ArticlePDF Available

Plant‐Centered Diet and Risk of Incident Cardiovascular Disease During Young to Middle Adulthood

Authors:

Abstract

Background The association between diets that focus on plant foods and restrict animal products and cardiovascular disease (CVD) is inconclusive. We investigated whether cumulative intake of a plant‐centered diet and shifting toward such a diet are associated with incident CVD. Methods and Results Participants were 4946 adults in the CARDIA (Coronary Artery Risk Development in Young Adults) prospective study. They were initially 18 to 30 years old and free of CVD (1985–1986, exam year [year 0]) and followed until 2018. Diet was assessed by an interviewer‐administered, validated diet history. Plant‐centered diet quality was assessed using the A Priori Diet Quality Score (APDQS), in which higher scores indicate higher consumption of nutritionally rich plant foods and limited consumption of high‐fat meat products and less healthy plant foods. Proportional hazards models estimated hazard ratios of CVD associated with both time‐varying average APDQS and a 13‐year change in APDQS score (difference between the year 7 and year 20 assessments). During the 32‐year follow‐up, 289 incident CVD cases were identified. Both long‐term consumption and a change toward such a diet were associated with a lower risk of CVD. Multivariable‐adjusted hazard ratio was 0.48 (95% CI, 0.28–0.81) when comparing the highest quintile of the time‐varying average ADPQS with lowest quintiles. The 13‐year change in APDQS was associated with a lower subsequent risk of CVD, with a hazard ratio of 0.39 (95% CI, 0.19–0.81) comparing the extreme quintiles. Similarly, strong inverse associations were found for coronary heart disease and hypertension‐related CVD with either the time‐varying average or change APDQS. Conclusions Consumption of a plant‐centered, high‐quality diet starting in young adulthood is associated with a lower risk of CVD by middle age.
Journal of the American Heart Association
J Am Heart Assoc. 2021;10:e020718. DOI: 10.1161/JAHA.120.020718 1
ORIGINAL RESEARCH
Plant- Centered Diet and Risk of Incident
Cardiovascular Disease During Young to
Middle Adulthood
Yuni Choi , PhD; Nicole Larson, PhD; Lyn M. Steffen, PhD; Pamela J. Schreiner , PhD; Daniel D. Gallaher, PhD;
Daniel A. Duprez, MD, PhD; James M. Shikany , DrPH; Jamal S. Rana, MD, PhD; David R. Jacobs, J r, P h D
BACKGROUND: The association between diets that focus on plant foods and restrict animal products and cardiovascular dis-
ease (CVD) is inconclusive. We investigated whether cumulative intake of a plant- centered diet and shifting toward such a diet
are associated with incident CVD.
METHODS AND RESULTS: Participants were 4946 adults in the CARDIA (Coronary Artery Risk Development in Young Adults) pro-
spective study. They were initially 18 to 30years old and free of CVD (1985– 1986, exam year [year 0]) and followed until 2018.
Diet was assessed by an interviewer- administered, validated diet history. Plant- centered diet quality was assessed using the
A Priori Diet Quality Score (APDQS), in which higher scores indicate higher consumption of nutritionally rich plant foods and
limited consumption of high- fat meat products and less healthy plant foods. Proportional hazards models estimated hazard
ratios of CVD associated with both time- varying average APDQS and a 13- year change in APDQS score (difference between
the year 7 and year 20 assessments). During the 32- year follow- up, 289 incident CVD cases were identified. Both long- term
consumption and a change toward such a diet were associated with a lower risk of CVD. Multivariable- adjusted hazard ratio
was 0.48 (95% CI, 0.28– 0.81) when comparing the highest quintile of the time- varying average ADPQS with lowest quintiles.
The 13- year change in APDQS was associated with a lower subsequent risk of CVD, with a hazard ratio of 0.39 (95% CI,
0.19– 0.81) comparing the extreme quintiles. Similarly, strong inverse associations were found for coronary heart disease and
hypertension- related CVD with either the time- varying average or change APDQS.
CONCLUSIONS: Consumption of a plant- centered, high- quality diet starting in young adulthood is associated with a lower risk
of CVD by middle age.
Key Words: cardiovascular disease plant- centered diet prospective cohort study
Heart disease remains the leading cause of death
in the United States.1 Suboptimal diet is a major
risk factor for morbidity and mortality.2 There is a
growing interest in the cardiovascular health benefits
of diets that focus on consuming only plant foods, ex-
cluding animal products. However, the evidence that
such diets actually confer a lower risk of incident car-
diovascular disease (CVD) is inconclusive.3 Recently,
an overall diet quality index that emphasizes healthful
plant- derived foods with restriction of all animal- derived
foods (plant- based diet quality index [PDI]) has been
studied for its association with risk of incident CVD and
mortality, but inconsistent results have been reported
across studies.4– 6 One study reported that improved
the healthful PDI scores over 12years was associated
with a lower subsequent risk of CVD- specific mortal-
ity and all- cause mortality.7 Otherwise, data regarding
the association between change in plant- centered diet
quality and subsequent risk of incident CVD are scarce.
Currently, little is known regarding the association
Correspondence to: David R. Jacobs Jr, PhD, Division of Epidemiology and Community Health, School of Public Health, University of Minnesota– Twin Cities,
Suite 300 West Bank Office Building, 1300 S. 2nd Street, Minnesota, MN 55454- 1015. E- mail: jacob004@umn.edu
Supplementary Material for this article is available at https://www.ahajo urnals.org/doi/suppl/ 10.1161/JAHA.120.020718
For Sources of Funding and Disclosures, see page 11.
© 2021 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley. This is an open access article under the terms of the Creat ive
Commo ns Attri butio n- NonCo mmerc ial- NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use
is non- commercial and no modifications or adaptations are made.
JAHA is available at: www.ahajournals.org/journal/jaha
Downloaded from http://ahajournals.org by on August 13, 2021
J Am Heart Assoc. 2021;10:e020718. DOI: 10.1161/JAHA.120.020718 2
Choi et al Plant- Centered Diet and Cardiovascular Disease
between overall diet quality and risk of incident CVD
during the transition period from young to middle
adulthood because most prospective cohort studies
are initiated in middle age. Yet young adulthood is a
key stage, in which modifying risk factors may greatly
reduce CVD risk in later adulthood.8
The present study evaluated the hypotheses that
long- term consumption of a plant- centered diet
and a shift toward a plant- centered diet starting in
young adulthood are associated with a lower risk of
incident CVD in midlife. Plant- centered diet quality
was assessed using the A Priori Diet Quality Score
(APDQS), in which higher scores represent greater
consumption of nutritionally rich plant foods and
lower consumption of high- fat meat products and
unhealthy plant foods. The APDQS has some re-
semblance to other diet quality indices that gener-
ally emphasize plant foods.4,9 The unique feature of
plant- centeredness in the APDQS is that higher con-
sumption of nutritionally rich plant foods and lower
consumption of unhealthy plant foods and high- fat
red meats are the main contributors to a higher
score; however, certain subsets of animal products
also contribute (eg, low- fat yogurt, cheese, nonfried
fish, or nonfried poultry). The underlying viewpoint of
the APDQS is that dietary practices with more flex-
ible options can ensure that the general population
achieves and maintains a daily healthy eating pat-
tern over long periods of life. Previous epidemiologic
studies support the validity of the APDQS by provid-
ing evidence of its linear associations with clinical
outcomes.10– 13
METHODS
The data that support the findings of this study are
available from the CARDIA Coordinating Center
(https://www.cardia.dopm.uab.edu) upon reasonable
request.
Study Population and Design
CARDIA (Coronary Artery Risk Development in Young
Adults) is a multicenter, prospective cohort study of
5115 Black and White men and women from 4 US cit-
ies. Participants were aged 18 to 30years who were
free of CVD at baseline (1985– 1986, exam year [year
0] clinic exam), with a retention rate of 71% among sur-
vivors at year 30 (2015– 2016).14 At baseline and dur-
ing 8 follow- up examinations, data collection included
laboratory tests, physical measurements, medical
histories, and lifestyle factors. Vital status and mor-
bidity were ascertained biennially through 2018, with
successful contact of >90% of participants over the
past 5years. For the present study, participants were
excluded who reported implausible energy intakes
(<800 or >8000kcal/d for men; <600 or >6000kcal/d
for women; n=133) at year 0, year 7, or year 20 or
who lacked information regarding physical activity
or smoking (n=36). Analyses of the time- varying av-
erage APDQS were based on 4946 participants. For
analysis of the 13- year change in APDQS (year 20
year 7), the events were followed up since year 20
(2005– 2006; mean age, 45 years); therefore, of the
3549 participants who attended the year 20 examina-
tion, those with CVD at or before year 20 (20052006;
n=57), those with no diet data at year 7 or year 20
(n=846), or those with no physical activity or no smok-
ing at year 7 or year 20 (n=25) were excluded from
the analysis, leaving 2621 participants. All participants
provided written informed consent at all examinations,
CLINICAL PERSPECTIVE
What Is New?
Our study expands on previous studies by ex-
ploring the time- varying relationship between
plant- centered diet quality and risk of car-
diovascular disease during the transition from
young to middle adulthood.
An important aspect is clarifying whether a flex-
ible, plant- centered diet improves cardiovas-
cular outcomes, where nutritionally rich plant
foods are the central component of the diet, and
subsets of animal products may be integrated.
Long- term consumption of a plant- centered
diet and shifting to such a diet, starting in young
adulthood, were associated with a lower cardio-
vascular disease risk.
What Are the Clinical Implications?
Our findings are consistent with assertions that
a nutritionally rich plant- centered diet help pre-
vent the development of cardiovascular disease.
However, it appears that the complete exclusion
of animal foods from diet is not necessary.
From a clinical and public health perspective,
our findings support a recommendation of eat-
ing primarily nutritionally rich plant foods, but al-
lowing small amounts of animal products (eg,
low- fat dairy products, nonfried fish, and non-
fried poultry), to prevent early cardiovascular
disease.
Nonstandard Abbreviations and Acronyms
APDQS A Priori Diet Quality Score
CARDIA Coronary Artery Risk Development in
Young Adults
PDI plant- based diet quality index
Downloaded from http://ahajournals.org by on August 13, 2021
J Am Heart Assoc. 2021;10:e020718. DOI: 10.1161/JAHA.120.020718 3
Choi et al Plant- Centered Diet and Cardiovascular Disease
and research protocols were approved by institutional
review boards at the coordinating center and each
CARDIA field center.
Assessment of Plant- Centered Diet
Quality
Diet was assessed via the interviewer- administered
CARDIA diet history questionnaire at year 0, year 7,
and year 20. The diet history established reproduc-
ibility and validity.15 ,16 Trained interviewers asked the
participants about consumption of foods and bev-
erages over the past month within 100 closed food
categories (“Do you eat meat?,” “Do you eat vegeta-
bles?,” etc) and recorded open- ended responses of
specific foods eaten (specific types of foods eaten,
brand names, preparation methods, frequency of
intake, and serving size). The number of food items
recorded in the CARDIA cohort was 950 at year 0,
1388 at year 7, and 4598 at year 20. CARDIA diet
data were analyzed using Nutrition Data System for
Research (University of Minnesota, Minneapolis, MN),
which includes over 18 000 foods of which about
7500 are brand name products and is updated an-
nually to reflect marketplace changes. The Nutrition
Data System for Research summarized foods in 166
food groups (invariant over calendar year), which
CARDIA collapsed into 46 food groups for the pur-
pose of creating the APDQS. Total energy intake was
derived through summing energy intake of all foods,
which was calculated by multiplying consumption of
food (frequency × serving size) by the energy con-
tent of each item using Nutrition Data System for
Research.
Plant- centered diet quality was assessed using the
APDQS, which is a hypothesis- driven index based
on 46 food groups, which are derived from individ-
ual foods collected. The APDQS reflects a theoreti-
cal concept that how foods affect human health does
not act in isolation, but in concert, where nutrients
and bioactive compounds in a mixture of individual
foods consumed over time work together to produce
health outcomes.17 The food groups were classified
into beneficial (20), adverse (13), and neutral (13) on
the basis of their presumed prior known association
with CVD.18,19 There was general, though not per-
fect, agreement of ratings of food groups done inde-
pendently by 4 experts in the field. These ratings used
only prior knowledge of the literature. The beneficially
rated food group includes fruit, avocado, beans/le-
gumes, green vegetables, yellow vegetables, toma-
toes, other vegetables, nuts and seeds, soy products,
whole grains, vegetable oil, fatty fish, lean fish, poultry,
alcohol (beer, wine, and liquor), coffee, tea, and low- fat
milk/cheese/yogurt. In practice, the amount of alcohol
consumed was rarely more than a moderate level. The
adversely rated food group includes fried potatoes,
grain dessert, salty snacks, pastries, sweets, high-
fat red meats, processed meats, organ meats, fried
fish/poultry, sauces, soft drink, whole- fat milk/cheese/
yogurt, and butter. The neutrally rated food group in-
cludes potatoes, refined grains, margarine, chocolate,
meal replacements, pickled foods, sugar substitutes,
lean meats, shellfish, eggs, soups, diet drinks, and
fruit juices. Each of the 46 food groups was divided
into quintiles of consumption and then scores of 0
(quintile 1) to 4 (quintile 5) were assigned to the bene-
ficially rated food groups, while scores of 4 (quintile 1)
to 0 (quintile 5) were assigned to the adversely rated
food groups. Zero points were assigned to the neu-
trally rated food groups. For the foods with many 0
servings/day, participants were divided into 5 groups
based on distribution of 0 and quartile (among con-
sumers). Change in diet of individuals over time were
tracked on the basis of specific cut points for each
food group that had been derived from year 0 CARDIA
data that were applied to the follow- up diet data at
year 7 and year 20. Forty- six component scores were
summed to form the total APDQS score, ranging from
0 (minimum) to 132 (maximum). A previous analysis
in CARDIA showed that participants with the great-
est improvement in the APDQS over time largely in-
creased consumption of beneficially rated plant foods
while reducing consumption of adversely rated meat
products.10
Outcome Ascertainment
Primary outcomes were incident CVD. Cases were
identified through August 31, 2018. CVD encompassed
myocardial infarction, non– myocardial infarction acute
coronary syndrome, stroke, heart failure, carotid or
peripheral artery disease, atherosclerotic coronary
heart disease, other atherosclerotic disease, and non-
atherosclerotic cardiac disease. Coronary heart dis-
ease (CHD) and hypertension- related CVD were also
examined as secondary outcomes. Occurrence of
death was determined by CARDIA staff on the basis
of biannual contact with participants or family mem-
bers and record linkage to the National Death Index.
