Abstract
The Healthy Eating Index-2005 (HEI-2005) measures adherence to the 2005 Dietary Guidelines for Americans, but the association between the HEI-2005 and risk of chronic disease is not known. The Alternative Healthy Eating Index (AHEI), which is based on foods and nutrients predictive of chronic disease risk, was associated inversely with chronic disease risk previously. We updated the AHEI, including additional dietary factors involved in the development of chronic disease, and assessed the associations between the AHEI-2010 and the HEI-2005 and risk of major chronic disease prospectively among 71,495 women from the Nurses’ Health Study and 41,029 men from the Health Professionals Follow-Up Study who were free of chronic disease at baseline. During ≥24 y of follow-up, we documented 26,759 and 15,558 incident chronic diseases (cardiovascular disease, diabetes, cancer, or nontrauma death) among women and men, respectively. The RR (95% CI) of chronic disease comparing the highest with the lowest quintile was 0.84 (0.81, 0.87) for the HEI-2005 and 0.81 (0.77, 0.85) for the AHEI-2010. The AHEI-2010 and HEI-2005 were most strongly associated with coronary heart disease (CHD) and diabetes, and for both outcomes the AHEI-2010 was more strongly associated with risk than the HEI-2005 (P-difference = 0.002 and <0.001, respectively). The 2 indices were similarly associated with risk of stroke and cancer. These findings suggest that closer adherence to the 2005 Dietary Guidelines may lower risk of major chronic disease. However, the AHEI-2010, which included additional dietary information, was more strongly associated with chronic disease risk, particularly CHD and diabetes.
Introduction
The Dietary Guidelines for Americans aim to provide science-based dietary advice that promotes good health and reduces major chronic diseases in the United States. The Dietary Guidelines are the most visible source of nutrition advice in the United States and the cornerstone of federal nutrition policy (1). Thus, it is imperative that they provide optimal guidance for preventing chronic disease. The Healthy Eating Index (HEI)11, which quantified adherence to the 1995 Guidelines, was associated with only a modest reduction in risk of major chronic disease [fatal and nonfatal cardiovascular disease (CVD) or cancer and nontraumatic death] (2, 3). In 2005, the 6th edition of the Dietary Guidelines and a new food guide, MyPyramid, were released, and the HEI-2005 quantifies adherence to these guidelines (4). Whether diets that are most consistent with the 2005 Dietary Guidelines are associated with lower risk of major chronic disease has not been evaluated.
The Alternate Healthy Eating Index (AHEI) was created in 2002 as an alternative to the HEI and was based on foods and nutrients predictive of chronic disease risk. Higher scores on the AHEI were strongly associated with lower risk of major chronic disease (5) as well as risk of CVD (5), diabetes (6), heart failure (7), colorectal (8) and estrogen-receptor-negative breast cancer (9), and total and cardiovascular mortality (10). Since the creation of the AHEI, substantial evidence has emerged to support a role of additional dietary factors in the development of chronic disease. Thus, we created the AHEI-2010, a new measure of diet quality that incorporates current scientific evidence on diet and health. In this analysis, we assessed the association between the AHEI-2010 and the HEI-2005 and risk of major chronic disease in the 2 large prospective cohorts in which the earlier scores had been evaluated.
Participants and Methods
Study population.
In 1976, 121,700 female nurses aged 30–55 y enrolled in the Nurses’ Health Study (NHS) (11). In 1984, 81,757 of these women completed an extensive FFQ. The Health Professionals Follow-Up Study (HPFS) is a prospective cohort of 51,529 U.S. men, aged 40–75 y, who returned a questionnaire about diet and medical history in 1986 (12). Participants of both cohorts provided information on diet lifestyle factors, medical history, and newly diagnosed diseases through self-administered mailed questionnaires at baseline and updated every 2–4 y.
We excluded women and men with previously diagnosed CVD (myocardial infarction, angina, stroke, transient ischemic attack, and revascularization), diabetes, and cancer at baseline. We also excluded participants with invalid FFQ data (13), leaving 71,495 women and 41,029 men for analysis. The institutional review boards at the Harvard School of Public Health and Brigham and Women’s Hospital approved the study protocol.
Dietary assessment.
We used a previously validated FFQ (14–16) to collect dietary data in the NHS in 1984 and 1986 and subsequently every 4 y through 2006. In the HPFS, dietary information has been collected every 4 y, from 1986 to 2006. For each food item, a commonly used portion size was specified and participants were asked how often, on average, he or she had consumed that quantity over the past year. We calculated nutrient intake by multiplying the frequency of intake for each food by its nutrient content and summing nutrient contributions across all food items (13).
The HEI-2005.
The HEI-2005 was based on criteria in the Technical Report of the Healthy Eating Index-2005 (4) and includes 12 components that represent the major food groups found in MyPyramid and recommendations from the 2005 Dietary Guidelines for Americans (Supplemental Table 1). Components in the HEI-2005 were energy-adjusted on a density basis (per 1000 kcal/d).
We modified the scoring for the sodium component from the published HEI-2005 due to the lack of brand specificity and information about discretionary use of salt on some questionnaires. As done previously (2, 3), we divided the participants into 11 equal groups on the basis of the distribution of reported sodium intake (mg/d) and assigned corresponding scores of 0–10 (higher score for less sodium consumed).
AHEI- 2010.
The AHEI-2010 was based on a comprehensive review of the relevant literature and discussions with other nutrition researchers to identify foods and nutrients that have been associated consistently with lower risk of chronic disease in clinical and epidemiologic investigations, including information from the original AHEI (5). The rationale for variable selection and scoring criteria for the AHEI-2010 is described in Table 1, and all variables and scoring decisions for the AHEI-2010 were determined a priori. All AHEI-2010 components were scored from 0 (worst) to 10 (best), and the total AHEI-2010 score ranged from 0 (nonadherence) to 110 (perfect adherence).
TABLE 1.
Component | Criteria for minimum score (0) | Criteria for maximum score (10) | AHEI-2010 in women | AHEI-2010 in men |
Vegetables,2 servings/d | 0 | ≥5 | 5.4 ± 2.4 | 5.6 ± 2.6 |
Fruit,3 servings/d | 0 | ≥4 | 3.4 ± 2.4 | 3.7 ± 2.6 |
Whole grains,4 g/d | 0 | 1.8 ± 1.7 | 2.4 ± 2.0 | |
Women | 75 | |||
Men | 90 | |||
Sugar-sweetened beverages and fruit juice,5 servings/d | ≥1 | 0 | 3.0 ± 3.6 | 2.6 ± 3.5 |
Nuts and legumes,6 servings/d | 0 | ≥1 | 2.7 ± 2.5 | 4.1 ± 3.2 |
Red/processed meat,7 servings/d | ≥1.5 | 0 | 3.5 ± 3.1 | 3.1 ± 3.0 |
trans Fat,8 % of energy | ≥4 | ≤0.5 | 6.0 ± 1.7 | 7.8 ± 1.4 |
Long-chain (n-3) fats (EPA + DHA),9 mg/d | 0 | 250 | 6.2 ± 3.2 | 7.6 ± 3.1 |
PUFA,10,% of energy | ≤2 | ≥10 | 5.6 ± 2.0 | 4.7 ± 1.8 |
Sodium,11 mg/d | Highest decile | Lowest decile | 5.0 ± 3.2 | 5.0 ± 3.2 |
Alcohol,12 drinks/d | 5.1 ± 3.1 | 5.8 ± 3.3 | ||
Women | ≥2.5 | 0.5–1.5 | ||
Men | ≥3.5 | 0.5–2.0 | ||
Total | 0 | 110 | 47.6 ± 10.8 | 52.4 ± 11.5 |
Values are means ± SD unless otherwise noted. Researchers are invited to re-create and use the AHEI-2010 score in their own data. AHEI, Alternate Healthy Eating Index.
Vegetable consumption has been associated with lower risk of cardiovascular disease (CVD) (28, 29) and some cancers (52, 53). Green leafy vegetables in particular may lower risk of diabetes (30). All vegetables on the FFQ were included, except for potatoes (including French fries) because they are not associated with lower risk of chronic disease risk in epidemiologic studies (52, 61) and are associated with increased risk of diabetes (62). We considered 5 servings/d as ideal, which reflects the upper range of current dietary guidelines and is consistent with intervention studies of intermediate CVD risk factors (63). One serving is 0.5 cup of vegetables or 1 cup of green leafy vegetables (1 cup = 236.59 g).
Fruit consumption has been associated with lower risk of CVD (28, 29) and some cancers (52, 53). We included only whole fruit in our definition, because fruit juice is not associated with lower risk of CVD (51, 61) or cancer (61) and may increase risk of diabetes (64). We considered 4 servings/d to be ideal, which is consistent with the upper range of current dietary guidelines. One serving is 1 medium piece of fruit or 0.5 cup of berries (1 cup = 236.59 g).
Greater consumption of whole grains is associated with lower risk of CVD (32), diabetes (31), and colorectal cancer (65). Conversely, refined grains are not associated with lower risk and may increase risk of diabetes, coronary heart disease (CHD), and other chronic diseases (32, 37, 38). We used grams of whole grains, which accounts for the variability of the percentages of whole grain in various “whole grain” products (66). One serving of a 100% whole-grain product (i.e., 0.5 cup of oatmeal or brown rice) contains ~15–20 g of whole grains (per dry weight). We considered 75 g/d to be optimal (~5 servings/d) for women and 90 g/d (~6 servings/d) to be optimal for men on the basis of current guidelines for total grains.
