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Introduction: Produce prescriptions are one of several approaches that have been receiving national attention to increase food security while also improving diet for patients with diet-related health challenges. Implementation of produce prescriptions vary widely, from food vouchers to tailored, pre-arranged weekly home deliveries. Our study focuses on sending weekly curated produce boxes, scaled by family size up to 5 members. We curated 5 different culturally themed boxes for participants to choose from with the ability to change theme at any time throughout the study period. It was our hypothesis that pre-curated, culturally varied boxes would allow to address patient food preferences to assure continued retention. Methods: This produce prescriptions pre-randomized clinical trial is being conducted at Kaiser Permanente Southern California, an integrated health care system with over 4.5M members. Adult members with uncontrolled diabetes with recent Hemoglobin A1c >7.5% or 8% (if >65 years or certain comorbid conditions) were pre-randomized into a high or low-dose (intervention) versus usual care group. Surveys are conducted at 4 different time points (2 and 8-week, 3 and 6 months) for participants pre-randomized to the intervention group. The eight week and 3 months survey that are now completed provide participant feedback on utility and satisfaction of both the food and recipes provided. Results: Recruitment has closed to enrollment; the intervention is slated to end January 2023. There were 150 participants enrolled in each arm for a total 450 participants. The average age at enrollment was 59 years. Over 62% reported currently being unemployed, retired or disabled. Just over half (51%), reported Spanish as their preferred language. Although diabetes was the main eligibility for this study, participants on average had 2-3 additional comorbidities, with 65% also being diagnosed with hypertension and 8.5% having congestive heart failure. Generally, respondents (N=187) considered the foods culturally appropriate with 69% indicating being familiar with the foods delivered and 70% knew how to prepare the foods. Recipes were moderately useful familiarizing participants with new foods (26%). Only 41% reported that of the foods new to them, they would use again in the future. Deliveries could be improved for future with participants overwhelmingly asking for more fruit, vegetables, legumes (98%, 94%, 71%), while also stating diary would be important to add to the deliveries (94%). Overall, 72% of participants reporting being very satisfied with the weekly produce deliveries and 81% stated the food helped them eat healthier throughout the week. Conclusions: Weekly produce deliveries are a promising approach to promote healthier eating providing more variety and autonomy in choices will likely increase use of produce and overall satisfaction in such programs.

Introduction: Previous studies have reported inverse associations of circulating and tissue levels of pentadecanoic acid (15:0), heptadecanoic acid (17:0) and trans -palmitoleic acid ( trans 16:1n-7), which have been proposed as potential biomarkers of dairy fat intake, with risk of type-2 diabetes and certain cardiovascular outcomes. Hypothesis: We assessed the hypothesis that circulating and tissue levels of 15:0, 17:0, trans 16:1n-7 are inversely associated with risk of incident coronary heart disease (CHD) and stroke in a global consortium of prospective studies. Methods: We used data from 15 prospective cohorts in the Fatty Acids and Outcomes Research Consortium. We included adults (age≥18 years) who were free of cardiovascular diseases and had blood or adipose tissue measurements of 15:0, 17:0 or trans 16:1n-7. We used a harmonized analysis protocol with each exposure standardized to the interquintile range (IQR): difference between the 10 th and 90 th percentiles of each fatty acid to conduct new individual participant-level analyses. We harmonized covariate definitions across studies to include demographic, lifestyle and health variables, and levels of other fatty acids associated with CHD or stroke. We used inverse-variance meta-analysis to calculate the pooled relative risks (RR) and 95% confidence intervals (CI) for each outcome. We also calculated Spearman correlation coefficients between levels of each fatty acid exposure and potential dietary determinants of their levels (intakes of total, high-fat and low-fat dairy, meat from ruminant animals, fish and dietary fiber) among 6 studies with dietary data. Results and Conclusions: Among 34,187 participants, 5,790 incident CHD and 3,098 stroke cases were documented during a maximum follow-up of 23.3 years. We did not observe significant associations of any of the fatty acid biomarkers with risk of CHD or stroke. The pooled multivariate RR and 95% CI of CHD per IQR were 0.97 (0.92, 1.02) for 15:0, 0.97 (0.92, 1.02) for 17:0, 1.11 (0.97, 1.26) for trans 16:1n-7, and 0.98 (0.92, 1.04) for the sum of the fatty acids. The respective RR and 95% of stroke were 1.01 (0.93, 1.09) for 15:0, 0.91 (0.81, 1.03) for 17:0, 0.99 (0.83, 1.18) for trans 16:1n-7, and 0.93 (0.85, 1.04) for the summed fatty acids. Additionally, we did not observe significant heterogeneity by age, sex, race/ethnicity, world region, baseline hypertension status or lipid compartment. Circulating and tissue levels of 15:0, 17:0 and trans 16:1n-7 were weakly correlated with intakes of total or high-fat dairy (Spearman correlations [ r = 0.05 to 0.37]) but were not correlated with intakes of low-fat dairy, ruminant meat, fish or dietary fiber [ r = -0.08 to 0.09]. In conclusion, circulating and tissue levels of 15:0, 17:0, trans 16:1n-7 were not associated with risk of CHD or stroke. Our study suggests a limited role for these fatty acids in the etiology of cardiovascular disease.

Background: Diet diversity and quality are each recommended to promote a healthy diet and prevent chronic disease. Yet, little is known on how diet diversity relates to diet quality or cardiometabolic health, particularly in underrepresented subgroups disproportionally affected by poor nutrition and CVD. Aims: To determine relationships of 1) dietary diversity with diet quality, and 2) diet diversity and quality with CVD risk factors (blood pressure, plasma LDL-C, HDL-C, triglycerides, total:HDL ratio, CRP, glucose) in a diverse population of U.S. adults. Methods: We evaluated 21,350 Black and White adults aged ≥45 years in REGARDS. A validated dietary questionnaire at baseline was used to estimate two distinct aspects of diet diversity: food count (no. of food items eaten at least once a week) and dissimilarity (Jaccard distance, capturing diversity of attributes of foods eaten). Diet quality was estimated using the AHA-2020 and AHEI-2010 scores. Cross-sectional associations with CVD risk factors were examined using multivariable linear regression. Results: Food count and dissimilarity each inversely correlated with diet quality scores (r ranging from -0.04 to -0.11). In multivariable models, diet diversity had mixed or mostly null associations with CVD risk factors (See Table). For instance, food count inversely associated with HDL-C and LDL-C; while dissimilarity inversely associated with plasma glucose but positively with triglycerides. In contrast, AHA-2020 and AHEI-2010 were consistently favorably associated with nearly all CVD risk factors. Associations of diet diversity were similar in Blacks and Whites, while most associations of diet quality were stronger among Whites ( P -interaction < 0.0015). Conclusion: Diet diversity metrics were not associated with diet healthfulness or most CVD risk factors among U.S. adults. Our findings support a focus on diet quality, with adequate intake of healthful food groups, rather than diversity, to promote cardiometabolic health.

Background: Evidence for the role of omega-3 fatty acids in the prevention of atrial fibrillation (AF) remain inconsistent, with some recent RCTs even suggesting possible harm. Whether long-term dietary intake of these fatty acids, as assessed using objective biomarkers, is related to AF is not known. Aims: To prospectively evaluate circulating and tissue levels of eicosapentaenoic acid (EPA), docosapentaenoic acid (DPA), docosahexaenoic acid (DHA), and the sum of EPA and DHA (also known as the omega-3 index), with respect to incident AF. Methods: We used data from a global consortium of 13 prospective cohort studies with measurements of EPA, DPA, or DHA in adults (age≥18) identified through March 2021. Participating studies conducted de novo participant-level analyses using a prespecified analytical plan with harmonized definitions for exposures, outcomes, covariates, and subgroups. Associations were pooled using inverse-variance weighted meta-analysis. Results: Among 45,910 participants, a total of 6,229 incident cases of AF were ascertained, with median follow-up ranging from 0.9 to 29.1 years. In the multivariable analysis, per interquintile range (difference between the 90 th and 10 th percentiles for each fatty acid), DPA, DHA, and EPA+DHA ( Figure 1 ) were associated with 11%, 13%, and 9% lower incidence of AF, respectively ( P I 2 ranged from 0% for DPA to 56.7% for EPA+DHA. Associations were broadly consistent irrespective of baseline cardiovascular risk, global region, age, sex, or lipid fraction. Conclusion: Biomarkers of omega-3 fatty acids including DPA, DHA, and EPA+DHA demonstrated an inverse association with incident AF. In the absence of RCTs examining long-term dietary omega-3 intake and AF risk, our results do not suggest that higher levels of these fatty acids are associated with harm.

Background: Sugar-sweetened beverage taxes are a rapidly growing policy tool and can be based on absolute volume, sugar content tiers, or absolute sugar content. Yet, their comparative health and economic impacts have not been quantified, in particular, tiered or sugar content taxes that provide industry incentives for sugar reduction. Methods: We estimated incremental changes in diabetes mellitus and cardiovascular disease, quality-adjusted life-years, costs, and cost-effectiveness of 3 sugar-sweetened beverage tax designs in the United States, on the basis of (1) volume ($0.01/oz), (2) tiers (20 g/8 oz: $0.02/oz), and (3) absolute sugar content ($0.01 per teaspoon added sugar), each compared with a base case of modest ongoing voluntary industry reformulation. A validated microsimulation model, CVD-PREDICT (Cardiovascular Disease Policy Model for Risk, Events, Detection, Interventions, Costs, and Trends), incorporated national demographic and dietary data from the National Health and Nutrition Examination Survey, policy effects and sugar-sweetened beverage-related diseases from meta-analyses, and industry reformulation and health-related costs from established sources. Results: Over a lifetime, the volume, tiered, and absolute sugar content taxes would generate $80.4 billion, $142 billion, and $41.7 billion in tax revenue, respectively. From a healthcare perspective, the volume tax would prevent 850 000 cardiovascular disease (95% CI, 836 000–864 000) and 269 000 diabetes mellitus (265 000–274 000) cases, gain 2.44 million quality-adjusted life-years (2.40–2.48), and save $53.2 billion net costs (52.3–54.1). Health gains and savings were approximately doubled for the tiered and absolute sugar content taxes. Results were robust for societal and government perspectives, at 10 years follow-up, and with lower (50%) tax pass-through. Health gains were largest in young adults, blacks and Hispanics, and lower-income Americans. Conclusions: All sugar-sweetened beverage tax designs would generate substantial health gains and savings. Tiered and absolute sugar content taxes should be considered and evaluated for maximal potential gains.