Following each death, the death certificate, autopsy,
and hospital records were requested with next- of- kin
consent. A panel of 2 physicians reviewed all col-
lected information and determined cause of death by
consensus.
Assessment of Covariates
Updated information regarding demographics, maxi-
mal educational attainment, smoking status, medica-
tion use, and parental history of CVD was self- reported
on standardized questionnaires. Physical activity lev-
els were estimated on the basis of a CARDIA physical
Downloaded from http://ahajournals.org by on August 13, 2021
J Am Heart Assoc. 2021;10:e020718. DOI: 10.1161/JAHA.120.020718 4
Choi et al Plant- Centered Diet and Cardiovascular Disease
activity history questionnaire administered by the in-
terviewer. Physical activity was measured in exercise
units as a product of intensity and frequency based on
13 different physical activities performed over the pre-
vious year.20 Body mass index (BMI) was calculated as
weight/height squared (kg/m2) on the basis of meas-
urements by trained technicians. Diabetes mellitus
was defined as fasting blood glucose ≥126 mg/dL, a
2- hour postchallenge glucose concentration ≥200mg/
dL, glycated hemoglobin ≥6.5%, or taking antidiabetic
medication. Hypertension was defined as systolic or
diastolic blood pressure of ≥130 or ≥80 mm Hg or
taking antihypertensive medications. Dyslipidemia
was defined as serum triglycerides ≥150 mg/dL or
high- density lipoprotein cholesterol <40 for men and
<50mg/dL for women.
Statistical Analysis
Cox proportional hazards regression models were
used to estimate hazard ratios (HRs) and 95% CIs
for CVD associated with the APDQS. Person- years
were calculated from the date of baseline examina-
tion to the date of initial diagnosis of CVD, death,
or the end of follow- up (August 31, 2018), whichever
occurred first. To account for potential changes in
diet over time, the APDQS was modeled as a time-
varying exposure: (1) the year 0, year 7, and year 20
values were cumulatively averaged over follow- up.21
Specifically, year 0 predicted events over follow- up
from year 0 to year 7, the average of year 0 and year
7 predicted events over follow- up from after year 7 to
year 20, and the average of year 0, year 7, and year
20 predicted events over follow- up from after year
20 to year 32. Note that if both year 7 and year 20
diet were missing, the model used year 0 data with
outcomes over all follow- up. This method carries for-
ward part or all of the previously observed values
and has the advantage of updating time trend and
retaining participants throughout follow- up (Data S1);
(2) the year 7 value was subtracted from the year
20 value to calculate the 13- year change in APDQS,
and it was evaluated with the outcomes occurring
after year 20. Analyses of the time- varying aver-
age APDQS evaluated the long- term impact of diet
throughout adulthood, and analyses of the APDQS
change evaluated the dynamic relationship between
an individual’s continuing dietary change during the
transition period from young to middle adulthood
and risk of later disease during midlife. We estimated
the risk of CVD using quintile variables as well as
the per 1- SD (13 points) increment in the APDQS as
continuous variables.
Initial analyses of the time- varying average APDQS
were adjusted for year 0 age, sex, race (White or
Black), total energy intake, and maximal educational
attainment (model 1), and were then further adjusted
for parental CVD history (yes versus no), year 0 smok-
ing status (never, former, and current), and physical
activity (model 2). Total energy intake and physi-
cal activity were treated as time- varying covariates.
Hypertension, diabetes mellitus, dyslipidemia, and
BMI as time- varying variables were further adjusted
for in the model (model 3) to examine whether the
association between APDQS and CVD was poten-
tially mediated by these comorbidities. The media-
tion effect of these clinical variables (cumulative data
through year 7) on the association between year 0
APDQS and CVD was quantified by comparing the
models with and without the mediating variables using
the formula: 1 − (βmediator model/βbase model) × 100.22
Next, we examined the association between the 13-
year change in APDQS and subsequent 12- year risk
of CVD outcomes, adjusting for the same covariates
as in the time- varying average diet analysis and, ad-
ditionally, adjustments for the year 7 APDQS and the
13- year change in total energy and physical activity.
CHD and hypertension- related CVD were also exam-
ined with the APDQS as time- varying or change in
secondary analyses.
We computed restricted cubic splines with 4 knots
to visually assess the shape of association between
ADPQS as a continuous variable (both time- varying
average and 13- year change) and risk of CVD.23 ,24
Statistical significance of nonlinearity (ie, curvature)
was tested by comparing the spline model with the
linear model, and P values of <0.05 were regarded as
statistically significant nonlinear relationship between
the exposure and the outcome. Statistical significance
of linearity was tested by comparing the linear model
to the model including only the covariates, both using
likelihood ratio tests.
Sensitivity analyses assessed the robustness
of the primary findings. First, 5- and 8- year lagged
analyses were performed to minimize the potential
impact of reverse causality attributable to preexist-
ing disease with individual diet variables at year 0,
year 7, and year 20, separately. Second, whether
the association differed by the past diagnoses of hy-
pertension, diabetes mellitus, and dyslipidemia was
evaluated by testing multiplicative terms of each past
diagnosis stratum (yes versus no) and the APDQS
(continuous) added in model 2 using the Wald test.
Also, stratified analyses according to race (White or
Black), sex (male or female), education (tertiles split),
physical activity (median split), and smoking (cur-
rent or noncurrent smoker) were performed and the
significance of the interaction were evaluated in the
same way.
All analyses were performed using SAS version 9.4
software (SAS Institute Inc., Cary, NC). The statistical
tests were 2- tailed, with P<0.05 considered to be sta-
tistically significant.
Downloaded from http://ahajournals.org by on August 13, 2021
J Am Heart Assoc. 2021;10:e020718. DOI: 10.1161/JAHA.120.020718 5
Choi et al Plant- Centered Diet and Cardiovascular Disease
RES ULTS
Participants Characteristics
We documented 289 incident CVD cases during
the 32- year follow- up. The mean cumulative APDQS
was 65.11.7 (range, 31– 101), and the mean 13- year
change in APDQS was 3.6±10.5 (range, −36 to 51).
Participants with higher APDQS tended to be older,
female, more educated, more physically active, con-
sumed more alcohol, and consumed less energy
as compared with participants with lower APDQS
(Table1). Additionally, participants with higher APDQS
were less likely to self- identify their race as Black,
smoke cigarettes, have a lower BMI, and have a his-
tory of dyslipidemia. The mean intake of each of the 46
food groups by quintiles of the year 0 APDQS is pre-
sented in Table2. To further specify the scoring sys-
tem, the cut points for each of the 46 food groups and
examples of the high and low scores of the APDQS
are shown in TableS1. One participant with a score
of 47 versus 1 participant with a score of 81 were ar-
bitrarily selected as examples of diets at the median
scores of the 2 extreme quintiles of the year 0 data.
While consuming more beneficially rated plant foods
and animal foods was the main driver in increasing
the diet quality score (12- point difference), consuming
less adversely rated plant foods and high- fat red and
processed meats was the driver of the score (22- point
difference).
Association of Plant- Centered Diet Quality
and Risk of Incident CVD outcomes
The time- varying average APDQS was inversely asso-
ciated with incident CVD (HR for quintile 5 versus quin-
tile 1=0.39; 95% CI, 0.23– 0.64; model 1 in Table 3).
Further adjustment for other covariates in model 2 did
not appreciably alter the association (HR for quintile 5
versus quintile 1=0.48; 95% CI, 0.28– 0.81). The asso-
ciation was slightly attenuated after additional adjust-
ment for time- varying hypertension, diabetes mellitus,
dyslipidemia, and BMI (HR for quintile 5 versus quintile
1=0.54; 95% CI, 0.32– 0.93; model 3). In mediation ef-
fect analyses, dyslipidemia explained some of the as-
sociation between the year 0 APDQS and risk of CVD
(15.8% explained; 95% CI, 5.6%– 37.1%; P<0.001), and
hypertension, diabetes mellitus, and BMI did not ex-
plain this association (<5% explained and P>0.05 for
all). Evaluation of specific CVD events showed that the
time- varying average APDQS was strongly associ-
ated with both CHD (HR for quintile 5 versus quintile
1=0.48; 95% CI, 0.24– 0.97) and hypertension- related
CVD (HR for quintile 5 versus quintile 1=0.48; 95% CI,
0.24– 0.94).
An increase in the APDQS over 13years was as-
sociated with a lower risk of CVD in the subsequent
12years in change analyses (HR for quintile 5 ver-
sus quintile 1=0.33; 95% CI, 0.16– 0.68; model 1 in
Table 4). This association was slightly attenuated in
Table 1. Baseline Characteristics ( Year 0) of the Participants According to Quintiles of the Year 0 APDQS* (n=4946)
Characteristics
Quintile 1 Quintile 2 Quintile 3 Quintile 4 Quintile 5
P Value
n=1026 n=999 n=984 n=9 91 n=946
Median of Year 0 APDQS (range) 47 (24 51) 55 (52– 58) 62 (59– 65) 7 0 (6 6 – 74) 81 (75 – 107 )
Age, y 23.1±3.7 24.4± 3.7 2 5.1±3. 6 2 5.7± 3.3 26.4±2.9 < 0.001
Female, N (%) 512 (4 9. 9) 527 (52.8) 526 (53.5) 52 6 (5 3.1) 623 (65.9) <0.001
Black race, N (%) 812 (79 .1) 677 (67.8) 5 22 (53.1 ) 365 (36.8) 133 (14.1) <0.001
Maximal educational attainment
(through ye ar 30), grades
14. 2. 3 14.5±2.5 15.1± 2 .6 15.9 ±2.6 16. 2.3 <0.001
Physical activit y, EU35 278 372±296 4 0 28 9 425 ±275 519 ±3 08 <0.001
Current s moker, N (%) 339 (33.0) 341 (34.1) 319 (3 2.4) 275 (27. 8) 196 (20.7 ) <0.0 01
Alcohol intake, drinks/d 0.4 ±1. 0 0.8±1.5 0 .9±1. 8 1.0±1.4 1. 0±1.1 <0.0 01
Energy intake, kcal/d 315 7±1382 2869±1388 28 8 2±146 3 26 92±124 5 2453±1033 <0.0 01
Parental history of CVD 395 (38.5) 398 (39.8) 419 (42 .6 ) 366 (36.9) 382 (4 0.4) 0.12
Prevalent disease
Diabetes mellitus, N (%) 8 (0.8) 5 (0.5) 9 (0.9) 7 (0.7) 4 (0.4) 0.65
Hyper tension, N (%) 40 (3.9) 5 1 (5 .1) 41 (4 .2) 33 (3.3) 28 (3.0) 0 .13
Dyslipidemia, N (%) 299 (29.3) 286 (28.7) 287 (29.4) 274 (27.7 ) 191 (20.3) <0.001
BMI, kg/m224.5±5.5 25±5.5 25.1±5.4 24.5±4.7 23.5±3.7 <0.001
APDQS indicates A Priori Diet Qualit y Score; BMI, body mass index; and CVD, cardiovascular disease.
Values are re ported as the mean±SD, unless noted as No. (percentage).
*Total score sums the 46 components (possible scores 0 – 132, with a range of 35– 95 in these data), with higher scores representing a nu tritionally rich, plant-
centered diet. A 1- point increment represents a one- categor y shif t in the presumed favorable direction.
Evaluated w ith chi- square tests for categoric al varia bles and ANOVA for continuous variables.
Exercise units, physical activity score der ived from the CARDIA physical activit y histor y.
