Background/Objectives Polyphenols are plant secondary metabolites with a large variability in their chemical structure and dietary occurrence that have been associated with some protective effects against several chronic diseases. To date, limited data exist on intake of polyphenols in populations. The current cross-sectional analysis aimed at estimating dietary intakes of all currently known individual polyphenols and total intake per class and subclass, and to identify their main food sources in the European Prospective Investigation into Cancer and Nutrition cohort. Methods Dietary data at baseline were collected using a standardized 24-h dietary recall software administered to 36,037 adult subjects. Dietary data were linked with Phenol-Explorer, a database with data on 502 individual polyphenols in 452 foods and data on polyphenol losses due to cooking and food processing. Results Mean total polyphenol intake was the highest in Aarhus—Denmark (1786 mg/day in men and 1626 mg/day in women) and the lowest in Greece (744 mg/day in men and 584 mg/day in women). When dividing the subjects into three regions, the highest intake of total polyphenols was observed in the UK health-conscious group, followed by non-Mediterranean (non-MED) and MED countries. The main polyphenol contributors were phenolic acids (52.5–56.9 %), except in men from MED countries and in the UK health-conscious group where they were flavonoids (49.1–61.7 %). Coffee, tea, and fruits were the most important food sources of total polyphenols. A total of 437 different individual polyphenols were consumed, including 94 consumed at a level >1 mg/day. The most abundant ones were the caffeoylquinic acids and the proanthocyanidin oligomers and polymers. Conclusion This study describes the large number of dietary individual polyphenols consumed and the high variability of their intakes between European populations, particularly between MED and non-MED countries.

Objective: The purpose was to determine whether obesity surgery is associated with a long-term increased risk of colorectal cancer. Background: Long-term cancer risk after obesity surgery is not well characterized. Preliminary epidemiological observations and human tissue biomarker studies recently suggested an increased risk of colorectal cancer after obesity surgery. Methods: A nationwide retrospective register-based cohort study in Sweden was conducted in 1980–2009. The long-term risk of colorectal cancer in patients who underwent obesity surgery, and in an obese no surgery cohort, was compared with that of the age-, sex- and calendar year-matched general background population between 1980 and 2009. Obese individuals were stratified into an obesity surgery cohort and an obese no surgery cohort. The standardized incidence ratio (SIR), with 95% confidence interval (CI), was calculated. Results: Of 77,111 obese patients, 15,095 constituted the obesity surgery cohort and 62,016 constituted the obese no surgery cohort. In the obesity surgery cohort, we observed 70 patients with colorectal cancer, rendering an overall SIR of 1.60 (95% CI 1.25–2.02). The SIR for colorectal cancer increased with length of time after surgery, with a SIR of 2.00 (95% CI 1.48–2.64) after 10 years or more. In contrast, the overall SIR in the obese no surgery cohort (containing 373 colorectal cancers) was 1.26 (95% CI 1.14–1.40) and remained stable with increasing follow-up time. Conclusions: Obesity surgery seems to be associated with an increased risk of colorectal cancer over time. These findings would prompt evaluation of colonoscopy surveillance for the increasingly large population who undergo obesity surgery.

The relations between tobacco, alcohol and risk of gastric cancer need to be established, and any gain from preventive measures should be estimated. We conducted a population‐based, prospective cohort study in Nord‐Trondelag county in Norway. During 1984–1986, adult residents were invited to a health survey and they answered questionnaires that assessed exposure to tobacco and alcohol, together with potential confounding factors. The exposure assessment regarding alcohol was limited to a 14‐day period. New gastric cancers that occurred during follow‐up (1984–2002) were identified by linkage to the Norwegian Cancer Registry. Cox proportion hazards regression models were used to calculate hazard ratios (HRs) with 95% confidence intervals (CI), adjusted for sex, education and body mass index. Follow‐up of 1,117,648 person‐years at risk among 69,962 cohort members revealed 251 gastric cancers, including 224 noncardia cancers. The risk was almost twice as high in daily smokers (HR = 1.88 [CI 95% = 1.33–2.67]) as in never smokers. Independent dose‐response relations were found with earlier age at initiation (p = 0.02), frequency (p = 0.00) and duration of smoking (p = 0.00). Attributable risk (AR) of gastric cancer among current smokers was 8.7/100,000 person‐years and the corresponding population AR was 18.4%. No statistically significant associations between various degrees of exposure to alcohol and risk of gastric cancer was revealed, but combined high use of cigarettes (>20/day) and alcohol (>5 occasions/14 days) increased the risk of noncardia gastric cancer nearly 5‐fold (HR = 4.90 [95% CI = 1.90–12.62]), compared to nonusers. It is concluded that smoking is a dose‐dependent risk factor for gastric cancer. Combined high exposure to smoking and alcohol further increases the risk. Successful preventive measures could considerably reduce the incidence of gastric cancer.

General obesity, as reflected by BMI, is an established risk factor for esophageal adenocarcinoma (EAC), a suspected risk factor for gastric cardia adenocarcinoma (GCC) and appears unrelated to gastric non‐cardia adenocarcinoma (GNCC). How abdominal obesity, as commonly measured by waist circumference (WC), relates to these cancers remains largely unexplored. Using measured anthropometric data from 391,456 individuals from the European Prospective Investigation into Cancer and Nutrition (EPIC) study and 11 years of follow‐up, we comprehensively assessed the association of anthropometric measures with risk of EAC, GCC and GNCC using multivariable proportional hazards regression. One hundred twenty‐four incident EAC, 193 GCC and 224 GNCC were accrued. After mutual adjustment, BMI was unrelated to EAC, while WC showed a strong positive association (highest vs. lowest quintile HR = 1.19; 95% CI, 0.63–2.22 and HR = 3.76; 1.72–8.22, respectively). Hip circumference (HC) was inversely related to EAC after controlling for WC, while WC remained positively associated (HR = 0.35; 0.18–0.68, and HR=4.10; 1.94‐8.63, respectively). BMI was not associated with GCC or GNCC. WC was related to higher risks of GCC after adjustment for BMI and more strongly after adjustment for HC (highest vs. lowest quintile HR = 1.91; 1.09–3.37, and HR = 2.23; 1.28–3.90, respectively). Our study demonstrates that abdominal, rather than general, obesity is an indisputable risk factor for EAC and also provides evidence for a protective effect of gluteofemoral (subcutaneous) adipose tissue in EAC. Our study further shows that general obesity is not a risk factor for GCC and GNCC, while the role of abdominal obesity in GCC needs further investigation.

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