Introduction: Findings on MRI of vascular brain injury, such as brain infarcts and white matter hyperintensities, are chronic manifestation of atherosclerosis. A gut-microbiome-generated metabolite, trimethylamine N-oxide (TMAO), is an independent predictor of clinical cardiovascular events. However, no study has examined associations between TMAO and subclinical vascular brain injury in the general population. Hypothesis: TMAO levels are positively associated with evidence of progressive subclinical vascular brain injury on serial MRI scans with incident brain infarcts and white matter worsening. Methods: The Cardiovascular Health Study (CHS) is a community-based prospective cohort study in adults aged >65 years. Plasma TMAO was measured using mass spectrometry from samples collected in 1992-1993 and 1996-1997. Brain MRI was performed at 1991-1994 and again at 1997-1999. White matter was graded on a 10-point scale, higher being worse, and white matter worsening (WMW) was defined by an increase of least one point comparing initial and follow up scans. In these analyses, participants with prior TIA or stroke were excluded. Those with serum TMAO and both MRI scans were included: n=1196 for incident brain infarct and n=1553 for white matter worsening. Logistic regression was used for the association of baseline TMAO levels and incident brain infarcts, and Poisson regression, for the change in TMAO levels and WMW. Models were adjusted for age, sex, race, alcohol use, intake of meat and vegetable, and vascular risk factors. Results: Between the two MRI scans, 191(15.9%) participants had subclinical incident brain infarcts, and 423 (27.2%) participants had WMW. Comparing the highest vs. lowest quartile, the first TMAO were not significantly associated with incident brain infarcts: odds ratio 0.78 (95% CI: 0.49 to 1.25). Again comparing the highest vs. lowest quartile, changes in TMAO were not associated with WMW: 1.08 (0.77 to 1.51). Conclusions: Baseline and changes in plasma TMAO levels were not associated with findings of subclinical vascular brain injury on MRI in older US adults. The associations of TMAO with the adverse clinical events seen in prior clinical samples of patients were not seen at the subclinical level in our population-based study.

Background: High intake of added sugar is linked to weight gain and cardiometabolic risk. In 2018, the US National Salt and Sugar Reduction Initiative proposed government-supported voluntary national sugar reduction targets. This intervention’s potential effects and cost-effectiveness are unclear. Methods: A validated microsimulation model, CVD-PREDICT (Cardiovascular Disease Policy Model for Risk, Events, Detection, Interventions, Costs, and Trends), coded in C++, was used to estimate incremental changes in type 2 diabetes, cardiovascular disease (CVD), quality-adjusted life-years (QALYs), costs, and cost-effectiveness of the US National Salt and Sugar Reduction Initiative policy. The model was run at the individual level, incorporating the annual probability of each person’s transition between health statuses on the basis of risk factors. The model incorporated national demographic and dietary data from the National Health and Nutrition Examination Survey across 3 cycles (2011 through 2016), added sugar-related diseases from meta-analyses, and policy costs and health-related costs from established sources. A simulated nationally representative US population was created and followed until age 100 years or death, with 2019 as the year of intervention start. Findings were evaluated over 10 years and a lifetime from health care and societal perspectives. Uncertainty was evaluated in a 1-way analysis by assuming 50% industry compliance and probabilistic sensitivity analyses through a second-order Monte Carlo approach. Model outputs included averted diabetes cases, CVD events and CVD deaths, QALYs gained, and formal health care cost savings, stratified by age, race, income, and education. Results: Achieving the US National Salt and Sugar Reduction Initiative sugar reduction targets could prevent 2.48 million CVD events, 0.49 million CVD deaths, and 0.75 million diabetes cases; gain 6.67 million QALYs; and save $160.88 billion net costs from a societal perspective over a lifetime. The policy became cost-effective ( Conclusions: Implementing and achieving the US National Salt and Sugar Reduction Initiative sugar reformation targets could generate substantial health gains, equity gains, and cost savings.

Background: Biomarker levels of very long-chain saturated fatty acids (VLCSFAs) have been found to be favorably associated with cardiovascular risk factors including lower risk of diabetes and reduced triglycerides. Few studies have examined the association between VLCSFAs and coronary heart disease (CHD). Aims: To assess the association of circulating arachidic acid (20:0), behenic acid (22:0), and lignoceric acid (24:0) with incident total, fatal, and nonfatal CHD. Methods: We used data from the Fatty Acids and Outcomes Research Consortium consisting of 15 prospective cohorts worldwide which included adults (age≥18 years) who were free of cardiovascular disease and had blood measurements of 20:0, 22:0, and 24:0 at baseline. A study protocol with standardized definitions of exposures, disease outcomes, and covariates was developed, for which each cohort conducted individual participant-level analysis. Cohort-specific associations were pooled using inverse variance-weighted meta-analysis to calculate the overall relative risk (RR) per interquintile range (difference between the 90 th and 10 th percentiles) and 95% confidence interval (CI). Results: Among 33,083 participants, 6,165 cases of total CHD were ascertained. The overall pooled RR and 95% CI were 0.96 (0.89, 1.02) for 20:0, 1.01 (0.92, 1.11) for 22:0, 0.94 (0.86, 1.02) for 24:0, and 0.96 (0.89, 1.04) for 20:0 + 22:0 + 24:0 ( Figure 1 ). However, we noted heterogeneity by lipid compartments, with significant inverse associations for higher 22:0 [0.77 (0.62, 0.96)], 24:0 [0.61 (0.49, 0.77)], and 20:0 + 22:0 + 24:0 [0.73 (0.60, 0.89)] in the total plasma/serum compartment but not in the phospholipid compartment. Similar associations were observed for fatal and nonfatal CHD and when using a random-effects model. Conclusion: Higher circulating VLCSFAs were not associated with total CHD in a global consortium of prospective studies. The finding of an inverse association with total CHD for VLCSFAs in the total plasma/serum compartment warrants further research.

Background: Several recent studies have linked higher blood levels of the long-chain omega-3 polyunsaturated fatty acids (PUFAs) with lower risk of certain disease outcomes, in particular cardiovascular disease (CVD). Limited studies have evaluated associations between n-3 PUFA levels and total and cause-specific mortality. Methods: We meta-analyzed the association of circulating omega-3 PUFAs with total and cause-specific mortality from 15 distinct cohorts in 10 countries following a total of 36,840 individuals (baseline average age 66 yrs; 47% female; median follow-up 13.7 yrs), with 11,635 deaths. Total mortality, and 3 cause-specific mortalities (CVD, cancer or other), were separately predicted by levels of the long chain omega-3 PUFAs eicosapentaenoic acid (EPA), docosapentaenoic acid (DPA), docosahexaenoic acid (DHA) and the Omega-3 index (EPA+DHA), as well as levels of alpha-linolenic acid (ALA, an intermediate chain n-3 PUFA). Using cohort-specific fatty acid levels (range from 10 th to 90 th percentiles), each cohort fit a Cox regression model adjusting for demographics, health related covariates, and n-6 PUFA levels. Cohort-specific estimates were pooled with inverse-variance weighted meta-analysis. Results: Higher levels of EPA, DPA, DHA and the Omega-3 index were all associated with lower all-cause mortality [EPA meta-analysis Hazard Ratio (HR)=0.90 (95% CI: 0.85, 0.95), DPA HR=0.84 (95% CI: 0.77, 0.91), DHA HR=0.84 (95% CI: 0.75, 0.93), Omega-3 index HR = 0.84 (95% CI 0.77, 0.92) (Figure)], as well as for each cause-specific mortality (CVD, cancer and other; HRs from 0.85 to 0.92). ALA showed no association with total-mortality or cause-specific mortality [HRs from 0.97 to 1.00)]. Conclusions: We have found strong evidence of inverse associations between long-chain omega-3 PUFA levels and all-cause and cause-specific mortality. Further controlled studies are needed in order to determine the extent to which these observations represent a causal or coincidental relationships.

Each decade, the American Heart Association (AHA) develops an Impact Goal to guide its overall strategic direction and investments in its research, quality improvement, advocacy, and public health programs. Guided by the AHA’s new Mission Statement, to be a relentless force for a world of longer, healthier lives, the 2030 Impact Goal is anchored in an understanding that to achieve cardiovascular health for all, the AHA must include a broader vision of health and well-being and emphasize health equity. In the next decade, by 2030, the AHA will strive to equitably increase healthy life expectancy beyond current projections, with global and local collaborators, from 66 years of age to at least 68 years of age across the United States and from 64 years of age to at least 67 years of age worldwide. The AHA commits to developing additional targets for equity and well-being to accompany this overarching Impact Goal. To attain the 2030 Impact Goal, we recommend a thoughtful evaluation of interventions available to the public, patients, providers, healthcare delivery systems, communities, policy makers, and legislators. This presidential advisory summarizes the task force’s main considerations in determining the 2030 Impact Goal and the metrics to monitor progress. It describes the aspiration that these goals will be achieved by working with a diverse community of volunteers, patients, scientists, healthcare professionals, and partner organizations needed to ensure success.

Background: Global dietary recommendations for and cardiovascular effects of linoleic acid, the major dietary omega-6 fatty acid, and its major metabolite, arachidonic acid, remain controversial. To address this uncertainty and inform international recommendations, we evaluated how in vivo circulating and tissue levels of linoleic acid (LA) and arachidonic acid (AA) relate to incident cardiovascular disease (CVD) across multiple international studies. Methods: We performed harmonized, de novo, individual-level analyses in a global consortium of 30 prospective observational studies from 13 countries. Multivariable-adjusted associations of circulating and adipose tissue LA and AA biomarkers with incident total CVD and subtypes (coronary heart disease, ischemic stroke, cardiovascular mortality) were investigated according to a prespecified analytic plan. Levels of LA and AA, measured as the percentage of total fatty acids, were evaluated linearly according to their interquintile range (ie, the range between the midpoint of the first and fifth quintiles), and categorically by quintiles. Study-specific results were pooled using inverse-variance–weighted meta-analysis. Heterogeneity was explored by age, sex, race, diabetes mellitus, statin use, aspirin use, omega-3 levels, and fatty acid desaturase 1 genotype (when available). Results: In 30 prospective studies with medians of follow-up ranging 2.5 to 31.9 years, 15 198 incident cardiovascular events occurred among 68 659 participants. Higher levels of LA were significantly associated with lower risks of total CVD, cardiovascular mortality, and ischemic stroke, with hazard ratios per interquintile range of 0.93 (95% CI, 0.88–0.99), 0.78 (0.70–0.85), and 0.88 (0.79–0.98), respectively, and nonsignificantly with lower coronary heart disease risk (0.94; 0.88–1.00). Relationships were similar for LA evaluated across quintiles. AA levels were not associated with higher risk of cardiovascular outcomes; in a comparison of extreme quintiles, higher levels were associated with lower risk of total CVD (0.92; 0.86–0.99). No consistent heterogeneity by population subgroups was identified in the observed relationships. Conclusions: In pooled global analyses, higher in vivo circulating and tissue levels of LA and possibly AA were associated with lower risk of major cardiovascular events. These results support a favorable role for LA in CVD prevention.