Downloaded from http://ahajournals.org by on August 13, 2021
J Am Heart Assoc. 2021;10:e020718. DOI: 10.1161/JAHA.120.020718 6
Choi et al Plant- Centered Diet and Cardiovascular Disease
Table 2. Mean Intake of 46 Individual Food Groups According to Quintiles of the APDQS at Year 0 (n= 494 6)
Food Group
Mean Int ake±SD in Serv ing/D ay
Quintile 1 Quintile 2 Quintile 3 Quintile 4 Quintile 5
Beneficially rated
1. Fruit 0. 9 6±1.38 1. 02 ±1.2 3 1. 27±1.4 5 1.5 6±1.55 2.05±1.64
2. Avoc ado 0.01±0.09 0.02±0.09 0.05±0.22 0 .11± 0 .30 0.24±0.47
3. Beans and legumes 0.17±0.35 0.21±0.44 0.21±0.38 0.19±0.32 0.24±0.4
4. Green vegetables 0.12±0.24 0.20±0.34 0.27±0.38 0.42±0.61 0 .9 0 ±1. 2 5
5. Yellow vegetables 0.07±0.21 0.12±0.22 0.2±0.65 0.28±0.52 0.60±0.97
6. Tomato 0.32±0.30 0.38±0.41 0.44±0.47 0.52±0.46 0.73±0.65
7. Other vegetable s 1.42 ±1.17 1.6 4±1.37 2 .0 1±1. 5 8 2 .28 ±1. 64 2.89±2.16
8. Nuts and seeds 0.39±0.84 0.53±1.04 0.79 ±1. 47 0.82±1.44 1.12±1.6 5
9. Soy products 0.09±0.44 0.18±0.65 0.21±0.70 0.23±0.65 0 . 47±1.0 6
10. Whole grains 1.01±1.3 4 1. 20 ±1.3 7 1.4 6±1.45 1.67±1.5 3 2.14±1.7 7
11. Vegetable oil 0. 8 7±1. 2 6 1.2 6±1.56 1.47±1.72 1.6 2±1.71 2.04±2.06
12. Fatty fish 0.01±0.07 0.02±0.09 0.03±0.27 0.03±0.13 0.08±0.25
13. Lean fish 0.44±0.90 0.52±0.79 0.64±1.02 0.84 ±1. 32 1.0 3±1.49
14. Poultry 1.07±1.14 1.0 6±1.0 6 1.17±1.36 1.3 3±1.7 7 1.4 2±1.71
15. B eer 0.29±0.85 0.53±1.24 0.54±1.24 0. 5 6±1.0 6 0.48±0.71
16. W in e 0.04±0.23 0.08±0.3 0 0.14±0.63 0.2±0.39 0.31±0.49
17. Liquor 0.10±0.52 0.16±0.55 0.24±0.63 0.26±0.56 0.18±0.45
18. C of fee 0.46±1.63 0 . 79 ± 2 .13 1.16 ± 2 .4 4 1. 43 ±2.3 1 1.8 2.71
19. Tea 0.3 2±1.27 0.62±5.98 0 . 57±1.46 0 .72±2.76 0.8 5 ± 2.15
20. Low- fat milk/
Cheese/Yogurt
0.55±1.06 0 . 89±1.4 8 1.18±1.96 1.4 6±1.85 1.6 5±1.52
Neutrally rated
1. Pot at oe s 0.38±0.53 0.42±0.59 0.46±0.76 0.41±0.58 0.34±0.40
2. Refined grains 5.62±3.28 4 .6 3 .12 4.32±3.03 3.8±2.70 3.1 2 . 22
3. Margarine 1. 67± 2 .48 1. 71±2 .2 7 1.77± 2 .19 1. 74±2 . 41 1.3 9 ±2.0 8
4. Chocolate 0.22±0.37 0.20±0.41 0.20±0.44 0.17±0.45 0.12±0.23
5. Meal replacements 0.01±0.13 0.0 0 .11 0 .01±0 .11 0.02±0.28 0.01±0.07
6. Pickled foods 0.29±0.71 0.29±0.73 0.34±0.55 0.39±0.70 0.40±0.63
7. Sugar substitutes 0.01±0.10 0.04±0.44 0.05±0.27 0.08±0.33 0.13±0.43
8. Lean red meats 0.82±1.10 0 .83 ±1. 0 2 0.92±1.28 0.70.99 0.48±0.75
9. Shellfish 0.14±0.38 0.17±0.33 0.21±0.42 0.31±0.94 0.27±0.42
10. Eggs 0.78±0.80 0.72±0.81 0.66±0.75 0.57±0.58 0.49±0.51
11. Soups 0.02±0.06 0.03±0.07 0.04±0.09 0. 0 5 ± 0.11 0.04±0.07
12. Diet soft drinks 0.11±0. 5 9 0.25±0.92 0 . 39 ±1. 0 8 0.55±1.38 0.6 8 ±1.4 4
13. Fruit juice 1.83 ±2 .3 6 1.81±2.58 1.88±2.3 1.9 2.20 1. 85 ±2 .2 7
Adversely rated
1. Fried potatoes 0.53±0.57 0.38±0.46 0.35±0.51 0.28±0.45 0.15±0.24
2. Grain des serts 0.9 7±1. 2 8 0.65±0.78 0.67±0.80 0.54±0.64 0.46±0.65
3. Salty snacks 0. 0 3 ± 0.11 0.0 4±0.22 0.03±0.12 0.03±0.23 0.04±0.18
4. Pastries 1.23±1.18 1. 02 ±1.12 0. 9 4±1.13 0.79±0.92 0.64±0.72
5. Sweets 2.00±2.46 2.03±2.56 1.8 2.4 4 1.48 ±2 .0 4 0. 9 6 ±1. 36
6. High- fat red meats 2.8 2 .11 2.59±2.32 2 .41± 2.11 2.09± 2.53 1.16 ±1.6 0
7. Processed meats 1.23 ±1.26 1.0 2±1.12 0.88±1.03 0.67±0.93 0.33±0.63
8. Organ me ats 0.06±0.19 0.05±0.16 0.05±0.18 0.04±0.14 0.02±0.07
9. Fried poultry and fish 0.15±0.84 0.12±0.75 0.11± 0 . 6 8 0.09±0.61 0.07±0.55
(Continued)
Downloaded from http://ahajournals.org by on August 13, 2021
J Am Heart Assoc. 2021;10:e020718. DOI: 10.1161/JAHA.120.020718 7
Choi et al Plant- Centered Diet and Cardiovascular Disease
model 2; the highest quintile of 13- year change in
APDQS was associated with a 61% (95% CI, 0.19–
0.81) lower subsequent 12- year risk of CVD as
compared with the lowest quintile. Strong inverse
associations were observed for CHD (HR for quintile
5 versus quintile 1=0.21; 95% CI, 0.06– 0.75; model
2) and hypertension- related CVD (HR for quintile 5
versus quintile 1=0.34; 95% CI, 0.16– 0.74; model 2).
These results were preserved after further adjustment
for comorbidity variables. A monotonic decrease
in CVD risk with time- varying average APDQS (P-
nonlinearity=0.12 and P- linearity<0.001; FigureA) and
the 13- year change in APDQS (P- nonlinearity=0.54
and P- linearity=0.04; FigureB) was observed in re-
stricted cubic splines. Associations between either the
time- varying average APDQS or the 13- year change
in APDQS with CVD did not differ by race, sex, educa-
tion, physical activity, or smoking (P- interaction >0.05
for each).
Sensitivity Analyses
In exam year– specific and exam- lagged analyses (5-
and 8- year lag), an inverse association between the
APDQS as a fixed baseline variable and CVD risk was
observed (TableS2). HR comparing the extreme quin-
tiles was stronger for the year 0 APDQS, although the
gradient of association across categories was more
consistent for the year 20 APDQS. Neither the as-
sociations of the time- varying average APDQS nor of
the 13- year change in APDQS with risk of CVD dif-
fered significantly by histories of hypertension, diabe-
tes mellitus, or dyslipidemia (P- interaction >0.05 for
each).
DISCUSSION
In this 32- year prospective cohort study, which fol-
lowed participants since young adulthood, long- term
consumption of a plant- centered, high- quality diet
that also incorporates subsets of animal products
was associated with a 52% lower risk of incident CVD.
Furthermore, an increase in plant- centered diet quality
over 13years was associated with a 61% lower risk of
incident CVD in the subsequent 12years.
There is increasing interest in understanding the
association between diets that emphasize plant foods
and limit most animal products and incident CVD out-
comes, but the evidence is inconclusive. A previous
meta- analysis showed that vegetarians (versus non-
vegetarians) had a lower risk of ischemic heart dis-
ease, but not incident CVD and all- cause mortality.3
The noted limitations were narrow definitions of popu-
lations, uncertain accuracy of the assessment of veg-
etarian status, and inconsistent results across studies
(the inverse associations were apparent in the US
Adventist cohorts but not in non- Adventist cohorts). In
addition, some studies have defined vegetarian diets
as non– meat eaters on the basis of food frequency in-
take or have self- identified as vegetarians, but neither
approach comprehensively captures an individual’s
overall diet quality. Recently, the healthful PDI has been
developed that focuses on healthy plant foods, limit-
ing all animal- derived foods. In a pooled analysis of 3
large cohorts, higher healthful PDI was associated with
a 14% lower risk of CVD, comparing the highest with
the lowest quintiles.4 Consistent with this, we found
that the time- varying APDQS was associated with a
lower risk of incident CVD, CHD, and hypertension-
related CVD. In contrast, however, another study found
no association with incident CVD.6 The PDI and the
APDQS share some commonalities. Both diet quality
indices assess the overall diet quality in holistic ap-
proaches, differentiating plant foods by their nutritional
quality. On the other hand, there are some differences.
All animal- derived products are rated adversely in the
PDI, while only high- fat processed/unprocessed red
meats, organ meats, and fried fish/poultry are rated
adversely in the APDQS. Additionally, the PDI does
not include alcoholic beverages in the index, while the
APDQS does. An important finding of our study was
to clarify whether eating nutritionally rich plant foods
while integrating subsets of animal products into diet
can improve future cardiovascular outcomes. The sen-
sitivity analyses of previous studies further support
the benefits of these flexible diet characteristics. The
reduced estimate of CHD or total mortality remained
similar when the modified healthful PDI was fitted as
the main exposure, where fish, poultry, dairy products,
or eggs were changed from their original adverse rating
Food Group
Mean Int ake±SD in Serv ing/D ay
Quintile 1 Quintile 2 Quintile 3 Quintile 4 Quintile 5
10. Sauces 4.62±4.18 4 .3 1±5 .51 4.67±6.39 4.3 9±5.97 4.72±9.27
11. Soft drinks 2.68±2.59 1. 95 ±2.2 5 1.4 0±1.76 0 .9 8 ±1. 43 0.43±0.74
12. Whole- fat milk/
Cheese/Yogurt
2.51± 2. 37 2 .0 1±1. 87 2.02±2.17 1.74±2.50 1.36 ±1.3 4
13. B utter 6.02±4.66 4.60±4.03 4.44±4.33 3.90±3.600 3.12±3.07
Table 2. Continued
Downloaded from http://ahajournals.org by on August 13, 2021
J Am Heart Assoc. 2021;10:e020718. DOI: 10.1161/JAHA.120.020718 8
Choi et al Plant- Centered Diet and Cardiovascular Disease
Table 3. HR (95% CI) of Incident CVD Outcomes ( Year 0Year 32) According to Q uintiles of t he Time- Varying Average APDQS*
Quintile 1 Quintile 2 Quintile 3 Quintile 4 Quintile 5
Each 1- SD increment
(13 - p oint) P for Trend
CVD
APDQS (median)50.0 58.0 64.3 71. 5 81.0
Unadjusted cumulative incidence % (n/N)9.0 (89/989) 7.8 (77/989) 5. 3 (51/9 61) 4.8 (49/1015) 2.3 (23/992)
Model 1§1 (ref) 0.86 (0.62– 1.17) 0.68 (0.48– 0.96) 0.6 9 ( 0.47– 1.01) 0.39 (0.23– 0.64) 0.74 (0.63– 0.87) <0.001
Model 2|| 1 (ref) 0.87 (0.63– 1.19) 0.73 (0.52– 1.04) 0.78 (0.53– 1.14) 0.48 (0.28– 0.81) 0.80 (0.67– 0.95) 0. 010
Model 3#1 (ref) 0.83 (0.60– 1.15) 0.72 (0.51– 1.03) 0.79 (0.53– 1.16) 0.54 (0.32– 0.93) 0.81 (0.68– 0.96) 0 .018
CHD
APDQS (median)50.0 58.0 64.3 71. 5 81.0
Unadjusted cumulative incidence % (n/N)3.7 (37/989) 3.6 (35/985) 3.2 (31/964) 2.2 (22/1016) 1.3 (13/992)
Model 1§1 (ref) 0.82 (0.51– 1.33) 0.82 (0.50– 1.34) 0.54 (0.30– 0.96) 0.38 (0.19– 0.75) 0.72 (0.57– 0.91) 0.006
Model 2|| 1 (ref) 0.84 (0.52– 1.36) 0.91 (0.55– 1.48) 0.63 (0.35– 1.12) 0.48 (0.24– 0.97) 0.78 (0.61– 1.00) 0 .0 51
Model 3#1 (ref) 0.89 (0.54– 1.45) 0.97 (0.59 – 1.61) 0.69 (0.38– 1.25) 0.61 (0.30– 1.25) 0.83 (0.65– 1.07) 0 .15
Hypertensive- related CVD
APDQS (median)50.0 58.0 64.3 71. 5 81.0
Unadjusted cumulative incidence % (n/N)7.1 (70/989) 5.4 (53/986) 3.4 (33/964) 3.0 (3 0/1014) 1.3 (13 /99 3)
Model 1§1 (ref) 0.79 (0.55 – 1.15) 0.61 (0.40– 0.93) 0 .7 0 (0. 4 4 – 1 .11) 0.39 (0.20– 0.76) 0.75 (0.61– 0.92) 0.0 06
Model 2|| 1 (ref) 0.80 (0.55– 1.16) 0.65 (0.43– 0.99) 0.78 (0.49– 1.23) 0.48 (0.24– 0.94) 0.80 (0.65– 0.99) 0.040
Model 3#1 (ref) 0.74 (0.51– 1.07) 0.60 (0.39– 0.92) 0.73 (0.46– 1.16) 0.50 (0.25– 0.99) 0.77 (0.62– 0.96) 0.022
APDQS indicates A Priori Diet Qualit y Score; CHD, coronar y hear t disease; CVD, cardiovascular disease; and HR, hazard ratio.
