Dietary intakes of flavanones, anthocyanidins, and certain foods rich in flavonoids were associated with reduced risk of death due to CHD, CVD, and all causes.

Objectives To estimate the prevalence of ideal cardiovascular health and its relation to incident cardiovascular disease (CVD). Background An American Heart Association committee recently set a goal to improve the cardiovascular heath of Americans by 20% by 2020. The committee developed definitions of “ideal,” “intermediate,” or “poor” cardiovascular health for adults and children based on seven CVD risk factors or health behaviors. Methods We used data from the Atherosclerosis Risk in Communities (ARIC) Study cohort, aged 45–64 years, to estimate the prevalence of ideal cardiovascular health in 1987–89 and the corresponding incidence rates of CVD. Incident CVD comprised stroke, heart failure, myocardial infarction, or fatal coronary disease. Results Among 12,744 participants initially free of CVD, only 0.1% had ideal cardiovascular health, 17.4% had intermediate cardiovascular health, and 82.5% had poor cardiovascular health. CVD incidence rates through 2007 showed a graded relation with the ideal, intermediate, and poor categories and with the number of ideal health metrics present: rates were one tenth as high in those with six ideal health metrics (3.9 per 1,000 person-years) compared with zero ideal health metrics (37.1 per 1,000 person-years). Conclusions In this community-based sample, few adults in 1987–9 had ideal cardiovascular health by the new AHA definition. Those who had the best levels of cardiovascular health nevertheless sustained relatively few events. Clearly, to achieve the AHA goal of improving cardiovascular health by 20% by 2020, we will need to redouble nationwide primordial prevention efforts at the population and individual levels.

Long-chain n-3 polyunsaturated fatty acids (PUFAs) can derive from diet or from α-linolenic acid (ALA) by elongation and desaturation. We investigated the association of common genetic variation with plasma phospholipid levels of the four major n-3 PUFAs by performing genome-wide association studies in five population-based cohorts comprising 8,866 subjects of European ancestry. Minor alleles of SNPs in FADS1 and FADS2 (desaturases) were associated with higher levels of ALA (p = 3×10−64) and lower levels of eicosapentaenoic acid (EPA, p = 5×10−58) and docosapentaenoic acid (DPA, p = 4×10−154). Minor alleles of SNPs in ELOVL2 (elongase) were associated with higher EPA (p = 2×10−12) and DPA (p = 1×10−43) and lower docosahexaenoic acid (DHA, p = 1×10−15). In addition to genes in the n-3 pathway, we identified a novel association of DPA with several SNPs in GCKR (glucokinase regulator, p = 1×10−8). We observed a weaker association between ALA and EPA among carriers of the minor allele of a representative SNP in FADS2 (rs1535), suggesting a lower rate of ALA-to-EPA conversion in these subjects. In samples of African, Chinese, and Hispanic ancestry, associations of n-3 PUFAs were similar with a representative SNP in FADS1 but less consistent with a representative SNP in ELOVL2. Our findings show that common variation in n-3 metabolic pathway genes and in GCKR influences plasma phospholipid levels of n-3 PUFAs in populations of European ancestry and, for FADS1, in other ancestries.

There is growing interest in understanding how food environments affect diet, but characterizing the food environment is challenging. The authors investigated the relation between global diet measures (an empirically derived "fats and processed meats" (FPM) dietary pattern and the Alternate Healthy Eating Index (AHEI)) and three complementary measures of the local food environment: 1) supermarket density, 2) participant-reported assessments, and 3) aggregated survey responses of independent informants. Data were derived from the baseline examination (2000-2002) of the Multi-Ethnic Study of Atherosclerosis, a US study of adults aged 45-84 years. A healthy diet was defined as scoring in the top or bottom quintile of AHEI or FPM, respectively. The probability of having a healthy diet was modeled by each environment measure using binomial regression. Participants with no supermarkets near their homes were 25-46% less likely to have a healthy diet than those with the most stores, after adjustment for age, sex, race/ethnicity, and socioeconomic indicators: The relative probability of a healthy diet for the lowest store density category versus the highest was 0.75 (95% confidence interval: 0.59, 0.95) for the AHEI and 0.54 (95% confidence interval: 0.42, 0.70) for FPM. Similarly, participants living in areas with the worst-ranked food environments (by participants or informants) were 22-35% less likely to have a healthy diet than those in the best-ranked food environments. Efforts to improve diet may benefit from combining individual and environmental approaches.

These results corroborate previous findings that empirically derived dietary patterns are associated with inflammation and show that these relations in an ethnically diverse population with unique dietary habits are similar to findings in more homogeneous populations.

OBJECTIVE We determined associations between diet soda consumption and risk of incident metabolic syndrome, its components, and type 2 diabetes in the Multi-Ethnic Study of Atherosclerosis. RESEARCH DESIGN AND METHODS Diet soda consumption was assessed by food frequency questionnaire at baseline (2000–2002). Incident type 2 diabetes was identified at three follow-up examinations (2002–2003, 2004–2005, and 2005–2007) as fasting glucose >126 mg/dl, self-reported type 2 diabetes, or use of diabetes medication. Metabolic syndrome (and components) was defined by National Cholesterol Education Program Adult Treatment Panel III criteria. Hazard ratios (HRs) with 95% CI for type 2 diabetes, metabolic syndrome, and metabolic syndrome components were estimated, adjusting for demographic, lifestyle, and dietary confounders. RESULTS At least daily consumption of diet soda was associated with a 36% greater relative risk of incident metabolic syndrome and a 67% greater relative risk of incident type 2 diabetes compared with nonconsumption (HR 1.36 [95% CI 1.11–1.66] for metabolic syndrome and 1.67 [1.27–2.20] for type 2 diabetes). Of metabolic syndrome components, only high waist circumference (men ≥102 cm and women ≥88 cm) and high fasting glucose (≥100 mg/dl) were prospectively associated with diet soda consumption. Associations between diet soda consumption and type 2 diabetes were independent of baseline measures of adiposity or changes in these measures, whereas associations between diet soda and metabolic syndrome were not independent of these factors. CONCLUSIONS Although these observational data cannot establish causality, consumption of diet soda at least daily was associated with significantly greater risks of select incident metabolic syndrome components and type 2 diabetes.

The authors examined associations among fast-food consumption, diet, and neighborhood fast-food exposure by using 2000-2002 Multi-Ethnic Study of Atherosclerosis data. US participants (n = 5,633; aged 45-84 years) reported usual fast-food consumption (never, <1 time/week, or > or =1 times/week) and consumption near home (yes/no). Healthy diet was defined as scoring in the top quintile of the Alternate Healthy Eating Index or bottom quintile of a Western-type dietary pattern. Neighborhood fast-food exposure was measured by densities of fast-food outlets, participant report, and informant report. Separate logistic regression models were used to examine associations of fast-food consumption and diet; fast-food exposure and consumption near home; and fast-food exposure and diet adjusted for site, age, sex, race/ethnicity, education, and income. Those never eating fast food had a 2-3-times higher odds of having a healthy diet versus those eating fast food > or =1 times/week, depending on the dietary measure. For every standard deviation increase in fast-food exposure, the odds of consuming fast food near home increased 11%-61% and the odds of a healthy diet decreased 3%-17%, depending on the model. Results show that fast-food consumption and neighborhood fast-food exposure are associated with poorer diet. Interventions that reduce exposure to fast food and/or promote individual behavior change may be helpful.

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