Intake of sugar-sweetened beverages, including soda and fruit drinks, is associated with increased risk of weight gain and obesity (67), CVD (35), and diabetes (34). We included intake of fruit juice in this category, given the positive association with risk of diabetes (64) and lack of beneficial effects on CVD (51) or cancer (61).The association with pancreatic cancer risk is not well established (68). We considered ≥1 serving/d to be the least optimal on the basis of the associations in the literature. One serving is 8 oz (1 oz = 28.35 g).
Nuts, legumes, and vegetable protein (e.g., tofu) are important sources of protein and contain important constituents such as unsaturated fat, fiber, copper, magnesium, plant sterols, and other nutrients. Nuts and other vegetable proteins have been associated with lower risk of CVD, especially when used as a substitute for other protein sources, such as red meat (41). Nuts are also associated with lower risk of diabetes (42) and weight gain (69), whereas their relation to cancer is inconclusive (70). We considered 1 serving/d to be ideal on the basis of the AHEI recommendations and the current literature. One serving is 1 oz (1 oz = 28.35 g) of nuts or 1 tablespoon (15 mL) of peanut butter.
Consumption of red meat and processed meats is associated with greater risk of CHD (48), especially when substituted for nuts, poultry, or fish (41). Red meat and/or processed meats are also associated with higher risk of stroke (45, 46), diabetes (47), and colorectal and other cancers (52, 55). Less than 1 serving/mo was considered to be ideal, with an upper limit of ≥1.5 servings/d. One serving is 4 oz of unprocessed meat or 1.5 oz of processed meat (1 oz = 28.35 g).
-Isomers of fatty acids, formed by partial hydrogenation of vegetable oils to produce margarines and vegetable shortening, are associated with higher risk of CHD (71) and diabetes (72). Cutoffs are consistent with original AHEI cutoffs for trans fat.
One serving of fish per week, specifically of species high in long-chain (n-3) fatty acids EPA + DHA, is strongly protective against fatal cardiac arrhythmias and sudden cardiac death (73) and may lower the incidence of other CVD (43, 74). EPA + DHA were associated with lower risk of diabetes in some (40, 44), but not all (75), studies, and the relation with cancer risk is unclear. Because of the strength and consistency of fish and EPA + DHA on cardiac arrhythmias and CVD, we included this nutrient in the AHEI-2010 score. The cutoff for optimal intake (250 mg/d) is ~2 4-oz servings of fish /wk, which is consistent with current guidelines (1 oz = 28.35 g).
Replacing saturated fats with polyunsaturated fats leads to positive changes in lipid profiles (63), is associated with a lower risk of CHD (36), and may lower risk of type 2 diabetes (76). Furthermore, a low-fat diet had no beneficial effects on CVD risk factors, lipid profile, or blood pressure and did not reduce the risk of CVD, breast cancer, colon cancer, or total mortality (77–79). We gave the highest score to individuals with ≥10% of total energy intake from PUFA on the basis of current guidelines from the USDA and the AHA (50, 80). PUFA does not include EPA or DHA intake.
High sodium intake has been associated with higher blood pressure (81), and salt-preserved foods are associated with greater risk of stomach cancer (52), CVD (54), and total mortality (82). Furthermore, sodium-reduced diets significantly lowered blood pressure (83) and CVD risk in clinical trials (84). Large reductions in sodium intake, to levels recommended by the USDA (60), may prevent a substantial number of new cases of CHD (33). The cutoffs for sodium were based on deciles of distribution in the population, due to lack of brand specificity in the FFQ to accurately estimate absolute intake. Values in lowest decile were ≤1112 mg/d in women and ≤1612 mg/d in men and in highest decile were ≥3337 mg/d in women and ≥5271 mg/d in men at baseline.
In moderation, alcohol may be consumed as a part of an overall healthy diet. Moderate alcohol consumption has been associated with lower risk of CHD (85), dementia (86), diabetes (87), and all-cause and CVD mortality (88). However, in heavier quantities, alcohol increases the risk of certain cancers (52) and has other health and social implications such as alcoholism and alcohol-related injuries (89). Furthermore, many adults choose not to drink for various reasons. Thus, we assigned the highest score to moderate, and the worst score to heavy, alcohol consumers. Nondrinkers received a score of 2.5. We used gender-specific cutoffs, because the health effects of alcohol are seen at lower quantities in women than in men. One drink is 4 oz of wine, 12 oz of beer, or 1.5 oz of liquor (1 oz = 28.35 g).
Outcome definition.
We included incident CVD, diabetes, cancer, and nontraumatic death in our endpoint of selected major chronic disease. CVD, cancer, and diabetes are the first, second, and seventh leading causes of death in the United States, respectively (17). We also included diabetes because of its high prevalence in the United States (8.3% of adults) and because it is a leading cause of CVD and other health complications (18).When a participant reported an incident event, we requested permission to review medical records, which were reviewed by study investigators blinded to the participant’s risk factor status.
We defined CVD as coronary heart disease (CHD); nonfatal myocardial infarction and fatal CHD, stroke, or angina. Myocardial infarction was defined according to WHO criteria and cardiac-specific troponin levels (19). Strokes were confirmed by using the National Survey of Stroke criteria, which requirie neurological deficit of rapid or sudden onset lasting ≥24 h or until death (20). Angina was confirmed when a participant reported “angina pectoris” on the questionnaire and met one of the following criteria: ≥70% occlusion, coronary artery bypass graft; percutaneous transluminal coronary angioplasty; or coronary stenting.
Type 2 diabetes was defined as self-reported diabetes confirmed by a validated supplementary questionnaire (21). We used criteria proposed by the National Diabetes Data Group (22) (before 1998) and the American Diabetes Association criteria (after 1998). We included all cancers, except for those with relatively low mortality [nonmelanoma skin cancer; low-grade, organ-confined prostate cancer (stage A or B and Gleason grade <7) and in situ breast cancer].
We included deaths, except for those resulting from external causes (e.g., injuries and suicides). Deaths were reported by next of kin, postal authorities, or through the National Death Index (23). We attempted to confirm each cause of death by reviewing medical records or autopsy reports.
Statistical analysis.
Each participant contributed follow-up time from the return of the baseline questionnaire until the date of diagnosis of the first event (CHD, stroke, angina, diabetes, or cancer), date of death, or end of follow-up (June 2008 in women, February 2008 in men). Cases were excluded from subsequent follow-up; thus, each person contributed only one diagnosed endpoint to the analysis.
We calculated the cumulative mean of the diet scores to optimize the use of repeated dietary questionnaires. Because changes in diet after the development of intermediate endpoints (hypercholesterolemia, hypertension, and transient ischemic attacks) may confound the associations between diet and disease, we stopped updating dietary information after these diagnoses.
We calculated the HR for disease by quintiles of the dietary scores using multivariate Cox proportional hazard models as an estimate of the RR, with adjustment for potential confounders (see Table 2 for full list of covariates). A test for linear trend across quintiles was performed by assigning the median values to each quintile and modeled as a single continuous variable. All variables, except for baseline hypertension and hypercholesterolemia, were included in models as time-varying covariates. The summary risk estimate was calculated by pooling the RR from the cohorts with the use of a random-effects model (24). Between-study heterogeneity was evaluated by using the Cochran Q statistic.
TABLE 2.