Background: Effects of omega-3 fatty acids on the prevention of type 2 diabetes (T2D) are unclear. Relatively few prospective studies have utilized objective omega-3 biomarkers to assess risk. Aims: To assess the prospective relationship between circulating and tissue levels of alpha linoleic acid (ALA), eicosapentaenoic acid (EPA), docosapentaenoic acid (DPA), and docosahexaenoic acid (DHA), with respect to risk of T2D. Methods: A global consortium of 20 prospective cohort studies from 14 nations with assessments of ALA, EPA, DPA, or DHA in adults (age > 18 years) were identified through July 2017 and included in this investigation. A pre-specified analytic protocol, including definitions for exposures, covariate list, disease outcome definitions, and subgroup analyses was developed and followed in new participant-level cohort analysis. Associations were pooled using inverse variance-weighted meta-analysis. Results: Among 65,147 participants, 16,693 incident cases of T2D occurred during follow-up (median follow-up in the cohorts ranged from 2.5 to 21.2 years). In pooled multivariate analysis, per interquintile range (difference between the midpoints of the first and fifth quintile for each fatty acid), EPA, DPA, DHA, and their sum ( Figure 1 ) were associated with 8%, 21%, 18%, and 19% lower risk of T2D, respectively (all P Conclusion: Higher circulating and tissue biomarkers of seafood-derived omega-3 fatty acids, EPA, DPA, and DHA, were associated with lower risk of T2D in a global consortium of prospective studies. Plant-derived ALA was not significantly associated with risk.

Introduction: Replacement of regular salt (NaCl) with potassium-based salt substitutes is a promising strategy to reduce blood pressure (BP) and prevent cardiovascular disease (CVD), especially in countries like China with high discretionary salt intake and low potassium intake. However, benefits of this strategy remain uncertain, and the risks of hyperkalemia and increased CVD mortality in persons with chronic kidney disease (CKD) are a concern. Hypothesis: In China, the estimated benefits of nationwide potassium-based salt substitution on CVD mortality will exceed potential risks. Methods: We used a comparative risk assessment framework to estimate potential benefits and risks of nationwide replacement of discretionary salt with potassium-based salt substitute (30±10% KCl) on CVD mortality in China. We incorporated existing data and corresponding uncertainties from randomized trials, the China National Survey of CKD, the Global Burden of Disease, and the CKD Prognosis Consortium ( Table ). We estimated averted CVD deaths from reduced BP subsequent to salt substitution in the adult population (benefits), and CVD deaths attributed to hyperkalemia from salt substitution in CKD patients (risks). Results: A nationwide implementation of potassium-based salt substitution in China, could prevent ~400,000 CVD deaths/year through BP lowering in the adult population, and increase ~10,000 CVD deaths/year through hyperkalemia among CKD patients (Table). For each additional death in CKD patients, around 40 CVD deaths could be averted in the adult population. Overall, the intervention could result in 369,258 (95% uncertainty interval: 160,702-576,680) net fewer deaths each year, corresponding to 9.4% (4.1-14.7) of annual CVD deaths in China. Conclusions: A nationwide potassium-based salt substitution in China could result in significant net benefits, preventing about 1 in 10 CVD deaths. Strategies to avoid potential hyperkalemic deaths among CKD patients could further improve the benefit:risk ratio.

Background: Polyunsaturated fatty acids (PUFA) are essential nutrients for normal brain function, constituting nearly 35% of brain lipids. Experimental studies suggest that omega-3 and omega-6 PUFA, present in plant foods and fish, may reduce risk of dementia. Most prior studies assessed self-reported estimates and used one baseline measure of objective PUFA biomarkers, which may lead to poor estimation of long-term risk. Aims: Investigate prospective associations of serial measures of plasma phospholipid omega-3 (ALA [18:3], EPA [20:5], DPA [22:5], DHA [22:6]) and omega-6 (LA [18:2], AA [20:4]) PUFA with risk of total dementia and dementia subtypes (Alzheimer’s Disease [AD] and vascular and mixed dementia [VaD]) in older adults in the Cardiovascular Health Study. Methods: Among 3,307 U.S. adults aged ≥65y and free of stroke, cognitive impairment or dementia at baseline, circulating levels were measured serially at baseline, 6 years and 13 years using standardized methods. Dementia was identified using neuropsychological tests or hospitalization records adjudicated by CHS Cognition Study investigators, and by ICD-9 codes from linked Medicare administrative data. Prospective associations were assessed by multivariate-adjusted Cox models incorporating time-varying fatty acid measures and covariates. Results: During 22,288 person-years of follow-up (1992-2015), 1,164 dementia cases were identified, with 530 AD and 256 VaD cases. After adjustment for demographic, lifestyle and dietary factors, higher circulating levels of AA were associated with lower risk of total dementia and AD (see Table). There were no statistically significant associations between circulating omega-3 PUFA or LA and incident dementia. Conclusion: In older adults, higher circulating AA was inversely associated with risk of total dementia and AD, but not other dementia subtypes. These findings highlight the need to identify mechanisms influencing circulating AA levels that could be effective for the prevention of dementia later in life.

“Eat a variety of foods,” or dietary diversity, is a widely accepted recommendation to promote a healthy, nutritionally adequate diet and to reduce the risk of major chronic diseases. However, recent evidence from observational studies suggests that greater dietary diversity is associated with suboptimal eating patterns, that is, higher intakes of processed foods, refined grains, and sugar-sweetened beverages and lower intakes of minimally processed foods, such as fish, fruits, and vegetables, and may be associated with weight gain and obesity in adult populations. This American Heart Association science advisory summarizes definitions for dietary diversity and reviews current evidence on its relationship with obesity outcomes, eating behavior, and food-based diet quality measures. Current data do not support greater dietary diversity as an effective strategy to promote healthy eating patterns and healthy body weight. Given the current state of the science on dietary diversity and the insufficient data to inform recommendations on specific aspects of dietary diversity that may be beneficial or detrimental to healthy weight, it is appropriate to promote a healthy eating pattern that emphasizes adequate intake of plant foods, protein sources, low-fat dairy products, vegetable oils, and nuts and limits consumption of sweets, sugar-sweetened beverages, and red meats.

Background— In prospective studies, the relationship of self-reported consumption of dairy foods with risk of diabetes mellitus is inconsistent. Few studies have assessed dairy fat, using circulating biomarkers, and incident diabetes mellitus. We tested the hypothesis that circulating fatty acid biomarkers of dairy fat, 15:0, 17:0, and t-16:1n-7, are associated with lower incident diabetes mellitus. Methods and Results— Among 3333 adults aged 30 to 75 years and free of prevalent diabetes mellitus at baseline, total plasma and erythrocyte fatty acids were measured in blood collected in 1989 to 1990 (Nurses’ Health Study) and 1993 to 1994 (Health Professionals Follow-Up Study). Incident diabetes mellitus through 2010 was confirmed by a validated supplementary questionnaire based on symptoms, diagnostic tests, and medications. Risk was assessed by using Cox proportional hazards, with cohort findings combined by meta-analysis. During mean±standard deviation follow-up of 15.2±5.6 years, 277 new cases of diabetes mellitus were diagnosed. In pooled multivariate analyses adjusting for demographics, metabolic risk factors, lifestyle, diet, and other circulating fatty acids, individuals with higher plasma 15:0 had a 44% lower risk of diabetes mellitus (quartiles 4 versus 1, hazard ratio, 0.56; 95% confidence interval, 0.37–0.86; P -trend=0.01); higher plasma 17:0, 43% lower risk (hazard ratio, 0.57; 95% confidence interval, 0.39–0.83; P -trend=0.01); and higher t-16:1n-7, 52% lower risk (hazard ratio, 0.48; 95% confidence interval, 0.33–0.70; P -trend Conclusions— In 2 prospective cohorts, higher plasma dairy fatty acid concentrations were associated with lower incident diabetes mellitus. Results were similar for erythrocyte 17:0. Our findings highlight the need to better understand the potential health effects of dairy fat, and the dietary and metabolic determinants of these fatty acids.

Background— Accurate forecasting of cardiovascular disease mortality is crucial to guide policy and programming efforts. Prior forecasts often have not incorporated past trends in rates of reduction in cardiovascular disease mortality. This creates uncertainties about future trends in cardiovascular disease mortality and disparities. Methods and Results— To forecast US cardiovascular disease mortality and disparities to 2030, we developed a hierarchical bayesian model to determine and incorporate prior age, period, and cohort effects from 1979 to 2012, stratified by age, sex, and race, which we combined with expected demographic shifts to 2030. Data sources included the National Vital Statistics System, Surveillance, Epidemiology, and End Results (SEER) single-year population estimates, and US Bureau of Statistics 2012 national population projections. We projected coronary disease and stroke deaths to 2030, first on the basis of constant age, period, and cohort effects at 2012 values, as is most commonly done (conventional), and then with the use of more rigorous projections incorporating expected trends in age, period, and cohort effects (trend based). We primarily evaluated absolute mortality. The conventional model projected total coronary and stroke deaths by 2030 to increase by ≈18% (67 000 additional coronary deaths per year) and 50% (64 000 additional stroke deaths per year). Conversely, the trend-based model projected that coronary mortality would decrease by 2030 by ≈27% (79 000 fewer deaths per year) and stroke mortality would remain unchanged (200 fewer deaths per year). Health disparities will be improved in stroke deaths but not coronary deaths. Conclusions— After prior mortality trends and expected demographic shifts are accounted for, total US coronary deaths are expected to decline, whereas stroke mortality will remain relatively constant. Health disparities in stroke but not coronary deaths will be improved but not eliminated. These age, period, and cohort approaches offer more plausible predictions than conventional estimates.

