ; INVESTIGATE ; 33 ; FORMALDEHYDE ; SPORADIC ALS
    Abstract: Objective: Cigarette smoking has been reported as "probable" risk factor for Amyotrophic Lateral Sclerosis (ALS), a poorly understood disease in terms of aetiology. The extensive longitudinal data of the European Prospective Investigation into Cancer and Nutrition (EPIC) were used to evaluate age-specific mortality rates from ALS and the role of cigarette smoking on the risk of dying from ALS. Methods: A total of 517,890 healthy subjects were included, resulting in 4,591,325 person-years. ALS cases were ascertained through death certificates. Cox hazard models were built to investigate the role of smoking on the risk of ALS, using packs/years and smoking duration to study dose-response. Results: A total of 118 subjects died from ALS, resulting in a crude mortality rate of 2.69 per 100,000/year. Current smokers at recruitment had an almost two-fold increased risk of dying from ALS compared to never smokers (HR = 1.89, 95% C.I. 1.14-3.14), while former smokers at the time of enrolment had a 50% increased risk (HR = 1.48, 95% C.I. 0.94-2-32). The number of years spent smoking increased the risk of ALS (p for trend = 0.002). Those who smoked more than 33 years had more than a two-fold increased risk of ALS compared with never smokers (HR = 2.16, 95% C.I. 1.33-3.53). Conversely, the number of years since quitting smoking was associated with a decreased risk of ALS compared with continuing smoking. Interpretation: These results strongly support the hypothesis of a role of cigarette smoking in aetiology of ALS. We hypothesize that this could occur through lipid peroxidation via formaldehyde exposure. Ann Neurol 2009;65:378-385
    Type of Publication: Journal article published
    PubMed ID: 19399866
    Signatur Availability
    BibTip Others were also interested in ...
  • 6
    Keywords: CANCER ; Germany ; MODEL ; MODELS ; FOLLOW-UP ; COHORT ; EPIDEMIOLOGY ; HISTORY ; RISK ; TIME ; ASSOCIATION ; HEALTH ; CIGARETTE-SMOKING ; smoking ; cancer risk ; ethanol ; NETHERLANDS ; ALCOHOL ; PROJECT ; ALCOHOL-CONSUMPTION ; CONSUMPTION ; EPIC ; nutrition ; pancreatic cancer ; LIFE-STYLE FACTORS ; pancreas ; PANCREATIC-CANCER ; WEIGHT ; DIETARY-INTAKE MEASUREMENTS ; BEER ; prospective ; CANCER-RISK ; MALE SMOKERS ; BEVERAGE CONSUMPTION ; COFFEE CONSUMPTION
    Abstract: To examine the association of baseline and lifetime ethanol intake with cancer of the pancreas in the European Prospective Investigation into Cancer and Nutrition (EPIC). Included in this analysis were 478,400 subjects, of whom detailed information on the intake of alcoholic beverages at baseline and over lifetime was collected between 1992 and 2000. During a median follow-up time of 8.9 years, 555 non-endocrine pancreatic cancer cases were observed. Multivariate Cox proportional hazard models were used to examine the association of ethanol intake at recruitment and average lifetime ethanol intake and pancreatic cancer adjusting for smoking, height, weight, and history of diabetes. Overall, neither ethanol intake at recruitment (relative risk (RR) = 0.94, 95% confidence interval (CI) 0.69-1.27 comparing 30+ g/d vs. 0.1-4.9 g/d) nor average lifetime ethanol intake (RR = 0.95, 95% CI 0.65-1.39) was associated with pancreatic cancer risk. High lifetime ethanol intake from spirits/liquor at recruitment tended to be associated with a higher risk (RR = 1.40, 95% CI 0.93-2.10 comparing 10+ g/d vs. 0.1-4.9 g/d), but no associations were observed for wine and beer consumption. These results suggest no association of alcohol consumption with the risk of pancreatic cancer
    Type of Publication: Journal article published
    PubMed ID: 19145468
    Signatur Availability
    BibTip Others were also interested in ...
