Dietary patterns within educational groups and their association with CHD and stroke in the European Prospective Investigation into Cancer and Nutrition-Netherlands cohort.

Higher-educated people often have healthier diets, but it is unclear whether specific dietary patterns exist within educational groups. We therefore aimed to derive dietary patterns in the total population and by educational level and to investigate whether these patterns differed in their composition and associations with the incidence of fatal and non-fatal CHD and stroke. Patterns were derived using principal components analysis in 36 418 participants of the European Prospective Investigation into Cancer and Nutrition-Netherlands cohort. Self-reported educational level was used to create three educational groups. Dietary intake was estimated using a validated semi-quantitative FFQ. Hazard ratios were estimated using Cox Proportional Hazard analysis after a mean follow-up of 16 years. In the three educational groups, similar 'Western', 'prudent' and 'traditional' patterns were derived as in the total population. However, with higher educational level a lower population-derived score for the 'Western' and 'traditional' patterns and a higher score on the 'prudent' pattern were observed. These differences in distribution of the factor scores illustrate the association between education and food consumption. After adjustments, no differences in associations between population-derived dietary patterns and the incidence of CHD or stroke were found between the educational groups (P interaction between 0·21 and 0·98). In conclusion, although in general population and educational groups-derived dietary patterns did not differ, small differences between educational groups existed in the consumption of food groups in participants considered adherent to the population-derived patterns (Q4). This did not result in different associations with incident CHD or stroke between educational groups.

Early life factors and adult mammographic density.

PURPOSE: Early life factors have shown to be related to breast cancer risk. The pathophysiological link could be mammographic density, a strong risk factor for breast cancer. Mammary gland development already starts in utero and early life factors might affect the number of mammary cells at risk. In this study, we investigated the association between early life factors and mammographic density in adulthood. METHODS: The study was conducted within 2,588, mainly postmenopausal women of the Prospect-European Prospective Investigation into Cancer and Nutrition cohort. This ongoing study recruited breast cancer screening participants who filled out extensive questionnaires. Information on the early life factors birth weight, gestational age, maternal and paternal age, multiple births, birth rank, exposure to parental smoking, and leg length as a proxy for growth at childhood was obtained using questionnaires. Generalized linear models and linear regression models were used to study the relation between early life factors and mammographic density. Analyses were adjusted for potential confounders. RESULTS: Women who had an older mother (p = 0.06) or father (p = 0.002) at birth tended to have a higher mammographic density. Furthermore, greater leg length seemed to be related to higher mammographic density, although not statistically significantly (p = 0.16). After adjustment for confounders, none of the early life factors showed any statistically significant relationship with mammographic density in adulthood. CONCLUSION: Although we cannot exclude small effects that go undetected due to measurement error in recall of early life factors, the results suggest that mammographic density is not a major pathway in any observed relationship between these early life events and breast cancer risk.

The association between dietary energy density and type 2 diabetes in Europe: results from the EPIC-InterAct Study.

BACKGROUND: Observational studies implicate higher dietary energy density (DED) as a potential risk factor for weight gain and obesity. It has been hypothesized that DED may also be associated with risk of type 2 diabetes (T2D), but limited evidence exists. Therefore, we investigated the association between DED and risk of T2D in a large prospective study with heterogeneity of dietary intake. METHODOLOGY/PRINCIPAL FINDINGS: A case-cohort study was nested within the European Prospective Investigation into Cancer (EPIC) study of 340,234 participants contributing 3.99 million person years of follow-up, identifying 12,403 incident diabetes cases and a random subcohort of 16,835 individuals from 8 European countries. DED was calculated as energy (kcal) from foods (except beverages) divided by the weight (gram) of foods estimated from dietary questionnaires. Prentice-weighted Cox proportional hazard regression models were fitted by country. Risk estimates were pooled by random effects meta-analysis and heterogeneity was evaluated. Estimated mean (sd) DED was 1.5 (0.3) kcal/g among cases and subcohort members, varying across countries (range 1.4-1.7 kcal/g). After adjustment for age, sex, smoking, physical activity, alcohol intake, energy intake from beverages and misreporting of dietary intake, no association was observed between DED and T2D (HR 1.02 (95% CI: 0.93-1.13), which was consistent across countries (I(2) = 2.9%). CONCLUSIONS/SIGNIFICANCE: In this large European case-cohort study no association between DED of solid and semi-solid foods and risk of T2D was observed. However, despite the fact that there currently is no conclusive evidence for an association between DED and T2DM risk, choosing low energy dense foods should be promoted as they support current WHO recommendations to prevent chronic diseases.