Author(s): Writing Group Members; Mozaffarian, Dariush; Benjamin, Emelia J; Go, Alan S; Arnett, Donna K; Blaha, Michael J; Cushman, Mary; Das, Sandeep R; de Ferranti, Sarah; Despres, Jean-Pierre; Fullerton, Heather J; Howard, Virginia J; Huffman, Mark D; Isasi, Carmen R; Jimenez, Monik C; Judd, Suzanne E; Kissela, Brett M; Lichtman, Judith H; Lisabeth, Lynda D; Liu, Simin; Mackey, Rachel H; Magid, David J; McGuire, Darren K; Mohler, Emile R; Moy, Claudia S; Muntner, Paul; Mussolino, Michael E; Nasir, Khurram; Neumar, Robert W; Nichol, Graham; Palaniappan, Latha; Pandey, Dilip K; Reeves, Mathew J; Rodriguez, Carlos J; Rosamond, Wayne; Sorlie, Paul D; Stein, Joel; Towfighi, Amytis; Turan, Tanya N; Virani, Salim S; Woo, Daniel; Yeh, Robert W; Turner, Melanie B; American Heart Association Statistics Committee; Stroke Statistics Subcommittee

Suboptimal nutrition is a leading cause of poor health. Nutrition and policy science have advanced rapidly, creating confusion yet also providing powerful opportunities to reduce the adverse health and economic impacts of poor diets. This review considers the history, new evidence, controversies, and corresponding lessons for modern dietary and policy priorities for cardiovascular diseases, obesity, and diabetes mellitus. Major identified themes include the importance of evaluating the full diversity of diet-related risk pathways, not only blood lipids or obesity; focusing on foods and overall diet patterns, rather than single isolated nutrients; recognizing the complex influences of different foods on long-term weight regulation, rather than simply counting calories; and characterizing and implementing evidence-based strategies, including policy approaches, for lifestyle change. Evidence-informed dietary priorities include increased fruits, nonstarchy vegetables, nuts, legumes, fish, vegetable oils, yogurt, and minimally processed whole grains; and fewer red meats, processed (eg, sodium-preserved) meats, and foods rich in refined grains, starch, added sugars, salt, and trans fat. More investigation is needed on the cardiometabolic effects of phenolics, dairy fat, probiotics, fermentation, coffee, tea, cocoa, eggs, specific vegetable and tropical oils, vitamin D, individual fatty acids, and diet-microbiome interactions. Little evidence to date supports the cardiometabolic relevance of other popular priorities: eg, local, organic, grass-fed, farmed/wild, or non–genetically modified. Evidence-based personalized nutrition appears to depend more on nongenetic characteristics (eg, physical activity, abdominal adiposity, gender, socioeconomic status, culture) than genetic factors. Food choices must be strongly supported by clinical behavior change efforts, health systems reforms, novel technologies, and robust policy strategies targeting economic incentives, schools and workplaces, neighborhood environments, and the food system. Scientific advances provide crucial new insights on optimal targets and best practices to reduce the burdens of diet-related cardiometabolic diseases.

Since the 2002 American Heart Association scientific statement “Fish Consumption, Fish Oil, Omega-3 Fatty Acids, and Cardiovascular Disease,” evidence from observational and experimental studies and from randomized controlled trials continues to emerge to further substantiate the beneficial effects of seafood long-chain n-3 polyunsaturated fatty acids and cardiovascular disease. A recent American Heart Association science advisory addressed the specific effect of n-3 polyunsaturated fatty acid supplementation on clinical cardiovascular events. This American Heart Association science advisory extends that review and offers further support to include n-3 polyunsaturated fatty acids from seafood consumption. Several potential mechanisms have been investigated, including antiarrhythmic, anti-inflammatory, hematologic, and endothelial, although for most, longer-term dietary trials of seafood are warranted to substantiate the benefit of seafood as a replacement for other important sources of macronutrients. The present science advisory reviews this evidence and makes a suggestion in the context of the 2015–2020 Dietary Guidelines for Americans and in consideration of other constituents of seafood and the impact on sustainability. We conclude that 1 to 2 seafood meals per week be included to reduce the risk of congestive heart failure, coronary heart disease, ischemic stroke, and sudden cardiac death, especially when seafood replaces the intake of less healthy foods.

Introduction: Unhealthful diet is one of the top contributors to the chronic disease burden in the U.S. There are growing concerns that socioeconomic disparities exist in Americans’ diets and this disparity may have widened over time. Aim: To characterize trends in dietary intake of key food groups and nutrients among low-income Americans who participated in the Supplemental Nutrition Assistance Program (SNAP), and assess whether disparities in U.S. diets have persisted, improved, or worsened over time. Methods: Nationally representative sample of 6,162 adults aged 20 years or older who participated in SNAP, 6,692 income-eligible nonparticipants, and 25,842 higher-income nonparticipants from 8 National Health and Nutrition Examination Survey (NHANES) cycles (1999-2014). Exposures are calendar year and SNAP participation status. Survey-weighted, energy-adjusted mean scores and proportion meeting the American Heart Association (AHA) 2020 Strategic Impact Diet Goals (5 primary components: fruits/vegetables, whole grains, fish/shellfish, sugar-sweetened beverages (SSBs), sodium; 3 secondary components: nuts/seeds/legumes, processed meats, saturated fat). Intakes of individual food groups and nutrients were also assessed. Results: From 2003-2004 to 2013-2014 among SNAP participants with data on two-day dietary recall, primary diet score (maximum of 50) modestly increased (15.6 to 16.6; P-trend =0.03) while the secondary diet score (maximum of 80 points) did not change (31.5 to 32.1; P-trend =0.11). The proportion of SNAP participants having a poor diet decreased from 74.3% to 68.6%, the proportion having an intermediate-quality diet increased from 25.5% to 31.2%, and the proportion of having an ideal diet remained unchanged (0.2%.). Among primary components, changes were strongest for SSBs (-0.43 servings/d, P-trend=0.001) and whole grains (+0.25 servings/d, P-trend nonparticipants, SNAP participants had weaker improvements in both primary and secondary diet scores. From 1999-2000 to 2013-2014, disparities persisted for most dietary components, worsened for nuts/seeds and added sugars, and weakened for sodium. Conclusion: Despite some improvements in diet quality, SNAP participants still fall far short of meeting the AHA Goals for a healthful diet, and dietary disparities persisted or worsened for most dietary components.

Introduction: Despite the clear association between poor diet and cardiometabolic diseases (CMD) and the overall economic burden of such conditions, the costs of an unhealthy diet pattern have not been assessed for the US population. Aim: Estimate the costs of CMD related to suboptimal intakes of 10 specific dietary factors in the US adult population. Methods: A validated microsimulation model (CVD PREDICT) was populated by weighted sampling (with replacement) of individuals aged 35–85y from the 2009-2010 and 2011-2012 National Health and Nutrition Examination Surveys (NHANES), in order to create an US representative model population. Consumption of 10 foods/nutrients associated with CMD were assessed: fruits, vegetables, nuts/seeds, whole grains, unprocessed red meats, processed meats, sugar-sweetened beverages, polyunsaturated fats, seafood omega-3 fats, and sodium. Cardiovascular disease progression and events were simulated and annual healthcare costs estimations were calculated. The model compared reported consumption of the 10 food/nutrients in the NHANES surveys to a hypothetical situation in which the consumption level of these nutrients were optimal. Each food/nutrient was assessed individually and combined. Estimates were stratified by gender, age, race and insurance. Results: The 2012 annual cost of an unhealthy diet was $USD 280 (Acute $USD 236, Chronic $USD 40 and Drug $USD 4) per adult. Individually the food/nutrient consumed below optimal levels that imposed the highest CMD economic burden was nuts/seeds ($USD 75) while non-optimal red meat consumption was associated with the lowest cost per person ($USD 3). Unhealthy diet costs of CMD by gender, age group, race and insurance are provided in table 1. The annual unhealthy diet cost of CMD in the US was $USD 44.9bn in 2012. Acute care costs represent 84.3% of this total ($USD 37.9bn). Conclusions: Suboptimal diet accounts for substantial CMD costs in the US, highlighting the need for timely implementation of diet policies to address these burdens.

Introduction: Taxes on sugar-sweetened beverage (SSB) purchases have emerged as a policy tool to lower obesity, diabetes and CVD risks. Prior cost-effectiveness analyses included SSB tax administration costs yet ignored tax payments as mere transfers from a societal perspective. Yet, tax payments could count as revenues for the government and as costs for consumers and the SSB industry. Corresponding health and economic impacts for different stakeholders, essential to guide decision-making, are not established. Aim: To estimate the health impact and cost-effectiveness of a national penny-per-ounce SSB tax from the healthcare perspective, societal perspective, and across 9 stakeholder groups: 6 consumer categories classified by insurance status (and reflecting varying SSB intake and risk factors), the government, the beverage industry, and other private sector. Methods: A validated microsimulation model (CVD PREDICT) was used to estimate CVD reductions, quality-adjusted life-years (QALYs) gained, costs, and cost-effectiveness among US adults (35+ years), evaluating both 100% and 50% price pass-through to consumers. Model inputs included dietary and demographic data from NHANES, policy effects on consumer intake and SSB-disease effects from meta-analyses, policy costs for tax administration based on the Berkeley tax, and validated healthcare costs. Findings were evaluated over a lifetime, with costs inflated to constant 2017 US dollars and outcomes discounted annually by 3%. Results: With 100% pass-through, the tax prevented 518,000 CVD events among US adults 35+ years over a lifetime and was cost-saving from a societal perspective. Lifetime discounted healthcare cost savings ($31.5bn) were 24 times as large as tax implementation costs ($1.3bn). Evaluating cost-effectiveness by stakeholder, for the 6 consumer categories, the tax was not cost saving, but incremental cost-effectiveness ratios (ICERs) each were Conclusions: A national SSB tax would improve health and be cost-saving nationally, with varying health impacts and costs across major stakeholders. These novel findings are relevant and timely for policy decisions on continuing expansion of SSB taxes.

Introduction: The 2018 Farm Bill represents a major opportunity to reduce disparities in diet and health. The largest component is the Supplemental Nutrition Assistance Program (SNAP), feeding 1 in 6 Americans. Potential options include subsidizing fruits & vegetables (F&V), restricting sugar-sweetened beverages (SSBs), or implementing a broader food incentive/disincentive framework that preserves choice. Their comparative health impacts and cost-effectiveness are not established. Methods: Using a validated microsimulation model (CVD PREDICT), we estimated changes in CVD events, quality-adjusted life-years (QALYs), costs, and cost-effectiveness of 3 policy scenarios in SNAP adults: 1) 30% subsidy on F&V; 2) 30% F&V subsidy + SSB restriction; and 3) 30% subsidy on F&V, whole grains, nuts/seeds, seafood, plant-based oils, and 30% disincentive on SSBs, junk food, and processed meats. Model inputs included national data from NHANES (2009-2014), policy effects from SNAP pilots and food pricing meta-analyses, diet-disease effects from meta-analyses, and policy, food subsidy, and healthcare costs. Results: From a societal perspective, all 3 scenarios were cost-savings at 5, 10, 20 y and lifetime ( Table ). At 5 y, a F&V subsidy would prevent 32,218 CVD events, gain 18,072 QALYs, and save $1.04B ($6.05B lifetime). Corresponding values for a F&V subsidy + SSB restriction were 63,898, 45,772, and $4.47B ($38.83B); and for a broader incentive/disincentive framework that preserved choice, 65,078, 26,663, and $3.98B ($29.90B). Government affordability varied by program duration and by whether subsidy costs for SNAP adults or all SNAP participants were included. Scenario 3 was generally most cost-effective or -saving, followed by scenario 2 and then scenario 1; all were cost-effective over a lifetime from a government affordability perspective. Conclusions: Financial incentives/disincentives through SNAP could generate substantial health benefits and be cost-effective or cost savings.

