Author + information
- Received February 14, 2017
- Revision received April 27, 2017
- Accepted May 23, 2017
- Published online July 17, 2017.
- Ambika Satija, ScDa,∗ (, )
- Shilpa N. Bhupathiraju, PhDa,b,
- Donna Spiegelman, ScDa,b,c,d,e,
- Stephanie E. Chiuve, ScDa,f,
- JoAnn E. Manson, MD, DrPHc,g,h,
- Walter Willett, MD, DrPHa,b,c,
- Kathryn M. Rexrode, MD, MPHi,
- Eric B. Rimm, ScDa,b,c and
- Frank B. Hu, MD, PhDa,b,c
- aDepartment of Nutrition, Harvard T.H. Chan School of Public Health, Boston, Massachusetts
- bChanning Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts
- cDepartment of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts
- dDepartment of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, Massachusetts
- eDepartment of Global Health, Harvard T.H. Chan School of Public Health, Boston, Massachusetts
- fBenefit-Risk Management, Innovative Platforms & Epidemiology, Pharmacovigilance & Patient Safety, AbbVie, North Chicago, Illinois
- gDepartment of Medicine, Brigham and Women’s Hospital, Boston, Massachusetts
- hDepartment of Medicine, Brigham and Womens' Hospital, Harvard Medical School, Boston, Massachusetts
- iDivision of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts
- ↵∗Address for correspondence:
Dr. Ambika Satija, Department of Nutrition, Harvard T.H. Chan School of Public Health, 665 Huntington Avenue, Boston, Massachusetts 02115.
Background Plant-based diets are recommended for coronary heart disease (CHD) prevention. However, not all plant foods are necessarily beneficial for health.
Objectives This study sought to examine associations between plant-based diet indices and CHD incidence.
Methods We included 73,710 women in NHS (Nurses’ Health Study) (1984 to 2012), 92,329 women in NHS2 (1991 to 2013), and 43,259 men in Health Professionals Follow-up Study (1986 to 2012), free of chronic diseases at baseline. We created an overall plant-based diet index (PDI) from repeated semiquantitative food-frequency questionnaire data, by assigning positive scores to plant foods and reverse scores to animal foods. We also created a healthful plant-based diet index (hPDI) where healthy plant foods (whole grains, fruits/vegetables, nuts/legumes, oils, tea/coffee) received positive scores, whereas less-healthy plant foods (juices/sweetened beverages, refined grains, potatoes/fries, sweets) and animal foods received reverse scores. To create an unhealthful PDI (uPDI), we gave positive scores to less-healthy plant foods and reverse scores to animal and healthy plant foods.
Results Over 4,833,042 person-years of follow-up, we documented 8,631 incident CHD cases. In pooled multivariable analysis, higher adherence to PDI was independently inversely associated with CHD (hazard ratio [HR] comparing extreme deciles: 0.92; 95% confidence interval [CI]: 0.83 to 1.01; p trend = 0.003). This inverse association was stronger for hDPI (HR: 0.75; 95% CI: 0.68 to 0.83; p trend <0.001). Conversely, uPDI was positively associated with CHD (HR: 1.32; 95% CI: 1.20 to 1.46; p trend <0.001).
Conclusions Higher intake of a plant-based diet index rich in healthier plant foods is associated with substantially lower CHD risk, whereas a plant-based diet index that emphasizes less-healthy plant foods is associated with higher CHD risk.
Plant-based diets have been associated with a lower risk of various diseases (1–3), including coronary heart disease (CHD) (4–9), the leading global cause of death (10). However, these studies suffer from key limitations. With the exception of a recent investigation (3), prior studies (4–9) have defined plant-based diets as “vegetarian” diets, which constitute a family of dietary patterns that exclude some or all animal foods. As recommendations based on incremental dietary changes are easier to adopt, it is important to understand how gradual reductions in animal food intake with concomitant increases in consumption of plant foods affect cardiovascular health. Additionally, in studies of vegetarian diets, all plant foods are treated equally, even though certain plant foods, such as refined grains and sugar-sweetened beverages (SSB) are associated with higher cardiometabolic risk (11–13).