HEI-2005 |
||||||
Q1 | Q2 | Q3 | Q4 | Q5 | P-linear trend2 | |
Major chronic disease | ||||||
Women | ||||||
Range | <53.5 | 53.5–60.0 | 60.1–65.3 | 65.4–71.3 | >71.3 | |
Median | 48.6 | 57.1 | 62.7 | 68.2 | 75.4 | |
Cases, n | 5901 | 5287 | 5224 | 5166 | 5181 | |
Age-adjusted | 1.0 (ref) | 0.84 (0.81, 0.88) | 0.80 (0.77, 0.83) | 0.75 (0.72, 0.78) | 0.68 (0.66, 0.71) | <0.001 |
Multivariate-adjusted3 | 1.0 (ref) | 0.91 (0.88, 0.95) | 0.90 (0.87, 0.94) | 0.88 (0.84, 0.91) | 0.84 (0.80, 0.87) | <0.001 |
Men | ||||||
Range | <53.6 | 52.6–60.0 | 60.0–66.3 | 66.3–73.2 | >73.2 | |
Median | 47.0 | 56.6 | 63.1 | 69.5 | 77.7 | |
Cases, n | 3373 | 3178 | 3052 | 2990 | 2965 | |
Age-adjusted | 1.0 (ref) | 0.90 (0.85, 0.94) | 0.83 (0.79, 0.87) | 0.80 (0.76, 0.84) | 0.74 (0.70, 0.78) | <0.001 |
Multivariate-adjusted | 1.0 (ref) | 0.95 (0.90,1.00) | 0.90 (0.85, 0.95) | 0.89 (0.85, 0.94) | 0.84 (0.80, 0.89) | <0.001 |
Pooled | ||||||
Multivariate-adjusted | 1.0 (ref) | 0.93 (0.89, 0.96) | 0.90 (0.87, 0.93) | 0.88 (0.85, 0.91) | 0.84 (0.81, 0.87) | <0.001 |
Cardiovascular disease | ||||||
Women | ||||||
Cases, n | 1168 | 980 | 932 | 896 | 892 | |
Multivariate-adjusted | 1.0 (ref) | 0.89 (0.82, 0.97) | 0.87 (0.79, 0.95) | 0.81 (0.74, 0.89) | 0.75 (0.68, 0.82) | <0.001 |
Men | ||||||
Cases, n | 1082 | 1057 | 1019 | 982 | 962 | |
Multivariate-adjusted | 1.0 (ref) | 0.97 (0.89, 1.06) | 0.91 (0.83, 1.00) | 0.89 (0.81, 0.98) | 0.84 (0.76, 0.92) | <0.001 |
Pooled | ||||||
Multivariate-adjusted | 1.0 (ref) | 0.93 (0.85, 1.02) | 0.89 (0.84, 0.95) | 0.85 (0.78, 0.93) | 0.79 (0.71, 0.88) | <0.0014 |
Coronary heart disease | ||||||
Women | ||||||
Cases, n | 469 | 376 | 375 | 337 | 329 | |
Multivariate-adjusted | 1.0 (ref) | 0.88 (0.77, 1.02) | 0.92 (0.80, 1.06) | 0.81 (0.70, 0.94) | 0.75 (0.64, 0.87) | <0.001 |
Men | ||||||
Cases, n | 548 | 495 | 472 | 475 | 433 | |
Multivariate-adjusted | 1.0 (ref) | 0.93 (0.82, 1.05) | 0.86 (0.75, 0.98) | 0.90 (0.79, 1.03) | 0.77 (0.67, 0.89) | 0.02 |
Pooled | ||||||
Multivariate-adjusted | 1.0 (ref) | 0.91 (0.83, 0.99) | 0.89 (0.81, 0.98) | 0.86 (0.78, 0.95) | 0.76 (0.68, 0.84) | <0.001 |
Stroke | ||||||
Women | ||||||
Cases, n | 380 | 345 | 353 | 332 | 351 | |
Multivariate-adjusted | 1.0 (ref) | 0.93 (0.80, 1.08) | 0.96 (0.82, 1.11) | 0.86 (0.74, 1.01) | 0.82 (0.70, 0.96) | 0.01 |
Men | ||||||
Cases, n | 218 | 218 | 200 | 186 | 189 | |
Multivariate-adjusted | 1.0 (ref) | 1.02 (0.84, 1.24) | 0.91 (0.74, 1.04) | 0.84 (0.68, 1.04) | 0.82 (0.66, 1.02) | 0.02 |
Pooled | ||||||
Multivariate-adjusted | 1.0 (ref) | 0.96 (0.86, 1.09) | 0.94 (0.83, 1.06) | 0.86 (0.75, 0.97) | 0.82 (0.72, 0.93) | <0.001 |
Diabetes | ||||||
Women | ||||||
Cases, n | 1367 | 1302 | 1171 | 1064 | 976 | |
Multivariate-adjusted | 1.0 (ref) | 0.97 (0.90, 1.05) | 0.91 (0.84, 0.99) | 0.84 (0.77, 0.92) | 0.83 (0.76, 0.90) | <0.001 |
Men | ||||||
Cases, n | 573 | 540 | 494 | 462 | 388 | |
Multivariate-adjusted | 1.0 (ref) | 0.96 (0.85, 1.08) | 0.91 (0.80, 1.03) | 0.89 (0.78, 1.01) | 0.82 (0.71, 0.94) | 0.003 |
Pooled | ||||||
Multivariate-adjusted | 1.0 (ref) | 0.97 (0.91, 1.03) | 0.91 (0.85, 0.98) | 0.86 (0.80, 0.92) | 0.82 (0.76, 0.89) | <0.001 |
Cancer | ||||||
Women | ||||||
Cases, n | 2510 | 2352 | 2387 | 2530 | 2590 | |
Multivariate-adjusted | 1.0 (ref) | 0.93 (0.88, 0.99) | 0.93 (0.88, 0.98) | 0.95 (0.90, 1.01) | 0.93 (0.87, 0.98) | 0.04 |
Men | ||||||
Cases, n | 1204 | 1067 | 1063 | 1113 | 1136 | |
Multivariate-adjusted | 1.0 (ref) | 0.87 (0.80, 0.95) | 0.86 (0.79, 0.93) | 0.89 (0.81, 0.97) | 0.86 (0.79, 0.94) | 0.003 |
Pooled | ||||||
Multivariate-adjusted | 1.0 (ref) | 0.91 (0.85, 0.97) | 0.90 (0.83, 0.97) | 0.93 (0.86, 0.99) | 0.90 (0.84, 0.96) | 0.001 |
HEI, Healthy Eating Index; Q, quintile; ref, reference.
Test for linear trend calculated by assigning the median value of diet score in each quintile and modeling this as a continuous variable in regression models.
Multivariate Cox proportional hazards models adjusted for age (in mo), energy (kcal/d, continuous), smoking status (5 categories), BMI (8 categories), aspirin (0, 1–6, ≥7 d/wk), physical activity (5 categories), vitamin E supplementation, family history of myocardial infarction, and family history of colon cancer; in the analysis in women, models adjusted for family history of breast cancer, menopausal status, and use of hormone therapy. All models were adjusted for history of hypertension and history of hypercholesterolemia, except where cancer was the only outcome.
-heterogeneity between studies <0.05 based on the Cochran Q statistic.
We formally compared the associations of the HEI-2005 and AHEI-2010 with disease risk, by including both diet scores in the model simultaneously and using a Wald test (see Supplemental Methods).
In addition, we examined the independent associations between the individual components of each diet score and risk of major chronic disease. Finally, we estimated the associations between the original HEI and the AHEI (5) and risk of chronic disease by using the same follow-up and definition of major chronic disease (including diabetes and angina). All analyses were carried out by using SAS version 9.2 (SAS Institute, Inc.), and a P value of <0.05 was considered significant.
Results
Among women in the NHS, we documented 26,759 incident chronic disease events (4868 CVD, 12,369 cancer, 5880 diabetes, and 3642 nontraumatic deaths) over 24 y of follow-up. Among men, we documented 15,558 chronic disease events (5102 CVD, 5583 cancers, 2457 diabetes, and 2416 nontraumatic deaths) over 22 y of follow-up. The correlation between HEI-2005 and AHEI-2010 scores was high, because the scores shared several important components such as a high intake of vegetables, whole fruit, and whole grains, and a low intake of sodium (r = 0.65, P < 0.001 in women; r = 0.68, P < 0.001 in men).
For both diet scores, participants with greater adherence tended to have lower BMI, to exercise more, and were less likely to be a current smoker;women were more likely to use hormone therapy (Supplemental Table 2).
Risk of major chronic disease.
The HEI-2005 was inversely associated with risk of major chronic disease among women and men (P-trend < 0.001) in age-adjusted models (Table 2). Although further adjustment for confounders attenuated the associations, the HEI-2005 remained significantly associated with lower risk (P-trend < 0.001). The pooled RR for major chronic disease comparing the highest with the lowest quintile of the original HEI was similar in magnitude [RR: 0.85 (95% CI: 0.82, 0.88)] (data not shown). The correlation between the HEI and HEI-2005 was 0.50 (P < 0.001) in women and 0.65 (P < 0.001) in men. The HEI-2005 was significantly inversely associated with risk of each of the major chronic diseases individually, including total CVD, CHD, stroke, diabetes, and total cancer, among both women and men (Table 2).
The AHEI-2010 was associated inversely with risk of major chronic disease in both women and men in age-adjusted and multivariate models (P-trend < 0.001 for both) (Table 3). The AHEI-2010 was strongly correlated with the AHEI (r = 0.67 in women and 0.77 in men, P < 0.001). For men and women combined, the RR of major chronic disease comparing the highest with the lowest quintile was 0.81 (95% CI: 0.77, 0.85) for both the AHEI and the AHEI-2010.
TABLE 3.
