Background: In the last decades, the incidence of oesophageal and gastric cardia adenocarcinoma has increased rapidly in the Western world. We investigated the association between body mass index (BMI), height and risk of oesophageal and gastric cardia adenocarcinoma. Methods: The Netherlands Cohort Study was initiated in 1986. All participants (n = 120 852), aged 55-69 years, completed a self administered questionnaire. Cases were identified through annual record linkage with the Netherlands Cancer Registry. After 13.3 years of follow-up, excluding the first follow-up year, complete data from 4552 subcohort members, 133 oesophageal and 163 gastric cardia adenocarcinomas were available for case-cohort analyses. Incidence rate ratios (RRs) and corresponding 95% confidence intervals were estimated using Cox proportional hazard models. Results: The RRs (95% CI) of oesophageal adenocarcinoma were 1.40 (0.95 to 2.04) and 3.96 (2.27 to 6.88) for overweight (BMI 25.0-29.9 kg/m 2 ) and obese subjects (BMI >30.0 kg/m 2 ), respectively, compared to subjects with normal weight (BMI 20.0-24.9 kg/m 2 ). For gastric cardia adenocarcinoma, these RRs were 1.32 (0.94 to 1.85) and 2.73 (1.56 to 4.79). Also change in BMI during adulthood was positively associated with the risk of oesophageal and gastric cardia adenocarcinoma (p trend 0.001 and 0.02, respectively), while no association was found with BMI in early adulthood (p trend 0.17 and 0.17, respectively). None of the tumour types investigated was significantly associated with height. Conclusions: These results confirm higher risks of oesophageal and gastric cardia adenocarcinoma with increasing BMI. This implies that the increasing prevalence of obesity may be one of the explanations for the rising incidence of oesophageal and gastric cardia adenocarcinoma in the Western world.

Incidence rates of cardiovascular diseases are often estimated by linkage to hospital discharge and mortality registries. The validity depends on the quality of the registries and the linkage. Therefore, we validated incidence rates of coronary heart disease (CHD), acute myocardial infarction, unstable angina pectoris, and heart failure, estimated by this method, against the disease registry of the cardiovascular registry Maastricht cohort study. The cohort consists of 21,148 persons, born between 1927 and 1977, who were randomly sampled from Maastricht and surrounding communities in 1987-1997. Incident cases were identified by linkage to the Netherlands causes of death registry and either the hospital discharge registry (HDR) or the cardiology information system (CIS) of the University Hospital Maastricht. Sensitivities and positive predictive values were calculated using the CIS-based registry as gold standard. Relatively high sensitivities and positive predictive values were found for CHD (72 and 91%, respectively) and acute myocardial infarction (84 and 97%, respectively). These values were considerably lower for unstable angina pectoris (53 and 78%, respectively) and heart failure (43 and 80%, respectively). A substantial number of cases (14-47%) were found only in the CISbased registry, because they were missed or miscoded in the HDR-based registry. As a consequence, the incidence rates in the HDR-based registry were considerably lower than in the CIS-based registry, especially for unstable angina pectoris and heart failure. Incidence rates based on hospital discharge and mortality data may underestimate the true incidence rates, especially for unstable angina pectoris and heart failure.

A metabolite score derived from a single-point metabolome measurement is associated with CHD, and metabolomics may be a promising tool for refining and improving the prediction of CHD.

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BackgroundIntakes of n-3 polyunsaturated fatty acids (PUFAs), especially EPA (C20∶5n-3) and DHA (C22∶6n-3), are known to prevent fatal coronary heart disease (CHD). The effects of n-6 PUFAs including arachidonic acid (C20∶4n-6), however, remain unclear. δ-5 and δ-6 desaturases are rate-limiting enzymes for synthesizing long-chain n-3 and n-6 PUFAs. C20∶4n-6 to C20∶3n-6 and C18∶3n-6 to C18∶2n-6 ratios are markers of endogenous δ-5 and δ-6 desaturase activities, but have never been studied in relation to incident CHD. Therefore, the aim of this study was to investigate the relation between these ratios as well as genotypes of FADS1 rs174547 and CHD incidence.MethodsWe applied a case-cohort design within the CAREMA cohort, a large prospective study among the general Dutch population followed up for a median of 12.1 years. Fatty acid profile in plasma cholesteryl esters and FADS1 genotype at baseline were measured in a random subcohort (n = 1323) and incident CHD cases (n = 537). Main outcome measures were hazard ratios (HRs) of incident CHD adjusted for major CHD risk factors.ResultsThe AA genotype of rs174547 was associated with increased plasma levels of C204n-6, C20∶5n-3 and C22∶6n-3 and increased δ-5 and δ-6 desaturase activities, but not with CHD risk. In multivariable adjusted models, high baseline δ-5 desaturase activity was associated with reduced CHD risk (P for trend = 0.02), especially among those carrying the high desaturase activity genotype (AA): HR (95% CI) = 0.35 (0.15–0.81) for comparing the extreme quintiles. High plasma DHA levels were also associated with reduced CHD risk.ConclusionIn this prospective cohort study, we observed a reduced CHD risk with an increased C20∶4n-6 to C20∶3n-6 ratio, suggesting that δ-5 desaturase activity plays a role in CHD etiology. This should be investigated further in other independent studies.