To overcome these limitations, we have created 3 versions of plant-based diet indices using a graded approach: an overall plant-based diet index (PDI), which emphasizes consumption of all plant food while reducing animal food intake; a healthful plant-based diet index (hPDI), which emphasizes intake of healthy plant foods associated with improved health outcomes such as whole grains, fruits, and vegetables; and an unhealthful plant-based diet index (uPDI), which emphasizes consumption of less healthy plant foods known to be associated with a higher risk of several diseases (14). In 3 U.S. cohorts, we previously documented that the PDI was inversely associated with type 2 diabetes risk with a stronger inverse association for hPDI and a positive association for uPDI (14). In the present study, we examined the associations of these plant-based diet indices with CHD incidence in more than 200,000 male and female health professionals in the United States.
The NHS (Nurses’ Health Study) started in 1976 with 121,701 female registered nurses (ages 30 to 55 years), the NHS2 started in 1989 with 116,686 female registered nurses (ages 25 to 42 years), and the HPFS (Health Professionals Follow-Up Study) started in 1986 with 51,529 male health professionals (ages 40 to 75 years). Participants receive a follow-up questionnaire every 2 years on lifestyle, health behaviors, and medical history, with a response rate of ∼90% at each cycle. Participants with CHD at baseline were excluded. Participants with cancer (except nonmelanoma skin cancer), stroke, and coronary artery surgery at baseline were also excluded, as diagnosis with these conditions can change diet. Lastly, individuals with implausible energy intake at baseline (<600 or >3,500 kcal/day for women and <800 or >4,200 kcal/day for men) were excluded. The final baseline sample included 73,710 women in NHS, 92,329 women in NHS2, and 43,259 men in HPFS (1984 for NHS, 1991 for NHS2, and 1986 for HPFS).
Study protocols for all cohorts were approved by the institutional review boards of Brigham and Women’s Hospital and the Harvard T.H. Chan School of Public Health; completion of the self-administered questionnaire was considered to imply informed consent.
Dietary assessment and the plant-based diet indices
Dietary data were collected using a semiquantitative food frequency questionnaire every 2 to 4 years. Participants were asked how often, on average, they consumed a defined portion of ∼130 food items over the previous year. There were 9 response categories ranging from “never or less than once/month” to “≥6 times/day.” The reliability and validity of the questionnaires have been described previously (15–18).
Using this dietary data, we created 3 versions of a plant-based diet for each food frequency questionnaire cycle for each cohort: PDI; hPDI; and uPDI (14). We created 18 food groups based on nutrient and culinary similarities within the larger categories of healthy plant foods, less healthy plant foods, and animal foods (Table 1). Given that alcoholic beverages have different directions of association for various health outcomes, and margarine’s fatty acid composition has changed over time from high trans to high unsaturated fats, we did not include these foods in the indices, but adjusted for them in the analysis. Food groups were ranked into quintiles and given positive or reverse scores. With positive scores, participants above the highest quintile of a food group received a score of 5, following on through to participants below the lowest quintile who received a score of 1. With reverse scores, this pattern of scoring was inversed. For creating PDI, plant food groups were given positive scores, and animal food groups were given reverse scores. For creating hPDI, positive scores were given to healthy plant food groups and reverse scores to less healthy plant food groups and animal food groups. Finally, for uPDI, positive scores were given to less healthy plant food groups and reverse scores to healthy plant food groups and animal food groups. The 18 food group scores were summed to obtain the indices. Higher intake of all indices reflected lower animal food intake (e.g., 5 to 6 vs. 3 servings/day comparing extreme PDI deciles).
CHD was defined as nonfatal myocardial infarction and fatal CHD. Participants self-reporting newly diagnosed CHD on the biennial questionnaires were asked permission to access their medical records to confirm diagnosis, which was done through blinded review by study physicians. To confirm diagnosis of nonfatal myocardial infarction, we used the World Health Organization criteria (19) of the presence of typical symptoms plus either elevated enzymes or diagnostic electrocardiographic findings. Cases that required hospital admission and were confirmed by interview or letter but for which medical records were unobtainable were included in the analysis as “probable.”