*Time- varying variables that were cumulatively averaged over follow- up at year 0, year 7, and year 20. Specifically, year 0 predicted events ove r follow- up from year 0 to year 7, the average of year 0 and year 7 predicted
events over follow- up from after year 7 to year 20, and the average of year 0, ye ar 7, and year 20 predicted events over follow- up from af ter year 20 to year 32. Note that if both year 7 and ye ar 20 diet was missing, the
model used year 0 data with outcomes over all follow- up.
Median A PDQS, number of cases, and numbers at risk are categories according to quintiles of the average of all available APDQS measu rements.
Statistical significance was estimated by modeling APDQS as a continuous variable in the model.
§Model 1: year 0 age, sex, race (White or Black), total energy intake (time- varying averag e), and maximal educational attainment.
||Model 2: model 1+parental history of CVD (yes vs no), year 0 smoking status (neve r, former, and current), and physic al activity level (time- varying average).
#Model 3: model 2+time- varying comorbidities (hypertension, diabetes mellitus, dyslipidemia [all yes vs no], and body mass index [continuous]).
Downloaded from http://ahajournals.org by on August 13, 2021
J Am Heart Assoc. 2021;10:e020718. DOI: 10.1161/JAHA.120.020718 9
Choi et al Plant- Centered Diet and Cardiovascular Disease
Table 4. HR (95% CI) of Incident CVD Outcomes ( Y20- Y32) Accord ing to Quintiles of the 13- year Change in APDQS*
Quintile 1 Quintile 2 Quintile 3 Quintile 4 Quintile 5
Each 1- SD increment
(13 - p oint) P for Trend
CVD
13- year change in APDQS
(median)
−9 −1 4 9 17
Unadjusted cumulative
incidence % (n/N)
5.6 (31/5 59 ) 4.2 (22/522) 2. 5 (13 /52 2) 4 (21/528) 2 . 2 (11/4 9 0 )
Model 11 (ref) 0.74 (0.43– 1.3) 0.42 (0.22– 0.81) 0.63 (0.35– 1.12) 0.33 (0.16 – 0.68) 0.69 (0.52– 0.90) 0.0 07
Model 2§1 (ref) 0.81 (0.46 – 1.43) 0.48 (0.25– 0.93) 0.74 (0.41– 1.33) 0.39 (0.19– 0.81) 0.75 (0.57– 1.00) 0.048
Model 3|| 1 (ref) 0.86 (0.49– 1.5) 0.47 (0.24– 0.92) 0.75 (0.41– 1.35) 0.36 (0.17– 0.75) 0.73 (0.56– 0.97) 0.028
CHD
13- year change in APDQS
(median)
−9 −1 4 9 17
Unadjusted cumulative
incidence % (n/N)
2.9 (16/5 59) 2.1 ( 11/ 522 ) 1.3 (7/5 22 ) 2.1 ( 11/ 528 ) 0.6 (3/490)
Model 11 (ref) 0.71 (0.32– 1.54) 0.43 (0.17– 1.06) 0.66 (0.30– 1.47) 0.18 (0.05– 0.64) 0.64 (0.43 – 0.9 5) 0.027
Model 2§1 (ref) 0.79 (0.36– 1.74) 0.50 (0.20 – 1.24) 0.75 (0.33– 1.69) 0.21 (0.06 – 0.75) 0.70 (0.47– 1.05) 0.084
Model 3|| 1 (ref) 0.83 (0.37– 1.82) 0.53 (0.21– 1.32) 0.77 (0. 34 – 1.75) 0.20 (0.06 – 0.72) 0.69 (0.46– 1.04) 0.076
Hypertensive- related CVD
13- year change in APDQS
(median)
−9 −1 4 9 17
Unadjusted cumulative
incidence % (n/N)
5.0 (28/557) 2.9 (15/ 521) 1.3 ( 7/5 2 2) 2.5 (13/5 27) 2.0 (10/4 90 )
Model 11 (ref) 0.54 (0.29– 1.03) 0.23 (0.10– 0.54) 0.38 (0.19– 0.76) 0.29 (0.14 – 0.64) 0.58 (0.42– 0.79) <0.001
Model 2+ 1 (ref) 0 . 5 8 (0 . 31– 1.11) 0.26 (0.11– 0.61) 0.44 (0.22– 0.89) 0.34 (0.16– 0.74) 0.63 (0.45– 0.86) 0.004
Model 3|| 1 (ref) 0.60 (0.32– 1.15) 0.23 (0.10– 0.54) 0.44 (0.22– 0.90) 0.31 (0.14– 0.68) 0.61 (0.44– 0.84) 0.003
APDQS indicates A Priori Diet Qualit y Score; CHD, coronar y hear t disease; CVD, cardiovascular disease; and HR, hazard ratio.
*The 13- year change in APDQS ( year 20 value minus year 7 value) was used to predict events occurred between year 20 and year 32.
Statistical significance was estimated by modelling APDQS as a continuous variable in the mode l.
Model 1: year 7 APDQS, year 0 age, sex, race (White or Black), total energy intake (year 7 and 13- year change), and ma ximal educational attainment.
§Model 2: model 1+parental history of CVD (yes vs no), year 7 s moking status (never, former, and current), and physical activity level ( year 7 and 13- year change).
||Model 3: model 2+hypertension (yes vs no), diabetes mellitus (yes vs no), dyslipidemia (yes vs no), and body mass index (continuous). The cumulative data through ye ar 20 were used.
Downloaded from http://ahajournals.org by on August 13, 2021
J Am Heart Assoc. 2021;10:e020718. DOI: 10.1161/JAHA.120.020718 10
Choi et al Plant- Centered Diet and Cardiovascular Disease
to a beneficial rating.7, 25 Furthermore, consumption of
these types of animal products has not generally been
associated with an increased risk of CVD outcomes
and mortality.26– 31
Longitudinal analyses can provide unique insights
as to whether late- life disease risk can be altered by
changing diet quality over time. Several long- term
prospective studies have demonstrated the relation-
ship between change in diet quality (assessed by the
Healthy Eating Index- 2015, the Alternative Healthy
Eating Index- 2010, the Dietary Approaches to Stop
Hypertension, or the Alternate Mediterranean Diet
score) and subsequent risk of CVD and mortality,
although results have varied.9,32,33 The timing and
duration of exposure to risk factors may differen-
tially affect the development of adult disease.34 Thus,
evaluating diet exposure in middle or older adulthood
may not completely explain the full spectrum of adult
disease development. Our study adds to the current
evidence on the association between diet quality and
CVD risk by indicating that improved plant- centered
diet quality, starting in young adulthood, is associ-
ated with a lower subsequent risk of CVD by middle
adulthood.
It is also worth noting that in the CARDIA sample,
there was a notable difference in the distribution of race
among the lowest versus the highest quintiles of the
APDQS (Black race, 79% versus 14%) and also there
was a difference in the maximal educational attainment
(14.2 versus 16.9 grades completed). We also ob-
served higher CVD cumulative incidence among Black
participants (7.7% for Black versus 3.9% for White)
and individuals with a lower educational level (8.6% for
≤13 grades versus 3.4% for ≥17 grades). Given the ob-
served higher risk of CVD with lower APDQS values,
the results of our study point out that the diet may help
to explain disparities in CVD, although the relationships
of the APDQS and incident CVD did not differ by race
or education. Further studies are warranted to explore
the association between a plant- centered diet and risk
of CVD events, considering these social parameters as
a potential mediator of the relationship.
It is not fully understood how a plant- centered diet has
a protective effect against the development of CVD. As
we previously described, the concerted action of nutri-
ents and bioactive compounds found in a combination
of plant foods may lead to a favorable cardiovascular
outcome.10,17 Numerous compounds, including ascorbic
Figure. Restricted cubic spline cur ves for the association of incident CVD wit h (A) the time- var ying average APDQS
(n=4946) and (B) the 13- year change in APDQS (n=2 621).
A, Time- varying average APDQS and incident CVD. B, 13- year change in APDQS and incident CVD. The solid line is the HR and the
dashed line represents the 95% CI. HR and 95% CI were calculated using restricted cubic splines with 4 knots within proportional
hazard regression models. Nonlinearity was tested by comparing the spline model with the linear model, and linearity was tested by
comparing the linear model to the model including only the covariates, both using likelihood ratio tests. A, Model was adjusted for year
0 age, sex, race (White or Black), total energy intake (time- varying average), maximal educational attainment, parental history of CVD
(yes vs no), year 0 smoking status (never, former, and current), and physical activit y level (time- var ying average). P- nonlinearity=0.12
and P- linearity<0.001. B, Model was adjusted for Y7 APDQS, Y0 age, sex, race (White or Black), total energy intake (year 7 and 13- year
change), and ma ximal educational attainment, parental history of CVD (yes vs no), year 7 smoking status (never, former, and current),
and physical activit y level (year 7 and 13- year change). P- nonlinearity=0.54 and P- linearity= 0.04. APDQS indicates A Priori Diet Quality
Score; CVD, cardiovascular disease; and HR, hazard ratio.
Downloaded from http://ahajournals.org by on August 13, 2021
J Am Heart Assoc. 2021;10:e020718. DOI: 10.1161/JAHA.120.020718 11
Choi et al Plant- Centered Diet and Cardiovascular Disease
acid, tocopherols, carotenoids, and phenolics, are abun-
dant in nuts and seeds, fruits, vegetables, and whole
grains. These compounds can trap free radicals and
reduce the levels of reactive oxygen molecules, thereby
protecting against tissue damage.35 Moreover, these sub-
stances may help inhibit plaque formation in the arteries
by reducing low- density lipoprotein oxidation, platelet ac-
tivation and aggregation, and inflammatory markers.36– 39
Experimental studies have also reported that a mixture of
compounds found in plant source foods had a synergistic
effect on enhancing antioxidant activity.40 ,41 Although the
mechanism remains to be established, our findings sup-
port a beneficial effect of a plant- centered diet on CVD
prevention at the general population level.
Study Strengths and Limitations
Because of the nature of the observational study de-
sign, we cannot rule out unmeasured or residual con-
founding. However, important potential confounding
factors were adjusted for regarding the association be-
tween diet and CVD. The results of this study may have
limited generalizability to other populations across dif-
ferent cultures, races/ethnicities, and periods of life.
Our study has several unique methodological fea-
tures that were used to evaluate the quality of plant-
centered diets. The CARDIA diet history questionnaire
measured comprehensively what specific foods were
eaten in the recent past, with an open- ended form. The
diet of the individuals with high APDQS score is cen-
tered on eating nutritionally rich plant foods, but with-
out excluding all animal products. Flexibility in dietary
choice may help maintain long- term stability in eating
healthfully. The APDQS allows choice by providing a
wide range of options in the way it is structured and
by emphasizing variety (46 groups). The components of
the APDQS were equally weighted with a maximum of
4 points, such that many food groups need to be part
of the diet to achieve a higher score. This is distinct from
other diet quality indices (eg, Healthy Eating Index- 2015
or Alternate Mediterranean Diet) that use a small num-
ber of food groups (≤13) within the scoring algorithm,
allowing a person to earn many points from single foods
and to avoid losing points for large consumption of less
healthy foods. Other strengths of this study include the
prospective design with the high retention rate during
a long follow- up, repeated measurements, and objec-
tively measured clinical data. Furthermore, the change
analysis allowed us to identify a clear temporality and
reduce the possibility of within- person confounding.
CONCLUSIONS
In summary, our study shows that long- term consump-
tion of a nutritionally rich plant- centered diet is associ-
ated with a lower risk of CVD. Furthermore, increased
plant- centered diet quality since young adulthood is as-
sociated with a lower subsequent risk of CVD through-
out middle age, independent of their earlier diet quality.
ARTICLE INFORMATION
Received December 30, 2020; accepted May 20, 2021.