  • 7
    Keywords: RISK ; RISK-FACTORS ; colorectal cancer ; COLORECTAL-CANCER ; CONSUMPTION ; nutrition ; NECK-CANCER ; EPIC PROJECT ; METAANALYSIS ; pooled analysis ; EPIDEMIOLOGY CONSORTIUM ; GLOBAL BURDEN ; INTERNATIONAL HEAD
    Abstract: Objective To compute the burden of cancer attributable to current and former alcohol consumption in eight European countries based on direct relative risk estimates from a cohort study. Design Combination of prospective cohort study with representative population based data on alcohol exposure. Setting Eight countries (France, Italy, Spain, United Kingdom, the Netherlands, Greece, Germany, Denmark) participating in the European Prospective Investigation into Cancer and Nutrition (EPIC) study. Participants 109 118 men and 254 870 women, mainly aged 37-70. Main outcome measures Hazard rate ratios expressing the relative risk of cancer incidence for former and current alcohol consumption among EPIC participants. Hazard rate ratios combined with representative information on alcohol consumption to calculate alcohol attributable fractions of causally related cancers by country and sex. Partial alcohol attributable fractions for consumption higher than the recommended upper limit (two drinks a day for men with about 24 g alcohol, one for women with about 12 g alcohol) and the estimated total annual number of cases of alcohol attributable cancer. Results If we assume causality, among men and women, 10% (95% confidence interval 7 to 13%) and 3% (1 to 5%) of the incidence of total cancer was attributable to former and current alcohol consumption in the selected European countries. For selected cancers the figures were 44% (31 to 56%) and 25% (5 to 46%) for upper aerodigestive tract, 33% (11 to 54%) and 18% (-3 to 38%) for liver, 17% (10 to 25%) and 4% (-1 to 10%) for colorectal cancer for men and women, respectively, and 5.0% (2 to 8%) for female breast cancer. A substantial part of the alcohol attributable fraction in 2008 was associated with alcohol consumption higher than the recommended upper limit: 33 037 of 178 578 alcohol related cancer cases in men and 17 470 of 397 043 alcohol related cases in women. Conclusions In western Europe, an important proportion of cases of cancer can be attributable to alcohol consumption, especially consumption higher than the recommended upper limits. These data support current political efforts to reduce or to abstain from alcohol consumption to reduce the incidence of cancer
    Type of Publication: Journal article published
    PubMed ID: 21474525
    Signatur Availability
    BibTip Others were also interested in ...
  • 8
    Keywords: CANCER ; COHORT ; ACIDS ; OBESITY ; VALIDITY ; PROJECT ; CALIBRATION ; ADULTS ; PARTICIPANTS ; CUTOFF
    Abstract: 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 344 757) 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 (95% CI 4.35, 7.06), 2.23 (95% CI 0.16, 4.31) and 11.12 (95% CI 8.17, 14.08) g/10 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 (95% CI 1.01, 1.02), 1.01 (95% CI 1.00, 1.02) and 1.02 (95% CI 1.01, 1.04) g/10 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 95% 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.
    Type of Publication: Journal article published
    PubMed ID: 22716915
    Signatur Availability
    BibTip Others were also interested in ...