Reports from next of kin or postal authorities were used to identify deaths, in addition to searching the National Death Index. Classification of CHD as the cause of death was done by examining autopsy reports, hospital records, or death certificates, using International Classification of Diseases-8th and -9th Revisions (20). CHD deaths were considered confirmed if fatal CHD was established through medical records or autopsy reports or if CHD was listed as the cause of death on the death certificate with prior medical record of CHD. If CHD was listed as the cause of death on the death certificate, but medical records were unavailable and no prior knowledge of CHD existed, the CHD death was included in the analysis as “probable.”
Assessment of covariates
We obtained updated information on participants’ smoking status, multivitamin use, CHD family history, and physical activity through self-report on the biennial questionnaires. Among women, updated information was assessed on menopausal status, post-menopausal hormone use, and oral contraceptive use (NHS2 only). Self-reported data on height were collected at baseline, with updated information on weight assessed every 2 years through the questionnaires. We also collected updated information on self-reported diagnosis of diseases such as hypertension, hypercholesterolemia, and diabetes, and on medication use.
We used Cox proportional hazards regression to estimate hazard ratios (HR) and 95% confidence intervals (CIs) evaluating, separately, the associations of deciles of each index with CHD. Person-time was calculated from questionnaire return date until CHD diagnosis, death, or end of follow-up (June 30, 2012, in NHS; June 30, 2013, in NHS2; and January 1, 2012, in HPFS). We used age (in years) as the time scale, with stratification by calendar time (in 2-year intervals). We adjusted for time-varying covariates including smoking status, alcohol intake, physical activity, CHD family history, multivitamin use, aspirin use, energy intake, margarine intake, body mass index (BMI), post-menopausal status and hormone use (women), and oral contraceptive use (NHS2). We additionally adjusted for baseline self-reported hypertension, hypercholesterolemia, and diabetes.
Indices were cumulatively averaged over follow-up to better capture long-term diet; for instance, for the 2001 to 2003 risk set, plant-based diet index scores in 1991, 1995, and 1999 were averaged to predict CHD risk. Because diagnosis of conditions such as type 2 diabetes, stroke, and cancer could change an individual’s diet and potentially be associated with the underlying risk of CHD, we stopped updating diet on diagnosis of these conditions. Values of other covariates were updated every 2 years to account for changes over time. A continuous variable for each index was created by assigning the median value to each decile and conducting tests for linear trend. To examine potential deviation from linearity, we fit restricted cubic splines to the fully adjusted model with the indices entered as continuous variables. The proportional hazards assumption was tested by including interaction terms between the indices, and age and calendar year. We examined potential effect modification by sex, BMI, physical activity, family history of CHD, and smoking status. We also evaluated the independent associations of the 3 food categories that constituted the diet indices (healthy plant foods, less healthy plant foods, animal foods) with CHD risk by entering all 3 simultaneously into the model in place of the diet indices. We also created a healthy omnivorous diet, by assigning positive scores to healthy plant foods and healthy animal foods (dairy products [except ice cream], egg, fish), and reverse scores to less healthy plant foods and less healthy animal foods (animal fat, ice cream, meat, miscellaneous animal-based foods). The analysis was carried out separately for each cohort and combined using a fixed-effects model; heterogeneity was examined using the Cochrane Q statistic (21) and the I2 statistic (22). All analyses were performed using SAS software version 9.2 (SAS Institute Inc., Cary, North Carolina), and statistical significance was set at a 2-tailed p value of <0.05.
At baseline, the indices ranged from a median of 42 to 44 in the lowest decile, to 66 to 68 in the highest decile (Online Table 1). Participants with higher scores on PDI and hPDI were older, more active, leaner, and less likely to smoke than were participants with lower scores. Conversely, high consumers of uPDI were younger, less active, and more likely to smoke than were low consumers. The proportion of participants with a history of diabetes decreased with increasing deciles of PDI and uPDI, but increased with higher hPDI intake. Animal food intake ranged from 5 to 6 servings per day in the highest decile to 3 to 4 servings per day in the lowest decile of the indices.
