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Dietary and policy recommendations frequently focus on reducing saturated fatty acid consumption for improving cardiometabolic health, based largely on ecologic and animal studies. Recent advances in nutritional science now allow assessment of critical questions about health effects of saturated fatty acids (SFA). We reviewed the evidence from randomized controlled trials (RCTs) of lipid and non-lipid risk factors, prospective cohort studies of disease endpoints, and RCTs of disease endpoints for cardiometabolic effects of SFA consumption in humans, including whether effects vary depending on specific SFA chain-length; on the replacement nutrient; or on disease outcomes evaluated. Compared with carbohydrate, the TC:HDL-C ratio is nonsignificantly affected by consumption of myristic or palmitic acid, is nonsignificantly decreased by stearic acid, and is significantly decreased by lauric acid. However, insufficient evidence exists for different chain-length-specific effects on other risk pathways or, more importantly, disease endpoints. Based on consistent evidence from human studies, replacing SFA with polyunsaturated fat modestly lowers coronary heart disease risk, with ~10% risk reduction for a 5% energy substitution; whereas replacing SFA with carbohydrate has no benefit and replacing SFA with monounsaturated fat has uncertain effects. Evidence for the effects of SFA consumption on vascular function, insulin resistance, diabetes, and stroke is mixed, with many studies showing no clear effects, highlighting a need for further investigation of these endpoints. Public health emphasis on reducing SFA consumption without considering the replacement nutrient or, more importantly, the many other food-based risk factors for cardiometabolic disease is unlikely to produce substantial intended benefits.

Reduced saturated fat (SFA) consumption is recommended to reduce coronary heart disease (CHD), but there is an absence of strong supporting evidence from randomized controlled trials (RCTs) of clinical CHD events and few guidelines focus on any specific replacement nutrient. Additionally, some public health groups recommend lowering or limiting polyunsaturated fat (PUFA) consumption, a major potential replacement for SFA. We systematically investigated and quantified the effects of increased PUFA consumption, as a replacement for SFA, on CHD endpoints in RCTs. RCTs were identified by systematic searches of multiple online databases through June 2009, grey literature sources, hand-searching related articles and citations, and direct contacts with experts to identify potentially unpublished trials. Studies were included if they randomized participants to increased PUFA for at least 1 year without major concomitant interventions, had an appropriate control group, and reported incidence of CHD (myocardial infarction and/or cardiac death). Inclusions/exclusions were adjudicated and data were extracted independently and in duplicate by two investigators and included population characteristics, control and intervention diets, follow-up duration, types of events, risk ratios, and SEs. Pooled effects were calculated using inverse-variance-weighted random effects meta-analysis. From 346 identified abstracts, eight trials met inclusion criteria, totaling 13,614 participants with 1,042 CHD events. Average weighted PUFA consumption was 14.9% energy (range 8.0%-20.7%) in intervention groups versus 5.0% energy (range 4.0%-6.4%) in controls. The overall pooled risk reduction was 19% (RR = 0.81, 95% confidence interval [CI] 0.70-0.95, p = 0.008), corresponding to 10% reduced CHD risk (RR = 0.90, 95% CI = 0.83-0.97) for each 5% energy of increased PUFA, without evidence for statistical heterogeneity (Q-statistic p = 0.13; I(2) = 37%). Meta-regression identified study duration as an independent determinant of risk reduction (p = 0.017), with studies of longer duration showing greater benefits. These findings provide evidence that consuming PUFA in place of SFA reduces CHD events in RCTs. This suggests that rather than trying to lower PUFA consumption, a shift toward greater population PUFA consumption in place of SFA would significantly reduce rates of CHD. Please see later in the article for the Editors' Summary.

The authors estimate that in 2010, a total of 1.65 million deaths from cardiovascular causes occurred as a result of excess sodium consumption. They assess correlations between sodium consumption and blood pressure and between blood pressure and cardiovascular events. A high dietary intake of sodium is associated with elevated blood pressure, a major risk factor for cardiovascular disease. 1 , 2 The United Nations, 3 World Health Organization, 4 Centers for Disease Control and Prevention, and other organizations have emphasized the relationship between dietary sodium and cardiovascular outcomes. 3 – 7 Yet the global effects of sodium consumption and the heterogeneity of these effects according to age, sex, and country have not been clearly established. Rates of sodium-associated cardiovascular disease have been estimated for only selected countries, 8 – 14 and these rates are often based on self-reported diet, without estimates of salt intake, or without considering . . .

