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  • cancer risk  (17)
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  • 1
    Keywords: CANCER ; FOLLOW-UP ; COHORT ; EXPOSURE ; RISK ; NITRIC-OXIDE ; INFECTION ; ASSOCIATION ; antibodies ; antibody ; PLASMA ; NUMBER ; cancer risk ; DIETARY ; INDIVIDUALS ; CARDIA ; CONSUMPTION ; EPIC ; GASTRIC-CANCER ; HELICOBACTER-PYLORI ; nutrition ; DIETARY-INTAKE ; INCREASE ; IRON ; LEVEL ; prospective ; MEAT INTAKE ; RED MEAT ; CANCER-RISK ; Helicobacter pylori ; N-NITROSO COMPOUNDS ; HEME ; processed meat
    Abstract: The risk of gastric cancer (GC) associated with dietary intake of nitrosodimethylamine (NDMA) and endogenous formation of nitroso compounds (NOCs) was investigated in the European Prospective Investigation into Cancer and Nutrition (EPIC). The study included 521 457 individuals and 314 incident cases of GC that had occurred after 6.6 average years of follow-up. An index of endogenous NOC (ENOC) formation was estimated using data of the iron content from meat intake and faecal apparent total NOC formation according to previous published studies. Antibodies to Helicobacter pylori and vitamin C levels were measured in a sub-sample of cases and matched controls included in a nested case-control within the cohort. Exposure to NDMA was 〈 1 mu g on average compared with 93 mu g on average from ENOC. There was no association between NDMA intake and GC risk (HR, 1.00; 95% CI, 0.7-1.43). ENOC was significantly associated with non-cardia cancer risk (HR, 1.42; 95% CI, 1.14-1.78 for an increase of 40 mu g/day) but not with cardia cancer (HR, 0.96; 95% CI, 0.69-1.33). Although the number of not infected cases is low, our data suggest a possible interaction between ENOC and H.pylori infection (P for interaction = 0.09). Moreover, we observed an interaction between plasma vitamin C and ENOC (P 〈 0.02). ENOC formation may account for our previously reported association between red and processed meat consumption and gastric cancer risk
    Type of Publication: Journal article published
    PubMed ID: 16571648
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  • 2
    Keywords: CANCER ; Germany ; LUNG ; FOLLOW-UP ; INFORMATION ; lung cancer ; LUNG-CANCER ; COHORT ; cohort study ; EPIDEMIOLOGY ; EXPOSURE ; MORTALITY ; occupation ; POPULATION ; RISK ; RISKS ; REDUCTION ; RISK-FACTORS ; ASSOCIATION ; HUMANS ; WOMEN ; MEN ; risk factors ; smoking ; COUNTRIES ; cancer risk ; POPULATIONS ; DIET ; VALIDITY ; EPIC ; nutrition ; SMOKERS ; RELATIVE RISK ; exercise ; physical activity ; REGRESSION ; ASSOCIATIONS ; PHYSICAL-ACTIVITY ; INTERVAL ; SUBTYPES ; prospective ; UNIT ; RISK-FACTOR ; CANCER-RISK ; sports ; occupations ; ACTIVITY QUESTIONNAIRE
    Abstract: Research conducted predominantly in male populations on physical activity and lung cancer has yielded inconsistent results. We examined this relationship among 416,277 men and women from the European Prospective Investigation into Cancer and Nutrition (EPIC). Detailed information on recent recreational, household and occupational physical activity, smoking habits and diet was assessed at baseline between 1992 and 2000. Relative risks (RR) were estimated using Cox regression. During 6.3 years of follow-up we identified 607 men and 476 women with incident lung cancer. We did not observe an inverse association between recent occupational, recreational or household physical activity and lung cancer risk in either males or females. However, we found some reduction in lung cancer risk associated with sports in males (adjusted RR = 0.71; 95% confidence interval 0.50-0.98; highest tertile vs. inactive group), cycling (RR = 0.73; 0.54-0.99) in females and non-occupational vigorous physical activity. For occupational physical activity, lung cancer risk was increased for unemployed men (adjusted RR = 1.57; 1.20-2.05) and men with standing occupations (RR = 1.35; 1.02-1.79) compared with sitting professions. There was no evidence of heterogeneity of physical activity associations across countries, or across any of the considered cofactors. For some histologic subtypes suggestive sex-specific reductions, limited by subgroup sizes, were observed, especially with vigorous physical activity. In total, our study shows no consistent protective associations of physical activity with lung cancer risk. It can be assumed that the elevated risks found for occupational physical activity are not produced mechanistically by physical activity itself but rather reflect exposure to occupation-related lung cancer risk factors. (c) 2006 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 16894558
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  • 3