Longitudinal changes in weight in relation to smoking cessation in participants of the EPIC-PANACEA study.

PURPOSE: We assessed the association between smoking cessation and prospective weight change in the European population of the European Prospective Investigation into Cancer and Nutrition-Physical Activity, Nutrition, Alcohol, Cessation of smoking, Eating out of home And obesity (EPIC-PANACEA) project. METHODS: The study involved more than 300,000 healthy volunteers, recruited between 1992 and 2000 in 9 European countries, who provided data on anthropometry and smoking habits at baseline and after a follow-up of 5 years on average. Adjusted mixed-effects linear regression models were used to obtain sex-specific summary estimates of the association between the change in smoking status and the annual change in weight. RESULTS: Smoking cessation tends to be followed by weight gain; when compared to stable smokers, annual weight gain was higher in men (0.44 kg (95%CI: 0.36; 0.52)) and women (0.46 kg (95%CI: 0.41; 0.52)) who stopped smoking during follow-up. When smokers who stopped smoking at least 1 year before recruitment were compared to never smokers, no major differences in annual weight gain were observed. The excess weight gain following smoking cessation appears to mainly occur in the first years following the cessation. CONCLUSIONS: When considering the benefits of smoking cessation, such findings strengthen the need for promoting cessation offering information on weight gain control and support to weight-concerned smokers in order to remove a barrier to quitting.

Physical activity and gain in abdominal adiposity and body weight: prospective cohort study in 288,498 men and women.

BACKGROUND: The protective effect of physical activity (PA) on abdominal adiposity is unclear. OBJECTIVE: We examined whether PA independently predicted gains in body weight and abdominal adiposity. DESIGN: In a prospective cohort study [the EPIC (European Prospective Investigation into Cancer and Nutrition)], we followed 84,511 men and 203,987 women for 5.1 y. PA was assessed by a validated questionnaire, and individuals were categorized into 4 groups (inactive, moderately inactive, moderately active, and active). Body weight and waist circumference were measured at baseline and self-reported at follow-up. We used multilevel mixed-effects linear regression models and stratified our analyses by sex with adjustments for age, smoking status, alcohol consumption, educational level, total energy intake, duration of follow-up, baseline body weight, change in body weight, and waist circumference (when applicable). RESULTS: PA significantly predicted a lower waist circumference (in cm) in men (ß = -0.045; 95% CI: -0.057, -0.034) and in women (ß = -0.035; 95% CI: -0.056, -0.015) independent of baseline body weight, baseline waist circumference, and other confounding factors. The magnitude of associations was materially unchanged after adjustment for change in body weight. PA was not significantly associated with annual weight gain (in kg) in men (ß = -0.008; 95% CI: -0.02, 0.003) and women (ß = -0.01; 95% CI: -0.02, 0.0006). The odds of becoming obese were reduced by 7% (P < 0.001) and 10% (P < 0.001) for a one-category difference in baseline PA in men and women, respectively. CONCLUSION: Our results suggest that a higher level of PA reduces abdominal adiposity independent of baseline and changes in body weight and is thus a useful strategy for preventing chronic diseases and premature deaths.

Dietary intake of folate and riboflavin, MTHFR C677T genotype, and colorectal adenoma risk: a Dutch case-control study.

We investigated the associations between dietary intake of folate and vitamin B2, MTHFR C677T genotype, and colorectal adenomas in a Dutch case-control study. Data of cases with at least one histologically confirmed colorectal adenoma (n = 768) and controls with no history of any type of colorectal polyp (n = 709) were included. Dietary intake was assessed using a food-frequency questionnaire. Multivariable models included age and, if appropriate, dietary folate and calcium intake. The adjusted odds ratio (OR) and 95% confidence interval (CI) for the highest compared with the lowest sex-specific tertile of intake were 1.32 (95% CI, 1.01-1.73) for folate and 0.51 (95% CI, 0.36-0.73) for vitamin B2. Folate seemed to be a risk factor, especially when vitamin B2 intake was low; vitamin B2 was inversely associated with adenomas, especially with relatively high folate intake. No association was observed between MTHFR C677T genotype and colorectal adenomas. The inverse association between vitamin B2 intake and colorectal adenoma risk seemed to be more pronounced among those with the MTHFR TT genotype. We conclude that this study does not provide evidence for a decreased colorectal adenoma risk for subjects with high dietary intake of folate. It suggests, however, an inverse association between vitamin B2 and colorectal adenomas, which may be more relevant for those with the MTHFR TT genotype.