The effect of dietary fats on cardiometabolic diseases, including cardiovascular diseases and type 2 diabetes mellitus, has generated tremendous interest. Many earlier investigations focused on total fat and conventional fat classes (such as saturated and unsaturated fats) and their influence on a limited number of risk factors. However, dietary fats comprise heterogeneous molecules with diverse structures, and growing research in the past two decades supports correspondingly complex health effects of individual dietary fats. Moreover, health effects of dietary fats might be modified by additional factors, such as accompanying nutrients and food-processing methods, emphasizing the importance of the food sources. Accordingly, the rapidly increasing scientific findings on dietary fats and cardiometabolic diseases have generated debate among scientists, caused confusion for the general public and present challenges for translation into dietary advice and policies. This Review summarizes the evidence on the effects of different dietary fats and their food sources on cell function and on risk factors and clinical events of cardiometabolic diseases. The aim is not to provide an exhaustive review but rather to focus on the most important evidence from randomized controlled trials and prospective cohort studies and to highlight current areas of controversy and the most relevant future research directions for understanding how to improve the prevention and management of cardiometabolic diseases through optimization of dietary fat intake.Dietary fats comprise heterogeneous molecules with diverse structures and complex health effects. This Review discusses the effects of different dietary fats on cell processes and cardiometabolic disease risk factors and clinical events, highlighting areas of controversy and future research directions to improve the prevention and management of cardiometabolic diseases through optimization of dietary fat intake.

Trans fatty acids, which are largely consumed from partially hydrogenated vegetable oils, adversely affect circulating lipid and lipoprotein levels and endothelial function, trigger systemic inflammation, and might increase visceral adiposity, body weight, and insulin resistance. The authors provide an overview of these adverse effects and their relationships with clinical endpoints, with a focus on potential effects on insulin resistance and diabetes. The major dietary sources of trans fatty acids (TFAs) in most countries are partially hydrogenated vegetable oils. TFA consumption is a modifiable dietary risk factor for metabolic syndrome, diabetes mellitus, and coronary heart disease. Here, we review the available data on various effects of TFAs, including metabolic and signaling pathways that mediate these effects, affected tissues, and relationships with clinical end points. TFA consumption causes metabolic dysfunction: it adversely affects circulating lipid levels, triggers systemic inflammation, induces endothelial dysfunction, and, according to some studies, increases visceral adiposity, body weight, and insulin resistance. Dietary TFAs influence the function of multiple cell types, including hepatocytes, adipocytes, macrophages and endothelial cells. Among dietary fats and nutrients, TFAs seem to have a unique cardiometabolic imprint that is linked to insulin-resistance and metabolic-syndrome pathways. Consistent with these adverse physiological effects, consumption of even small amounts of TFAs (2% of total energy intake) is consistently associated with a markedly increased incidence of coronary heart disease. Relationships between TFA consumption and diabetes mellitus have been less consistent, possibly owing to differences in study designs. Nevertheless, the documented adverse effects of TFAs underscore their potential to cause harm and the importance of policy measures to minimize consumption of industrially produced TFAs. Key Points Dietary trans fatty acids (TFAs) derive from industrial, partial hydrogenation of vegetable oils or from ruminant products Dietary TFAs influence the function of multiple cell types, including hepatocytes, adipocytes, macrophages and endothelial cells TFA consumption affects multiple metabolic risk factors, including lipid and lipoprotein levels, systemic inflammation, endothelial function, adiposity, and glucose–insulin homeostasis TFA consumption increases risk of clinical coronary heart disease and likelihood of development of diabetes mellitus

School food environment policies may be a critical tool to promote healthy diets in children, yet their effectiveness remains unclear. To systematically review and quantify the impact of school food environment policies on dietary habits, adiposity, and metabolic risk in children. We systematically searched online databases for randomized or quasi-experimental interventions assessing effects of school food environment policies on children's dietary habits, adiposity, or metabolic risk factors. Data were extracted independently and in duplicate, and pooled using inverse-variance random-effects meta-analysis. Habitual (within+outside school) dietary intakes were the primary outcome. Heterogeneity was explored using meta-regression and subgroup analysis. Funnel plots, Begg's and Egger's test evaluated potential publication bias. From 6,636 abstracts, 91 interventions (55 in US/Canada, 36 in Europe/New Zealand) were included, on direct provision of healthful foods/beverages (N = 39 studies), competitive food/beverage standards (N = 29), and school meal standards (N = 39) (some interventions assessed multiple policies). Direct provision policies, which largely targeted fruits and vegetables, increased consumption of fruits by 0.27 servings/d (n = 15 estimates (95%CI: 0.17, 0.36)) and combined fruits and vegetables by 0.28 servings/d (n = 16 (0.17, 0.40)); with a slight impact on vegetables (n = 11; 0.04 (0.01, 0.08)), and no effects on total calories (n = 6; -56 kcal/d (-174, 62)). In interventions targeting water, habitual intake was unchanged (n = 3; 0.33 glasses/d (-0.27, 0.93)). Competitive food/beverage standards reduced sugar-sweetened beverage intake by 0.18 servings/d (n = 3 (-0.31, -0.05)); and unhealthy snacks by 0.17 servings/d (n = 2 (-0.22, -0.13)), without effects on total calories (n = 5; -79 kcal/d (-179, 21)). School meal standards (mainly lunch) increased fruit intake (n = 2; 0.76 servings/d (0.37, 1.16)) and reduced total fat (-1.49%energy; n = 6 (-2.42, -0.57)), saturated fat (n = 4; -0.93%energy (-1.15, -0.70)) and sodium (n = 4; -170 mg/d (-242, -98)); but not total calories (n = 8; -38 kcal/d (-137, 62)). In 17 studies evaluating adiposity, significant decreases were generally not identified; few studies assessed metabolic factors (blood lipids/glucose/pressure), with mixed findings. Significant sources of heterogeneity or publication bias were not identified. Specific school food environment policies can improve targeted dietary behaviors; effects on adiposity and metabolic risk require further investigation. These findings inform ongoing policy discussions and debates on best practices to improve childhood dietary habits and health.

