Table 1.
Dietary Factors in the Analysis, Consumption Levels Among Adults Aged ≥ 25 Years in 1999–2002 and 2009–2012, Optimal Consumption Levels, Related Cardiometabolic Disease Outcomes, and Relative Risks at Ages 50 and 70 Years
| Dietary Targetsa | Mean (SD)/Median (IQR) | Optimal Consumption, Meanc | Cardiometabolic Outcome | Unit of RRd | RR (95% Cl) | ||
|---|---|---|---|---|---|---|---|
| Consumption in 1999–2002b | Consumption in 2009–2012b | Age 50 ye | Age 70 ye | ||||
| Fruits excluding fruit juices, g/d | 96.4 (89.1)/14.2 (0–141.8) | 115.0 (107.5)/71.2 (3.5–174.9) | 300 | Decreased CHD | Per 100 g/d | 0.93 (0.89–0.97) | 0.95 (0.92–0.98) |
| Decreased ischemic stroke | 0.86 (0.80–0.92) | 0.90 (0.86–0.94) | |||||
| Decreased hemorrhagic stroke | 0.69 (0.56–0.84) | 0.77 (0.67–0.89) | |||||
| Vegetables including legumes, g/d | 179.8 (98.4)/136.5 (50.1–259.7) | 182.5 (106.2)/154.0 (83.6–243.2) | 400 | Decreased CHD | Per 100 g/d | 0.94 (0.91–0.97) | 0.96 (0.94–0.98) |
| Decreased ischemic stroke | 0.80 (0.70–0.92) | 0.86 (0.78–0.94) | |||||
| Decreased hemorrhagic stroke | 0.80 (0.67–0.96) | 0.86 (0.76–0.97) | |||||
| Nuts/seeds, g/d | 7.3 (11.8)/0 (0–4.1) | 11.7 (21.1)/1.5 (0–12.6) | 20.2 (5 1–oz servings/wk) | Decreased CHD | Per 1 oz/wk | 0.91 (0.87–0.94) | 0.93 (0.91–0.96) |
| Decreased diabetes | 0.96 (0.94–0.98) | 0.97 (0.96–0.99) | |||||
| Whole grains, g/d | 15.3 (15.6)/0.7 (0–19.5) | 21.2 (18.7)/12.4 (0–32.1) | 125 (2.5 50–g servings/d) | Decreased CHD | Per 50 g/d | 0.96 (0.93–0.99) | 0.97 (0.95–0.99) |
| Decreased ischemic stroke | 0.90 (0.83–0.97) | 0.93 (0.88–0.98) | |||||
| Decreased hemorrhagic stroke | 0.90 (0.83–0.97) | 0.93 (0.88–0.98) | |||||
| Decreased diabetes | 0.86 (0.80–0.92) | 0.90 (0.86–0.94) | |||||
| Red meats, unprocessed, g/d | 50.5 (22.6)/8.7 (0–84.2) | 47.4 (23.6)/34.4 (0–74) | 14.3 (1 100–g serving/wk) | Increased diabetes | Per 100 g/d | 1.24 (1.04–1.47) | 1.16 (1.03–1.30) |
| Processed meats, g/d | 29.9 (17.8)/0 (0–43.5) | 30.8 (19.0)/17.6 (0–47.6) | No intake | Increased CHD | Per 50 g/d | 1.47 (1.14–1.88) | 1.30 (1.09–1.54) |
| Increased diabetes | 1.65 (1.30–2.08) | 1.41 (1.20–1.65) | |||||
| SSBs, 8-oz servings/d | 1.52 (1.53)/0.6 (0–2.4) | 1.14 (1.44)/0.4 (0–1.7) | No intake | Increased BMI (baseline BMI <25)f | Per 8 oz/d | 0.10 (0.05–0.15) | 0.10 (0.05–0.15) |
| Increased BMI (baseline BMI ≥25)f | 0.23 (0.14–0.32) | 0.23 (0.14–0.32) | |||||
| Increased CHD (BMI adjusted)f | 1.26 (1.15–1.37) | 1.17 (1.10–1.24) | |||||
| Increased diabetes (BMI adjusted)f | 1.27 (1.11–1.46) | 1.18 (1.07–1.29) | |||||
| PUFAs, % energy replacing carbohydrates or saturated fatsg | 7.0 (1.4)/6.4 (4.7–8.6) | 7.7 (1.5)/7.4 (5.9–9.2) | 11 | Decreased CHD | Per 5% energy/d | 0.88 (0.83–0.94) | 0.92 (0.88–0.96) |
| Seafood omega-3 fats, mg/d | 117 (85)/27.5 (0–72) | 100 (69)/37.9 (15.1–88.5) | 250h | Decreased CHD | Per 100 mg/d | 0.82 (0.75–0.90) | 0.87 (0.82–0.93) |
| Sodium, mg/d | 3400 (552)/3261 (2636–3963) | 3480 (605)/3355 (2874–3933) | 2000 | Increased SBP, white, normotensivei | Per 2300 mg/d | 3.74 mm Hg (2.30–5.17) | 5.84 mm Hg (4.01–7.66) |