Affiliations
Depar tment of Food Science and Nutrition ( Y.C., D.D.G.), University of
Minnes ota–Twin Cities, St Paul, M N; Division of Ep idemiolog y and Communi ty
Health (N.L., L.M.S., P.J.S., D.R.J.), and Cardiovascular Division, Department
of Medicine (D.A.D.), University of Minnesota– Twin Cities, Minneapolis, MN;
Division of Preventive Medicine, School of Medicine, University of Alabama
at Birmingham, Birmingham, AL (J.M.S.); Divisions of Cardi ology and
Research, Kaiser Permanente Northern California, Oakland, CA (J.S.R.); and
Depar tment of Medicine, University of California, San Francisco, CA (J.S.R.).
Acknowledgments
Author contributions: Drs Choi and Jacobs conceived and designed the
study. Dr Choi did the statistical analysis a nd drafted the manuscript. All
authors c ontributed to data interpretation and critical rev iew of the report.
Drs Choi, Shikany, and Schreiner obtained funding for this study. Dr Jacobs
supervised the study.
Sources of Funding
CARDIA is supported by contracts HHSN268201800003I, HHSN2682018
00004I, HHSN268201800005I, HHSN268201800006I, and HHSN268
201800007I from the National Heart, Lung, and Blood Institute (NHLBI),
Bethesda, Maryland. The sponsor, NHLBI has a representative on the Steering
Commit tee of CARDIA and par ticipated in study design, data collection, and
scientific review of this paper. The sponsor had no role in data analysis, data
interpretation, or writing of this repor t. Dr Choi is suppor ted by Graduate and
Professional Research Grant from the Healthy Food Healthy Lives Institute and
from the MnDRIVE Global Food Ventures Professional Development Program,
University of Minnesota, Minneapolis, Minnesota.
Disclosures
Dr Jacobs has been a paid consultant to the California Walnut C ommiss ion.
Dr Galla her is a paid member of the Nutrition Advisory Council for the
California Prune Board. Dr Steffen received a grant ending Febru ary 2020
with Dairy Management about dairy products. The remaining authors have
no disclosures to report.
Supplementary Material
Data S1
Tab l es S1 S2
REFERENCES
1. Rana JS, Kha n SS, Lloyd- Jones DM, Sidney S. Changes in mor tality in
top 10 causes of de ath from 2011 to 2018. J Gen Intern Med. 2020;1– 2.
Jul 23 [Epub ahead of print]. DOI: 10.1007/s1160 6- 020- 06070 - z.
2. GBD 2017 Risk Factor Collaborators. Global, regional, and national
comparative risk assessment of 84 be havioural, enviro nmental and oc-
cupational, and metabolic risks or clusters of risks for 195 countries
and territories, 1990 2017: a systematic analysis for the Global Burden
of Disease Study. Lancet. 2018;392:1923– 1994. DOI: 10.1016/S0140
- 6736(18)32225 - 6.
3. D inu M, Abbate R, Gensini GF, Casini A, Sofi F. Vegetarian, vegan diets
and multiple health outcomes: a systematic review with meta- analysis
of obser vational studies. Crit Rev Food Sci Nutr. 2 017; 57: 36 4 0 364 9.
DOI: 10.1080/10408 398.2016.1138447.
4. Shan Z, Li Y, Baden MY, Bhupathiraju SN, Wang DD, Sun QI, Rexrode
KM, Rimm EB, Q i LU, Willett WC, et al. Association between he althy
eating patterns and risk of cardiovascular disease. JAMA Inte rn Med.
2020;180:1090– 1100. DOI: 10.1001/ jamai ntern m ed.2020.2176.
5. Kim H, Caulfield LE, Rebholz CM. Healthy plant- based diets are as-
sociated with lower risk of all- cau se mortality in US adults. J N utr.
2018;148:624– 631. D OI : 10.109 3/ jn /n xy 019.
Downloaded from http://ahajournals.org by on August 13, 2021
J Am Heart Assoc. 2021;10:e020718. DOI: 10.1161/JAHA.120.020718 12
Choi et al Plant- Centered Diet and Cardiovascular Disease
6. Kim H, Caulfield LE, Garcia- Larsen V, Steffen LM, Coresh J, Re bholz
CM. Plant- based diets are associated with a lower risk of incident car-
diovascular disease, cardiovascular disease mortality, and all- cause
mortality in a general population of middle- aged adults. J Am Heart
Assoc. 2019;8:e012865. DOI: 10.1161/JAHA .119.012865.
7. Baden MY, Liu G, Satija A, Li Y, Sun Q, Fung TT, Rimm EB, Willett WC,
Hu FB, Bhupathiraju SN. Change s in plant- based diet quality and total
and cause- specific mortality. Circulation. 2019;140:979– 991. DOI:
10 .116 1/ C I RCU L ATIO NA H A .11 9.0 41 014.
8. Spri ng B, Moller AC, Colang elo LA, Siddique J, Roeh rig M, Daviglus ML,
Polak JF, Reis JP, Sidney S, Liu K. Healthy lifestyle change and subclin-
ical athe rosclerosis in young adults: Coronar y Artery Risk D evelopm ent
in Young Adults (CARDIA) study. Circulation. 2014;130:10– 17. DOI:
10 .116 1/ C I RCU L ATIO NA H A .11 3.0 0 5 4 4 5 .
9. Sotos- Prieto M, Bhupathiraju SN, Mattei J, Fung TT, Li Y, Pan A,
Willett WC, Rimm EB, Hu FB. Changes in diet quality scores and risk
of cardiovascular disease among US men and women. Circulation.
20 15 ;1 32: 2 212– 2 2 19 . DOI: 10.11 61 /C I R C U L ATIO N A H A .11 5. 0 171 58.
10. Choi Y, Larson N, Gall aher DD, Odegaard AO, Rana JS, Shikany JM,
Steffen LM, Jacobs DR. A shif t toward a plant- centered diet from young
to middle adulthood a nd subsequent risk of type 2 diabetes and weight
gain: the Coronary Arter y Risk Development in Young Adults (CARDIA)
stud y. Diabetes Care. 2020;43:2796– 2803. DOI: 10.2337/dc20- 1005.
11. Hu T, Ja cobs DR, Larson NI, Cutler G J, Laska M N, Neumark- Sztai ner D.
Higher diet quality in adolescen ce and dietary improvements are related
to less weight gain during the transition from adolescence to adulthood.
J Pediatr. 2016;178:188– 193 . DOI: 10.1016/ j. jp ed s. 2016 .08.0 26.
12. Mursu J, Steffen LM, Meyer K A, Duprez D, Jacobs DR. Diet quality
indexes and mortality in postmenopausal women: the Iowa Women’s
Health Study. Am J Clin Nutr. 2013;98:444– 453. D OI: 10.3945/
ajcn.112.055681.
13. Jacobs DR, Orlich MJ. Diet pattern and longevity: do simple rules
suffice? A commentary. Am J Cl in Nutr. 2014;100:313S 319S. DOI:
10 .394 5 / ajcn.11 3. 0 71 340 .
14. Frie dman GD, Cutter GR, Do nahue RP, Hughes GH, Hulley SB,
Jacobs DR, Liu K, Savage PJ. CARDIA: study design, recruitment,
and some characteristics of the examined subjects. J Clin Epidemiol.
19 8 8;41 :110 5 – 1116 . D O I: 1 0.1 016 /089 5 - 4 3 5 6 ( 8 8)9 0 08 0 - 7.
15. McD onald A, Van Horn L, Slattery M, Hilner J, Bragg C, Caan B,
Jacobs D, Liu K, Huber t H, Gernhofer N, et al. T he CARDIA dietar y
history: development, implementation, and evaluation. J Am Diet Assoc.
19 91;91: 110 4 1112.
16. Liu K, Slattery M, Jacobs D, Cut ter G, McDo nald A, Van Horn L, Hilner
JE, Caan B, Bragg C, Dyer A. A study of the re liability and comparative
validit y of the cardia dietary history. Ethn Dis. 19 9 4; 4 :1 5 2 7.
17. Jacobs DR, Steffen LM. Nutrients, foods, and dietar y patterns as ex-
posures in research: a framework for food synergy. Am J Cl in Nutr.
2003;78:508S– 513S. DOI: 10.1093/ajcn/78.3.508S.
18. Sijtsma FP, Meyer KA , Steffe n LM, Shikany JM, Van Horn L, Harnack
L, Kromhout D, Jacobs DR. Longitu dinal tre nds in diet and effects of
sex, race, and education on dietary qua lity score change: the Coronary
Arter y Risk Development in Young Adults study. Am J Clin N utr.
20 12 ; 95: 5 8 0 – 58 6. D OI : 10 .39 45 /a jc n.111.02 0719 .
19. Lockhear t MS, Stef fen LM, Rebnord HM, Fimreite RL, Ringstad J,
Thelle DS, Pedersen JI, Jacobs DR. Dietary pat terns, food groups and
myocardial infarction: a case - control study. Br J Nutr. 2007;98:380–
387. DOI: 10.1017/S 0007 11450 7701654.
20. Jacobs DR, Hahn LP, Haskell WL, Pirie P, Sidney S. Validit y and re-
liability of short physical activity history: CARDIA and the Minnesota
Heart Health program. J Cardiopulm Rehabil. 1989;9:448– 459. DOI:
10.1097/00008 483- 19891 1000- 00003.
21. Satija A, Bhupathiraju SN, Rimm EB, Spiegelman D, Chiuve SE, Borgi
L, Willet t WC, Manson JE, Sun Q, Hu FB. Plant- based dietar y patterns
and incidence of type 2 diabetes in US men and women: results from
three prospective cohort studies. PLoS Med. 2016;13:e10 02039. DOI:
10.1371/journ al.pmed.1002039.
22. Hertzmark E, Paz aris M, Spiegelm an D. The SAS me diate macro. 2018.
https://w ww.hsph.harva rd.edu/donna - spieg elman/ softw are/media te/.
Accessed April 15, 2021.
23. Durrleman S, Simon R. Flexible regression models with cubic splines.
Stat Med. 1989;8:551– 561. DOI: 10.1002/sim.4780 0 80504.
24. Li R, Her tzmark E, Louie M, Chen L, Spiegelma n D. T he SAS lgtphcurv9
Macro. 2011. https://www.hsph.har va rd.edu/donna - spieg elman/ softw
are/lgtph curv9/. Accessed October 15, 2020.
25. Satija A , Bhupathiraju SN, S piegelman D, Chiu ve SE, Manson JE, Willett
W, Rexrode KM, Rimm EB, Hu FB. Healthful and unhealthful plant-
based diets and the risk of coronary heart disease in U.S. Adults. J Am
Coll Cardiol. 2017;70:411– 422. DOI: 10.1016/j.ja cc.2017.0 5.047.
26. Zhong VW, Van Horn L, Greenland P, Carnethon MR, Ning H, Wilkins
JT, Lloyd- Jones DM, Allen NB. Associations of processed meat, un-
processed red meat, poultr y, or fish intake with incident cardiovascular
disease and all- cause mortality. JAMA Intern Med. 2020;180:503– 512.
DOI: 10.1001/ jamai ntern med.2019.6969.
27. Kim K, Hyeon J, Lee SA, Kwon SO, Lee H, Keum N, Lee JK, Park SM.
Role of total, re d, proces sed, and white meat consumption in stroke
incidence and mortality: a systematic review and meta- a nalysis of
prospective cohort studies. J Am Heart Asso c. 2017;6:e005983. DOI:
10 .116 1/JA H A .117.0 0 5 9 8 3.
28. Jayedi A, Shab- Bidar S, Eimeri S, Djafarian K. Fish consumption and
risk of all- cause and cardiovascular mortality: a dose- re sponse meta-
analysis of prospective observational studies. Public Health Nutr.
2018;21:1297– 130 6. DO I: 10.1017/S136 8 9 80 01 70 038 34.
29. Drouin- Char tier JP, Chen S, Li Y, Schwab AL, Stampfer MJ, Sacks
FM, Rosner B, Willet t WC, Hu FB, Bhupathiraju SN. Egg consump-
tion and risk of cardiovascular disease: three large prospective US
cohor t studies, systematic review, and updated meta- analysis. BMJ.
2020;368:m513. DOI: 10.1136/bmj.m513.
30. Drou in- Chartie r JP, Bras sard D, Te ssier- Grenier M, C ôté JA, Labonté M,
Desroches S, Couture P, Lamarche B. Systematic review of the asso-
ciation between dairy product consumptio n and risk of cardiovascular-
related clinical outcomes. Adv Nutr. 2016;7:10261040. DO I: 10.39 45 /
an.11 5. 0 114 0 3 .
31. Key TJ, Appleby PN, Bradbury KE, Sweeting M, Wood A, Johansson
I, Kühn T, Steur M, Weiderpass E, Wennberg M, et al. Consumption
of meat, fish, dairy products, and eggs and risk of ischemic h eart dis-
ease. Circulation. 2019;139:2835– 2845. DOI: 10.1161/CIRCU LATIO
NAHA .118. 0 3 8 813 .
32. Sotos- Prieto M, Bhupathiraju SN, Mattei J, Fung T T, Li Y, Pan A, Willett
WC, Rimm EB, Hu FB. Association of changes in diet qualit y with total
and cause- specific mortality. N Engl J Med. 2017;377:143– 153. DOI:
10.1056/NEJMo a1613502.