AHEI-2010 |
||||||
Q1 | Q2 | Q3 | Q4 | Q5 | P-linear trend2 | |
Major chronic disease | ||||||
Women | ||||||
Range | <40.3 | 40.3–46.0 | 46.1–51.3 | 51.4–57.8 | >57.8 | |
Median | 36.2 | 43.4 | 48.6 | 54.3 | 62.7 | |
Cases, n | 5879 | 5414 | 5333 | 5092 | 5041 | |
Age-adjusted | 1.0 (ref) | 0.85 (0.82, 0.88) | 0.80 (0.77, 0.83) | 0.73 (0.70, 0.76) | 0.67 (0.65, 0.70) | <0.001 |
Multivariate-adjusted3 | 1.0 (ref) | 0.90 (0.87, 0.94) | 0.87 (0.84, 0.90) | 0.82 (0.79, 0.85) | 0.79 (0.76, 0.82) | <0.001 |
Men | ||||||
Range | <42.6 | 42.6–49.2 | 49.3–55.2 | 55.3–62.3 | >62.3 | |
Median | 38.0 | 46.1 | 52.2 | 58.4 | 67.6 | |
Cases, n | 3210 | 3137 | 3119 | 3077 | 3016 | |
Age-adjusted | 1.0 (ref) | 0.92 (0.87, 0.96) | 0.86 (0.82, 0.90) | 0.81 (0.77, 0.85) | 0.74 (0.70, 0.78) | <0.001 |
Multivariate-adjusted | 1.0 (ref) | 0.96 (0.91, 1.00) | 0.91 (0.86, 0.96) | 0.88 (0.83, 0.93) | 0.83 (0.79, 0.87) | <0.001 |
Pooled | ||||||
Multivariate-adjusted | 1.0 (ref) | 0.93 (0.88, 0.98) | 0.89 (0.85, 0.92) | 0.85 (0.79, 0.91)4 | 0.81 (0.77, 0.85) | <0.0014 |
Cardiovascular disease | ||||||
Women | ||||||
Cases, n | 1101 | 1010 | 938 | 915 | 904 | |
Multivariate-adjusted | 1.0 (ref) | 0.91 (0.84, 0.99) | 0.82 (0.75, 0.89) | 0.79 (0.72, 0.86) | 0.74 (0.67, 0.81) | <0.001 |
Men | ||||||
Cases, n | 1062 | 1062 | 1029 | 989 | 960 | |
Multivariate-adjusted | 1.0 (ref) | 0.96 (0.88, 1.05) | 0.89 (0.81, 0.97) | 0.84 (0.77, 0.92) | 0.78 (0.71, 0.86) | <0.001 |
Pooled | ||||||
Multivariate-adjusted | 1.0 (ref) | 0.94 (0.88, 1.00) | 0.85 (0.79, 0.93) | 0.81 (0.76, 0.87) | 0.76 (0.71, 0.81) | <0.001 |
Coronary heart disease | ||||||
Women | ||||||
Cases, n | 453 | 406 | 351 | 343 | 333 | |
Multivariate-adjusted | 1.0 (ref) | 0.89 (0.78, 1.02) | 0.74 (0.64, 0.86) | 0.72 (0.62, 0.84) | 0.67 (0.58, 0.78) | <0.001 |
Men | ||||||
Cases, n | 522 | 548 | 465 | 455 | 433 | |
Multivariate-adjusted | 1.0 (ref) | 1.01 (0.89, 1.14) | 0.81 (0.71, 0.92) | 0.78 (0.68, 0.89) | 0.70 (0.61, 0.80) | <0.001 |
Pooled | ||||||
Multivariate-adjusted | 1.0 (ref) | 0.50 (0.85, 1.05) | 0.78 (0.71, 0.86) | 0.75 (0.68, 0.83) | 0.69 (0.62, 0.76) | <0.001 |
Stroke | ||||||
Women | ||||||
Cases, n | 361 | 346 | 372 | 331 | 351 | |
Multivariate-adjusted | 1.0 (ref) | 0.92 (0.79, 1.07) | 0.95 (0.82, 1.11) | 0.83 (0.71, 0.97) | 0.83 (0.71, 0.97) | 0.01 |
Men | ||||||
Cases, n | 215 | 200 | 201 | 203 | 192 | |
Multivariate-adjusted | 1.0 (ref) | 0.90 (0.74, 1.11) | 0.86 (0.70, 1.05) | 0.85 (0.70, 1.04) | 0.76 (0.62, 0.94) | 0.01 |
Pooled | ||||||
Multivariate-adjusted | 1.0 (ref) | 0.92 (0.81, 1.03) | 0.92 (0.82, 1.03) | 0.84 (0.74, 0.95) | 0.80 (0.71, 0.91) | <0.001 |
Diabetes | ||||||
Women | ||||||
Cases, n | 1569 | 1312 | 1171 | 1006 | 822 | |
Multivariate-adjusted | 1.0 (ref) | 0.88 (0.81, 0.94) | 0.81 (0.75, 0.87) | 0.74 (0.68, 0.80) | 0.65 (0.59, 0.71) | <0.001 |
Men | ||||||
Cases, n | 598 | 527 | 491 | 464 | 397 | |
Multivariate-adjusted | 1.0 (ref) | 0.89 (0.78, 1.00) | 0.85 (0.75, 0.96) | 0.84 (0.74, 0.95) | 0.72 (0.63, 0.82) | <0.001 |
Pooled | ||||||
Multivariate-adjusted | 1.0 (ref) | 0.88 (0.82, 0.94) | 0.82 (0.77, 0.87) | 0.78 (0.69, 0.88) | 0.67 (0.61, 0.74) | <0.0014 |
Cancer | ||||||
Women | ||||||
Cases, n | 2412 | 2389 | 2512 | 2429 | 2627 | |
Multivariate-adjusted | 1.0 (ref) | 0.94 (0.89, 1.00) | 0.96 (0.91, 1.02) | 0.90 (0.85, 0.95) | 0.93 (0.88, 0.99) | 0.01 |
Men | ||||||
Cases, n | 1066 | 1079 | 1115 | 1118 | 1205 | |
Multivariate-adjusted | 1.0 (ref) | 0.97 (0.89, 1.05) | 0.96 (0.88, 1.04) | 0.93 (0.85, 1.01) | 0.94 (0.87, 1.03) | 0.13 |
Pooled | ||||||
Multivariate-adjusted | 1.0 (ref) | 0.95 (0.91, 1.00) | 0.96 (0.91, 1.01) | 0.91 (0.87, 0.95) | 0.94 (0.89, 0.98) | 0.003 |
AHEI, Alternative Healthy Eating Index; Q, quintile; ref, reference.
Test for linear trend calculated by assigning the median value of diet score in each quintile and modeling this as a continuous variable in regression models.
Multivariate Cox proportional hazards models adjusted for age (in mo), energy (kcal/d, continuous), smoking status (5 categories), BMI (8 categories),aspirin (0, 1–6, ≥7 d/wk), physical activity (5 categories), vitamin E supplementation, family history of myocardial infarction, and family history of colon cancer; in the analysis in women, models adjusted for family history of breast cancer, menopausal status, and use of hormone therapy. All models were adjusted for history of hypertension and history of hypercholesterolemia, except where cancer was the only outcome.
-heterogeneity between studies < 0.05 based on the Cochran Q statistic.
Higher AHEI-2010 scores were inversely associated with risk of CVD (P-trend < 0.001), and the AHEI-2010 was more strongly associated with risk of CHD than stroke (Table 3). The AHEI-2010 was inversely associated with risk of diabetes (Table 3). The AHEI-2010 was inversely associated with risk of total cancer in women (P-trend = 0.01) but not in men (P-trend = 0.13). However, in pooled analysis, the AHEI-2010 was inversely associated with cancer (P-trend = 0.003) (Table 3).
Comparison of the HEI-2005 and AHEI-201.
When included in the same model, the AHEI-2010 was more strongly associated with the risk of major chronic disease than the HEI-2005 (P-difference in diet scores < 0.001) (Table 4). The association between the AHEI-2010 and risk of major chronic disease was minimally attenuated when the HEI-2005 was included in the model. For the HEI-2005, the RR for chronic disease was attenuated, although remained significant after adjustment for the AHEI-2010.
TABLE 4.
Dietary score |
P-similar effects of diet scores3 | ||||||
Q1 | Q2 | Q3 | Q4 | Q5 | P-linear trend2 | ||
Major chronic disease | |||||||
HEI-20054 | 1.0 (ref) | 0.96 (0.93, 0.99) | 0.96 (0.93, 0.99) | 0.96 (0.93, 0.99) | 0.94 (0.90, 0.98) | 0.003 | <0.001 |
AHEI-20105 | 1.0 (ref) | 0.94 (0.88, 0.99) | 0.90 (0.86, 0.95) | 0.87 (0.80, 0.94)6 | 0.83 (0.78, 0.90) | <0.0016 | |
Cardiovascular disease | |||||||
HEI-2005 | 1.0 (ref) | 0.96 (0.89, 1.04) | 0.96 (0.89, 1.03) | 0.95 (0.86, 1.04) | 0.91 (0.80, 1.04) | 0.17 | 0.06 |
AHEI-2010 | 1.0 (ref) | 0.95 (0.89, 1.01) | 0.87 (0.81, 0.93) | 0.84 (0.78, 0.90) | 0.80 (0.74, 0.86) | <0.001 | |
Coronary heart disease | |||||||
HEI-2005 | 1.0 (ref) | 0.97 (0.88, 1.07) | 1.01 (0.91, 1.12) | 1.03 (0.92, 1.16) | 0.97 (0.86, 1.10) | 0.99 | 0.002 |
AHEI-2010 | 1.0 (ref) | 0.95 (0.85, 1.06) | 0.78 (0.70, 0.86) | 0.75 (0.67, 0.84) | 0.69 (0.61, 0.78) | <0.001 | |
Stroke | |||||||
HEI-2005 | 1.0 (ref) | 0.99 (0.88, 1.12) | 0.98 (0.86, 1.12) | 0.91 (0.79, 1.05) | 0.90 (0.77, 1.05) | 0.12 | 0.87 |
AHEI-2010 | 1.0 (ref) | 0.93 (0.82, 1.05) | 0.94 (0.83, 1.07) | 0.87 (0.76, 1.00) | 0.86 (0.74, 1.00) | 0.03 | |
Diabetes | |||||||
HEI-2005 | 1.0 (ref) | 1.03 (0.97, 1.11) | 1.03 (0.95, 1.10) | 1.02 (0.94, 1.10) | 1.06 (0.96, 1.16) | 0.38 | <0.001 |
AHEI-2010 | 1.0 (ref) | 0.87 (0.82, 0.93) | 0.81 (0.75, 0.87) | 0.77 (0.67, 0.89) | 0.66 (0.57, 0.76) | <0.0016 | |
Cancer | |||||||
HEI-2005 | 1.0 (ref) | 0.91 (0.84, 0.99) | 0.91 (0.82, 1.01) | 0.94 (0.84, 1.05) | 0.91 (0.81, 1.03) | 0.16 | 0.23 |
AHEI-2010 | 1.0 (ref) | 0.97 (0.92, 1.02) | 0.98 (0.93, 1.03) | 0.95 (0.86, 1.03) | 0.97 (0.90, 1.05) | 0.10 |
Values were estimated from Cox proportional hazards models adjusted for age (in mo), energy (kcal/d, continuous), smoking status (5 categories), BMI (8 categories), aspirin (0, 1–6, ≥7 d/wk), physical activity (5 categories), vitamin E supplementation, family history of myocardial infarction, and family history of colon cancer; in the analysis in women, models additionally adjusted for family history of breast cancer, menopausal status, and use of hormone therapy. All models were adjusted for history of hypertension and history of hypercholesterolemia, except where cancer was the only outcome. The risk estimates from each cohort were pooled by using the DerSimonian and Laird random-effects model. AHEI, Alternative Healthy Eating Index; HEI, Healthy Eating Index; Q, quintile; ref, reference.