| Increased SBP, additional effect among black patientsi | 2.49 mm Hg (0.13–4.85) | 2.49 mm Hg (0.13–4.85) | |||||
| Increased SBP, additional effect among patients with hypertensioni | 1.87 mm Hg (0.12–3.63) | 1.87 mm Hg (0.12–3.63) | |||||
Abbreviations: IQR, interquartile range; PUFA, polyunsaturated fat; RR, relative risk; SBP, systolic blood pressure; SSB, sugar-sweetened beverage.
From 17 dietary factors with probable or convincing evidence, based on criteria for assessing causality,10–12 for etiologic relationships with cardiometabolic outcomes including coronary heart disease (CHD), stroke, type 2 diabetes, body mass index (BMI), or SBP (eTable 1 in the Supplement).9 Of these, beans/legumes were summed with vegetables; dietary fiber, glycemic load, and potassium were not included because of overlap with major food sources (eg, fruits, vegetables, legumes, whole grains), fish/seafood because of overlap with seafood omega-3 fats, yogurt because of lack of data on generalized least-squares dose-response relationships, and trans fats because of limited national data on intakes as well as rapidly declining US levels due to policy interventions.
Based on the National Health and Nutrition Examination Survey (see Methods and eTables 7–10 in the Supplement).
Based on observed levels at which the lowest disease risk occurs, with further considerations of feasibility and consistency with major guidelines (eTable 3 in the Supplement).13
Based on published or de novo dose-response meta-analyses of prospective cohorts or randomized clinical trials (eAppendix 2 and eTables 2 and 5 in the Supplement).
For SSBs and BMI, data are change in BMI calculated as weight in kilograms divided by height in meters squared; for sodium and SBP,change in SBP in mm Hg. Effect sizes correspond to associations between increased consumption of each dietary factor and cardio metabolic risk. Analyses used age-specific RRs (eAppendix 2 and eTable 5 in the Supplement).5,14
Evidence suggests that SSBs are associated with increased cardiometabolic risk through relationships with BMI plus additional BMI-independent relationships of SSBs with CHD and type 2 diabetes (eAppendix 1 and eTable 5 in the Supplement).15
Estimated RRs are similar for PUFAs replacing carbohydrates (49.4% of US calories in 2012) or saturated fats (10.7% of US calories in 2012); the former is reported herein. For comparison, in sensitivity analyses we also evaluated estimated mortality associated with excess saturated fats in place of PUFAs.
A linear reduction in risk was modeled until 250 mg/d, with no additional benefit thereafter.
Evidence suggests that sodium is associated with increased mortality due to heart disease and stroke through effects on SBP.7,14 Effects of sodium on SBP, including evidence for larger effects among older adults, blacks, and hypertensiveindividuals,weredeterminedfromrandomizedclinicaltrials(eAppendix1andeTable5intheSupplement).7