The impact of egg consumption, a major source of dietary cholesterol, on the risk of atherosclerotic cardiovascular diseases (ASCVD) is controversial. Venous thromboembolism (VTE) is a CVD which shares common risk factors and mechanistic pathways with ASCVD. However, there is no data on the relationship between egg or cholesterol intake and VTE risk. Therefore, we evaluated the prospective associations of egg and cholesterol intakes with VTE risk and whether the apoE4 phenotype, which influences cholesterol metabolism, could modify the associations. Data involving 1852 men aged 42–61 years at baseline without a history of VTE or CHD in the population-based Kuopio Ischaemic Heart Disease Risk Factor Study were analysed. Dietary intakes were assessed with 4-d food records. Incident VTE events were identified by record linkage to hospital discharge registries. Hazard ratios (95 % CI) for incident VTE were estimated using Cox regression. During a median follow-up of 28·8 years, 132 VTE events occurred. Comparing the top (> 38 g/d) v. bottom (< 20 g/d) tertiles of egg consumption, the hazard ratio (95 % CI) for VTE was 0·99 (0·64, 1·53) in analysis adjusted for several established risk factors and other dietary factors. There was also no evidence of an association between cholesterol intake and VTE risk. Imputed results were consistent with the observed results. The apoE4 phenotype did not modify the associations. In middle-aged and older Finnish men, egg or cholesterol intakes were not associated with future VTE risk. Other large-scale prospective studies are needed to confirm or refute these findings.

The risk of Alzheimer's disease is increased for carriers of apoE4 (E4) or the PPAR-α L162V polymorphism (L162V), but it is decreased in fish and seafood consumers. The link between high fish intake and reduced risk of cognitive decline in the elderly appears not to hold in carriers of E4, possibly because better cognition is linked to EPA+DHA in the blood, but only in non-carriers of E4. As yet, no such studies exist in carriers of L162V. Our objective was to determine whether the plasma fatty acid response to a dietary supplement of EPA+DHA was altered in carriers of L162V and/or E4. This was an add-on project; in the original study, men were selected based on whether or not they were carriers of L162V (n 14 per group). E4 status was determined afterwards. All subjects received an EPA+DHA supplement for 6 weeks. L162V polymorphism did not interact with the supplement in a way to alter EPA and DHA incorporation into plasma lipids. However, when the groups were separated based on the presence of E4, baseline EPA and DHA in plasma TAG were 67 and 60 % higher, respectively, in E4 carriers. After the supplementation, there were significant gene × diet interactions in which only non-carriers had increased EPA and DHA in plasma NEFA and TAG, respectively.

Drawing on previous research on geneticization and the clinical uptake of pharmacogenetics, this article argues for the use of the concept of clinical usefulness, in preference to the idea of clinical resistance to such testing. A general framework for clinical usefulness is sketched out, looking at how a number of features (clinicians’ knowledge, the differing interests of clinicians and researchers, how context influences the value of tests’ accuracy, the economic aspects of such tests and general cultural aspects of the clinic) influence how ‘useful’ a genetic or pharmacogenetic test will be seen to be by clinicians.