De novo lipogenesis (DNL) is a crucial metabolic pathway that convert excess carbohydrates to fatty acids (FA) for energy and storage. Both DNL and the synthesized FA have biologic effects that may affect cardiometabolic risk. Yet, the association between DNL FA and mortality and CVD are not well-established in older adults, especially using serial biomarkers which objectively allow more accurate estimates of long-term FA exposure, as well as changes over time. We investigated the longitudinal association between serial levels of circulating DNL FA and total mortality, cause-specific mortality, and total CVD among 3,869 older U.S. adults (mean age 75 y) free of prevalent CVD at baseline. Levels of plasma phospholipid palmitic (16:0), palmitoleic (16:1n-7), stearic (18:0), and oleic acid (18:1n-9) were quantified at baseline, year 6, and year 13. Outcomes were centrally adjudicated using multiple sources. Risk was assessed in multivariable-adjusted Cox models with time-varying FA and covariates. During 46,974 person-years, 3,227 deaths (including 1,131 from CVD, 2,096 from non-CVD causes) and 1,754 incident total CVD events occurred. After multivariable-adjustment, cumulative levels of 16:0, 16:1n-7 and 18:1n-9 were each positively, while 18:0 was inversely, associated with total mortality ( Table ). Associations were generally similar for CVD vs. non-CVD mortality, and vs. total incident CVD (not shown). Among non-CVD deaths, associations for dementia and pulmonary deaths were generally similar to total mortality; while only 16:0 and 18:1n-9 were positively associated with cancer mortality. Higher long-term levels of circulating 16:0, 16:1n-7 and 18:1n-9 were positively, while 18:0 was inversely, associated with total mortality in older adults. Novel findings highlight the potential relevance of DNL later in life, and the need for further experimental research and interventions on the relevant underlying physiology and long-term health effects of DNL FA. Findings for FA changes over time to be presented.

Background: Sodium consumption is a leading modifiable risk factor for CVD mortality and morbidity in the US. In 2016, the US Food and Drug Administration (FDA), following recent effective examples in several other countries, proposed voluntary sodium targets for industry to reduce sodium in processed foods. Aim: We aimed to estimate the potential CVD, equity and economic impacts of implementing this policy. Methods: We used the validated US IMPACT Food Policy microsimulation model to estimate the CVD cases averted, quality-adjusted life-years (QALYs) gained and cost-effectiveness from 2017-2036 of the FDA sodium reformulation policy in US adults (30+ years). Model inputs included national demographics and sodium intakes from NHANES, FDA short- and long-term sodium reformulation targets, sodium effects on blood pressure and of blood pressure on CVD from meta-analyses, government costs to administer and monitor the policy and industry reformulation costs, and validated healthcare and productivity costs. We modelled 3 scenarios: a) Optimal, 100% compliance of 10-year reformulation targets b) Modest, 50% compliance of 10-year reformulation targets c) Pessimistic, 100% compliance of 2-year reformulation targets with no further progress Costs were inflated to 2017 US dollars and outputs were discounted annually by 3%. We took a societal perspective for this analysis. Rigorous probabilistic sensitivity analyses were conducted. Results: The optimal scenario achieving the 10-year sodium reduction targets could prevent ~ 450,000 CVD cases (95% Uncertainty Interval: 240,000-740,000), gain 2.1 million QALYs (1.7m-2.4m), and produce $41billion ($14bn-$81bn) cost-savings from 2017-2036. The modest and pessimistic scenarios were also cost-saving, with both health gains and savings about one half and one quarter, respectively, of the optimal scenario. Relative disparities between non-Hispanic white and non-Hispanic black populations would be reduced in all scenarios. The pessimistic scenario yielded the largest reduction in absolute disparities (70,000 CVD cases (33,000-120,000) prevented in non-Hispanic blacks vs. 13,000 (0-54,000) in non-Hispanic whites). The optimal scenario would prevent approximately 4.6% (130,000 cases (65,0000-220,000)) of all CVD cases in non-Hispanic blacks compared to 1.5% (220,000 cases (120,000-360,000)) in non-Hispanic whites. Despite a smaller population, total net savings would be over 50% larger in non-Hispanic blacks than non-Hispanic whites ($19bn vs $12bn) in the optimal scenario. Conclusions: Implementing and even partly achieving the FDA sodium reduction targets could generate substantial health gains and net cost savings. Crucially, this policy could also reduce CVD disparities between non-Hispanic black and non-Hispanic white populations.

Introduction: De novo lipogenesis (DNL) is an endogenous pathway for converting excess carbohydrates and proteins into fatty acids (FAs). While elevated DNL is linked to several metabolic abnormalities, little is known about associations of longitudinal changes in DNL FAs with incident congestive heart failure (CHF), a growing condition in older adults. Methods: We investigated relations of longitudinal changes in DNL FAs, measured at year 0, year 6, and year 13, with incident CHF using serial measures of plasma phospholipid myristic acid (14:0), palmitic acid (16:0), 7-hexadecenoic acid (16:1n-9), palmitoleic acid (16:1n-7), stearic acid (18:0), oleic acid (18:1n-9), and cis-vaccenic acid (18:1n-7). Time-varying covariates were measured using standardized methods in 2,005 older adults with two or more FA measures and free of CHF at baseline. Incident CHF was centrally adjudicated using medical records. Risk was assessed by multivariable-adjusted Cox proportional hazards. Results: During 14,628 person-years, 553 CHF events occurred. After multivariate adjustment, serial changes in 16:0, 16:1n-9, and 18:1n-7 were positively associated with incident CHF, with HRs (95% CI) for each 30% change in levels of 2.84 (1.50, 5.37), 1.16 (1.00, 1.33), and 1.42 (1.15, 1.77), respectively ( Table ). Findings were similar in sensitivity analyses excluding individuals with prevalent coronary heart disease (not shown). In analyses evaluating absolute, rather than changes in, DNL FA levels, the associations of 16:0, 16:1n-9, and 18:1n-7 with incident CHF were no longer statistically significant although with consistent directions of association (not shown). Neither changes nor absolute levels of 14:0, 16:1n-7, 18:0, and 18:1n-9 were associated with CHF. Conclusion: Serial changes in plasma phospholipid 16:0, 16:1n-9, and 18:1n-7 were associated with an elevated risk of CHF in older adults. These results indicate that potential mechanisms of risk, especially related to DNL, deserve further investigation.

Background: While economic incentives through health insurance are being considered to promote healthy behaviors, little is known about health or financial impacts of incentivizing diet, a leading risk factor for CVD. We estimated health and economic impacts of programs to incentivize healthful foods through Medicare and Medicaid over a 5, 10, and 20 y horizon. Methods: A validated microsimulation model, CVD PREDICT, was used to estimate reductions in CVD events, gains in quality-adjusted life-years (QALYs), costs, and cost-effectiveness of two policy scenarios within Medicare and Medicaid: (1) 20% subsidy on fruits and vegetables (F&V), and (2) 20% subsidy on broader healthful foods including F&V, whole grains, nuts/seeds, seafood and plant-based oils. Model inputs included national demographic and dietary data from NHANES 2009-2014, policy effects from pricing meta-analyses, diet-disease effects from meta-analyses, and policy costs including program and healthcare costs, inflated to constant 2017 US dollars and discounted at 3% annually. Productivity gains were conservatively excluded. Results: Both incentive programs were cost-effective from a healthcare (government affordability) perspective ( Table ). Over 20 y, a 20% F&V subsidy could prevent 1.24M CVD events; while a broader 20% healthful food subsidy could prevent 1.91M CVD events. Incremental cost-effectiveness ratios for the F&V program ranged from $19,773/QALY for dual eligible to $26,862/QALY for Medicaid beneficiaries; and for the broader healthful food program, from $9,020/QALY for dual eligible to $13,484/QALY for Medicare beneficiaries. Findings were robust to a range of sensitivity analyses; within Medicare, the incentive program was more cost-effective among individuals with lower income. These incentive programs were also cost-effective at 5 and 10 y (not shown). Conclusions: Economic incentives for healthier foods through either Medicare or Medicaid could generate substantial health gains and healthcare cost savings.

Introduction: Circulating very long-chain saturated fatty acids (VLSFA) are biomarkers of diet and metabolism which impart different biological activities to sphingolipids and may influence physiological pathways relevant to aging. Higher levels of circulating VLSFAs have been associated with lower risk of all-cause mortality, cardiovascular outcomes, and diabetes. Apart from these associations, it is unknown whether these biomarkers are related to the maintenance of healthy aging. Hypothesis: Higher levels of circulating VLSFA are associated with lower risk of unhealthy aging. Methods: Phospholipid fatty acids were measured in serial plasma samples collected among participants of the Cardiovascular Health Study (CHS) in 1992-93, 1998-99, and 2005-06. Incident unhealthy aging was defined as the onset of cardiovascular disease (CVD), cancer, lung disease, severe chronic kidney disease, ≥1 difficulties with activities of daily living (ADL), or reduced cognitive function (Mini-Mental State Examination Results: Among 2,183 CHS participants with one or more fatty acid measure and healthy aging up to the time of their first VLSFA measurement, mean age at baseline was 75 years, 62% were female, and 12% were black. During median follow-up of 8 years, all but 198 participants failed to age successfully. The most common conditions marking the first occurrence of unhealthy aging were ADL difficulties and CVD (27% each). In analyses adjusted for major risk factors, higher levels of 22:0 and 24:0 were associated with lower risk of unhealthy aging (Table). Conclusions: Higher levels of two circulating VLSFA, 22:0 and 24:0, are associated with lower risk of unhealthy aging. These findings open a new avenue of research into these saturated fatty acids and their possible beneficial role in promoting better aging.

Introduction: Ceramides and sphingomyelins (sphingolipids) are circulating lipids involved in multiple physiological pathways relevant to heart failure (HF) and atrial fibrillation (AF), including apoptosis, oxidative stress, and inflammation. Experimental studies suggest that sphingolipids with different saturated fatty acids exhibit different biological activities, but their relationships with HF and AF are unknown. Hypothesis: Higher levels of plasma ceramide and sphingomyelin that contain the fatty acid 16:0 are associated with higher risks of HF and AF; and higher levels of ceramides and sphingomyelins that contain the fatty acid 20:0, 22:0 or 24:0 are associated with lower risks. Methods: We measured sphingolipids in the Cardiovascular Health Study (CHS) in plasma samples from 1994-95 (N=4026) or from 1992-93 (N=586). We assessed the separate associations of the levels of 8 sphingolipids with risks of incident HF and incident AF using Cox regression. A p-value threshold of 0.006 was used to account for multiple testing. Results: Among 4,612 participants, 1179 incident HF and 1198 incident AF occurred during >40,000 person-years of follow-up. In adjusted analyses, higher levels of Cer-16 (ceramide with 16:0) and SM-16 (sphingomyelin with 16:0) were associated with higher risk of incident HF, but not with risk of incident AF (Table). In contrast, higher levels of Cer-20, Cer-22 and Cer-24 were each associated with lower risk of AF, but not with risk of HF. Higher levels of SM-20, SM-22, and SM-24 tended to be associated with lower risks of AF and HF, with only the association of SM-20 with AF significant. Conclusions: Plasma levels of ceramide and sphingomyelin with 16:0 show different associations with HF and AF than species with 20:0, 22:0 or 24:0. Associations of Cer-16 and SM-16 specifically with higher risk of HF may be due to a role of apoptosis in HF. The novel findings that Cer-20, Cer-22, and Cer-24 are associated with lower risk of AF warrant further examination of the role of these sphingolipids in protecting from AF.

