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  • HEALTH  (19)
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  • 1
    Keywords: CANCER ; BLOOD ; EXPOSURE ; RISK ; BINDING ; ASSOCIATION ; BREAST ; breast cancer ; BREAST-CANCER ; hormone ; HEALTH ; WOMEN ; DIETARY ; UNITED-STATES ; ALCOHOL ; ALCOHOL-CONSUMPTION ; CONSUMPTION ; EPIC ; nutrition ; QUESTIONNAIRE ; IMMUNOASSAYS ; immunoassay ; LIFE-STYLE FACTORS ; dehydroepiandrosterone ; POSTMENOPAUSAL WOMEN ; SERUM ; ONCOLOGY ; RE ; EPIC PROJECT ; LEVEL ; methods ; PREMENOPAUSAL WOMEN ; SERUM-LEVELS ; alcohol consumption ; PREMENOPAUSAL ; prospective ; BINDING GLOBULIN ; CIRCULATING LEVELS ; intake ; steroids ; HORMONE CONCENTRATIONS ; alcohol intake ; ESTRADIOL LEVELS ; post-menopausal women ; pre-menopausal ; SERUM HORMONE CONCENTRATIONS ; sex steroids
    Abstract: Objective Women with a moderate intake of alcohol have higher concentrations of sex steroids in serum, and higher risk of developing breast cancer, compared to non-drinkers. In the present study, we investigate the relationships between alcohol consumption and serum levels of sex steroids and sex-hormone binding globulin (SHBG) in 790 pre- and 1,291 post-menopausal women, who were part of the European Prospective Investigation into Cancer and Nutrition (EPIC). Methods Serum levels of testosterone (T), androstenedione (Delta(4)), dehydroepiandrosterone sulphate (DHEAS), estrone (E-1), estradiol (E-2) and SHBG were measured by direct immunoassays. Free T (fT) and free E-2 (fE(2)) were calculated according to mass action laws. Current alcohol intake exposure to alcohol was assessed from dietary questionnaires. Results Pre-menopausal women who consumed more than 25 g/day of alcohol had about 30% higher DHEAS, T and fT, 20% higher Delta(4) and about 40% higher E-1, concentrations compared to women who were non-consumers. E-2, fE(2) and SHBG concentrations showed no association with current alcohol intake. In post-menopausal women, DHEAS, fT, T, Delta(4), and E-1 concentrations were between 10% and 20% higher in women who consumed more than 25 g/day of alcohol compared to non-consumers. E-2 or fE(2) were not associated with alcohol intake at all. SHBG levels were about 15% lower in alcohol consumers compared to non-consumers. Conclusion This study supports the hypothesis of an influence of alcohol intake on sex hormone concentrations in blood
    Type of Publication: Journal article published
    PubMed ID: 16933054
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  • 2
    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
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  • 3
    Keywords: CANCER ; carcinoma ; FOLLOW-UP ; INFORMATION ; COHORT ; RISK ; INFECTION ; ASSOCIATION ; PATTERNS ; HEALTH ; MEN ; COUNTRIES ; DIET ; NETHERLANDS ; STOMACH ; adenocarcinoma ; EPIC ; GASTRIC-CANCER ; HELICOBACTER-PYLORI ; nutrition ; physical activity ; ONCOLOGY ; POPULATION-BASED COHORT ; SCALE ; PHYSICAL-ACTIVITY ; METAANALYSIS ; SUBTYPES ; prospective ; CANCERS ; VARIABLES ; Helicobacter pylori ; stomach cancer ; BODY-MASS ; tumours ; gastric adenocarcinoma ; Type ; EURGAST ; REGISTER ; Oesophagus cancer
    Abstract: To analyse the association between types of physical activity (occupational, recreational and household, vigorous and overall) and risk of primary oesophageal (OAC) or gastric adenocarcinoma (GAC). From nine European countries, 420,449 participants were recruited between 1991 and 2000 and followed-up for a mean of 8.8 years to register incident GAC and OAC. Information on physical activity (PA), diet, lifestyle and health-related variables was obtained at baseline. Helicobacter pylori infection status was considered in a subset of 1,211 participants. Analyses were repeated by tumour site (cardia/non-cardia) and histological type (intestinal/diffuse). During the follow-up, 410 GAC and 80 OAC occurred. A lower risk of overall and non-cardia GAC was found for increasing levels of a PA index which combined occupational PA with weekly time spent in sports and cycling. The hazard ratio (HR) of GAC was 0.69, 95% CI: 0.50-0.94, for the comparison between active and inactive participants according to the PA index (HR = 0.44, 95% CI:0.26-0.74, for non-cardia GAC). No effect was found for cardia tumours or histological subtypes of GAC. PA of any kind was not associated with OAC. Overall and distal (non-cardia) gastric tumours were inversely associated with time spent on cycling and sports and a total PA index. No association was found for any type of PA and risk of cardia cancers of the stomach