Dietary habits are major contributors to coronary heart disease, stroke, and diabetes. However, comprehensive evaluation of etiologic effects of dietary factors on cardiometabolic outcomes, their quantitative effects, and corresponding optimal intakes are not well-established. To systematically review the evidence for effects of dietary factors on cardiometabolic diseases, including comprehensively assess evidence for causality; estimate magnitudes of etiologic effects; evaluate heterogeneity and potential for bias in these etiologic effects; and determine optimal population intake levels. We utilized Bradford-Hill criteria to assess probable or convincing evidence for causal effects of multiple diet-cardiometabolic disease relationships. Etiologic effects were quantified from published or de novo meta-analyses of prospective studies or randomized clinical trials, incorporating standardized units, dose-response estimates, and heterogeneity by age and other characteristics. Potential for bias was assessed in validity analyses. Optimal intakes were determined by levels associated with lowest disease risk. We identified 10 foods and 7 nutrients with evidence for causal cardiometabolic effects, including protective effects of fruits, vegetables, beans/legumes, nuts/seeds, whole grains, fish, yogurt, fiber, seafood omega-3s, polyunsaturated fats, and potassium; and harms of unprocessed red meats, processed meats, sugar-sweetened beverages, glycemic load, trans-fats, and sodium. Proportional etiologic effects declined with age, but did not generally vary by sex. Established optimal population intakes were generally consistent with observed national intakes and major dietary guidelines. In validity analyses, the identified effects of individual dietary components were similar to quantified effects of dietary patterns on cardiovascular risk factors and hard endpoints. These novel findings provide a comprehensive summary of causal evidence, quantitative etiologic effects, heterogeneity, and optimal intakes of major dietary factors for cardiometabolic diseases, informing disease impact estimation and policy planning and priorities.

ObjectiveTo quantify global intakes of key foods related to non-communicable diseases in adults by region (n=21), country (n=187), age and sex, in 1990 and 2010.DesignWe searched and obtained individual-level intake data in 16 age/sex groups worldwide from 266 surveys across 113 countries. We combined these data with food balance sheets available in all nations and years. A hierarchical Bayesian model estimated mean food intake and associated uncertainty for each age-sex-country-year stratum, accounting for differences in intakes versus availability, survey methods and representativeness, and sampling and modelling uncertainty.Setting/populationGlobal adult population, by age, sex, country and time.ResultsIn 2010, global fruit intake was 81.3 g/day (95% uncertainty interval 78.9–83.7), with country-specific intakes ranging from 19.2–325.1 g/day; in only 2 countries (representing 0.4% of the world's population), mean intakes met recommended targets of ≥300 g/day. Country-specific vegetable intake ranged from 34.6–493.1 g/day (global mean=208.8 g/day); corresponding values for nuts/seeds were 0.2–152.7 g/day (8.9 g/day); for whole grains, 1.3–334.3 g/day (38.4 g/day); for seafood, 6.0–87.6 g/day (27.9 g/day); for red meats, 3.0–124.2 g/day (41.8 g/day); and for processed meats, 2.5–66.1 g/day (13.7 g/day). Mean national intakes met recommended targets in countries representing 0.4% of the global population for vegetables (≥400 g/day); 9.6% for nuts/seeds (≥4 (28.35 g) servings/week); 7.6% for whole grains (≥2.5 (50 g) servings/day); 4.4% for seafood (≥3.5 (100 g) servings/week); 20.3% for red meats (≤1 (100 g) serving/week); and 38.5% for processed meats (≤1 (50 g) serving/week). Intakes of healthful foods were generally higher and of less healthful foods generally lower at older ages. Intakes were generally similar by sex. Vegetable, seafood and processed meat intakes were stable over time; fruits, nuts/seeds and red meat, increased; and whole grains, decreased.ConclusionsThese global dietary data by nation, age and sex identify key challenges and opportunities for optimising diets, informing policies and priorities for improving global health.