    Keywords: CANCER ; PROSTATE ; COHORT ; DISEASE ; RISK ; CELL-LINES ; ASSOCIATION ; ALPHA ; NO ; STAGE ; TRIAL ; prevention ; DESIGN ; DIFFERENCE ; PLASMA ; MEN ; smoking ; prostate cancer ; PROSTATE-CANCER ; cancer risk ; MULTIVARIATE ; case-control studies ; PREDICTORS ; EPIC ; nutrition ; NESTED CASE-CONTROL ; RELATIVE RISK ; VITAMIN-E ; case-control study ; GRADE ; SUPPLEMENTATION ; USA ; prospective ; CANCER-RISK ; ENGLAND ; SUBSEQUENT RISK ; DIETARY SELENIUM ; European Prospective Investigation into Cancer ; SERUM SELENIUM
    Abstract: Background: Some evidence indicates that a low selenium intake may be associated with an increased risk of prostate cancer. Objective: The aim of this study was to investigate the association of plasma selenium concentration with subsequent prostate cancer risk and to examine this association by stage and grade of disease and other factors. Design: A nested case-control study was performed among men in the European Prospective Investigation into Cancer and Nutrition (EPIC). The association between plasma selenium concentration and prostate cancer risk was assessed in 959 men with incident prostate cancer and 1059 matched controls. Results: Overall, plasma selenium concentration was not associated with prostate cancer risk; the multivariate relative risk for men in the highest fifth of selenium concentration compared with the lowest fifth was 0.96 (95% CI: 0.70, 1.31; P for trend = 0.25). There were no significant differences in the association of plasma selenium with risk when analyzed by stage or grade of disease. Similarly, the association of selenium with risk did not differ by smoking status or by plasma alpha- or gamma-tocopherol concentration. Conclusion: Plasma selenium concentration was not associated with prostate cancer risk in this large cohort of European men. Am J Clin Nutr 2008; 88:1567-75
    Type of Publication: Journal article published
    PubMed ID: 19064517
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  • 4
    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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  • 5
    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
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  • 6
    Keywords: CANCER ; GROWTH ; IN-VITRO ; human ; VITRO ; FOLLOW-UP ; COHORT ; incidence ; RISK ; RISK-FACTORS ; ASSOCIATION ; BREAST ; breast cancer ; BREAST-CANCER ; ACIDS ; HUMANS ; WOMEN ; risk factors ; cancer risk ; RECRUITMENT ; fatty acids ; DIETARY ; CONSUMPTION ; EPIC ; nutrition ; CALIBRATION ; RELATIVE RISK ; DIETARY-INTAKE ; SERUM PHOSPHOLIPIDS ; ADIPOSE-TISSUE ; POLYUNSATURATED FATTY-ACIDS ; POSTMENOPAUSAL WOMEN ; ASSOCIATIONS ; INTERVAL ; prospective ; MEAT INTAKE ; RISK-FACTOR ; CANCERS ; CANCER-RISK ; fish consumption ; N-3
    Abstract: There is current interest in fish consumption and marine omega-3 (n-3) fatty acids and breast cancer risk. Some in vitro and animal studies have suggested an inhibitory effect of marine n-3 fatty acids on breast cancer growth, but the results from epidemiological studies that have examined the association between fish consumption and breast cancer risk in humans are inconsistent. We examined fish consumption and breast cancer risk in 310,671 women aged between 25 and 70 yr at recruitment into the European Prospective Investigation Into Cancer and Nutrition (EPIC). The participants completed a dietary questionnaire between 1992-98 and were followed up for incidence of breast cancer for a median of 6.4 yr. Hazard ratio for breast cancer by intake of total and lean and fatty fish were estimated, stratified by study centre and adjusted for established breast cancer risk factors. During follow-up, 4,776 invasive incident breast cancers were reported. No significant associations between intake of total fish and breast cancer risk were observed, hazard ratio (HR) 1.01 (95% confidence interval [CI] 0.99-1.02; p = 0.28 per 10 g fish/day). When examining lean and ratty fish separately, we round a positive significant association only in the highest quintile for fatty fish (HR 1.13, 95% CI 1.01-1.26), but test for trend was not significant (p = 0.10). No associations with breast cancer risk were observed when the study participants were subdivided by menopausal status. Although the period of follow-up is relatively short, the results provide no evidence for an association between fish intake and breast cancer risk. (c) 2006 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 16470807
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  • 7
    Keywords: CANCER ; evaluation ; Germany ; LUNG ; MODEL ; MODELS ; FOLLOW-UP ; INFORMATION ; lung cancer ; LUNG-CANCER ; COHORT ; EPIDEMIOLOGY ; incidence ; POPULATION ; RISK ; ASSOCIATION ; FREQUENCY ; FREQUENCIES ; NO ; smoking ; cancer risk ; MEASUREMENT ERROR ; MULTIVARIATE ; DIET ; INDIVIDUALS ; CONSUMPTION ; EPIC ; European Prospective Investigation into Cancer and Nutrition ; FRUIT ; nutrition ; VEGETABLES ; CALIBRATION ; LIFE-STYLE ; BETA-CAROTENE ; FOOD FREQUENCY QUESTIONNAIRE ; ALPHA-TOCOPHEROL ; ONCOLOGY ; ASSOCIATIONS ; RE ; INCREASE ; NONSMOKING WOMEN ; VITAMIN-C ; pooled analysis ; USA ; CANCER INCIDENCE ; prospective ; CANCER-RISK ; comparison ; ERROR ; CHINESE WOMEN ; DIETARY CAROTENOIDS