    Type of Publication: Journal article published
    PubMed ID: 20052611
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  • 4
    Keywords: CANCER ; CELLS ; BLOOD ; LUNG ; lung cancer ; LUNG-CANCER ; RISK ; BIOMARKERS ; ASSOCIATION ; HEALTH ; EPIC ; nutrition ; molecular epidemiology ; physical activity ; PHYSICAL-ACTIVITY ; biomarker ; BODY-MASS INDEX ; prospective ; NEVER SMOKERS ; BLOOD GLUTATHIONE CONCENTRATIONS ; BULKY DNA-ADDUCTS ; EX-SMOKERS ; FORMER SMOKERS ; LIFE HABITS ; SMOKING-RELATED DISEASE
    Abstract: The association between physical activity, potential intermediate biomarkers and lung cancer risk was investigated in a study of 230 cases and 648 controls nested within the European Prospective Investigation of Cancer and Nutrition. Data on white blood cell aromatic-DNA adducts by 〈SU32〈/SUP-post-labelling and glutathione (GSH) in red blood cells were available from a subset of cases and controls. Compared with the first quartile, the fourth quartile of recreational physical activity was associated with a lower lung cancer risk (odds ratio (OR) 0.56, 95% confidence interval (CI) 0.35-0.90), higher GSH levels (+1.87 mu mol GSH g〈SU-1〈/SU haemoglobin, p = 0.04) but not with the presence of high levels of adducts (OR 1.05, 95% CI 0.38-2.86). Despite being associated with recreational physical activity, in these small-scale pilot analyses GSH levels were not associated with lung cancer risk (OR 0.95, 95% CI 0.84-1.07 per unit increase in GSH levels). Household and occupational activity was not associated with lung cancer risk or biomarker levels.〈/
    Type of Publication: Journal article published
    PubMed ID: 20050820
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  • 5
    Keywords: SURVIVAL ; ASSOCIATION ; HEALTH ; WOMEN ; nutrition ; DETERMINANTS ; SOCIOECONOMIC INEQUALITIES ; CARDIOVASCULAR RISK ; LUNG-CANCER INCIDENCE ; EDUCATIONAL INEQUALITIES
    Abstract: BACKGROUND: Socio-economic inequalities in mortality are observed at the country level in both North America and Europe. The purpose of this work is to investigate the contribution of specific risk factors to social inequalities in cause-specific mortality using a large multi-country cohort of Europeans. METHODS: A total of 3,456,689 person/years follow-up of the European Prospective Investigation into Cancer and Nutrition (EPIC) was analysed. Educational level of subjects coming from 9 European countries was recorded as proxy for socio-economic status (SES). Cox proportional hazard model's with a step-wise inclusion of explanatory variables were used to explore the association between SES and mortality; a Relative Index of Inequality (RII) was calculated as measure of relative inequality. RESULTS: Total mortality among men with the highest education level is reduced by 43% compared to men with the lowest (HR 0.57, 95% C.I. 0.52-0.61); among women by 29% (HR 0.71, 95% C.I. 0.64-0.78). The risk reduction was attenuated by 7% in men and 3% in women by the introduction of smoking and to a lesser extent (2% in men and 3% in women) by introducing body mass index and additional explanatory variables (alcohol consumption, leisure physical activity, fruit and vegetable intake) (3% in men and 5% in women). Social inequalities were highly statistically significant for all causes of death examined in men. In women, social inequalities were less strong, but statistically significant for all causes of death except for cancer-related mortality and injuries. DISCUSSION: In this European study, substantial social inequalities in mortality among European men and women which cannot be fully explained away by accounting for known common risk factors for chronic diseases are reported.