Test for linear trend calculated by assigning the median value of diet score in each quintile and modeling this as a continuous variable in regression models.
-value based on the Wald test evaluating the hypothesis that the β-coefficient in quintile 5 for the AHEI-2010 equals the β-coefficient in quintile 5 for the HEI-2005.
Additionally adjusted for the AHEI-2010 (quintiles).
Additionally adjusted for the HEI-2005 (quintiles).
-heterogeneity between studies <0.05 based on the Cochran Q statistic.
The AHEI-2010 was more strongly associated with risk of CHD (P-difference between diet scores = 0.002) and diabetes (P-difference between diet scores < 0.001) (Table 4). The association between the AHEI-2010 and risk of CHD and diabetes was not attenuated and remained significant after adjustment for the HEI-2005. Conversely, the HEI-2005 was not significantly associated with risk of CHD or diabetes after adjustment for the AHEI-2010 (Table 4). For both stroke and cancer, we did not detect significance differences in association between the diet scores (P-difference in diet scores: 0.87 for stroke and 0.23 for cancer).
Individual components of the HEI-2005 and AHEI-2010 and risk of disease.
The components of the HEI-2005 that were independently associated with lower risk of major chronic disease were dark-green and orange vegetables, whole fruit, and whole grains and to a lesser extent total grains, milk, vegetable oils, and a low intake of sodium (Supplemental Table 3). For the AHEI-2010, a higher intake of whole grains, nuts, and alcoholic beverages and a lower intake of sugar-sweetened beverages and red/processed meats were associated with lower risk of major chronic disease.
For the HEI-2005, dark-green and orange vegetables, whole grains, and energy from solid fat, alcohol, and added sugar were significantly associated with lower risk of CHD and diabetes. The inverse association for the solid fat, alcohol, and added sugar component was driven by alcohol intake. In addition, a high intake of whole fruit, milk, and oils and a low intake of sodium and saturated fat were associated with risk of diabetes. Vegetable oils were associated with risk of CHD among women only. For the AHEI-2010, whole grains and alcoholic beverages were inversely associated, and red and processed meats were positively associated with risk of CHD and diabetes; in addition, sugar-sweetened beverages, sodium, and EPA + DHA were also associated with greater risk of diabetes.
Discussion
In these 2 large prospective cohorts, women and men whose diets most closely matched the goals of the 2005 Dietary Guidelines, as assessed by the HEI-2005, had a 16% lower risk of major chronic disease, which was attributable to a 23% lower risk of CHD and 18% lower risk of diabetes. Higher scores on an alternative dietary index, the AHEI-2010, were associated with a 19% lower risk of chronic disease, a 31% lower risk of CHD, and a 33% lower risk of diabetes. When modeled simultaneously, the AHEI-2010 was associated more strongly with risk of major chronic disease, CHD, and diabetes than was the HEI-2005. There were no significant differences in the association between the AHEI-2010 and HEI-2005 and risk of either stroke or cancer.
The inverse association between the HEI-2005 and CHD and diabetes is consistent with previous studies in which greater adherence to the 2005 Dietary Guidelines was associated with lower prevalence of the metabolic syndrome (25), reduced atherosclerotic progression (26), and lower insulin resistance (among women only) (27). The HEI-2005 was not associated with lower risk of CHD and diabetes after adjustment for the AHEI-2010; however, the inverse association between the AHEI-2010 and risk remained strong after adjustment for the HEI-2005. Although there are common and beneficial components of both diet scores—with their emphasis on increasing vegetables (28–30), fruit (28, 29), and whole grains (31, 32) and reducing sodium (33), added sugar (34, 35), and saturated fat (36)—the AHEI-2010 captures additional information on diet quality that may lower the risk of metabolic diseases further. For example, the AHEI-2010 emphasizes intake of whole, not total, grains; refined grains are not associated with lower risk of metabolic diseases and may increase risk (37, 38). The AHEI-2010 provides separate recommendations for protein sources, given their different effects on health; nuts, legumes, and fish, specifically those high in EPA + DHA, are associated with lower risk of metabolic diseases (39–44), whereas red and processed meats are associated with greater risk (41, 45–48). The AHEI-2010 promotes a high intake of PUFA, at levels consistent with current recommendations from the American Heart Association (49, 50). Finally, the AHEI-2010 provides quantitative guidance for reduction in sugar-sweetened beverages, separate from other discretionary calories, given their positive association with risk of CHD (35, 51) and diabetes (34). One or more of these components may contribute to the additional benefits of the AHEI-2010 on CHD and diabetes risk.
Many of the components of the diet scores were included because of their associations with CHD and diabetes specifically, because fewer optimal dietary factors have been established for the prevention of stroke and cancer. Yet, the AHEI-2010 and HEI-2005 were both associated with lower risk of cancer and stroke as well. Both diet scores emphasize high intakes of fruit, vegetables, and whole grains and low sodium intake, because these have been associated with lower risk of cancer (52, 53) and/or stroke (29, 32, 54). In addition, the AHEI-2010 emphasizes a low intake of red and processed meats, which is a risk factor for certain cancers (52, 55), whereas dairy foods, a component of the HEI-2005, may lower risk of colon cancer (56).
Total cancer is a heterogeneous endpoint, and dietary factors may play a stronger role in the etiology of certain cancers. For example, the HEI-2005 was associated with lower risk of colorectal (8, 57), but not endometrial (58), cancer, whereas the AHEI was associated with lower risk of colorectal cancer (8) and estrogen-receptor-negative, but not estrogen-receptor-positive, breast cancer (9). Thus, future studies should assess the association between the HEI-2005 and AHEI-2010 diet scores and other organ-specific cancers.
Greater adherence to the 2005 Dietary Guidelines predicted lower risk of chronic disease to a similar degree as adherence to the prior guidelines, as assessed by the HEI. In the current analysis, the magnitude of association between the original HEI and risk of major chronic disease (RR for quintile 5 vs. quintile 1: 0.85) was consistent with the prior association observed for major chronic disease risk (without diabetes) in the HPFS after 8 y of follow-up (RR for quintile 5 vs. quintile 1: 0.89) (2). The inclusion of diabetes in the major chronic disease endpoint increased the proportion of metabolic diseases and may have strengthened the association among women, which was null previously (3). The association between the AHEI and the AHEI-2010 and risk of major chronic disease was also similar in magnitude. Although some components differ, the AHEI and AHEI-2010 captured a similar dietary pattern, as was evident in the strong correlations between the diet scores.
The Dietary Guidelines aim to provide a dietary pattern that, if followed, could lower major chronic disease. From an etiologic standpoint, it may not be appropriate to pool all chronic diseases. However, from a public health perspective, the prevention of all chronic diseases is important. Therefore, it is necessary to assess dietary scores on risk of total chronic disease, to identify the most scientifically sound dietary recommendations.
We included components in the AHEI-2010 on the basis of diet-disease relationships in the current literature, including reports from these cohorts. However, associations between individual components of the AHEI-2010 and chronic disease have been observed in many other populations, and the AHEI, which was derived in a similar fashion, was strongly predictive of CVD risk in several independent populations (7, 10). Nevertheless, further testing of the AHEI-2010 in independent study populations is warranted.