33. Xu Z, Steffen LM, Selvin E, Rebholz CM. Diet quality, change in diet
qualit y and risk of incident CVD and diabetes. Public Health Nutr.
2020;23:329 338. DOI: 10.1017/S1368 98 001 900212X.
34. Lynch J, Smith GD. A life course approach to chronic disease epide-
miology. Annu Rev Pu blic Hea lth. 2005;26:1– 35. DOI: 10.1146/annur
ev.publh ealth.26.021304.144505.
35. Packer L. Protective role of vitamin E in biological systems. Am J Clin
Nutr. 1991;53 (4 S uppl):105 0S 1055 S. DOI: 10.1093/ajcn/53 .4.105 0S.
36. Santhakumar AB, Bulm er AC, Singh I. A review of the me chanis ms and
effectivenes s of dietar y polyphenols in reducing oxidati ve stress and
thrombotic risk. J Hum Nutr Diet. 20 14;2 7:1 – 21. D OI: 10.1111/ jh n .12177.
37. Freedman JE, Keaney JF. Vitamin E inhibition of platelet aggregation is
independent of antioxidant activity. J Nutr. 2001;131:374S– 377S. DOI:
10.1093 /j n/ 131.2.374S.
38. Schinella GR, Tournier HA, Prieto JM, Mordujovich de Buschiazzo P,
Ríos JL. Antioxidant activity of anti- inflammatory plant extracts. Life Sci.
2002;70:10 23 – 103 3. DOI: 10.1016/S0 024 - 32 05(01)01482 - 5.
39. Kiokias S, Proestos C, Oreopoulou V. Effect of natural food antioxi-
dants against LDL and DNA oxidative changes. Antioxidants (Basel).
2018;7:133. DOI: 10.3390/antio x7100133.
40. Fuhrman B, Volkova N, Rosenblat M, Aviram M. Lycopene synergis-
tically inhibits LDL oxidation in combination with vitamin E, glabri-
din, rosmarinic acid, carnosic acid, or garlic. Antioxid Redox Signal.
2000;2:491– 506. DOI: 10.1089/15230 86005 0192279.
41. Ninfali P, Mea G, Giorgini S, Rocchi M, Bacchio cca M. Antioxidant c a-
pacity of vegetables, spic es and dre ssings relevant to nu trition. Br J
Nutr. 2005;93:257– 266. D OI: 10.1079/B JN20 041327.
Downloaded from http://ahajournals.org by on August 13, 2021
SUPPLEMENTAL MATERIAL
Downloaded from http://ahajournals.org by on August 13, 2021
Data S1.
Supplemental Methods: Details of time-varying covariates in proportional hazards regression
Algebraically, suppose a covariate is called COV(t) (meaning that COV is repeatedly measured at CARDIA times t Y0, Y7 and Y20) and the time to
event variable is TIME, meaning time in study until event or censoring.
For the continuous covariates (total energy intake, physical activity level and BMI), we created a MEAN TO DATE function, that is, for each
variable, the covariate enters the regression as COV(1) for the time interval Y0-Y7, as mean[COV(1),COV(2)] for the time interval Y7-Y20, and as
mean[COV(1),COV(2),COV(3)] for the time interval Y20-Y32. We did this for each of the 3 continuous covariates.
For the disease status (hypertension, diabetes, and dyslipidemia), binary variables (0 or 1) was coded, with 0 meaning never diagnosed to date and 1
meaning ever diagnosed to date. For each variable, the diagnostic history covariate enters the model as COV (1) for the time interval Y0-Y7,
max[COV (1), COV (2)] for the time interval Y7-Y20, and max [COV (1), COV (2), COV (3)] for the time interval Y20-Y32. We did this for each of
the 3 binary covariates.
We used the SAS functions mean() and max(). These functions use whatever data are available. Thus if a person were missing COV(2), their value
in the interval Y0-Y7 would be COV(1), their value in the interval Y7-Y20 would also be COV(1) (because COV(2) is missing), and their value in
the interval Y20-Y32 would be mean[COV(1), COV(2), COV(3)].
Downloaded from http://ahajournals.org by on August 13, 2021
Table S1. Quintile cutpoints* of 46 individual food groups for total score computation of the APDQS and empirical examples of low (47) vs. high score
(81)†
Cutpoints (servings/day)
Low score
(APDQS=47 points)
High score
(APDQS=81 points)
Cutpoint 1
(20th
percentile)
Cutpoint 3
(60th
percentile)
Cutpoint 4
(80th
percentile)
Servings/day
Quintile
category
assigned
Score
Servings/day
Quintile
category
assigned
Score
Beneficially-rated
1. Fruit
0.3
1.23
2.18
0
1
0
0.81
3
2
2. Avocado
0
0.15
0.39
0
1
0
0
1
0
3. Beans and legumes
0
0.14
0.31
0.48
5
4
0.12
3
2
4. Green vegetables
0.01
0.23
0.53
0.44
4
3
0.08
2
1
5. Yellow vegetables
0
0.13
0.32
0
1
0
0
1
0
6. Tomato
0.14
0.42
0.71
1.27
5
4
0.99
5
4
7. Other vegetables
0.84
1.96
2.98
2.59
4
3
3.07
5
4
8. Nuts and seeds
0
0.46
1.10
0.03
2
1
0.75
4
3
9. Soy products
0
0.20
0.76
0
1
0
0
1
0
10. Whole grains
0.27
1.41
2.43
0.60
2
1
1.51
4
3
11. Vegetable oil
0.27
1.20
2.25
1.77
4
3
3.43
5
4
12. Fatty fish
0
0.15
0.29
0
1
0
0
1
0
13. Lean fish
0.02
0.49
1.05
0
1
0
0.33
3
2
14. Poultry
0.33
1.01
1.82
0.22
1
0
0.85
3
2
15. Beer
0
0.45
1.10
1.70
5
4
0.85
4
3
16. Wine
0
0.16
0.38
0
1
0
0
1
0
17. Liquor
0
0.20
0.45
0
1
0
0
1
0
18. Coffee
0
1.16
2.59
0
1
0
1.27
4
3
19. Tea
0
0.42
1.09
3.87
5
4
3.04
5
4
20.Low-fat
milk/Cheese/Yogurt
0.12
0.78
1.87
0.1
1
0
0.32
3
2
Neutrally-rated
1. Potatoes
0.07
0.32
0.62
0.22
3
0
0.94
5
0
2. Refined grains
1.90
4.42
6.52
3.81
3
0
2.15
2
0
3. Margarine
0.02
1.32
2.90
1.32
3
0
1.63
4
0
4. Chocolate
0
0.16
0.36
0
1
0
0
1
0
5. Meal replacements
0
0.26
0.56
0
1
0
0
1
0
6. Pickled foods
0
0.19
0.42
0.63
5
0
0.34
4
0
Downloaded from http://ahajournals.org by on August 13, 2021
7. Sugar substitutes
0
0.26
0.71
0
1
0
0.75
5
0
8. Lean red meats
0.02
0.61
1.24
0.22
2
0
1.20
4
0
9. Shellfish
0
0.16
0.38
0.19
4
0
0
1
0
10. Eggs
0
0.48
0.93
0.59
4
0
0.81
4
0
11. Soups
0
0.04
0.09
0
1
0
0
1
0
12. Diet soft drinks
0
0.83
1.62
0
1
0
1.52
4
0
13. Fruit juice
0.36
1.64
2.91
0
1
0
1.81
4
0
Adversely-rated
1. Fried potatoes
0
0.25
0.52
0.31
4
1
0.31
4
1
2. Grain desserts
0.11
0.55
1.05
0
1
4
0.51
3
2
3. Salty snacks
0
0.08
0.17
0.08
3
2
0
1
4
4. Pastries
0.20
0.83
1.49
3.70
5
0
0.35
2
3
5. Sweets
0.24
1.38
2.73
0.05
1
4
0.03
1
4
6. High-fat red meats
0.69
2.12
3.48
3.68
5
0
1.12
2
3
7. Processed meats
0.10
0.69
1.38
0.75
4
1
0.13
2
3
8. Organ meats
0
0.18
0.35
0.39
5
0
0
1
4
9. Fried poultry and
fish
0
0.08
1.15
0
1
4
0
1
4
10. Sauces
1.41
3.81
6.35
2.83
3
2
1.59
2
3
11. Soft drinks
0.12
1.30
2.45
5.80
5
0
0
1
4
12.Whole-fat
milk/Cheese/Yogurt
0.62
1.71
2.95
2.11
4
1
0.88
2
3
13. Butter
1.47
4.23
7.03
4.24
4
1
0.88
1
4
*The cutoffs of food group derived from the Y0 diet data was applied to follow-up data at Y7 and Y20 to track change in diet quality of individuals over time.
†To illustrate the scoring system, the two individuals were arbitrarily selected based on the median scores of the bottom and top quintiles of the Y0 data.
Downloaded from http://ahajournals.org by on August 13, 2021
Table S2. HR (95% CI) of incident CVD according to quintiles of the exam year-specific APDQS and for APDQS at a lagged
examination
Quintile 1
Quintile 2
Quintile 3
Quintile 4
Quintile 5
Each 1-SD
increment
(13 points)
P for
trend*
Y0 APDQS predicting CVD
over 32-years of follow-up
APDQS (median)
47
55
62
70
81
Unadjusted
cumulative
incidence % (n/N)
7.4 (76/1,026)
7.2 (72/999)
6.2 (61/984)
5.9 (58/991)
2.3 (22/946)
Model 1†
1 (ref)
0.92
(0.671.28)
0.85
(0.601.20)
0.92
(0.641.33)
0.44
(0.260.75)
0.80
(0.690.93)
0.003
Model 2‡
1 (ref)
0.92
(0.661.27)
0.85
(0.601.20)
0.99
(0.691.43)
0.50
(0.290.84)
0.83
(0.710.97)
0.016
5-year lag, after Y5
1 (ref)
0.91
(0.661.27)
0.84
(0.591.19)
0.96
(0.671.39)
0.49
(0.290.83)
0.82
(0.700.96)
0.012
Y7 APDQS predicting CVD
over 25-years of follow-up,
after Y7
APDQS (median)
51
60
67
74
83
Unadjusted
cumulative
incidence % (n/N)
7.2 (52/722)
8.0 (67/839)
5.0 (38/755)
4.1 (28/686)
2.8 (22/797)
Model 1†
1 (ref)
1.19
(0.831.72)
0.80
(0.521.23)
0.74
(0.461.20)
0.59
(0.341.02)
0.84
(0.710.99)
0.041
Model 2‡
1 (ref)
1.16
(0.811.68)
0.85
(0.551.31)
0.77
(0.481.26)
0.66
(0.381.15)
0.87
(0.731.04)
0.14
8-year lag, after Y15
1 (ref)
1.05
(0.701.58)
0.88
(0.551.41)
0.82
(0.481.39)
0.59
(0.311.10)
0.87
(0.721.06)
0.16
Downloaded from http://ahajournals.org by on August 13, 2021
Y20 APDQS predicting CVD
over 12-years of follow-up,
after Y20
APDQS (median)
54
64
70
78
88
Unadjusted
cumulative
incidence % (n/N)
6.4 (40/626)
4.7 (29/619)
3.7 (20/538)
2.7 (18/666)
1.7 (10/576)
Model 1†
1 (ref)
0.85
(0.521.37)
0.73
(0.421.26)
0.57
(0.321.04)
0.42
(0.200.88)
0.71
(0.570.87)
0.001
Model 2‡
1 (ref)
0.89
(0.551.44)
0.86
(0.491.50)
0.72
(0.391.31)
0.59
(0.271.28)
0.79
(0.630.99)
0.041
5-year lag, after Y25
1 (ref)
0.82
(0.451.52)
0.81
(0.401.62)
0.68
(0.321.43)
0.57
(0.221.45)
0.79
(0.601.04)
0.10
APDQS = A Priori Diet Quality Score; CI = confidence interval; HR = hazard ratio.
Note: Each APDQS variable measured in a different exam year was set at the baseline.
*Statistical significance was estimated by modeling APDQS as a continuous variable in the model.
†Model 1: Baseline age (continuous), sex, race (White and Black), baseline total energy intake (continuous), and maximal educational
attainment (continuous).
‡Model 2: Model 1 + parental history of CVD (yes vs no), baseline smoking status (never, former, and current), and baseline physical activity
level (continuous).
Downloaded from http://ahajournals.org by on August 13, 2021
... In another prospective cohort study conducted by Choi et al., a plant-centered over the long term was linked to a 52% decreased risk of incident CVD in people who were tracked since young adulthood [11]. Additionally, a 13-year rise in the quality of a plant-based diet was linked to a 61% decreased risk of CVD occurrences in the next 12-year period [11]. ...
... In another prospective cohort study conducted by Choi et al., a plant-centered over the long term was linked to a 52% decreased risk of incident CVD in people who were tracked since young adulthood [11]. Additionally, a 13-year rise in the quality of a plant-based diet was linked to a 61% decreased risk of CVD occurrences in the next 12-year period [11]. However, since there are other risk factors relevant to the incidence of CVDs, the timing and length of exposure to these risk factors may differ in how this illness manifests in adults. ...