Over 4,833,042 person-years of follow-up, 8,631 participants developed CHD (3,233 cases over 1,876,942 person-years in NHS; 667 cases over 1,999,945 person-years in NHS2; and 4,731 cases over 956,155 person-years in HPFS). In the pooled fully adjusted model, PDI was modestly inversely associated with CHD incidence (HR comparing extreme deciles: 0.92; 95% CI: 0.83 to 1.01; HR per 10-U increase: 0.93; 95% CI: 0.90 to 0.97; p trend = 0.003) (Table 2). When we analyzed hPDI (Table 3) and uPDI (Table 4) separately, we found a stronger inverse association between hPDI and CHD incidence (HR comparing extreme deciles: 0.75; 95% CI: 0.68 to 0.83; HR per 10-U increase: 0.88; 95% CI: 0.85 to 0.91; p trend <0.001) and a positive association for uPDI (HR comparing extreme deciles: 1.32; 95% CI: 1.20 to 1.46; HR per 10-U increase: 1.10; 95% CI: 1.06 to 1.14; p trend <0.001). The association of uPDI with CHD was nonlinear (p for test of curvature = 0.01; p for nonlinear association <0.001) (Central Illustration, panel A, and Online Figure 1). We found no evidence of deviation from linearity for PDI and hPDI (p for test of curvature >0.20 for both; p for linearity = 0.001 for PDI, and <0.001 for hPDI). Further adjustment for ethnicity, marital status, recent physical exam, diet beverage intake, and indicators of socioeconomic status did not appreciably alter the results (pooled HR for extreme deciles of [PDI: 0.93; 95% CI: 0.84 to 1.03; p trend = 0.01; hPDI: 0.76; 95% CI: 0.69 to 0.84; p trend <0.001; uPDI: 1.30; 95% CI: 1.18 to 1.44; p trend <0.001]).
The associations of hPDI and uPDI with risk of CHD were consistently observed across strata defined by age, BMI, family history of CHD, and sex (Figure 1). Associations of both indices were significantly stronger among more active relative to less active participants (p interaction = 0.002 for both); the association of uPDI with CHD was slightly stronger among ever smokers compared with never smokers (p interaction = 0.04). There was no evidence of significant effect modification by calendar year in any of the cohorts for hPDI or uPDI (all p values for interaction >0.20).
When, in place of the indices, we entered variables for the 3 food categories together into the fully adjusted model, we found an inverse association for healthy plant foods, and positive associations for animal foods and less healthy plant foods (Central Illustration, panel B, Online Figure 1, and Online Table 2). To quantify the benefit of hPDI that was due to lower intake of red meat or SSB, we individually adjusted for these foods in the final model. The results were largely unchanged on red meat adjustment: (pooled HR for extreme deciles of PDI: 0.93; 95% CI: 0.84 to 1.03; p trend = 0.01; hPDI: 0.76; 95% CI: 0.68 to 0.84; p trend <0.001; uPDI: 1.32; 95% CI: 1.19 to 1.46; p trend <0.001) and changed in expected directions with SSB adjustment (pooled HR for extreme deciles of PDI: 0.90; 95% CI: 0.81 to 0.99; p trend = 0.001; hPDI: 0.79; 95% CI: 0.71 to 0.88; p trend <0.001; uPDI: 1.22; 95% CI: 1.10 to 1.36; p trend = 0.005). Given the previously observed inverse association between fish intake and CHD (23), we modified hPDI to score fish intake positively and found similar results (pooled HR for extreme deciles: 0.74; 95% CI: 0.67 to 0.81; p trend <0.001). The results were slightly attenuated when we modified hPDI to score healthy animal foods positively (dairy except ice cream, egg, and fish) (pooled HR comparing extreme deciles: 0.78; 95% CI: 0.71 to 0.86; HR per 10-U increase: 0.91; 95% CI: 0.89 to 0.94; p trend <0.001).