    Type of Publication: Journal article published
    PubMed ID: 22848347
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  • 6
    Keywords: POPULATION ; RISK ; IMPACT ; HEALTH ; MEN ; OXIDATIVE STRESS ; CALIBRATION ; HEART-DISEASE ; DIETARY ASSESSMENT ; CARDIOVASCULAR-DISEASE
    Abstract: In this study, the relation between fruit and vegetable consumption and mortality was investigated within the European Prospective Investigation Into Cancer and Nutrition. Survival analyses were performed, including 451,151 participants from 10 European countries, recruited between 1992 and 2000 and followed until 2010. Hazard ratios, rate advancement periods, and preventable proportions to respectively compare risk of death between quartiles of consumption, to estimate the period by which the risk of death was postponed among high consumers, and to estimate proportions of deaths that could be prevented if all participants would shift their consumption 1 quartile upward. Consumption of fruits and vegetables was inversely associated with all-cause mortality (for the highest quartile, hazard ratio = 0.90, 95% confidence interval (CI): 0.86, 0.94), with a rate advancement period of 1.12 years (95% CI: 0.70, 1.54), and with a preventable proportion of 2.95%. This association was driven mainly by cardiovascular disease mortality (for the highest quartile, hazard ratio = 0.85, 95% CI: 0.77, 0.93). Stronger inverse associations were observed for participants with high alcohol consumption or high body mass index and suggested in smokers. Inverse associations were stronger for raw than for cooked vegetable consumption. These results support the evidence that fruit and vegetable consumption is associated with a lower risk of death.
    Type of Publication: Journal article published
    PubMed ID: 23599238
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  • 7
    Keywords: RISK ; HEALTH ; OBESITY ; COUNTRIES ; VALIDITY ; QUESTIONNAIRE ; CARDIOVASCULAR-DISEASE ; PARTICIPANTS ; LIFE EXPECTANCY ; COLLEGE
    Abstract: BACKGROUND: The higher risk of death resulting from excess adiposity may be attenuated by physical activity (PA). However, the theoretical number of deaths reduced by eliminating physical inactivity compared with overall and abdominal obesity remains unclear. OBJECTIVE: We examined whether overall and abdominal adiposity modified the association between PA and all-cause mortality and estimated the population attributable fraction (PAF) and the years of life gained for these exposures. DESIGN: This was a cohort study in 334,161 European men and women. The mean follow-up time was 12.4 y, corresponding to 4,154,915 person-years. Height, weight, and waist circumference (WC) were measured in the clinic. PA was assessed with a validated self-report instrument. The combined associations between PA, BMI, and WC with mortality were examined with Cox proportional hazards models, stratified by center and age group, and adjusted for sex, education, smoking, and alcohol intake. Center-specific PAF associated with inactivity, body mass index (BMI; in kg/m(2)) (〉30), and WC (〉/=102 cm for men, 〉/=88 cm for women) were calculated and combined in random-effects meta-analysis. Life-tables analyses were used to estimate gains in life expectancy for the exposures. RESULTS: Significant interactions (PA x BMI and PA x WC) were observed, so HRs were estimated within BMI and WC strata. The hazards of all-cause mortality were reduced by 16-30% in moderately inactive individuals compared with those categorized as inactive in different strata of BMI and WC. Avoiding all inactivity would theoretically reduce all-cause mortality by 7.35% (95% CI: 5.88%, 8.83%). Corresponding estimates for avoiding obesity (BMI 〉30) were 3.66% (95% CI: 2.30%, 5.01%). The estimates for avoiding high WC were similar to those for physical inactivity. CONCLUSION: The greatest reductions in mortality risk were observed between the 2 lowest activity groups across levels of general and abdominal adiposity, which suggests that efforts to encourage even small increases in activity in inactive individuals may be beneficial to public health.