... As a result, an assessment in middle or advanced age may not provide a comprehensive view of the whole spectrum of illness development in adulthood. This study demonstrated a link between a higher quality plant-based diet starting in early adulthood and a decreased risk of CVDs in adulthood [11]. Social parameters like race and educational background were also found to be mediators of the relationship between a plant-based diet and CVD incidence. ...
Article
Full-text available
Coronary heart disease (CHD) is one of the leading causes of morbidity and mortality worldwide. Dietary modifications in the form of a vegetarian diet can perhaps be the key to the prevention and management of cardiovascular diseases. The aims of this review are to determine the association between a vegetarian diet and CHD, to compare the risk of CHD in different types of vegetarian diets, and to assess variability in the biochemical predictors of CHD in the various vegetarian diets. Our study inferred that adherence to a plant-based diet was inversely related to the incidence of heart failure risk. Our research further supports the idea that a vegetarian diet is advantageous for the secondary prevention of CHD since it alters lipid profiles, lowers body mass index (BMI), and increases plasma antioxidant micronutrient concentrations. Additionally, eating a plant-based diet starting in adolescence is linked to a decreased risk of cerebrovascular disease (CVD) by middle age. An increase in sensitization and education efforts is imperative to ensure that people are appropriately informed about this option to significantly improve their quality of life.
... In recent years a plant-based diet, which is high in consumption of leafy greens, whole grains, vegetables, nuts, fruits and whole grains and has also a high content in cereal, beans, poultry, fish and yogurt, has received much attention. This kind of diet, often called Vegetarian as well, constitutes a dietary pattern that (almost) excludes some or all animal foods 10 . ...
... When it comes to a plant-based diet, the concerted action of nutrients, including ascorbic acid, tocopherols, carotenoids, and phenolics, are abundant in vegetables and fruits, whole grains, nuts and seeds and bioactive compounds found in a combination of plant foods may lead to a beneficial cardiovascular outcome 10,12,[33][34][35] as they can trap free radicals and reduce the levels of reactive oxygen molecules, thus protecting against tissue damage 10 . Similarly, higher DASH diet scores trended toward a lower risk of CVD rate among the studies referring to that particular kind of diet 6,7,[36][37][38] . ...
... When it comes to a plant-based diet, the concerted action of nutrients, including ascorbic acid, tocopherols, carotenoids, and phenolics, are abundant in vegetables and fruits, whole grains, nuts and seeds and bioactive compounds found in a combination of plant foods may lead to a beneficial cardiovascular outcome 10,12,[33][34][35] as they can trap free radicals and reduce the levels of reactive oxygen molecules, thus protecting against tissue damage 10 . Similarly, higher DASH diet scores trended toward a lower risk of CVD rate among the studies referring to that particular kind of diet 6,7,[36][37][38] . ...
Article
Full-text available
Aim: The fact that the role of various dietary patterns on cardiovascular disease (CVD) incidence has not yet been well established, reveals the need to estimate the association of dietary patterns and CVD risk. Material and Methods: A review of English language articles, archived in PubMed (2000-2021) was performed. Additional studies were identified by searching the bibliographies of the eligible articles at the start of the review. Search items included: coronary heart/cardiovascular disease, dietary patterns, diet, Mediterranean, DASH, prudent, western, vegan, plant-based. Only prospective cohort studies with adult participants that had no underlying disease at baseline were included. Independent extraction of articles by 2 authors using predefined data fields, including study quality indicators. Guidelines of the Prisma statement were kept. Results: 1,249,644 participants and 31,709 CVD fatal or non-fatal events were observed out of 29 studies that were included. The Mediterranean, the DASH-style, the Prudent, and the Plant-based dietary patterns were consistently associated with reduced risk of a CVD event, while the western dietary pattern was associated with an increase or did not show any significant relationship with CVD outcomes. Conclusions: Based on the present findings and the fact that the role of diet has been underestimated in CVD prevention guidelines, a dietary pattern rich in fruits and vegetables, whole grains, nuts, fish, and vegetable oils, with alcohol in moderation, if at all, and avoids red and processed meats, refined carbohydrates, foods and beverages with added sugar, sodium, and trans, should be further promoted.
... Neutrally rated food groups received a score of 0. The cut points used to define the quintiles for the individual 46 food groups are presented in Table S3. 24 For food groups with many recordings of 0 servings per day, the participants' values were grouped into 5 categories: category 1 (nonconsumers) and categories 2 to 5 (consumers divided into quartiles). For example, for avocado, the 0 is the first category, >0 to <0.06 is the second category, 0.06 to <0.14 is the third category, 0.14 to <0.31 is the fourth category, and ≥0.31 is the fifth category. ...
... The APDQS has been validated with various clinical outcomes. [23][24][25][26] Body Mass Index ...
Article
Full-text available
BACKGROUND Little attention has been paid to how well the American Heart Association's cardiovascular health (CVH) score predicts early‐onset diabetes in young adults. We investigated the association of CVH score with early‐ and later‐onset diabetes and with subsequent complications of diabetes. METHODS AND RESULTS Our sample included 4547 Black and White adults in the CARDIA (Coronary Artery Risk Development in Young Adults) study without diabetes at baseline (1985–1986; aged 18–30 years) with complete data on the CVH score at baseline, including smoking, body mass index, physical activity, diet quality, total cholesterol, blood pressure, and fasting blood glucose. Incident diabetes was determined based on fasting glucose, 2‐hour postload glucose, hemoglobin A1c, or self‐reported medication use throughout 8 visits for 30 years. Multinomial logistic regression was used to assess the association between CVH score and diabetes onset at age <40 years (early onset) versus age ≥40 years (later onset). Secondary analyses assessed the association between CVH score and risk of complications (coronary artery calcium, clinical cardiovascular disease, kidney function markers, diabetic retinopathy, and diabetic neuropathy) among a subsample with diabetes. We identified 116 early‐ and 502 later‐onset incident diabetes cases. Each 1‐point higher CVH score was associated with lower odds of developing early‐onset (odds ratio [OR], 0.64 [95% CI, 0.58–0.71]) and later‐onset diabetes (OR, 0.78 [95% CI, 0.74–0.83]). Lower estimates of diabetic complications were observed per 1‐point higher CVH score: 19% for coronary artery calcification≥100, 18% for cardiovascular disease, and 14% for diabetic neuropathy. CONCLUSIONS Higher CVH score in young adulthood was associated with lower early‐ and later‐onset diabetes as well as diabetic complications.
... The NDSR summarized foods into 166 food groups (the same in each exam), which CARDIA then collapsed into 46 food groups for the purpose of creating APDQS, a hypothesisdriven index. APDQS has been validated with varying degrees of predictive ability for obesity, diabetes, kidney function decline, myocardial infarction (MI), and mortality [10][11][12]16,17]. We calculated the diet quality score of plant-centered diets using APDQS. ...
... Expanding on our previous finding that APDQS predicted incident CVD outcomes [10], we conducted a head-to-head comparison of predictiveness for CHD and stroke of APDQS vs. Keys score (strongly based in theory and representing a blood cholesterol-lowering diet), total fat restriction, and total carbohydrate restriction. In so doing, we interpreted observed long-term diet features as indicative of different dietary recommendations. ...
Article
Full-text available
To better understand nutrition paradigm shift from nutrients to foods and dietary patterns, we compared associations of a nutrient-based blood cholesterol-lowering diet vs. a food-based plant-centered diet with risk of coronary heart disease (CHD) and stroke. Participants were 4701 adults aged 18–30 years and free of cardiovascular disease at baseline, followed for clinical events from 1985 and 86 to 2018. A plant-centered diet was represented by higher A Priori Diet Quality Score (APDQS). A blood cholesterol-lowering diet was represented by lower Keys Score. Proportional hazards regression was used to calculate hazard ratios (HR). Higher APDQS showed a nutrient-dense composition that is low in saturated fat but high in fiber, vitamins and minerals. Keys Score and APDQS changes were each inversely associated with concurrent plasma low-density lipoprotein cholesterol (LDL-C) change. Over follow-up, 116 CHD and 80 stroke events occurred. LDL-C predicted CHD, but not stroke. APDQS, but not Keys Score, predicted lower risk of CHD and of stroke. Adjusted HRs (95% CIs) for each 1-SD higher APDQS were 0.73 (0.55–0.96) for CHD and 0.70 (0.50–0.99) for stroke. Neither low dietary fat nor low dietary carbohydrate predicted these events. Our findings support the ongoing shift in diet messages for cardiovascular prevention.
... 8 Early adverse health-related behaviors, including smoking, physical inactivity, and poor diets, additionally contribute to premature CVD event risk. [9][10][11] Early implementation of lifelong prevention measures may hinder initial development and progression of risk factors and reduce their differential prevalence rates across sociodemographics. 12,13 However, broad implementation of prevention measures is typically costly and may have varied engagement. ...
Article
Background Favorable cardiovascular health (CVH) in young adulthood has been associated with lower future cardiovascular risk. We determined whether CVH and its sex differences in young adults have changed from 2007 to 2018. Methods and Results We identified 10 206 individuals, aged 20 to 39 years, from the National Health Examination and Nutrition Survey data. CVH was assessed on the basis of the American Heart Association’s Life’s Simple 7 metrics (of 7). Changes in the mean number of ideal CVH components and the ideal proportion of individual components were calculated using linear regression analysis. Changes in sex difference trends were assessed with an interaction term between sex and calendar year. The mean (SD) age of the study population was 29.3 (5.8) years, and 5260 (51.5%) individuals were women. The mean (SD) ideal CVH component remained unchanged for both women (4.40 [1.22] to 4.48 [1.15]; P =0.94) and men (3.97 [1.27] to 3.93 [1.24]; P =0.87), with stable sex differences ( P for interaction=0.94). Nonetheless, sex differences in blood pressure widened as ideal blood pressure decreased in men (54.0% to 46.9%; P =0.03) but not in women ( P for interaction <0.001). Concurrently, the proportion with ideal physical activity declined in women (57.3% to 49.4%; P =0.04) but remained stable in men ( P for interaction=0.03). Nonsmoking increased to a greater extent in women (64.1% to 70.5%; P =0.05) than in men ( P for interaction=0.01). Conclusions Sex disparities in CVH have persisted with exacerbated differences in blood pressure, physical activity, and smoking. These insights provide opportunities to promote equitable CVH.
... Adolescence is a time of increased energy and nutrient requirements due to accelerated growth and development [9] and, therefore, achieving an adequate and well-balanced diet is of increased importance. Dietary patterns developed over this time are also likely to be maintained through adulthood [10], and recent research indicates that young adults who follow a high-quality plant-based diet experience~50% lower risk of developing cardiovascular disease in later adulthood [11]. Similar to research in adults, much of the evidence on the eating patterns of vegetarian adolescents is close to 20 years old [12][13][14][15]. ...
Article
Full-text available
This study aimed to describe the intake and food sources of macronutrients in vegetarian and non-vegetarian adolescent females. Cross-sectional data was collected between February and September 2019. Adolescent females, aged 15 to 18 years old, were recruited throughout New Zealand. Intakes were assessed via two 24-h diet recalls, adjusted to represent usual intake using the multiple source method. Of the 254 participants, 38 self-identified as vegetarian. Vegetarians had similar carbohydrate and fat intakes compared to non-vegetarians; however, their protein intakes were 2.1% kJ lower (95% confidence interval (CI) −3.0 to −1.1%). Vegetarians also consumed 1.1% kJ less saturated fat (95% CI –2.1 to −0.1%), 1.3% kJ (95% CI 0.7 to 1.9) more polyunsaturated fat, and 5 g/day (95% CI 1.8 to 8.0) more fiber than non-vegetarians. When consumed, bread-based dishes and discretionary foods were the highest sources of energy, fat, and carbohydrate in both vegetarians and non-vegetarians. This suggests that some adolescents, including vegetarians, were obtaining high amounts of fat and carbohydrate from food groups associated with poorer dietary quality. We recommend further research to assess how the changing food environment is influencing vegetarian eating patterns and their associations with health outcomes in the wider population.
... Fast changes in the life style of people have lead to lifestyle ailments like hypertension, diabetes mellitus, dyslipidemia and overweight which are life threatening to human race. Yuni et al. (2021) reported that starting from young adulthood, if plant centered high quality food is consumed, there is a very low risk of cardiovascular disease (CVD) by the middle age in humans. The extracts from Yacon (Smallanthus sonchifolius), an underutilized crop is shown to enhance the antioxidant activity and reduce the levels of cardiac markers in serum (Oliveira et al., 2018). ...
Article
Sufficient amount of minerals, vitamins, and proteins in human diet play indispensable role in maintaining the active metabolism for better human health. All the essential nutrients that are requisite for an individual's survival are acquired from plants as well as animals. Micronutrients and macronutrients directly influence the metabolic pathways and their deficiencies play a substantial role in development of manifold disorders. In addition to environmental factors, quality and quantity of foods are key factors in maintaining the human health. Transition from healthy to diseased state is concurrent with the pattern of gene expression that is largely influenced by nutrition and environment. A combined approach to study the influence of nutrition on expression of numerous genes can be well explored through nutrigenomic studies. Nutrigenomics includes studies wherein applied genomics is used to investigate nutritional science to understand the compartmentalization of genes that influence the cause of diet-related complications. This review describes the role of underutilized crops as frontline foods to circumvent the health complications through the nutrigenomic studies. Further dynamics of nutrigenomic tools to study the impact of nutrition on the changing pattern of genome stability and gene expression for developing precise safety measures against wide range of health ailments linked to metabolic networks. Additionally, this review provides detailed information on nutrigenomic studies undertaken to unravel the potential of underutilized crops to augment the human health and to carry the agronomic/genomic approaches to enhance nutritional profile of underutilized crops to overcome diet-related disorders.