The dietary quality within these cohorts of mostly white, well-educated health professionals may not be representative of the dietary quality in the United States. The mean HEI-2005 in these cohorts (mean: 62.3 in women; 62.7 in men) is slightly higher compared with the HEI-2005 in the general U.S. population (mean score = 57.5) (59). In addition, these analyses were based on the 2005 Dietary Guidelines, which were recently updated (60). The HEI-2010 has not been released, and thus we cannot assess adherence to the most recent guidelines. The impact of adherence to the new guidelines should be evaluated in future studies. Finally, many lifestyle factors play an important role in the development of chronic disease and may confound the association between diet quality and disease risk. Although we controlled for these factors in our analysis, residual confounding remains possible. Importantly, the educational and occupational homogeneity of this population minimizes variation in factors related to socioeconomic status that are associated with diet quality and could potentially confound our results.
In summary, the HEI-2005 was inversely associated with risk of major chronic disease, including CHD, stroke, diabetes, and total cancer. Thus, greater adherence to the 2005 Guidelines may reduce risk of major chronic disease. The AHEI-2010, which explicitly emphasizes high intakes of whole grains, PUFA, nuts, and fish and reductions in red and processed meats, refined grains, and sugar-sweetened beverages, was also associated with lower risk of chronic diseases; in models that adjusted for both scores, the AHEI-2010 was more strongly associated with CHD and diabetes. These results suggest that future revisions of Dietary Guidelines may consider special emphasis on selecting the healthiest choices within each food group, specifically high-quality grains (whole vs. refined grains) and protein sources (nuts/beans/fish vs. red/processed meats), and encouraging greater intake of PUFA and reducing intake of sugar-sweetened beverages. Adherence to dietary guidelines that include such modifications could potentially reduce risk of chronic disease even further, especially CHD and diabetes.
Supplementary Material
Acknowledgments
The authors thank Donna Spiegelman and Ellen Hertzmark for helpful comments and guidance in the statistical analysis. S.E.C., T.T.F., E.B.R., F.B.H., M.J.S., and W.C.W. designed the research; S.E.C. performed statistical analysis and holds primary responsibility for the final content; S.E.C. drafted the manuscript; and all of the authors contributed intellectual content to the manuscript. All authors read and approved the final manuscript.
Footnotes
Supported by research grants HL35464, HL34594, HL088521, CA55075, CA87969, HL60712, and CA58895from the National Institutes of Health. S.E.C. is supported by NIH grant K99 HL097068 and a Clinical Research Program Award from the American Heart Association.
Supplemental Tables 1–3 and Supplemental Methods are available from the “Online Supporting Material” link in the online posting of the article and from the same link in the online table of contents at http://jn.nutrition.org.
Abbreviations used: AHEI, Alternate Healthy Eating Index; CHD, coronary heart disease; CVD, cardiovascular disease; HEI, Healthy Eating Index; HPFS, Health Professionals Follow-Up Study; NHS, Nurses’ Health Study.
Literature Cited
- 1.U.S. Department of Health and Human Services, U. S. Department of Agriculture Dietary guidelines for Americans, 2005. 6th ed Washington, DC: U.S. Government Printing Office; 2005 [Google Scholar]
- 2.McCullough ML, Feskanich D, Rimm EB, Giovannucci E, Ascherio A, Variyam JN, Spiegelmen D, Stampfer MJ, Willett WC. Adherence to the Dietary Guidelines for Americans and risk of major chronic disease in men. Am J Clin Nutr. 2000;72:1223–31 [DOI] [PubMed] [Google Scholar]
- 3.McCullough ML, Feskanich D, Stampfer MJ, Rosner BA, Hu FB, Hunter DJ, Variyam JN, Colditz GA, Willett WC. Adherence to the Dietary Guidelines for Americans and risk of major chronic disease in women. Am J Clin Nutr. 2000;72:1214–22 [DOI] [PubMed] [Google Scholar]
- 4.Guenther PM, Reedy J, Krebs-Smith SM. Development of the Healthy Eating Index-2005. J Am Diet Assoc. 2008;108:1896–901 [DOI] [PubMed] [Google Scholar]
- 5.McCullough ML, Feskanich D, Stampfer MJ, Giovannucci EL, Rimm EB, Hu FB, Spiegelman D, Hunter DJ, Colditz GA, Willett WC. Diet quality and major chronic disease risk in men and women: moving toward improved dietary guidance. Am J Clin Nutr. 2002;76:1261–71 [DOI] [PubMed] [Google Scholar]
- 6.Fung TT, McCullough M, van Dam RM, Hu FB. A prospective study of overall diet quality and risk of type 2 diabetes in women. Diabetes Care. 2007;30:1753–7 [DOI] [PubMed] [Google Scholar]
- 7.Belin RJ, Greenland P, Allison M, Martin L, Shikany JM, Larson J, Tinker L, Howard BV, Lloyd-Jones D, Van Horn L. Diet quality and the risk of cardiovascular disease: the Women's Health Initiative (WHI). Am J Clin Nutr. 2011;94:49–57 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 8.Reedy J, Mitrou PN, Krebs-Smith SM, Wirfalt E, Flood A, Kipnis V, Leitzmann M, Mouw T, Hollenbeck A, Schatzkin A, et al. Index-based dietary patterns and risk of colorectal cancer: the NIH-AARP Diet and Health Study. Am J Epidemiol. 2008;168:38–48 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 9.Fung TT, Hu FB, McCullough ML, Newby PK, Willett WC, Holmes MD. Diet quality is associated with the risk of estrogen receptor-negative breast cancer in postmenopausal women. J Nutr. 2006;136:466–72 [DOI] [PubMed] [Google Scholar]
- 10.Akbaraly TN, Ferrie JE, Berr C, Brunner EJ, Head J, Marmot MG, Singh-Manoux A, Ritchie K, Shipley MJ, Kivimaki M. Alternative Healthy Eating Index and mortality over 18 y of follow-up: results from the Whitehall II cohort. Am J Clin Nutr. 2011;94:247–53 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 11.Willett WC, Green A, Stampfer MJ, Speizer FE, Colditz GA, Rosner B, Monson R, Stason W, Hennekens CH. Relative and absolute excess risks of coronary heart disease among women who smoke cigarettes. N Engl J Med. 1987;317:1303–9 [DOI] [PubMed] [Google Scholar]
- 12.Colditz GA, Rimm EB, Giovannucci E, Stampfer MJ, Rosner BA, Willett WC. A prospective study of parental history of myocardial infarction and coronary artery disease in men. Am J Cardiol. 1991;67:933–8 [DOI] [PubMed] [Google Scholar]
- 13.Giovannucci E, Stampfer MJ, Colditz GA, Rimm EB, Willett WC. Relationship of diet to risk of colorectal adenoma in men. J Natl Cancer Inst. 1992;84:91–8 [DOI] [PubMed] [Google Scholar]
- 14.Rimm EB, Giovannucci EL, Stampfer MJ, Colditz GA, Litin LB, Willett WC. Reproducibility and validity of an expanded self-administered semiquantitative food frequency questionnaire among male health professionals. Am J Epidemiol. 1992;135:1114–26 [DOI] [PubMed] [Google Scholar]
- 15.Feskanich D, Rimm EB, Giovannucci EL, Colditz GA, Stampfer MJ, Litin LB, Willett WC. Reproducibility and validity of food intake measurements from a semiquantitative food frequency questionnaire. J Am Diet Assoc. 1993;93:790–6 [DOI] [PubMed] [Google Scholar]
- 16.Giovannucci E, Colditz G, Stampfer MJ, Rimm EB, Litin L, Sampson L, Willett WC. The assessment of alcohol consumption by a simple self-administered questionnaire. Am J Epidemiol. 1991;133:810–7 [DOI] [PubMed] [Google Scholar]
- 17.Heron M. Deaths: leading causes for 2007. Natl Vital Stat Rep. 2011;59:1–95 [PubMed] [Google Scholar]
- 18.Centers for Disease Control and Prevention National diabetes fact sheet: national estimates and general information on diabetes and prediabetes in the United States, 2011. Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention; 2011 [Google Scholar]
- 19.Alpert JS, Thygesen K, Antman E, Bassand JP. Myocardial infarction redefined–a consensus document of The Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction. J Am Coll Cardiol. 2000;36:959–69 [DOI] [PubMed] [Google Scholar]
- 20.Walker AE, Robins M, Weinfeld FD. The National Survey of Stroke: clinical findings. Stroke. 1981;12: supp 1:I13–44 [PubMed] [Google Scholar]
- 21.Manson JE, Colditz GA, Stampfer MJ, Willett WC, Krolewski AS, Rosner B, Arky RA, Speizer FE, Hennekens CH. A prospective study of maturity-onset diabetes mellitus and risk of coronary heart disease and stroke in women. Arch Intern Med. 1991;151:1141–7 [PubMed] [Google Scholar]
