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Leukocyte DNA methylation patterns associated with habitual diet may reveal molecular mechanisms involved in the pathogenesis of diet-related chronic diseases and highlight targets for prevention and treatment. We aimed to examine peripheral blood derived leukocyte DNA methylation signatures associated with diet quality. We meta-analyzed epigenome-wide associations between diet quality and DNA methylation levels at over 400,000 cytosine-guanine dinucleotides (CpGs). We conducted analysis primarily in 6,662 European ancestry (EA) participants and secondarily in a group additionally including 3,062 participants of non-European ancestry from five population-based cohort studies. DNA methylation profiles were measured in whole blood, CD4 + T-cells, or CD14 + monocytes. We used food frequency questionnaires to assess habitual intake and constructed two diet quality scores: the Mediterranean-style diet score (MDS) and Alternative Healthy Eating Index (AHEI). Our primary analysis identified 32 diet-associated CpGs, 12 CpGs for MDS and 24 CpGs for AHEI (at FDR < 0.05, corresponding p-values = 1.2×10-6 and 3.1×10-6, respectively) in EA participants. Four of these CpGs were associated with both MDS and AHEI. In addition, Mendelian randomization analysis indicated that seven diet-associated CpGs were causally linked to at least one of the CVD risk factors. For example, hypermethylation of cg11250194 (FADS2), which was associated with higher diet quality scores, was also associated with lower fasting triglycerides concentrations (p-value = 1.5×10-14) and higher high-density lipoprotein cholesterol concentrations (p-value = 1.7×10-8). Transethnic meta-analysis identified nine additional CpGs associated with diet quality (either MDS or AHEI) at FDR < 0.05. Overall quality of habitual diet was associated with differential peripheral leukocyte DNA methylation levels of 32 CpGs in EA participants. The diet-associated CpGs may serve as biomarkers and targets for preventive measures in CVD health. Future studies are warranted to examine diet-associated DNA methylation patterns in larger, ethnically diverse study samples.
Sufficient protein intake has been suggested to be important for preventing physical frailty, but studies show conflicting results which may be explained because not all studies address protein source and intake of other macronutrients and total energy. Therefore, we studied 2504 subjects with data on diet and physical frailty, participating in a large population-based prospective cohort among subjects aged 45+ years (the Rotterdam Study). Dietary intake was assessed with a FFQ. Frailty was defined according to the frailty phenotype as the presence of at least three out of the following five symptoms: weight loss, low physical activity, weakness, slowness and fatigue. We used multinomial logistic regression models to evaluate the independent association between protein intake and frailty using two methods: nutrient residual models and energy decomposition models. With every increase in 10 g total, plant or animal protein per d, the odds to be frail were 1·06 (95 % CI 0·98, 1·15), 0·87 (95 % CI 0·71, 1·07) and 1·07 (95 % CI 0·99, 1·15), respectively, using the nutrient residual method. Using the energy partition model, we observed that the odds to be frail were lower with higher vegetable protein intake (OR per 418·4 kJ (100 kcal): 0·61, 95 % CI 0·39, 0·97), however, results disappeared when adjusting for physical activity. For energy intake from any source we observed that with every 418·4 kJ (100 kcal) increase, the odds to be frail were 5 % lower (OR: 0·95, 95 % CI 0·93, 0·97). Our results suggest that energy intake, but not protein specifically, is associated with less frailty. Considering other macronutrients, physical activity and diet quality seems to be essential for future studies on protein and frailty.
High protein intake in early childhood is associated with obesity, suggesting possible adverse effects on other cardiometabolic outcomes. However, studies in adults have suggested beneficial effects of protein intake on blood pressure (BP) and lipid profile. Whether dietary protein intake is associated with cardiovascular and metabolic health in children is unclear. Therefore, we aimed to systematically review the evidence on the associations of protein intake with BP, insulin sensitivity and blood lipids in children. We searched the databases Medline, Embase, Cochrane Central and PubMed for interventional and observational studies in healthy children up to the age of 18 years, in which associations of total, animal and/or vegetable protein intake with one or more of the following outcomes were reported: BP; measures of insulin sensitivity; cholesterol levels; or TAG levels. In the search, we identified 6636 abstracts, of which fifty-six studies met all selection criteria. In general, the quality of the included studies was low. Most studies were cross-sectional, and many did not control for potential confounders. No overall associations were observed between protein intake and insulin sensitivity or blood lipids. A few studies suggested an inverse association between dietary protein intake and BP, but evidence was inconclusive. Only four studies examined the effects of vegetable or animal protein intake, but with inconsistent results. In conclusion, the literature, to date provides insufficient evidence for effects of protein intake on BP, insulin sensitivity or blood lipids in children. Future studies could be improved by adequately adjusting for key confounders such as energy intake and obesity.
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