  • 9
    Keywords: MODELS ; RISK ; DIETARY ; meat ; CALIBRATION ; CORONARY-HEART-DISEASE ; METAANALYSIS ; CONTAMINANTS ; DANISH ADULTS ; FISHERMEN
    Abstract: Fish is a source of important nutrients and may play a role in preventing heart diseases and other health outcomes. However, studies of overall mortality and cause-specific mortality related to fish consumption are inconclusive. We examined the rate of overall mortality, as well as mortality from ischaemic heart disease and cancer in relation to the intake of total fish, lean fish, and fatty fish in a large prospective cohort including ten European countries. More than 500,000 men and women completed a dietary questionnaire in 1992-1999 and were followed up for mortality until the end of 2010. 32,587 persons were reported dead since enrolment. Hazard ratios and their 99 % confidence interval were estimated using Cox proportional hazard regression models. Fish consumption was examined using quintiles based on reported consumption, using moderate fish consumption (third quintile) as reference, and as continuous variables, using increments of 10 g/day. All analyses were adjusted for possible confounders. No association was seen for fish consumption and overall or cause-specific mortality for both the categorical and the continuous analyses, but there seemed to be a U-shaped trend (p 〈 0.000) with fatty fish consumption and total mortality and with total fish consumption and cancer mortality (p = 0.046).
    Type of Publication: Journal article published
    PubMed ID: 25377533
    Signatur Availability
    BibTip Others were also interested in ...
  • 10
    Keywords: CANCER ; FOLLOW-UP ; COHORT ; POPULATION ; RISK ; INFECTION ; CARCINOGENESIS ; ASSOCIATION ; WOMEN ; MEN ; cancer risk ; DOSE-RESPONSE ; DIETARY ; adenocarcinoma ; ADENOCARCINOMAS ; case-control studies ; CARDIA ; CONSUMPTION ; EPIC ; GASTRIC-CANCER ; HELICOBACTER-PYLORI ; nutrition ; case-control study ; DIETARY FACTORS ; ASSOCIATIONS ; INCREASE ; case control studies ; INTERVAL ; prospective ; MEAT INTAKE ; RED MEAT ; JAPANESE ; Helicobacter pylori ; N-NITROSO COMPOUNDS
    Abstract: Background. Dietary factors are thought to have an important role in gastric and esophageal carcinogenesis, but evidence from cohort studies for such a role is lacking. We examined the risks of gastric cancer and esophageal adenocarcinoma associated with meat consumption within the European Prospective Investigation Into Cancer and Nutrition (EPIC) cohort. Methods: A total of 521 457 men and women aged 35-70 years in 10 European countries participated in the EPIC cohort. Dietary and lifestyle information was collected at recruitment. Cox proportional hazard models were used to examine associations between meat intake and risks of cardia and gastric noncardia cancers and esophageal adenocarcinoma. Data from a calibration substudy were used to correct hazard ratios (HRs) and 95% confidence intervals (CIs) for diet measurement errors. In a nested case-control study, we examined interactions between Helicobacter pylori infection status (i.e., plasma H. pylori antibodies) and meat intakes. All statistical tests were two-sided. Results: During a mean follow-up of 6.5 years, 330 gastric adenocarcinoma and 65 esophageal adenocarcinomas were diagnosed. Gastric noncardia cancer risk was statistically significantly associated with intakes of total meat (calibrated HR per 100-g/day increase = 3.52, 95%, CI = 1.96 to 6.34), red meat (calibrated HR per 50-g/day increase = 1.73; 95% CI = 1.03 to 2.88), and processed meat (calibrated HR per 50-g/day increase = 2.45; 95% CI = 1.43 to 4.21). The association between the risk of gastric noncardia cancer and total meat intake was especially large in H. pylori-infected subjects (odds ratio per 100-g/day increase = 5.32; 95% CI = 2.10 to 13.4). Intakes of total, red, or processed meat were not associated with the risk of gastric cardia cancer. A positive but non-statistically significant association was observed between esophageal adenocarcinoma cancer risk and total and processed meat intake in the calibrated model. In this study population, the absolute risk of development of gastric adenocarcinoma within 10 years for a study subject aged 60 years was 0.26% for the lowest quartile of total meat intake and 0.33% for the highest quartile of total meat intake. Conclusion: Total, red, and processed meat intakes were associated with an increased risk of gastric noncardia cancer, especially in H. pylori antibody-positive subjects, but not with cardia gastric cancer
    Type of Publication: Journal article published
    PubMed ID: 16507831
    Signatur Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...