Introduction: Excess added sugars, particularly from sugar-sweetened beverages (SSBs), are linked to cardiometabolic risk including obesity, type 2 diabetes (T2D) and CVD. Despite recent declines in SSB intake in the US, added sugar intake from SSBs and foods remains high and exceeds dietary recommendations. In May 2016, the US Food and Drug Administration (FDA) announced major revisions to the Nutrition Facts panel, including mandatory labeling of added sugar content, as a strategy to target added sugars from packaged foods and beverages. Yet, potential health effects remain unclear; and the FDA recently announced delays in implementation. Aim: To estimate the cardiometabolic and economic effects of implementing FDA’s added sugar labeling policy over a 20-year horizon. Methods: A validated microsimulation model, the US IMPACT Food Policy Model, was used to estimate the T2D and CVD cases averted and quality-adjusted life-years (QALYs) gained from the FDA policy for US adults age 30+ years. Model inputs included: nationally representative demographics and added sugar intakes from NHANES; policy effects on consumer intake from labeling intervention studies; obesity-mediated effects and direct independent effects of added sugars from SSBs and other foods, considered separately, on T2D and CVD from meta-analyses; policy costs including government administrative costs and industry compliance costs from federal government reports; national health statistics from the CDC; and healthcare costs including medical, productivity, and indirect costs from the AHA and American Diabetes Association. All costs were inflated to constant 2017 US dollars, discounted annually at 3%. We took a societal perspective and assumed a willingness to pay of $100,000 per QALY. Probabilistic sensitivity analysis accounted for model parameter uncertainty and population heterogeneity. Results: Between 2018 and 2037, the FDA added sugar labeling policy could prevent approximately 580,000 (95% UI: 270,000–960,000) T2D cases and 210,000 (96,000–440,000) CVD cases, generating 600,000 (290,000–970,000) discounted QALYs. The policy would produce discounted net cost savings (health savings minus policy costs) of $47.3bn (21.7-78.6), including $25.6bn (11.9-43.1) from direct healthcare cost reductions. Most (>60%) savings were driven by costs related to T2D. Incorporating modelling and input uncertainty, the FDA added sugar label was estimated with >80% probability to be cost-effective by 2020 and cost-saving by 2022. Potential additional reductions from industry reformulations were not included and could further increase cost-savings. Conclusions: Implementing the FDA added sugar labeling mandate would generate substantial health gains and cost savings for the US population, highlighting the need for timely implementation, monitoring and evaluation.

Author(s): Mozaffarian, Dariush; Benjamin, Emelia J; Go, Alan S; Arnett, Donna K; Blaha, Michael J; Cushman, Mary; de Ferranti, Sarah; Despres, Jean-Pierre; Fullerton, Heather J; Howard, Virginia J; Huffman, Mark D; Judd, Suzanne E; Kissela, Brett M; Lackland, Daniel T; Lichtman, Judith H; Lisabeth, Lynda D; Liu, Simin; Mackey, Rachel H; Matchar, David B; McGuire, Darren K; III, Mohler Emile R; Moy, Claudia S; Muntner, Paul; Mussolino, Michael E; Nasir, Khurram; Neumar, Robert W; Nichol, Graham; Palaniappan, Latha; Pandey, Dilip K; Reeves, Mathew J; Rodriguez, Carlos J; Sorlie, Paul D; Stein, Joel; Towfighi, Amytis; Turan, Tanya N; Virani, Salim S; Willey, Joshua Z; Woo, Daniel; Yeh, Robert W; Turner, Melanie B; Comm, Amer Heart Assoc Stat; Subcomm, Stroke Stat

Quantifying reductions in US cardiovascular deaths and disparities by different diet policies Background: Large disparities exist in US dietary habits and cardiovascular disease (CVD) mortality. While economic incentives have demonstrated success in improving dietary choices, the quantitative impact of different dietary policies on CVD disparities is not well-established Methods: Using a US IMPACT Food Policy Model and probabilistic sensitivity analyses, we estimated and compared the reductions in CVD mortality and disparities in the US population potentially achievable from 2015 to 2030 with specific dietary policy scenarios a) a national mass media campaign (Media campaign) aimed to increase consumption of fruits and vegetables (F&V) or reduce sugar sweetened beverages (SSBs), b) national fiscal policies to tax SSB and increase price by 10% and subsidize F&V to reduce prices by 10%; and c) a targeted policy, to subsidize F&V to reduce prices by 30% among Supplemental Nutrition Assistance Programme (SNAP) participants only. We also evaluated a combined multi-component approach, combining each of the above policies. Results: Among individual policy options, a national 10% F&V subsidy was estimated to be most effective, resulting in approximately 150,500 (95% CI, 142,700-157,900) CVD deaths potentially prevented or postponed (DPPs) by 2030. This far exceed the approximately 35,100 (32,000-37,900) DPPs from a 30% F&V subsidy targeting SNAP participants, or some 23,000 (21,700-24,600) DPPs from a 1-year Media campaign or approximately 21,400 (19,500-23,600) DPPs from a 10% SSB tax. Neither the Media campaign nor individual national economic policies would significantly reduce CVD disparities. However, the SNAP-targeted intervention would significantly reduce CVD disparities between SNAP participants and SNAP-ineligible individuals, by approximately 7% (10 DPPs per 100,000 population). The combined policy approach would save more lives than any single policy studied (approximately 215,500 DPPs by 2030) while also significantly reducing disparities by approximately 5% (7 DPPs per 100,000 population). Conclusions: Fiscal strategies targeting diet could reduce CVD burdens. A national 10% F&V subsidy would save by far the most lives, while a SNAP-targeted 30% F&V subsidy would most reduce disparities. A combined policy would have the greatest overall impact on both mortality and disparities.

Introduction: The neighborhood food environment - locations and density of different types of stores and restaurants - is of great interest to reduce obesity. However, prior meta-analyses have focused on cross-sectional studies, for which reverse causation is a major limitation. Meta-analyses restricted to longitudinal study designs evaluating the food environment and change in BMI have yet to be conducted. Hypothesis: We hypothesized that increased exposure to fast food restaurants would be associated with increased change in BMI. Methods: Eleven databases were searched for longitudinal studies evaluating convenience stores, fast food restaurants, grocery stores, or supermarkets and change in BMI. Inclusion criteria consisted of: (1) interventional, quasi-experimental, or cohort studies; (2) adult or children populations; (3) any country; (4) geographic density or distance of food outlets; (5) a multivariable-adjusted change in BMI over time and corresponding uncertainty. Data were extracted independently and in duplicate, and studies pooled using fixed and random-effects models. Heterogeneity was quantified using Cochrane’s Q, and publication bias using funnel plots, Egger’s test, and Begg’s test. Results: 13 studies including 98,268 subjects were identified. In random effects models, no significant association was seen between food environments and change in BMI ( Figure ). A nonsignificant trend was seen toward lower BMI with increasing density of supermarkets; however, a similar nonsignificant trend was also observed between increasing density of fast food restaurants and lower BMI. Evidence for publication bias was not identified. Conclusion: In available longitudinal studies,no significant relationships were identified between food environments and change in BMI. Our novel findings support the need for further longitudinal and especially interventional studies of how the built food environment, including new measures related to cost and accessibility, may influence health and weight.

Introduction: Worksites are promising venues for promoting health, given considerable time spent at work and opportunities for environmental change. Yet, the impact of worksite wellness programs (WWPs) on diet and adiposity, as well as the most relevant WWP components, are not established. Methods: Following MOOSE and PRISMA guidelines, we conducted a systematic review and meta-analysis of the impact of multi-component WWP trials (RCT or quasi-experimental) on diet and adiposity. Data were extracted in duplicate and pooled using inverse variance random effects meta-analysis. Pre-specified sources of heterogeneity (study design, world region, worksite type, duration, WWP components) were analyzed by meta-regression and subgroup analysis. Funnel plots, Begg’s, and Egger’s tests evaluated potential publication bias. Results: From 6612 abstracts, we identified 48 studies assessing WWPs and diet or adiposity. Most were in the US (54%) or Europe (23%), with diet (64%) and exercise/weight loss (20%) as main targets. Intervention components were variable (Figure). Most common outcomes were intakes of fruits and vegetables (F&V) (19 studies), total fat or fat subtypes (18), and dietary fiber (4); and BMI (35) and waist circumference (WC) (10). Median duration was 12 months (range: 1-48 mo). In pooled analyses, WWP increased intake of F&V, especially fruits (Figure). Significant effects were not identified for dietary fiber, total fat, or fat subtypes. WWP also reduced BMI (Figure) and WC (-2.03 cm, 95% CI:-3.88,-0.20). Trial duration significantly modified effects on BMI (2 ; 12+ mo: -0.16 kg/m 2 ; P-interaction=0.046); but not WC or F&V intake. Additional findings for heterogeneity, including WWP components, and publication bias will be presented. Conclusions: These novel findings support effectiveness of WWP for increasing F&V and reducing BMI and WC.

Background: The US population is rapidly aging, with concurrent increases in chronic disease burdens, particularly CVD. Yet, to-date, the spatial, temporal, and demographic distributions and trends in CVD incidence in the US elderly have not been characterized in detail using data with full coverage of this population. Objective: To characterize trends, 1991-2004, in CVD hospitalizations among US elderly, by single year of age/ sex/race/county/state using records from US Centers for Medicare and Medicaid (CMS), which provide full coverage of the US population aged 65+. Methods: We abstracted 108,357,431 hospitalization records compiled by CMS indicating CVD in any of 10 diagnosis codes, and tabulated total cases of CVD by sex, single year of age, state and calendar year (1991-2004). CVD incidence rates were calculated using stratum-specific population data from the US Census in conjunction with CMS records. We characterized distributions of CVD cases by single year of age for the US and further by state and calendar year, determining the sex-specific age at which the largest number of incident CVD cases were registered (peak age). Results: CVD hospitalization rates increased from 1991-2004 for women aged 65-90 and men aged 65-80, but declined in the oldest-old. In 1991, CVD hospitalization rates for women aged 75 were 48 per 100,000 population, rising to 70 per 100,000 in 2004; men aged 75 had rates of 66 per 100,000 in 1991 versus 87 per 100,000 in 2004. Nationally, peak age of CVD hospitalizations increased 1991-2004, from 77 to 83 years of age for women and from 70 to 77 years of age for men. Men and women in Southern states had among the lowest peak ages of CVD in the nation in 1991 as well as 2004. ( Figure ) Trends by race/CVD subtype are forthcoming. Conclusions: Emerging national trends and regional heterogeneity in CVD hospitalization rates and peak age of CVD hospitalization in the US elderly emphasize the need for targeted population-level policy/interventions to reduce CVD burdens and promote healthy aging.