    Type of Publication: Journal article published
    PubMed ID: 25733647
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  • 8
    Keywords: CANCER ; BLOOD ; COMMON ; COHORT ; RISK ; GENE ; TIME ; MARKER ; primary ; GENETIC POLYMORPHISMS ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; ACID ; NO ; HEALTH ; PLASMA ; AGE ; etiology ; cancer risk ; case-control studies ; European Prospective Investigation into Cancer and Nutrition ; GASTRIC-CANCER ; nutrition ; STOMACH-CANCER ; SINGLE ; DEFICIENCY ; ONCOLOGY ; case control study ; case-control study ; REGRESSION ; ASSOCIATIONS ; VARIANT ; INCREASE ; SINGLE NUCLEOTIDE POLYMORPHISMS ; prospective studies ; gastric cancer ; METHYLENETETRAHYDROFOLATE REDUCTASE ; MTHFR ; LEVEL ; biomarker ; case control studies ; HELICOBACTER-PYLORI INFECTION ; GENOTYPE ; LOCUS ; single-nucleotide ; USA ; C677T POLYMORPHISM ; prospective ; prospective study ; INCREASED RISK ; odds ratio ; cancer research ; CANCER-RISK ; CHINESE POPULATION ; nested case-control study ; case control ; LOGISTIC-REGRESSION ; MENDELIAN RANDOMIZATION ; PLASMA-CONCENTRATION ; chronic atrophic gastritis ; gastric ; pepsinogen ; MTHFR POLYMORPHISMS ; 5,10-METHYLENETETRAHYDROFOLATE REDUCTASE ; EPIC-EURGAST ; MICROBIOLOGICAL ASSAY
    Abstract: Previous studies have shown inconsistent associations of folate intake and polymorphisms of the methylenetetrahydrofolate reductase (MTHFR) gene with gastric cancer risk. Our nested case-control study within the European Prospective Investigation into Cancer and Nutrition cohort is the first prospective study of blood folate levels and gastric cancer. Gastric cancer cases (n = 247) and controls (n = 631) were matched for study center, age, sex, and time of blood donation. Two common single nucleotide polymorphisms of the MTHFR gene were determined, as were plasma concentrations of folate, cobalamin (vitamin B12), total homocysteine, and methylmalonic acid (cobalamin deficiency marker) in prediagnostic plasma. Risk measures were calculated with conditional logistic regression. Although no relations were observed between plasma folate or total homocysteine concentrations and gastric cancer, we observed a trend toward lower risk of gastric cancer with increasing cobalamin concentrations (odds ratio, 0.79 per SD increase in cobalamin; P = 0.01). Further analyses showed that the inverse association between cobalamin and gastric cancer was confined to cancer cases with low pepsinogen A levels (marker of severe chronic atrophic gastritis) at the time of blood sampling. The 677 C -〉 T MTHFR polymorphism was not associated with gastric cancer, but we observed an increased risk with the variant genotype of the 1298 A -〉 C polymorphism (odds ratio, 1.47 for CC versus AA; P = 0.04). In conclusion, we found no evidence of a role of folate in gastric cancer etiology. However, we observed increased gastric cancer risk at low cobalamin levels that was most likely due to compromised cobalamin status in atrophic gastritis preceding gastric cancer
    Type of Publication: Journal article published
    PubMed ID: 18006931
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  • 9
    Keywords: CANCER ; LUNG-CANCER ; SUPPORT ; COHORT ; RISK ; GENE ; GENES ; validation ; DNA ; CARCINOGENESIS ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; antibodies ; antibody ; NO ; HEALTH ; REPAIR ; COLORECTAL-CANCER ; cancer risk ; microsatellite instability ; adenocarcinoma ; EPIC ; GASTRIC-CANCER ; HELICOBACTER-PYLORI ; DNA repair ; TP53 ; RE ; prospective studies ; XPD POLYMORPHISMS ; gastric cancer ; XRCC1 ; GC ; ALLELES ; LEVEL ; DNA repair genes ; prospective ; prospective study ; CANCER-RISK ; Helicobacter pylori ; intestinal metaplasia ; ENGLAND ; CHINESE POPULATION ; HOGG1 SER326CYS POLYMORPHISM ; OGG1 ; chronic atrophic gastritis ; pepsinogen ; RATIO ; GENE POLYMORPHISMS ; GENE POLYMORPHISM ; neoplasm ; gastric adenocarcinoma ; severe chronic atrophic gastritis