The associations of PDI, hPDI, and uPDI with risk of CHD did not vary based on how we modeled diet. For example, we found similar results when we continuously updated the indices throughout follow-up, used baseline values of the indices, used the most recent index scores before CHD diagnosis, and stopped updating the indices once intermediate conditions such as hypertension and hypercholesterolemia developed (Online Table 3). When we created the plant-based diet indices with quintiles of energy-adjusted food groups (instead of with quintiles of unadjusted food groups as we had originally done), the association of PDI with CHD became slightly stronger, but that of uPDI with CHD was slightly attenuated (Online Table 4). Removing potential intermediates (BMI and aspirin use) from the model strengthened the association of PDI with CHD (pooled HR for extreme deciles of PDI: 0.86; 95% CI: 0.78 to 0.95; p trend <0.001; hPDI: 0.73; 95% CI: 0.66 to 0.81; p trend <0.001; uPDI: 1.27; 95% CI: 1.15 to 1.40; p trend <0.001). Adjustment for additional potential intermediates in the causal pathway, (updated history of hypertension, hypercholesterolemia, and diabetes instead of baseline history) slightly attenuated associations of hPDI and uPDI with CHD (pooled HR for extreme deciles of PDI: 0.92; 95% CI: 0.83 to 1.02; p trend = 0.003; hPDI: 0.80; 95% CI: 0.73 to 0.89; p trend <0.001; uPDI: 1.24; 95% CI: 1.12 to 1.37; p trend = 0.001; proportion of the association with hPDI explained by these intermediates ranged from 9.5% in NHS to 4.9% in HPFS, with all p < 0.01). Finally, the results did not change when we excluded participants who had diabetes at baseline (pooled HR for extreme deciles of PDI: 0.93; 95% CI: 0.84 to 1.03; p trend = 0.002; hPDI: 0.74; 95% CI: 0.66 to 0.82; p trend <0.001; uPDI: 1.35; 95% CI: 1.21 to 1.50; p trend <0.001) or when we pooled results across the cohorts using a random-effects model (pooled HR for extreme deciles of PDI: 0.92; 95% CI: 0.83 to 1.01; p trend = 0.01; hPDI: 0.71; 95% CI: 0.57 to 0.88; p trend <0.001; uPDI: 1.40; 95% CI: 1.13 to 1.73; p trend <0.001).
In 3 ongoing prospective cohort studies, higher adherence to PDI was modestly associated with lower CHD incidence (HR comparing extreme deciles: 0.92; 95% CI: 0.83 to 1.01). This inverse association was considerably stronger for adherence to a healthier version (hPDI) (HR: 0.75; 95% CI: 0.68 to 0.83), but positive for adherence to a less healthy version (uPDI) (HR: 1.32; 95% CI: 1.20 to 1.46) of a plant-based diet index. These associations remained robust to adjustment for multiple confounders and were consistently observed in various subgroups.
In a previous analysis (14), we found similar associations of these 3 indices with type 2 diabetes. Our current analysis extends the potentially protective association with hPDI to CHD. The mechanisms through which hPDI could reduce CHD risk are likely shared with the mechanisms for type 2 diabetes risk reduction (2,24–32). Specifically, greater adherence to hPDI would lead to diets high in dietary fiber, antioxidants, unsaturated fat, and micronutrient content, and low in saturated fat and heme iron content (Online Table 1), all of which could aid in weight loss/maintenance, enhance glycemic control and insulin regulation, improve lipid profile, reduce blood pressure, improve vascular health, decrease inflammation, and foster more favorable diet-gut microbiome interactions (e.g., through lowered levels of trimethylamine N-oxide), thereby lowering CHD risk. Greater adherence to uPDI, on the other hand, leads to diets with higher glycemic load and index; added sugar; and lower levels of dietary fiber, unsaturated fats, micronutrients, and antioxidants, which could result in higher CHD risk through the above-mentioned pathways. This is also illustrated in the fact that the associations of hPDI and uPDI with CHD incidence were slightly attenuated on adjustment for some of these pathways, specifically hypercholesterolemia, hypertension, and diabetes.