Background: Circulating saturated fatty acids are biomarkers of diet and metabolism that may influence the pathogenesis of diabetes. Unlike palmitic acid (16:0), which has been extensively studied, little is known of the relationship of very long-chain saturated fatty acids (VLSFAs), with 20 carbons or more, to diabetes risk. Objective: To investigate the associations of circulating levels of VLSFA with incident diabetes. Methods: A meta-analysis was conducted within a consortium of prospective (cohort or nested case-control) studies having circulating measures of one or more VLSFAs, including arachidic acid (20:0), behenic acid (22:0) and lignoceric acid (24:0). Standardized analysis was conducted in each study using pre-specified models, exposures, outcomes, and covariates. Study-specific estimates were pooled using fixed effects meta-analysis. Results: Current findings were based on 9 participating studies, including 46,549 total participants and 13,750 incident diabetes. In multivariable-adjusted analyses, higher levels of all 3 VLSFAs were associated with lower risk of incident diabetes. Pooled RRs (95% CI) per interquintile range were 0.80 (0.71-0.90) for 20:0; 0.83 (0.76-0.91) for 22:0; and 0.70 (0.63-0.79) for 24:0, after adjustment for demographics, lifestyle factors and clinical conditions. Additional adjustments for circulating palmitic acid and triglyceride levels moved the RRs toward the null (illustrated for 24:0, in model 3 of the Figure ). Conclusions: Based on meta-analysis of results from several studies around the world, biomarker levels of VLSFA are associated with lower risk of incident diabetes, potentially mediated by effects on circulating triglycerides and 16:0.

Introduction: Promising school food environment policies include providing fresh fruits and vegetables (F&V provision) and competitive food restrictions on sugar-sweetened beverages (SSB restriction). Yet, the impact of these policies on diet and BMI in children and future cardiometabolic disease (CMD) outcomes is not established. Methods: We used a comparative risk assessment model to estimate the effects of F&V provision and SSB restriction on diet and BMI in US children age 5-18 yrs. We used national data from NHANES 2009-12 on baseline BMI and intakes of fruits, vegetables, and SSBs; impacts of these policies on diet from meta-analyses of interventions; and estimated effects of dietary changes on BMI from trials and cohorts. We also estimated the effects of these school policies on CMD in current US adults if such policies had been implemented in their childhood, based on meta-analysis of long-term within-person correlations of childhood and adult diets, meta-analyses of diet and CMD, and data on national CMD deaths. Model inputs were stratified by age, sex, and race, where appropriate. Point estimates and 95% uncertainty intervals were derived from probabilistic sensitivity analyses using 1000 Monte Carlo simulations. Results: F&V provision would increase overall fruit intake in children by ~ 14-21% and would not significantly increase vegetable intake ( Table ). SSB restriction would decrease overall SSB intake by ~ 6-11% and BMI (kg/m 2 ) by 0.2-0.3%. Among these dietary factors, reducing SSBs had the largest estimated impact on CMD (2418 deaths averted/year), followed by providing fruits (2121) and vegetables (165). If US adults had been exposed to both policies, an estimated 4703 CMD deaths/year would be averted, representing 0.67% of all CMD deaths. Conclusions: Specific US school food environment policies involving F&V provision and SSB restriction would modestly improve diet and BMI in children, and could prevent up to 0.7% of all CMD deaths.

Background: Controversy has emerged about cardiovascular benefits versus harms of dairy fat consumption. Further, little data are available on potential long-term noncardiovascular effects. In addition, most observational studies to date assessed self-reported estimates of dairy fat consumption, which may not capture all dietary sources; and the few studies using objective biomarkers included only one baseline measure, which may lead to poor estimation of long-term risk. Aims: To investigate prospective associations of serial measures of dairy plasma phospholipid fatty acids (15:0, 17:0, trans 16:1n-7) with cause-specific and total mortality among older adults in the Cardiovascular Health Study. Methods: Among 2,638 U.S. adults aged ≥65y and free of CVD at baseline, circulating fatty acid levels were measured serially at baseline, 6 years and 13 years using standardized methods. All-cause and cause-specific deaths were assessed and adjudicated centrally. Prospective associations were assessed by multivariate-adjusted Cox models incorporating time-dependent fatty acid measures and covariates. Results: During 36,486 person-years of follow-up (1992-2015), 2,619 deaths occurred (930 CVD deaths, 1,689 non-CVD deaths), with 603 CHD deaths and 208 stroke deaths. After adjustment for demographic and lifestyle factors, higher plasma phospholipid 17:0 and trans 16:1n-7 were associated with lower cause-specific and total mortality (see Table). There were no statistically significant associations with 15:0. Conclusion: Plasma phospholipid 17:0 and trans 16:1n-7, two objective biomarkers of dairy fat consumption, measured serially over 13 years, were associated with lower all-cause and especially CVD mortality among older adults. A third biomarker, 15:0, was not significantly associated with mortality. These novel findings highlight the need for detailed mechanistic and interventional investigation of long-term health effects of dairy fat, dairy-specific fatty acids, and dairy foods.

Author(s): Go, Alan S; Mozaffarian, Dariush; Roger, Veronique L; Benjamin, Emelia J; Berry, Jarett D; Blaha, Michael J; Dai, Shifan; Ford, Earl S; Fox, Caroline S; Franco, Sheila; Fullerton, Heather J; Gillespie, Cathleen; Hailpern, Susan M; Heit, John A; Howard, Virginia J; Huffman, Mark D; Judd, Suzanne E; Kissela, Brett M; Kittner, Steven J; Lackland, Daniel T; Lichtman, Judith H; Lisabeth, Lynda D; Mackey, Rachel H; Magid, David J; Marcus, Gregory M; Marelli, Ariane; Matchar, David B; McGuire, Darren K; Mohler, Emile R; Moy, Claudia S; Mussolino, Michael E; Neumar, Robert W; Nichol, Graham; Pandey, Dilip K; Paynter, Nina P; Reeves, Matthew J; Sorlie, Paul D; Stein, Joel; Towfighi, Amytis; Turan, Tanya N; Virani, Salim S; Wong, Nathan D; Woo, Daniel; Turner, Melanie B; American Heart Association Statistics Committee and Stroke Statistics Subcommittee

Background— Decades-old animal experiments suggested that dietary long-chain monounsaturated fatty acids (LCMUFAs) caused cardiotoxicity, leading, for example, development of Canola oil (Canadian oil low in erucic acid) from rapeseed. However, potential cardiotoxicity in humans and contemporary dietary sources of LCMUFAs are unknown. Methods and Results— We prospectively investigated the associations of plasma phospholipid LCMUFAs (20:1, 22:1, and 24:1), assessed as objective biomarkers of exposure, with incidence congestive heart failure in 2 independent cohorts: 3694 older adults (mean age, 75.2±5.2 years) in the Cardiovascular Health Study (CHS; 1992–2006) and 3577 middle-aged adults (mean age, 54.1±5.8 years) in the Atherosclerosis Risk in Communities Study, Minnesota subcohort (ARIC; 1987–2008). We further examined dietary correlates of circulating LCMUFAs in CHS and ARIC and US dietary sources of LCMUFAs in the 2003–2010 National Health and Nutrition Examination Survey (NHANES). In CHS, 997 congestive heart failure events occurred during 39 238 person-years; in ARIC, 330 events congestive heart failure events occurred during 64 438 person-years. After multivariable adjustment, higher levels of 22:1 and 24:1 were positively associated with greater incident congestive heart failure in both CHS and ARIC; hazard ratios were 1.34 (95% confidence interval, 1.02–1.76) and 1.57 (95% confidence interval, 1.11–2.23) for highest versus lowest quintiles of 22:1, respectively, and 1.75 (95% confidence interval, 1.23–2.50) and 1.92 (95% confidence interval, 1.22–3.03) for 24:1, respectively ( P for trend ≤0.03 each). A variety of foods were related to circulating LCMUFAs in CHS and ARIC, consistent with food sources of LCMUFAs in NHANES, including fish, poultry, meats, whole grains, and mustard. Conclusions— Higher circulating levels of 22:1 and 24:1, with apparently diverse dietary sources, were associated with incident congestive heart failure in 2 independent cohorts, suggesting possible cardiotoxicity of LCMUFAs in humans.

Author(s): Go, Alan S; Mozaffarian, Dariush; Roger, Veronique L; Benjamin, Emelia J; Berry, Jarett D; Borden, William B; Bravata, Dawn M; Dai, Shifan; Ford, Earl S; Fox, Caroline S; Franco, Sheila; Fullerton, Heather J; Gillespie, Cathleen; Hailpern, Susan M; Heit, John A; Howard, Virginia J; Huffman, Mark D; Kissela, Brett M; Kittner, Steven J; Lackland, Daniel T; Lichtman, Judith H; Lisabeth, Lynda D; Magid, David; Marcus, Gregory M; Marelli, Ariane; Matchar, David B; McGuire, Darren K; Mohler, Emile R; Moy, Claudia S; Mussolino, Michael E; Nichol, Graham; Paynter, Nina P; Schreiner, Pamela J; Sorlie, Paul D; Stein, Joel; Turan, Tanya N; Virani, Salim S; Wong, Nathan D; Woo, Daniel; Turner, Melanie B; American Heart Association Statistics Committee and Stroke Statistics Subcommittee

Autier and colleagues suggest that disease burdens attributable to individual dietary factors such as sugar-sweetened beverages (SSBs) are unquantifiable. Decades of robust research have established methods to evaluate population-health impacts of modifiable risk factors as diverse as air pollution, smoking, blood pressure, and poor diet.1 We agree that such factors often cluster: Like any other cause of disease, SSB consumption combines with multiple factors to characterize individuals’ lifestyles and population health. However, the multifactorial nature of disease does not preclude reasonable estimation of the impact of any single factor, and well-designed prevention strategies are unattainable without knowledge of the contributions of the individual risk factors to disease. As a result of clustering of risks, we agree that crude correlations of exposure and disease often result in …

Background: Dietary habits are major contributors to cardiometabolic diseases. Estimating the impact of diet on these conditions requires identification and quantification of evidence for causal effects. Objectives: To comprehensively evaluate the current evidence and quantify the effects of major dietary factors on CHD, stroke, and diabetes as part of the Global Burden of Diseases (GBD) 2015 study. Methods: We assessed probable or convincing evidence for causal effects based on Bradford-Hill, World Health Organization, and WCRF/AICR criteria. We searched PubMed through April 2015 to identify systematic reviews and meta-analyses of well-designed observational studies and clinical trials. Meta-analyses were evaluated and selected based on design, number of studies and events, definition of dietary exposure and disease outcomes, length of follow-up, statistical methods, evidence of bias, and control for confounders. Effect sizes and uncertainty were quantified per standardized units. We focused on dose-response meta-analyses. When necessary, original data were extracted from individual studies within each meta-analysis to perform de novo dose-response meta-analyses using generalized least squares for trend estimation. Results: We identified 11 dietary factors with probable or convincing evidence for causal effects on CHD, 4 on stroke, and 7 on diabetes. ( Table ). Examples of other factors not yet meeting probable or convincing evidence for causal effects included coffee and tea (consistent dose-response, yet plausible biology not well-established), eggs, and dietary cholesterol. Conclusion: This evaluation provides the best current evidence-based quantitative estimates of effects of major dietary factors on CHD, stroke, and diabetes. These findings enable quantitative estimation of disease burdens of suboptimal diet in the US and globally, and also inform policy planning and priorities.