    Abstract: Background The contribution of genetic variation in DNA repair genes to gastric cancer (GC) risk remains essentially unknown. The aim of this study was to explore the relative contribution of DNA repair gene polymorphisms to GC risk and severe chronic atrophic gastritis (SCAG). Method A nested case control study within the EPIC cohort was performed including 246 gastric adenocarcinomas and 1175 matched controls. Controls with SCAG (n 91), as defined by low pepsinogen A (PGA) levels, and controls with no SCAG (n 1061) were also compared. Twelve polymorphisms at DNA repair genes (MSH2, MLH1, XRCC1, OGG1 and ERCC2) and TP53 gene were analysed. Antibodies against Helicobacter pylori were measured. Results No association was observed for any of these polymorphisms with stomach cancer risk. However, ERCC2 K751Q polymorphism was associated with an increased risk for non-cardial neoplasm [odds ratio (OR) 1.78; 95 confidence interval (CI) 1.023.12], being ERCC2 K751Q and D312N polymorphisms associated with the diffuse type. ERCC2 D312N (OR 2.0; 95 CI 1.093.65) and K751Q alleles (OR 1.82; 95 CI 1.013.30) and XRCC1 R399Q (OR 1.69; 95 CI 1.022.79) allele were associated with an increased risk for SCAG. Conclusion Our study supports a role of ERCC2 in non-cardial GC but not in cardial cancer. A concordant result was observed for subjects with low PGA levels. XRCC1 allele was associated also with SCAG. This is the first prospective study suggesting that individual variation in DNA repair may be relevant for gastric carcinogenesis, a finding that will require further confirmation validation in larger independent studies
    Type of Publication: Journal article published
    PubMed ID: 18641418
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  • 10
    Keywords: CANCER ; RISK ; GENE ; GENES ; DNA ; BIOMARKERS ; ASSOCIATION ; polymorphism ; HEALTH ; AGE ; adenocarcinoma ; STOMACH-CANCER ; METHYLATION ; nutrient intake ; HELICOBACTER-PYLORI INFECTION ; prospective ; PERNICIOUS-ANEMIA ; MTHFR POLYMORPHISMS ; ATROPHIC GASTRITIS ; Genetic ; FOLATE-DEFICIENCY ; HOMOCYSTEINE METABOLISM ; METHYLENETETRAHYDROFOLATE-REDUCTASE ; UPPER GASTROINTESTINAL-TRACT
    Abstract: B vitamins and polymorphisms in genes coding for enzymes involved in one-carbon metabolism may affect DNA synthesis and methylation and thereby be implicated in carcinogenesis. Previous data on vitamins B2 and B6 and genetic polymorphisms other than those involving MTHFR as risk factors for gastric cancer (GC) are sparse and inconsistent. In this case-control study nested within the European Prospective Investigation into Cancer and Nutrition cohort, cases (n = 235) and controls (n = 601) were matched for study center, age, sex, and time of blood sampling. B2 and B6 species were measured in plasma, and the sum of riboflavin and flavin mononucleotide was used as the main exposure variable for vitamin 132 status, whereas the sum of pyridoxal 5'-phosphate, pyridoxal, and 4-pyridoxic acid was used to define vitamin B6 status. In addition, we determined eight polymorphisms related to one-carbon metabolism. Relative risks for CC risk were calculated with conditional logistic regression, adjusted for Helicobacter pylori infection status and smoking status. Adjusted relative risks per quartile (95% confidence interval, P-trend) were 0.85 (0.72-1.01, 0.06) for vitamin B2 and 0.78 (0.65-0.93, 〈0.01) for vitamin B6. Both relations were stronger in individuals with severe chronic atrophic gastritis. The polymorphisms were not associated with CC risk and did not modify the observed vitamin-cancer associations. In summary, results from this large European cohort study showed an inverse association between vitamin B2 and CC risk, which is borderline significant, and a significant inverse association between vitamin B6 and CC risk. Cancer Epidemiol Biomarkers Prev; 19(1); 28-38. (C)2010 AACR
    Type of Publication: Journal article published
    PubMed ID: 20056620
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