Prospective cohort studies examining the association of plant-based diets with CHD have focused on CHD mortality. Most of these studies have been carried out in Europe, with only 3 studies in the United States (Adventist Health Studies ). A pooled analysis of 5 of the above-mentioned cohorts found a 24% lower risk of CHD mortality (95% CI: 6% to 38%) comparing vegetarians with nonvegetarians (5). A recent meta-analysis found similar results with vegetarians experiencing a 29% lower risk of CHD mortality (95% CI: 13% to 43%) relative to nonvegetarians (6). The EPIC (European Prospective Investigation into Cancer and Nutrition)-Oxford study, 1 of the few studies to examine the association of a vegetarian diet with CHD incidence in addition to mortality, found a 32% lower 11-year CHD incidence (95% CI: 19% to 42%) among vegetarians relative to nonvegetarians (8).
These studies have defined plant-based diets dichotomously as being vegetarian or not. Our study adds to the evidence base by examining the association of gradations of adherence to PDI with CHD incidence. For instance, those in the lowest decile of PDI consumed 5 to 6 servings of animal foods per day, whereas those in the highest decile consumed 3 servings of animal foods per day. This approach has the advantage of being easily translatable, as we found that even a slightly lower intake of animal foods combined with higher intake of healthy plant foods is associated with lower CHD risk. One other study adopted this approach with respect to cardiovascular disease mortality and found similar results (3). However, these studies have examined plant-based diets at a single time point, making it difficult to fully capture the association of a time-varying exposure such as diet on the development of CHD, which has a long etiologic period. Our study adds to the existing reports by demonstrating the associations of long-term cumulative intake of a plant-based diet index with more than 20-year CHD incidence.
We also found that a healthier version of a plant-based diet index, which emphasizes plant foods known to be associated with improved health outcomes, is associated with substantially lower CHD risk. Contrarily, when intake of less healthy plant foods is emphasized, the opposite association was observed. When we examined associations of the 3 food categories with CHD risk, less healthy plant foods and animal foods were both associated with increased risk, with a potentially stronger association for less healthy plant foods. This highlights the wide variation in nutritional quality of plant foods, making it crucial to consider the quality of plant foods consumed in plant-rich diets.
When we examined a diet that emphasized both healthy plant and healthy animal foods, the association with CHD was only slightly attenuated relative to that with hPDI. Thus, the moderate reductions in animal foods suggested here can be largely achieved by lowering intake of less healthy animal foods such as red and processed meats. The results of this study are in line with the recently released 2015 Dietary Guidelines for Americans (33), which recommends higher consumption of high-quality plant foods. Dietary recommendations based on the hPDI would also be environmentally sustainable, as plant-based food systems use fewer resources than food systems that are heavily reliant on animal foods (34).
This is one of the largest prospective investigations of plant-based diet indices and incident CHD in the world, with periodic data on diet, lifestyle, and medical history collected over more than 2 decades. However, measurement error in diet assessment is likely, although evaluating cumulatively averaged intake reduces random errors (17) while allowing for the examination of long-term dietary intake. Given the observational nature of the study, residual and unmeasured confounding are possible; thus, we should interpret modest effect sizes such as those we observed for PDI with caution. However, the results were largely unchanged when we adjusted for additional covariates, including markers of socioeconomic status. Additionally, randomized controlled trial evidence showing the protective effect of plant-based diets on intermediate outcomes, including weight change, lipid profile, glycemic control, and blood pressure lends further support to our findings (35–38).
We found a modest inverse association of higher adherence to PDI with CHD incidence in 3 prospective cohort studies in the United States. While this inverse association was stronger for a plant-based diet index that emphasized healthy plant foods, CHD risk was significantly elevated for a plant-based diet index that emphasized less healthy plant foods. Dietary guidelines and lifestyle interventions could recommend increasing intake of healthy plant foods, while reducing intake of less healthy plant foods and certain animal foods for improved cardiometabolic health.