    Abstract: The association of fruit and vegetable consumption and lung cancer incidence was evaluated using the most recent data from the European Prospective Investigation into Cancer and Nutrition (EPIC), applying a refined statistical approach (calibration) to account for measurement error potentially introduced by using food frequency questionnaire data. Between 1992 and 2000, detailed information on diet and life-style of 478,590 individuals participating in EPIC was collected. During a median follow-up of 6.4 years, 1,126 lung cancer cases were observed. Multivariate Cox proportional hazard models were applied for statistical evaluation. In the whole study population, fruit consumption was significantly inversely associated with lung cancer risk while no association was found for vegetable consumption. In current smokers, however, lung cancer risk significantly decreased with higher vegetable consumption; this association became more pronounced after calibration, the hazard ratio (HR) being 0.78 (95% CI 0.620.98) per 100 g increase in daily vegetable consumption. In comparison, the HR per 100 g fruit was 0.92 (0.85-0.99) in the entire cohort and 0.90 (0.81-0.99) in smokers. Exclusion of cases diagnosed during the first 2 years of follow-up strengthened these associations, the HR being 0.71 (0.55-0.94) for vegetables (smokers) and 0.86 (0.78-0.95) for fruit (entire cohort). Cancer incidence decreased with higher consumption of apples and pears (entire cohort) as well as root vegetables (smokers). In addition to an overall inverse association with fruit intake, the results of this evaluation add evidence for a significant inverse association of vegetable consumption and lung cancer incidence in smokers. (C) 2007 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 17487840
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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 ; LUNG-CANCER ; COHORT ; DNA adducts ; EXPOSURE ; RISK ; DNA ; BIOMARKERS ; colon ; RATS ; CONTRAST ; BINDING ; ASSOCIATION ; COLORECTAL-CANCER ; BLADDER-CANCER ; cancer risk ; POLYCYCLIC AROMATIC-HYDROCARBONS ; COLON-CANCER ; MULTIVARIATE ; ADDUCTS ; CARCINOGENS ; DIET ; DIETARY ; ALCOHOL ; EPIC ; nutrition ; SMOKERS ; FOOD ; GUIDELINES ; VITAMIN-E ; DNA-ADDUCTS ; REGRESSION ; air pollution ; prospective studies ; N-NITROSAMINES ; LEVEL ; biomarker ; analysis ; prospective ; prospective study ; correlation ; BMI ; CANCER-RISK ; ENGLAND ; non-smokers ; AMINE ; gastrointestinal ; European Prospective Investigation into Cancer ; fibre intake ; haemoglobin adducts ; RESISTANT STARCH
    Abstract: In contrast to some extensively examined food mutagens, for example, aflatoxins, N-nitrosamines and heterocyclic amines, some other food contaminants, in particular polycyclic aromatic hydrocarbons (PAH) and other aromatic compounds, have received less attention. Therefore, exploring the relationships between dietary habits and the levels of biomarkers related to exposure to aromatic compounds is highly relevant. We have investigated in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort the association between dietary items (food groups and nutrients) and aromatic DNA adducts and 4-aminobiphenyl-Hb adducts. Both types of adducts are biomarkers of carcinogen exposure and possibly of cancer risk, and were measured, respectively, in leucocytes and erythrocytes of 1086 (DNA adducts) and 190 (Hb adducts) non-smokers. An inverse. statistically significant, association has been found between DNA adduct levels and dietary fibre intake (P=0.02), vitamin E (P =0.04) and alcohol (P=0.03) but not with other nutrients or food groups. Also, an inverse association between fibre and fruit intake, and BMI and 4-aminobiphenyl-Hb adducts (P=0.03, 0.04, and 0.03 respectively) was observed. After multivariate regression analysis these inverse correlations remained statistically significant, except for the correlation adducts v. fruit intake. The present study suggests that fibre intake in the usual range can modify the level of DNA or Hb aromatic adducts, but Such role seems to be quantitatively modest. Fibres could reduce the formation of DNA adducts in different manners, by diluting potential food mutagens and carcinogens in the gastrointestinal tract, by speeding their transit through the colon and by binding carcinogenic substances
    Type of Publication: Journal article published
    PubMed ID: 18275627
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