- 22.National Diabetes Data Group Classification and diagnosis of diabetes mellitus and other categories of glucose intolerance. Diabetes. 1979;28:1039–57 [DOI] [PubMed] [Google Scholar]
- 23.Stampfer MJ, Willett WC, Speizer FE, Dysert DC, Lipnick R, Rosner B, Hennekens CH. Test of the National Death Index. Am J Epidemiol. 1984;119:837–9 [DOI] [PubMed] [Google Scholar]
- 24.DerSimonian R, Laird N. Meta-analysis in clinical trials. Control Clin Trials. 1986;7:177–88 [DOI] [PubMed] [Google Scholar]
- 25.Fogli-Cawley JJ, Dwyer JT, Saltzman E, McCullough ML, Troy LM, Meigs JB, Jacques PF. The 2005 Dietary Guidelines for Americans and risk of the metabolic syndrome. Am J Clin Nutr. 2007;86:1193–201 [DOI] [PubMed] [Google Scholar]
- 26.Imamura F, Jacques PF, Herrington DM, Dallal GE, Lichtenstein AH. Adherence to 2005 Dietary Guidelines for Americans is associated with a reduced progression of coronary artery atherosclerosis in women with established coronary artery disease. Am J Clin Nutr. 2009;90:193–201 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 27.Fogli-Cawley JJ, Dwyer JT, Saltzman E, McCullough ML, Troy LM, Meigs JB, Jacques PF. The 2005 Dietary Guidelines for Americans and insulin resistance in the Framingham Offspring Cohort. Diabetes Care. 2007;30:817–22 [DOI] [PubMed] [Google Scholar]
- 28.He FJ, Nowson CA, Lucas M, MacGregor GA. Increased consumption of fruit and vegetables is related to a reduced risk of coronary heart disease: meta-analysis of cohort studies. J Hum Hypertens. 2007;21:717–28 [DOI] [PubMed] [Google Scholar]
- 29.He FJ, Nowson CA, MacGregor GA. Fruit and vegetable consumption and stroke: meta-analysis of cohort studies. Lancet. 2006;367:320–6 [DOI] [PubMed] [Google Scholar]
- 30.Carter P, Gray LJ, Troughton J, Khunti K, Davies MJ. Fruit and vegetable intake and incidence of type 2 diabetes mellitus: systematic review and meta-analysis. BMJ. 2010;341:c4229. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 31.de Munter JS, Hu FB, Spiegelman D, Franz M, van Dam RM. Whole grain, bran, and germ intake and risk of type 2 diabetes: a prospective cohort study and systematic review. PLoS Med. 2007;4:e261. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 32.Mellen PB, Walsh TF, Herrington DM. Whole grain intake and cardiovascular disease: a meta-analysis. Nutr Metab Cardiovasc Dis. 2008;18:283–90 [DOI] [PubMed] [Google Scholar]
- 33.Bibbins-Domingo K, Chertow GM, Coxson PG, Moran A, Lightwood JM, Pletcher MJ, Goldman L. Projected effect of dietary salt reductions on future cardiovascular disease. N Engl J Med. 2010;362:590–9 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 34.Schulze MB, Manson JE, Ludwig DS, Colditz GA, Stampfer MJ, Willett WC, Hu FB. Sugar-sweetened beverages, weight gain, and incidence of type 2 diabetes in young and middle-aged women. JAMA. 2004;292:927–34 [DOI] [PubMed] [Google Scholar]
- 35.Fung TT, Malik V, Rexrode KM, Manson JE, Willett WC, Hu FB. Sweetened beverage consumption and risk of coronary heart disease in women. Am J Clin Nutr. 2009;89:1037–42 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 36.Jakobsen MU, O'Reilly EJ, Heitmann BL, Pereira MA, Balter K, Fraser GE, Goldbourt U, Hallmans G, Knekt P, Liu S, et al. Major types of dietary fat and risk of coronary heart disease: a pooled analysis of 11 cohort studies. Am J Clin Nutr. 2009;89:1425–32 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 37.Sun Q, Spiegelman D, van Dam RM, Holmes MD, Malik VS, Willett WC, Hu FB. White rice, brown rice, and risk of type 2 diabetes in US men and women. Arch Intern Med. 2010;170:961–9 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 38.Barclay AW, Petocz P, McMillan-Price J, Flood VM, Prvan T, Mitchell P, Brand-Miller JC. Glycemic index, glycemic load, and chronic disease risk–a meta-analysis of observational studies. Am J Clin Nutr. 2008;87:627–37 [DOI] [PubMed] [Google Scholar]
- 39.Flight I, Clifton P. Cereal grains and legumes in the prevention of coronary heart disease and stroke: a review of the literature. Eur J Clin Nutr. 2006;60:1145–59 [DOI] [PubMed] [Google Scholar]
- 40.Djoussé L, Biggs ML, Lemaitre RN, King IB, Song X, Ix JH, Mukamal KJ, Siscovick DS, Mozaffarian D. Plasma omega-3 fatty acids and incident diabetes in older adults. Am J Clin Nutr. 2011;94:527–33 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 41.Bernstein AM, Sun Q, Hu FB, Stampfer MJ, Manson JE, Willett WC. Major dietary protein sources and risk of coronary heart disease in women. Circulation. 2010;122:876–83 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 42.Jiang R, Manson JE, Stampfer MJ, Liu S, Willett WC, Hu FB. Nut and peanut butter consumption and risk of type 2 diabetes in women. JAMA. 2002;288:2554–60 [DOI] [PubMed] [Google Scholar]
- 43.Mozaffarian D, Rimm EB. Fish intake, contaminants, and human health: evaluating the risks and the benefits. JAMA. 2006;296:1885–99 [DOI] [PubMed] [Google Scholar]
- 44.Villegas R, Xiang YB, Elasy T, Li HL, Yang G, Cai H, Ye F, Gao YT, Shyr Y, Zheng W, et al. Fish, shellfish, and long-chain n–3 fatty acid consumption and risk of incident type 2 diabetes in middle-aged Chinese men and women. Am J Clin Nutr. 2011;94:543–51 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 45.Larsson SC, Virtamo J, Wolk A. Red meat consumption and risk of stroke in Swedish men. Am J Clin Nutr. 2011;94:417–21 [DOI] [PubMed] [Google Scholar]
- 46.Larsson SC, Virtamo J, Wolk A. Red meat consumption and risk of stroke in Swedish women. Stroke. 2011;42:324–9 [DOI] [PubMed] [Google Scholar]
- 47.Pan A, Sun Q, Bernstein AM, Schulze MB, Manson JE, Willett WC, Hu FB. Red meat consumption and risk of type 2 diabetes: 3 cohorts of US adults and an updated meta-analysis. Am J Clin Nutr. 2011;94:1088–96 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 48.Micha R, Wallace SK, Mozaffarian D. Red and processed meat consumption and risk of incident coronary heart disease, stroke, and diabetes mellitus: a systematic review and meta-analysis. Circulation. 2010;121:2271–83 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 49.Kris-Etherton PM, Harris WS, Appel LJ. Omega-3 fatty acids and cardiovascular disease: new recommendations from the American Heart Association. Arterioscler Thromb Vasc Biol. 2003;23:151–2 [DOI] [PubMed] [Google Scholar]
- 50.Harris WS, Mozaffarian D, Rimm E, Kris-Etherton P, Rudel LL, Appel LJ, Engler MM, Engler MB, Sacks F. Omega-6 fatty acids and risk for cardiovascular disease: a science advisory from the American Heart Association Nutrition Subcommittee of the Council on Nutrition, Physical Activity, and Metabolism; Council on Cardiovascular Nursing; and Council on Epidemiology and Prevention. Circulation. 2009;119:902–7 [DOI] [PubMed] [Google Scholar]
- 51.Hansen L, Dragsted LO, Olsen A, Christensen J, Tjonneland A, Schmidt EB, Overvad K. Fruit and vegetable intake and risk of acute coronary syndrome. Br J Nutr. 2010;104:248–55 [DOI] [PubMed] [Google Scholar]
- 52.World Cancer Research Fund, American Institute for Cancer Research Food, nutrition, physical activity and the prevention of cancer: a global perspective. Washington, DC: American Institute for Cancer Research; 2007 [Google Scholar]
- 53.Gonzalez CA, Riboli E. Diet and cancer prevention: contributions from the European Prospective Investigation into Cancer and Nutrition (EPIC) study. Eur J Cancer. 2010;46:2555–62 [DOI] [PubMed] [Google Scholar]
- 54.Strazzullo P, D'Elia L, Kandala NB, Cappuccio FP. Salt intake, stroke, and cardiovascular disease: meta-analysis of prospective studies. BMJ. 2009;339:b4567. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 55.Cross AJ, Leitzmann MF, Gail MH, Hollenbeck AR, Schatzkin A, Sinha R. A prospective study of red and processed meat intake in relation to cancer risk. PLoS Med. 2007;4:e325. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 56.Huncharek M, Muscat J, Kupelnick B. Colorectal cancer risk and dietary intake of calcium, vitamin D, and dairy products: a meta-analysis of 26,335 cases from 60 observational studies. Nutr Cancer. 2009;61:47–69 [DOI] [PubMed] [Google Scholar]
