Milk intake and incident stroke and CHD in populations of European descent: a Mendelian randomisation study.

Higher milk intake has been associated with a lower stroke risk, but not with risk of CHD. Residual confounding or reverse causation cannot be excluded. Therefore, we estimated the causal association of milk consumption with stroke and CHD risk through instrumental variable (IV) and gene-outcome analyses. IV analysis included 29 328 participants (4611 stroke; 9828 CHD) of the European Prospective Investigation into Cancer and Nutrition (EPIC)-CVD (eight European countries) and European Prospective Investigation into Cancer and Nutrition-Netherlands (EPIC-NL) case-cohort studies. rs4988235, a lactase persistence (LP) SNP which enables digestion of lactose in adulthood was used as genetic instrument. Intake of milk was first regressed on rs4988235 in a linear regression model. Next, associations of genetically predicted milk consumption with stroke and CHD were estimated using Prentice-weighted Cox regression. Gene-outcome analysis included 777 024 participants (50 804 cases) from MEGASTROKE (including EPIC-CVD), UK Biobank and EPIC-NL for stroke, and 483 966 participants (61 612 cases) from CARDIoGRAM, UK Biobank, EPIC-CVD and EPIC-NL for CHD. In IV analyses, each additional LP allele was associated with a higher intake of milk in EPIC-CVD (ß = 13·7 g/d; 95 % CI 8·4, 19·1) and EPIC-NL (36·8 g/d; 95 % CI 20·0, 53·5). Genetically predicted milk intake was not associated with stroke (HR per 25 g/d 1·05; 95 % CI 0·94, 1·16) or CHD (1·02; 95 % CI 0·96, 1·08). In gene-outcome analyses, there was no association of rs4988235 with risk of stroke (OR 1·02; 95 % CI 0·99, 1·05) or CHD (OR 0·99; 95 % CI 0·95, 1·03). Current Mendelian randomisation analysis does not provide evidence for a causal inverse relationship between milk consumption and stroke or CHD risk.

Substitution among milk and yogurt products and the risk of incident type 2 diabetes in the EPIC-NL cohort.

BACKGROUND: Higher dairy consumption has been associated with lower type 2 diabetes (T2D) risk, whereas dairy product subtypes appear to differ in their T2D risk association. We investigated whether replacing one type of milk or yogurt product with another is associated with T2D incidence. METHODS: Participants of the European Prospective Investigation into Cancer and Nutrition-Netherlands (EPIC-NL) cohort (n = 35 982) were included in the present study. Information on milk and yogurt consumption at baseline was obtained by a validated food frequency questionnaire. T2D cases were identified by self-report or linkage to the hospital discharge registry, and validated by consulting the general practitioner. Multivariable Cox proportional hazard models were used to estimate associations. RESULTS: During a mean of 15 years of follow-up, 1467 indecent T2D cases were validated. Median total milk and yogurt intake was 1.5 servings (25th percentile to 75th percentile: 0.8-2.4). After adjustment for demographic and cardiovascular risk factors, replacement of one serving (200 g) of whole-fat milk [hazard ratio (HR) = 0.93, 95% confidence interval (CI) = 0.60-1.44], buttermilk (HR = 0.88, 95% CI = 0.58-1.34), skimmed milk (HR = 0.87, 95% CI = 0.57-1.32) or skimmed fermented milk (HR = 0.99, 95% CI = 0.63-1.54) with whole-fat yogurt was not associated with T2D risk. Substitutions among other milk and yogurt products were also not associated with T2D risk. Sensitivity analysis investigating T2D risk halfway follow-up suggested a lower risk for substitutions with whole-fat yogurt. CONCLUSIONS: No evidence was found for the association between substitutions among milk and yogurt products and the risk of incident T2D, although we cannot exclude possible attenuation of results as a result of dietary changes over time. This analysis should be repeated in a population with a wider consumption range of whole-fat yogurt.

A pro-inflammatory diet is associated with increased risk of developing hypertension among middle-aged women.

BACKGROUND AND AIMS: A pro-inflammatory diet is thought to lead to hypertension through oxidative stress and vessel wall inflammation. We therefore investigated the association between the dietary inflammatory index (DII) and developing hypertension in a population-based cohort of middle-aged women. METHODS AND RESULTS: The Australian Longitudinal Study on Women's Health included 7169 Australian women, aged 52 years (SD 1 year) at baseline in 2001, who were followed up through 4 surveys until 2013. The DII, a literature-derived dietary index that has been validated against several inflammatory markers, was calculated based on data collected via a validated food-frequency questionnaire administered at baseline. Hypertension was defined as new onset of doctor-diagnosed hypertension, ascertained through self-report between 2001 and 2013. Generalised Estimating Equation analyses were used to investigate the association between the DII and incident hypertension. The analyses were adjusted for demographic and hypertension risk factors. During 12-years follow-up we identified 1680 incident cases of hypertension. A more pro-inflammatory diet was associated with higher risk of hypertension in dichotomised analyses with an ORfully adjusted of 1.24, 95% CI: 1.06-1.45. CONCLUSION: A pro-inflammatory diet might lead to a higher risk of developing hypertension. These results need to be replicated in other studies.