Objective To quantify the cost effectiveness of a government policy combining targeted industry agreements and public education to reduce sodium intake in 183 countries worldwide.Design Global modeling study.Setting 183 countries.Population Full adult population in each country.Intervention A “soft regulation” national policy that combines targeted industry agreements, government monitoring, and public education to reduce population sodium intake, modeled on the recent successful UK program. To account for heterogeneity in efficacy across countries, a range of scenarios were evaluated, including 10%, 30%, 0.5 g/day, and 1.5 g/day sodium reductions achieved over 10 years. We characterized global sodium intakes, blood pressure levels, effects of sodium on blood pressure and of blood pressure on cardiovascular disease, and cardiovascular disease rates in 2010, each by age and sex, in 183 countries. Country specific costs of a sodium reduction policy were estimated using the World Health Organization Noncommunicable Disease Costing Tool. Country specific impacts on mortality and disability adjusted life years (DALYs) were modeled using comparative risk assessment. We only evaluated program costs, without incorporating potential healthcare savings from prevented events, to provide conservative estimates of cost effectivenessMain outcome measure Cost effectiveness ratio, evaluated as purchasing power parity adjusted international dollars (equivalent to the country specific purchasing power of US$) per DALY saved over 10 years.Results Worldwide, a 10% reduction in sodium consumption over 10 years within each country was projected to avert approximately 5.8 million DALYs/year related to cardiovascular diseases, at a population weighted mean cost of I$1.13 per capita over the 10 year intervention. The population weighted mean cost effectiveness ratio was approximately I$204/DALY. Across nine world regions, estimated cost effectiveness of sodium reduction was best in South Asia (I$116/DALY); across the world’s 30 most populous countries, best in Uzbekistan (I$26.08/DALY) and Myanmar (I$33.30/DALY). Cost effectiveness was lowest in Australia/New Zealand (I$880/DALY, or 0.02×gross domestic product (GDP) per capita), although still substantially better than standard thresholds for cost effective (<3.0×GDP per capita) or highly cost effective (<1.0×GDP per capita) interventions. Most (96.0%) of the world’s adult population lived in countries in which this intervention had a cost effectiveness ratio <0.1×GDP per capita, and 99.6% in countries with a cost effectiveness ratio <1.0×GDP per capita.Conclusion A government “soft regulation” strategy combining targeted industry agreements and public education to reduce dietary sodium is projected to be highly cost effective worldwide, even without accounting for potential healthcare savings.

Poor diet is a leading risk factor for cardiometabolic disease (CMD) in the United States, but its economic costs are unknown. We sought to estimate the cost associated with suboptimal diet in the US. A validated microsimulation model (Cardiovascular Disease Policy Model for Risk, Events, Detection, Interventions, Costs, and Trends [CVD PREDICT]) was used to estimate annual cardiovascular disease (fatal and nonfatal myocardial infarction, angina, and stroke) and type 2 diabetes costs associated with suboptimal intake of 10 food groups (fruits, vegetables, nuts/seeds, whole grains, unprocessed red meats, processed meats, sugar-sweetened beverages, polyunsaturated fats, seafood omega-3 fats, sodium). A representative US population sample of individuals aged 35-85 years was created using weighted sampling from National Health And Nutrition Examination Surveys (NHANES) 2009-2012 cycles. Estimates were stratified by cost type (acute, chronic, drug), sex, age, race, education, BMI, and health insurance. Annual diet-related CMD costs were $301/person (95% CI $287-$316). This translates to $50.4 billion in CMD costs (18.2% of total) for the whole population, of which 84.3% are attributed to acute care ($42.6 billion). The largest annual per capita costs are attributed to low consumption of nuts/seeds ($81; 95% CI $74-$86) and seafood omega-3 fats ($76; 95% CI $70-$83), and the lowest are attributed to high consumption of red meat ($3; 95% CI $2.8-$3.5) and polyunsaturated fats ($20; 95% CI $19-$22). Individual costs are highest for men ($380), those aged ≥65 years ($408), blacks ($320), the less educated ($392), and those with Medicare ($481) or dual-eligible ($536) insurance coverage. A limitation of our study is that dietary intake data were assessed from 24-hour dietary recall, which may not fully capture a diet over a person's life span and is subject to measurement errors. Suboptimal diet of 10 dietary factors accounts for 18.2% of all ischemic heart disease, stroke, and type 2 diabetes costs in the US, highlighting that timely implementation of diet policies could address these health and economic burdens.