- 57.Miller PE, Lazarus P, Lesko SM, Muscat JE, Harper G, Cross AJ, Sinha R, Ryczak K, Escobar G, Mauger DT, et al. Diet index-based and empirically derived dietary patterns are associated with colorectal cancer risk. J Nutr. 2010;140:1267–73 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 58.Chandran U, Bandera EV, Williams-King MG, Sima C, Bayuga S, Pulick K, Wilcox H, Zauber AG, Olson SH. Adherence to the Dietary Guidelines for Americans and endometrial cancer risk. Cancer Causes Control. 2010;21:1895–904 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 59.Guenther PM, Juan W, Lino M, Hiza HA, Fungwe T, Lucas R. Diet quality of low-income and higher income Americans in 2003–04 as measured by the Healthy Eating Index-2005. Washington, DC: Center for Nutrition Policy and Promotion, USDA; 2008 [Google Scholar]
- 60.U.S. Department of Agriculture, U.S. Department of Health and Human Services Dietary guidelines for Americans, 2010. 7th ed Washington, DC: U.S. Government Printing Office; 2010 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 61.Hung HC, Joshipura KJ, Jiang R, Hu FB, Hunter D, Smith-Warner SA, Colditz GA, Rosner B, Spiegelman D, Willett WC. Fruit and vegetable intake and risk of major chronic disease. J Natl Cancer Inst. 2004;96:1577–84 [DOI] [PubMed] [Google Scholar]
- 62.Halton TL, Willett WC, Liu S, Manson JE, Stampfer MJ, Hu FB. Potato and French fry consumption and risk of type 2 diabetes in women. Am J Clin Nutr. 2006;83:284–90 [DOI] [PubMed] [Google Scholar]
- 63.Appel LJ, Sacks FM, Carey VJ, Obarzanek E, Swain JF, Miller ER, 3rd, Conlin PR, Erlinger TP, Rosner BA, Laranjo NM, et al. Effects of protein, monounsaturated fat, and carbohydrate intake on blood pressure and serum lipids: results of the OmniHeart randomized trial. JAMA. 2005;294:2455–64 [DOI] [PubMed] [Google Scholar]
- 64.Bazzano LA, Li TY, Joshipura KJ, Hu FB. Intake of fruit, vegetables, and fruit juices and risk of diabetes in women. Diabetes Care. 2008;31:1311–7 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 65.Haas P, Machado MJ, Anton AA, Silva AS, De Francisco A. Effectiveness of whole grain consumption in the prevention of colorectal cancer: meta-analysis of cohort studies. Int J Food Sci Nutr. 2009;Mar 21.:1–13 [DOI] [PubMed] [Google Scholar]
- 66.Koh-Banerjee P, Franz M, Sampson L, Liu S, Jacobs DR, Jr, Spiegelman D, Willett W, Rimm E. Changes in whole-grain, bran, and cereal fiber consumption in relation to 8-y weight gain among men. Am J Clin Nutr. 2004;80:1237–45 [DOI] [PubMed] [Google Scholar]
- 67.Malik VS, Schulze MB, Hu FB. Intake of sugar-sweetened beverages and weight gain: a systematic review. Am J Clin Nutr. 2006;84:274–88 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 68.Bao Y, Stolzenberg-Solomon R, Jiao L, Silverman DT, Subar AF, Park Y, Leitzmann MF, Hollenbeck A, Schatzkin A, Michaud DS. Added sugar and sugar-sweetened foods and beverages and the risk of pancreatic cancer in the National Institutes of Health–AARP Diet and Health Study. Am J Clin Nutr. 2008;88:431–40 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 69.Bes-Rastrollo M, Sabate J, Gomez-Gracia E, Alonso A, Martinez JA, Martinez-Gonzalez MA. Nut consumption and weight gain in a Mediterranean cohort: the SUN study. Obesity (Silver Spring). 2007;15:107–16 [DOI] [PubMed] [Google Scholar]
- 70.Sabaté J, Ang Y. Nuts and health outcomes: new epidemiologic evidence. Am J Clin Nutr. 2009;89:1643S–8S [DOI] [PubMed] [Google Scholar]
- 71.Mozaffarian D, Katan MB, Ascherio A, Stampfer MJ, Willett WC. Trans fatty acids and cardiovascular disease. N Engl J Med. 2006;354:1601–13 [DOI] [PubMed] [Google Scholar]
- 72.Salmerón J, Hu FB, Manson JE, Stampfer MJ, Colditz GA, Rimm EB, Willett WC. Dietary fat intake and risk of type 2 diabetes in women. Am J Clin Nutr. 2001;73:1019–26 [DOI] [PubMed] [Google Scholar]
- 73.Albert CM, Campos H, Stampfer MJ, Ridker PM, Manson JE, Willett WC, Ma J. Blood levels of long-chain n-3 fatty acids and the risk of sudden death. N Engl J Med. 2002;346:1113–8 [DOI] [PubMed] [Google Scholar]
- 74.He K, Song Y, Daviglus ML, Liu K, Van Horn L, Dyer AR, Goldbourt U, Greenland P. Fish consumption and incidence of stroke: a meta-analysis of cohort studies. Stroke. 2004;35:1538–42 [DOI] [PubMed] [Google Scholar]
- 75.Kaushik M, Mozaffarian D, Spiegelman D, Manson JE, Willett WC, Hu FB. Long-chain omega-3 fatty acids, fish intake, and the risk of type 2 diabetes mellitus. Am J Clin Nutr. 2009;90:613–20 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 76.Risérus U, Willett WC, Hu FB. Dietary fats and prevention of type 2 diabetes. Prog Lipid Res. 2009;48:44–51 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 77.Howard BV, Van Horn L, Hsia J, Manson JE, Stefanick ML, Wassertheil-Smoller S, Kuller LH, LaCroix AZ, Langer RD, Lasser NL, et al. Low-fat dietary pattern and risk of cardiovascular disease: the Women's Health Initiative Randomized Controlled Dietary Modification Trial. JAMA. 2006;295:655–66 [DOI] [PubMed] [Google Scholar]
- 78.Prentice RL, Caan B, Chlebowski RT, Patterson R, Kuller LH, Ockene JK, Margolis KL, Limacher MC, Manson JE, Parker LM, et al. Low-fat dietary pattern and risk of invasive breast cancer: the Women's Health Initiative Randomized Controlled Dietary Modification Trial. JAMA. 2006;295:629–42 [DOI] [PubMed] [Google Scholar]
- 79.Beresford SA, Johnson KC, Ritenbaugh C, Lasser NL, Snetselaar LG, Black HR, Anderson GL, Assaf AR, Bassford T, Bowen D, et al. Low-fat dietary pattern and risk of colorectal cancer: the Women's Health Initiative Randomized Controlled Dietary Modification Trial. JAMA. 2006;295:643–54 [DOI] [PubMed] [Google Scholar]
- 80.Harris WS, Mozaffarian D, Rimm E, Kris-Etherton P, Rudel LL, Appel LJ, Engler MM, Engler MB, Sacks F. Omega-6 fatty acids and risk for cardiovascular disease: a science advisory from the American Heart Association Nutrition Subcommittee of the Council on Nutrition, Physical Activity, and Metabolism; Council on Cardiovascular Nursing; and Council on Epidemiology and Prevention. Circulation. 2009;119:902–7 [DOI] [PubMed] [Google Scholar]
- 81.Intersalt Cooperative Research Group Intersalt: an international study of electrolyte excretion and blood pressure. Results for 24-hour urinary sodium and potassium excretion. BMJ. 1988;297:319–28 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 82.Yang Q, Liu T, Kuklina EV, Flanders WD, Hong Y, Gillespie C, Chang MH, Gwinn M, Dowling N, Khoury MJ, et al. Sodium and potassium intake and mortality among US adults: prospective data from the Third National Health and Nutrition Examination Survey. Arch Intern Med. 2011;171:1183–91 [DOI] [PubMed] [Google Scholar]
- 83.Sacks FM, Svetkey LP, Vollmer WM, Appel LJ, Bray GA, Harsha D, Obarzanek E, Conlin PR, Miller ER, Simons-Morton D, et al. Effects on blood pressure of reduced dietary sodium and the dietary approaches to stop hypertension (DASH) diet. N Engl J Med. 2001;344:3–10 [DOI] [PubMed] [Google Scholar]
- 84.Cook NR, Cutler JA, Obarzanek E, Buring JE, Rexrode KM, Kumanyika SK, Appel LJ, Whelton PK. Long term effects of dietary sodium reduction on cardiovascular disease outcomes: observational follow-up of the trials of hypertension prevention (TOHP). BMJ. 2007;334:885–8 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 85.Corrao G, Rubbiati L, Bagnardi V, Zambon A, Poikolainen K. Alcohol and coronary heart disease: a meta-analysis. Addiction. 2000;95:1505–23 [DOI] [PubMed] [Google Scholar]
- 86.Mukamal KJ, Kuller LH, Fitzpatrick AL, Longstreth WT, Jr, Mittleman MA, Siscovick DS. Prospective study of alcohol consumption and risk of dementia in older adults. JAMA. 2003;289:1405–13 [DOI] [PubMed] [Google Scholar]
- 87.Wannamethee SG, Camargo CA, Jr, Manson JE, Willett WC, Rimm EB. Alcohol drinking patterns and risk of type 2 diabetes among younger women. Arch Intern Med. 2003;163:1329–36 [DOI] [PubMed] [Google Scholar]
- 88.Ronksley PE, Brien SE, Turner BJ, Mukamal KJ, Ghali WA. Association of alcohol consumption with selected cardiovascular disease outcomes: a systematic review and meta-analysis. BMJ. 2011;342:d671. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 89.Thun MJ, Peto R, Lopez AD, Monaco JH, Henley SJ, Heath CW, Jr, Doll R. Alcohol consumption and mortality among middle-aged and elderly U.S. adults. N Engl J Med. 1997;337:1705–14 [DOI] [PubMed] [Google Scholar]
Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.