COMPETENCY IN PATIENT CARE AND PROCEDURAL SKILLS: Medical and health professionals should guide patients to increase intake of healthy plant foods, such as whole grains, fruits, vegetables, and nuts, and reduce intake of animal foods and less healthy plant foods such as SSB for CHD prevention.
TRANSLATIONAL OUTLOOK: Future research should replicate these findings in other racial/ethnic, occupational, and socioeconomic groups and explore biological mechanisms involved in the potentially cardioprotective effects of hPDI to identify personalized clinical interventions and therapies for CHD prevention.
For supplemental tables and a figure, please see the online version of this article.
Supported by research grants from the National Institutes of Health (UM1 CA186107, UM1 CA176726, UM1 CA167552, HL034594, HL60712, and HL35464). Dr. Chiuve is an employee of AbbVie, Inc. Dr. Rimm has received a research grant from the U.S. Department of Agriculture/Blueberry Highbush Council; and has served on the Scientific Advisory Committees of IKEA, Take C/O, and SPE. Dr. Hu has received research support from the California Walnut Commission and Metagenics. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Abbreviations and Acronyms
- body mass index
- coronary heart disease
- confidence interval
- healthful plant-based diet index
- hazard ratio
- overall plant-based diet index
- sugar-sweetened beverages
- unhealthful plant-based diet index
- Received February 14, 2017.
- Revision received April 27, 2017.
- Accepted May 23, 2017.
- 2017 American College of Cardiology Foundation
- Fraser G.E.
- Martinez-Gonzalez M.A.,
- Sanchez-Tainta A.,
- Corella D.,
- et al.,
- for the PREDIMED Group
- Key T.J.,
- Fraser G.E.,
- Thorogood M.,
- et al.
- Kwok C.S.,
- Umar S.,
- Myint P.K.,
- Mamas M.A.,
- Loke Y.K.
- Orlich M.J.,
- Singh P.,
- Sabaté J.,
- et al.
- Crowe F.L.,
- Appleby P.N.,
- Travis R.C.,
- Key T.J.,
- Risk of hospitalization or death from ischemic heart disease among British vegetarians and nonvegetarians: results from the EPIC-Oxford cohort study
- Fraser G.E.,
- Lindsted K.D.,
- Beeson W.L.
- ↵World Health Organization. The global burden of disease: 2004 update. Geneva, Switzerland: World Health Organization, 2008. Available at: http://www.who.int/healthinfo/global_burden_disease/2004_report_update/en/. Accessed February 1, 2017.
- Hu E.A.,
- Pan A.,
- Malik V.,
- Sun Q.
- Rimm E.B.,
- Giovannucci E.L.,
- Stampfer M.J.,
- Colditz G.A.,
- Litin L.B.,
- Willett W.C.
- Willett W.C.,
- Sampson L.,
- Stampfer M.J.,
- et al.
- Willett W.
- Yuan C.,
- Spiegelman D.,
- Rimm E.B.,
- et al.
- ↵(1979) Nomenclature and criteria for diagnosis of ischemic heart disease: report of the Joint International Society and Federation of Cardiology/World Health Organization task force on standardization of clinical nomenclature. Circulation 59:607–609.
- Higgins J.P.,
- Thompson S.G.,
- Deeks J.J.,
- Altman D.G.
- Jenkins D.J.,
- Kendall C.W.,
- Marchie A.,
- et al.
- Hu F.B.
- Salonen J.T.,
- Nyyssönen K.,
- Korpela H.,
- Tuomilehto J.,
- Seppänen R.,
- Salonen R.
- Hunnicutt J.,
- He K.,
- Xun P.
- Baer H.J.,
- Glynn R.J.,
- Hu F.B.,
- et al.
- Song M.,
- Fung T.T.,
- Hu F.B.,
- et al.
- ↵U.S. Department of Health and Human Services and U.S. Department of Agriculture. 2015–2020 Dietary Guidelines for Americans 2015. Available at: http://health.gov/dietaryguidelines/2015/guidelines/. Accessed June 10, 2017.
- Pimentel D.,
- Pimentel M.
- Barnard N.D.,
- Levin S.M.,
- Yokoyama Y.