Introduction: The associations of individual seafood n-3 polyunsaturated fatty acids with incident ischemic stroke, and its subtypes (atherothrombotic and cardioembolic stroke), are not well-established. Individual n-3 fatty acids, which are best assessed by circulating biomarkers, may also have differential effects on atherothrombotic vs. cardioembolic stroke. Objective: To prospectively investigate the relationship of circulating eicosapentaenoic acid (EPA), docosapentaenoic acid (DPA), and docosahexaenoic acid (DHA) with risk of total ischemic, atherothrombotic, and cardioembolic stroke. Methods: We measured circulating phospholipid fatty acids (erythrocyte or plasma) at baseline in the Cardiovascular Health Study (CHS), Nurses’ Health Study (NHS) and Health Professionals Follow-Up Study (HPFS). Ischemic stroke was prospectively adjudicated and classified into atherothrombotic (large and small vessel infarctions) or cardioembolic (cardiac mural thrombi, valvular heart disease, atrial fibrillation, other sources) stroke by imaging studies and medical records. Risk was assessed using conditional logistic regression (for prospective nested case-control studies: NHS, HPFS) or Cox proportional hazards model (full cohort: CHS). Findings were pooled by fixed-effects meta-analysis. Results: A total of 953 incident ischemic strokes were identified that included 408 atherothrombotic and 256 cardioembolic strokes, during mean follow-up of 11.4 (CHS) and 8.3 (NHS,HPFS) years (the remaining 289 ischemic strokes could not be sub-classified). After adjustment for age, race, sex, smoking, physical activity, alcohol intake, family history of MI and diabetes, menopausal status, BMI, aspirin use and intakes of fruits, vegetables, and meats, lower risk of total ischemic stroke was seen with DPA (highest vs. lowest-quartiles, pooled HR=0.74, 95%CI=0.58-0.92) and DHA (0.80, 0.64-1.00), but not EPA (0.94, 0.77-1.19). Among stroke subtypes, DHA was associated with substantially lower risk of atherothrombotic (0.53, 0.34-0.83), but not cardioembolic stroke; and DPA with substantially lower risk of cardioembolic (0.58, 0.37-0.92), but not atherothrombotic stroke. Findings in each individual cohort were similar to the pooled results. Conclusions: In 3 US cohorts, higher circulating levels of DHA were inversely associated with incident atherothrombotic stroke, and DPA, with cardioembolic stroke. EPA was not associated with ischemic stroke. These novel findings highlight the importance of separately evaluating ischemic stroke subtypes as well as specific individual fatty acids, and suggest differential pathways of benefit for DHA, DPA, and EPA.

Background: Cardiometabolic (CMB) risk factors are major mediators of the effects of diet on health. Multiple foods are often consumed in tandem, yet CMB effects of individual dietary factors are often studied in isolation, leading to estimates that may not represent true effects as part of diet patterns. Objective: To quantify the effects of major foods (fruits, vegetables, nuts/seeds, whole grains, fish) and dietary fiber, when consumed within the context of overall diet patterns, on systolic BP, serum lipids, and glucose-insulin homeostasis. Methods: PubMed was searched through Oct 2015 to identify randomized controlled feeding studies evaluating effects of major dietary patterns on CMB factors. We included trials evaluating major dietary patterns including fruits, vegetables, nuts/seeds, whole grains, fish, and dietary fiber as major components and evaluating effects on systolic BP, serum lipids (total cholesterol, LDL-C, HDL-C, or triglycerides), or markers of glucose-insulin homeostasis (fasting plasma glucose, HbA1c, postprandial glucose, or fasting insulin). Multivariate metaregression was used to estimate food-specific effects on CMB factors. Results: Among 15 included trials, diet-pattern related decreases in SBP ranged from -2.2 to -9.5 mmHg; and in LDL-C, from -5.0 to -14.7 mg/dL. Each specific food had different, independent, and additive effects on these risk factors ( Figure ). Results for measures of glucose-insulin homeostasis are in progress. Conclusions: Each of these foods independently influences major CMB risk factors, even when consumed in tandem as part of overall diet patterns . Such quantification more accurately reflects the complementary effects of diverse dietary components and highlights the importance of integrated approaches to investigating dietary factors and implementing relevant dietary policies.

Background: Food taxes and subsidies are promising strategies for improving diets and reducing cardiometabolic diseases (CMD). Both dietary habits and CMD burdens are unequally distributed in the US, with major disparities by socioeconomic status (SES). Information on impacts of national food price policies on disparities is lacking. Aim: To estimate the impact on CMD deaths and health disparities in US adults of price interventions (taxes, subsidies) targeting 7 key dietary factors. Methods: Using nationally representative data, we conducted comparative risk assessment analysis to estimate the impact of a 10% price subsidy on fruits, vegetables, whole grains, and nuts and a 10% tax on processed meat, unprocessed red meat, and sugar-sweetened beverages, on CMD deaths and disparities in SES subgroups. We evaluated 18% (based on global price elasticity data) and 50% (based on recent experience from soda taxes in Mexico) greater price responsiveness in lowest vs. highest SES groups. Results: Each separate price intervention would reduce CMD deaths (Figure). Jointly subsidizing and taxing these 7 dietary factors (10% price change each) and assuming 18% greater price-responsiveness in lowest vs. highest SES, this intervention would prevent 5.27% of CMD deaths in those with Conclusions: Introducing modest price changes on key dietary factors could reduce CMD burdens and improve disparities in the US. Policy-based strategies targeting disparities will require considering both baseline dietary habits as well as price responsiveness in specific population subgroups.

Introduction: Changes in food prices can lead to healthier dietary patterns. Recent meta-analyses suggest the responses differ by food category with respect to impact on disease outcome. Hypothesis: We tested the hypothesis that a 10% subsidy on price of fruits, vegetables and whole grains, and a 10% tax on sugar-sweetened beverages, would have differential effects on CVD mortality, non-fatal MI and stroke, and diabetes over a 5-year period through a 20-year period in the U.S. Methods: We used an individual-based microsimulation CVD risk prediction model of a million adults created from NHANES sample (aged 35+). Model inputs included patient risk factor information, CVD risk equations, and intervention effectiveness data. The baseline cohort was expanded by adding additional groups of 35-year olds annually to produce cross-sectional outcomes from 2015-2035. Results: Using a conservative estimate of population growth, we project that the subsidy-increased consumption of fruits and vegetables would lead to 5- and 20-year reductions of CVD deaths by 8% and 10%, reductions in non-fatal MI by 16% and 18%, and reductions in non-fatal stroke by 25% and 24%, respectively. Subsidy-increased whole grain consumption would have corresponding reductions of 2.5% and 3% for CVD deaths and 9.1% and 9.7% for MI (Table). Tax-induced decreased consumption of sugar sweetened beverages would reduce 5- and 20-year CVD deaths by 0.8% and 1.3%, MI by 2.5% and 2.5%, stroke by 1.8% and 2.3%, and diabetes by 2.6% and 9.8%. Combined these numbers translate to prevention of over 3.5 million CVD deaths and over 4 million combined CVD events by 2035, assuming independent benefits for each food group. Conclusions: Pricing interventions resulting in differential changes in dietary habits can significantly reduce CVD outcomes in the U.S by different amounts. Further research should be done in assessing the cost-effectiveness of applying these price changes, as well as the compliance of the population to maintain healthy dietary habits over the 20-year horizon.

Introduction: Dietary guidelines recommend avoiding foods high in saturated fat. Yet, emerging evidence suggests potential cardiometabolic benefits of dairy products and dairy fat. Evidence on the role of butter, with high saturated dairy fat content, for total mortality, CVD, and diabetes remains unclear. Objective: To systematically investigate the prospective association of butter consumption with all-cause mortality, CVD, and type 2 diabetes. Methods: We searched 9 databases from inception to May 2015 without restriction on publication year, setting, or language, using keywords related to butter intake and outcomes of interest. We included prospective cohorts or randomized clinical trials providing estimates of effects of butter intake on mortality, CVD (including CHD or stroke), or diabetes in general adult populations. Inclusion decisions and data extractions were performed independently and in duplicate, including on study and participant characteristics, exposure and outcome definitions and assessments, analysis methods, and adjusted risk estimates and uncertainty of prospective multivariate associations. Study quality was evaluated by a modified Newcastle-Ottawa score. Findings were pooled by random and fixed effects meta-analysis, with heterogeneity assessed by the I2 statistic and publication bias by Egger’s test and funnel plots. Results: We identified 9 publications including 15 country-specific cohorts, with 636,151 unique participants, 6.5 million person-years of follow-up, and 28,271 total deaths, 9,783 cases of incident CVD, and 23,954 cases of incident diabetes. Quality ratings were high for all studies. Butter consumption was weakly associated with all-cause mortality (N=9 country-specific cohorts; per 14 g (1 tablespoon)/day: RR=1.01, 95%CI=1.00, 1.03, P=0.045); was not significantly associated with any CVD (N=4; RR=1.00, 95%CI=0.98, 1.02; P=0.79), CHD (N=3; RR=0.99, 95%CI=0.96, 1.03; P=0.605), or stroke (N=3; RR=1.00, 95%CI=0.98, 1.03; P=0.79), and was inversely associated with incidence of diabetes (N=11; RR=0.96, 95%CI=0.93, 0.99; P=0.02). We did not identify evidence for heterogeneity nor publication bias. Conclusions: This systematic review and meta-analysis identified a weak association of butter intake with total mortality, no association with CVD, and a modest protective association with diabetes. The studies identified indicate that many global cohorts have not reported on these associations; if publication bias exists, it would likely be for unpublished reports with null findings, rather than significant associations. In sum, these results suggest relatively neutral effects of butter consumption on major health outcomes, with a possible modest benefit for diabetes.