Background-The role of diet in the origin of metabolic syndrome (MetSyn) is not well understood; thus, we sought to evaluate the relationship between incident MetSyn and dietary intake using prospective data from 9514 participants (age, 45 to 64 years) enrolled in the Atherosclerosis Risk in Communities (ARIC) study. Methods and Results-Dietary intake was assessed at baseline via a 66-item food frequency questionnaire. We used principal-components analysis to derive "Western" and "prudent" dietary patterns from 32 food groups and evaluated 10 food groups used in previous studies of the ARIC cohort. MetSyn was defined by American Heart Association guidelines. Proportional-hazards regression was used. Over 9 years of follow-up, 3782 incident cases of MetSyn were identified. After adjustment for demographic factors, smoking, physical activity, and energy intake, consumption of a Western dietary pattern (P trend ϭ0.03) was adversely associated with incident MetSyn. After further adjustment for intake of meat, dairy, fruits and vegetables, refined grains, and whole grains, analysis of individual food groups revealed that meat (P trend Ͻ0.001), fried foods (P trend ϭ0.02), and diet soda (P trend ϭϽ 0.001) also were adversely associated with incident MetSyn, whereas dairy consumption (P trend ϭ0.006) was beneficial. No associations were observed between incident MetSyn and a prudent dietary pattern or intakes of whole grains, refined grains, fruits and vegetables, nuts, coffee, or sweetened beverages. Conclusions-These prospective findings suggest that consumption of a Western dietary pattern, meat, and fried foods promotes the incidence of MetSyn, whereas dairy consumption provides some protection. The diet soda association was not hypothesized and deserves further study.

Abstract-High intakes of dietary sugars in the setting of a worldwide pandemic of obesity and cardiovascular disease have heightened concerns about the adverse effects of excessive consumption of sugars. In 2001 to 2004, the usual intake of added sugars for Americans was 22.2 teaspoons per day (355 calories per day). Between 1970 and 2005, average annual availability of sugars/added sugars increased by 19%, which added 76 calories to Americans' average daily energy intake. Soft drinks and other sugar-sweetened beverages are the primary source of added sugars in Americans' diets. Excessive consumption of sugars has been linked with several metabolic abnormalities and adverse health conditions, as well as shortfalls of essential nutrients. Although trial data are limited, evidence from observational studies indicates that a higher intake of soft drinks is associated with greater energy intake, higher body weight, and lower intake of essential nutrients. National survey data also indicate that excessive consumption of added sugars is contributing to overconsumption of discretionary calories by Americans. On the basis of the 2005 US Dietary Guidelines, intake of added sugars greatly exceeds discretionary calorie allowances, regardless of energy needs. In view of these considerations, the American Heart Association recommends reductions in the intake of added sugars. A prudent upper limit of intake is half of the discretionary calorie allowance, which for most American women is no more than 100 calories per day and for most American men is no more than 150 calories per day from added sugars. (Circulation. 2009; 120:1011-1020.)Key Words: AHA Scientific Statements Ⅲ cardiovascular diseases Ⅲ carbohydrates, dietary Ⅲ diet Ⅲ beverages Ⅲ carbonated beverages Ⅲ lipids N ew evidence on the relationship between intake of sugars and cardiovascular health has emerged since the last American Heart Association (AHA) scientific statement was published in 2002. 1 In 2006, the AHA published revised diet and lifestyle recommendations that recommend minimizing the intake of beverages and foods with added sugars. 2 The present statement expands on that recommendation by reviewing the evidence for recommending a specific upper limit of intake for added sugars. Because the focus of the present statement is on added sugars, recommendations for intake of naturally occurring sugars and complex carbohydrates are beyond its scope. Consumption of Sugars in the United StatesSugars are a ubiquitous component of our food supply and are consumed as a naturally occurring component of many foods and as additions to foods during processing, preparation, or at the table. 3 There are various definitions for sugar. Table 1 The American Heart Association makes every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside relationship or a personal, professional, or business interest of a member of the writing panel. Specifically, all members of the writing group are required to complete and submit a Disclos...

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.

National Institutes of Health.

Evidence is synthesized that foods and food patterns act synergistically to influence the risk of several chronic diseases. Whole-grain consumption and risk of disease are presented as a model of food synergy. Food synergy is defined as additive or more than additive influences of foods and food constituents on health. Risk appears to be lower with consumption of whole grain than of refined grain; that is, benefit accrues when all edible parts of the grain are included (bran, germ, and endosperm). It appears that phytochemicals that are located in the fiber matrix, in addition to or instead of the fiber itself, are responsible for the reduced risk. Risk is further reduced if whole-grain foods are consumed in a diet otherwise high in plant foods. To gain full understanding of the pathways by which food synergies work, it is desirable to use several "top down" approaches, starting with the larger units, namely foods or food patterns, and working down to smaller units that provide protection from disease. Study of foods, food patterns, and individual nutrients or food components in reducing disease risk is seen as complementary. Epidemiologic, clinical trial, and in vitro approaches to such research are needed.

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.

Background Prior studies on intake of linoleic acid (LA), the predominant n-6 fatty acid, and coronary heart disease (CHD) risk have generated inconsistent results. We performed a systematic review and meta-analysis of prospective cohort studies to summarize the evidence regarding the relation of dietary LA intake and CHD risk. Methods and Results We searched MEDLINE and EMBASE databases through June, 2013 for prospective cohort studies that reported the association between dietary LA and CHD events. In addition, we utilized unpublished data from cohort studies in a previous pooling project. We pooled the multivariate-adjusted relative risk (RR) comparing the highest with the lowest categories of LA intake using fixed-effect meta-analysis. We identified 13 published and unpublished cohort studies with a total of 310,602 individuals and 12,479 total CHD events including 5,882 CHD deaths. Comparing the highest to the lowest category, dietary LA was associated with a 15% lower risk of CHD events (pooled RR, 0.85; 95% confidence intervals (95% CI): 0.78–0.92; I2=35.5%) and a 21% lower risk of CHD deaths (pooled RR, 0.79; 95% CI, 0.71–0.89; I2=0.0%). A 5% of energy increment in LA intake replacing energy from saturated fat intake was associated with a 9% lower risk of CHD events (RR, 0.91; 95% CI, 0.86–0.96) and a 13% lower risk of CHD deaths (RR, 0.87; 95% CI, 0.82–0.94). Conclusion In prospective observational studies, dietary LA intake is inversely associated with CHD risk in a dose-response manner. These data provide support for current recommendations to replace saturated fat with polyunsaturated fat for primary prevention of CHD.

These observational findings suggest a beneficial effect of whole-grain and fruit and vegetable consumption on the risks of total mortality and incident CAD but not on the risk of ischemic stroke.