Article
Full-text available
Public higher education institutions (PHEIs) have a unique and important role in responding to the public and planetary health crisis—they are centers of research on public and planetary health and of learning for young people, and have a public good mission. Yet, PHEI campus food environments are predominantly unhealthy and environmentally unsustainable, and associated with unhealthy food choices and unhealthy students. PHEIs are addressing high levels of student food insecurity (FI) that disproportionately affect the most vulnerable groups. Yet, because student FI is measured as individual access to adequate quantities of food, campus responses to FI often overlook unhealthy food environments. These environments result from neoliberal PHEI business policies that prioritize short-term revenue and encourage superfluous consumption, and unhealthy, environmentally harmful diets. PHEIs need to move beyond neoliberalism to honor their public good mission, including prioritizing health, the environment, and equity, in decisions about food on campus. My goal in this perspective is to encourage inclusive campus discussion about why this change is required to adequately respond to the crisis of student, public, and planetary health, and about how to begin.
Article
The human gut microbiome is linked to metabolic and cardiovascular disease risk. Dietary modulation of the human gut microbiome offers an attractive pathway to manipulate the microbiome to prevent microbiome-related disease. However, this promise has not been realized. The complex system of diet and microbiome interactions is poorly understood. Integrating observational human diet and microbiome data can help researchers and clinicians untangle the complex systems of interactions that predict how the microbiome will change in response to foods. The use of dietary patterns to assess diet-microbiome relations holds promise to identify interesting associations and result in findings that can directly translate into actionable dietary intake recommendations and eating plans. In this article, we first highlight the complexity inherent in both dietary and microbiome data and introduce the approaches generally used to explore diet and microbiome simultaneously in observational studies. Second, we review the food group and dietary pattern-microbiome literature focusing on dietary complexity-moving beyond nutrients. Our review identified a substantial and growing body of literature that explores links between the microbiome and dietary patterns. However, there was very little standardization of dietary collection and assessment methods across studies. The 54 studies identified in this review used ≥7 different methods to assess diet. Coupled with the variation in final dietary parameters calculated from dietary data (e.g., dietary indices, dietary patterns, food groups, etc.), few studies with shared methods and assessment techniques were available for comparison. Third, we highlight the similarities between dietary and microbiome data structures and present the possibility that multivariate and compositional methods, developed initially for microbiome data, could have utility when applied to dietary data. Finally, we summarize the current state of the art for diet-microbiome data integration and highlight ways dietary data could be paired with microbiome data in future studies to improve the detection of diet-microbiome signals.
Article
In cardiology clinic visits, the discussion of optimal dietary patterns for prevention and management of cardiovascular disease is usually very limited. Herein, we explore the benefits and risks of various dietary patterns including intermittent fasting (IF), low carbohydrate, Paleolithic, whole food plant based diet and Mediterranean dietary patterns within the context of cardiovascular disease to empower clinicians with the evidence and information they need to maximally benefit their patients.
Article
Full-text available
Objective To evaluate the association between egg intake and cardiovascular disease risk among women and men in the United States, and to conduct a meta-analysis of prospective cohort studies. Design Prospective cohort study, and a systematic review and meta-analysis of prospective cohort studies. Setting Nurses’ Health Study (NHS, 1980-2012), NHS II (1991-2013), Health Professionals’ Follow-Up Study (HPFS, 1986-2012). Participants Cohort analyses included 83 349 women from NHS, 90 214 women from NHS II, and 42 055 men from HPFS who were free of cardiovascular disease, type 2 diabetes, and cancer at baseline. Main outcome measures Incident cardiovascular disease, which included non-fatal myocardial infarction, fatal coronary heart disease, and stroke. Results Over up to 32 years of follow-up (>5.54 million person years), 14 806 participants with incident cardiovascular disease were identified in the three cohorts. Participants with a higher egg intake had a higher body mass index, were less likely to be treated with statins, and consumed more red meats. Most people consumed between one and less than five eggs per week. In the pooled multivariable analysis, consumption of at least one egg per day was not associated with incident cardiovascular disease risk after adjustment for updated lifestyle and dietary factors associated with egg intake (hazard ratio for at least one egg per day v less than one egg per month 0.93, 95% confidence interval 0.82 to 1.05). In the updated meta-analysis of prospective cohort studies (33 risk estimates, 1 720 108 participants, 139 195 cardiovascular disease events), an increase of one egg per day was not associated with cardiovascular disease risk (pooled relative risk 0.98, 95% confidence interval 0.93 to 1.03, I ² =62.3%). Results were similar for coronary heart disease (21 risk estimates, 1 411 261 participants, 59 713 coronary heart disease events; 0.96, 0.91 to 1.03, I ² =38.2%), and stroke (22 risk estimates, 1 059 315 participants, 53 617 stroke events; 0.99, 0.91 to 1.07, I ² =71.5%). In analyses stratified by geographical location (P for interaction=0.07), no association was found between egg consumption and cardiovascular disease risk among US cohorts (1.01, 0.96 to 1.06, I ² =30.8%) or European cohorts (1.05, 0.92 to 1.19, I ² =64.7%), but an inverse association was seen in Asian cohorts (0.92, 0.85 to 0.99, I ² =44.8%). Conclusions Results from the three cohorts and from the updated meta-analysis show that moderate egg consumption (up to one egg per day) is not associated with cardiovascular disease risk overall, and is associated with potentially lower cardiovascular disease risk in Asian populations. Systematic review registration PROSPERO CRD42019129650.
Article
Full-text available
Objective The objective of this study was to assess the prospective association between diet quality, as well as a 6-year change in diet quality, and risk of incident CVD and diabetes in a community-based population. Design We used Cox regression models to estimate the prospective association between diet quality, assessed using the Healthy Eating Index (HEI)-2015 and the Alternative HEI (AHEI)-2010 scores, as well as change in diet quality, and incident CVD and diabetes. Setting The ARIC Study recruited 15 792 black and white men and women (45–64 years) from four US communities. Participants We included 10 808 study participants who reported usual dietary intake via FFQ at visit 1 (1987–1989) and who had not developed CVD, diabetes, or cancer at baseline. Results Overall, 3070 participants developed CVD (median follow-up of 26 years) and 3452 developed diabetes (median follow-up of 22 years) after visit 1. Higher diet score at the initial visit was associated with a significantly lower risk of CVD (HR per 10 % higher HEI-2015 diet quality score: 0·90 (95 % CI: 0·86, 0·95) and HR per 10 % higher AHEI-2010 diet quality score: 0·96 (95 % CI: 0·93, 0·99)). We did not observe a significant association between initial diet score and incident diabetes. There were no significant associations between change in diet score and CVD or diabetes risk in the overall study population. Conclusions Higher diet quality assessed using HEI-2015 and AHEI-2010 was strongly associated with lower CVD risk but not diabetes risk within a middle-aged, community-based US population.
Article
Full-text available
Background Previous studies have documented the cardiometabolic health benefits of plant‐based diets; however, these studies were conducted in selected study populations that had narrow generalizability. Methods and Results We used data from a community‐based cohort of middle‐aged adults (n=12 168) in the ARIC (Atherosclerosis Risk in Communities) study who were followed up from 1987 through 2016. Participants’ diet was classified using 4 diet indexes. In the overall plant‐based diet index and provegetarian diet index, higher intakes of all or selected plant foods received higher scores; in the healthy plant‐based diet index, higher intakes of only the healthy plant foods received higher scores; in the less healthy plant‐based diet index, higher intakes of only the less healthy plant foods received higher scores. In all indexes, higher intakes of animal foods received lower scores. Results from Cox proportional hazards models showed that participants in the highest versus lowest quintile for adherence to overall plant‐based diet index or provegetarian diet had a 16%, 31% to 32%, and 18% to 25% lower risk of cardiovascular disease, cardiovascular disease mortality, and all‐cause mortality, respectively, after adjusting for important confounders (all P <0.05 for trend). Higher adherence to a healthy plant‐based diet index was associated with a 19% and 11% lower risk of cardiovascular disease mortality and all‐cause mortality, respectively, but not incident cardiovascular disease ( P <0.05 for trend). No associations were observed between the less healthy plant‐based diet index and the outcomes. Conclusions Diets higher in plant foods and lower in animal foods were associated with a lower risk of cardiovascular morbidity and mortality in a general population.
Article
Full-text available
Background There is uncertainty about the relevance of animal foods to the pathogenesis of ischemic heart disease (IHD). We examined meat, fish, dairy products, and eggs and risk for IHD in the pan-European EPIC cohort (European Prospective Investigation Into Cancer and Nutrition). Methods In this prospective study of 409 885 men and women in 9 European countries, diet was assessed with validated questionnaires and calibrated with 24-hour recalls. Lipids and blood pressure were measured in a subsample. During a mean of 12.6 years of follow-up, 7198 participants had a myocardial infarction or died of IHD. The relationships of animal foods with risk were examined with Cox regression with adjustment for other animal foods and relevant covariates. Results The hazard ratio (HR) for IHD was 1.19 (95% CI, 1.06–1.33) for a 100-g/d increment in intake of red and processed meat, and this remained significant after exclusion of the first 4 years of follow-up (HR, 1.25 [95% CI, 1.09–1.42]). Risk was inversely associated with intakes of yogurt (HR, 0.93 [95% CI, 0.89–0.98] per 100-g/d increment), cheese (HR, 0.92 [95% CI, 0.86–0.98] per 30-g/d increment), and eggs (HR, 0.93 [95% CI, 0.88–0.99] per 20-g/d increment); the associations with yogurt and eggs were attenuated and nonsignificant after exclusion of the first 4 years of follow-up. Risk was not significantly associated with intakes of poultry, fish, or milk. In analyses modeling dietary substitutions, replacement of 100 kcal/d from red and processed meat with 100 kcal/d from fatty fish, yogurt, cheese, or eggs was associated with ≈20% lower risk of IHD. Consumption of red and processed meat was positively associated with serum non–high-density lipoprotein cholesterol concentration and systolic blood pressure, and consumption of cheese was inversely associated with serum non–high-density lipoprotein cholesterol. Conclusions Risk for IHD was positively associated with consumption of red and processed meat and inversely associated with consumption of yogurt, cheese, and eggs, although the associations with yogurt and eggs may be influenced by reverse causation bias. It is not clear whether the associations with red and processed meat and cheese reflect causality, but they were consistent with the associations of these foods with plasma non–high-density lipoprotein cholesterol and for red and processed meat with systolic blood pressure, which could mediate such effects.
Article
Full-text available
Background The Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2017 comparative risk assessment (CRA) is a comprehensive approach to risk factor quantification that offers a useful tool for synthesising evidence on risks and risk–outcome associations. With each annual GBD study, we update the GBD CRA to incorporate improved methods, new risks and risk–outcome pairs, and new data on risk exposure levels and risk–outcome associations. Methods We used the CRA framework developed for previous iterations of GBD to estimate levels and trends in exposure, attributable deaths, and attributable disability-adjusted life-years (DALYs), by age group, sex, year, and location for 84 behavioural, environmental and occupational, and metabolic risks or groups of risks from 1990 to 2017. This study included 476 risk–outcome pairs that met the GBD study criteria for convincing or probable evidence of causation. We extracted relative risk and exposure estimates from 46 749 randomised controlled trials, cohort studies, household surveys, census data, satellite data, and other sources. We used statistical models to pool data, adjust for bias, and incorporate covariates. Using the counterfactual scenario of theoretical minimum risk exposure level (TMREL), we estimated the portion of deaths and DALYs that could be attributed to a given risk. We explored the relationship between development and risk exposure by modelling the relationship between the Socio-demographic Index (SDI) and risk-weighted exposure prevalence and estimated expected levels of exposure and risk-attributable burden by SDI. Finally, we explored temporal changes in risk-attributable DALYs by decomposing those changes into six main component drivers of change as follows: (1) population growth; (2) changes in population age structures; (3) changes in exposure to environmental and occupational risks; (4) changes in exposure to behavioural risks; (5) changes in exposure to metabolic risks; and (6) changes due to all other factors, approximated as the risk-deleted death and DALY rates, where the risk-deleted rate is the rate that would be observed had we reduced the exposure levels to the TMREL for all risk factors included in GBD 2017. Findings In 2017, 34·1 million (95% uncertainty interval [UI] 33·3–35·0) deaths and 1·21 billion (1·14–1·28) DALYs were attributable to GBD risk factors. Globally, 61·0% (59·6–62·4) of deaths and 48·3% (46·3–50·2) of DALYs were attributed to the GBD 2017 risk factors. When ranked by risk-attributable DALYs, high systolic blood pressure (SBP) was the leading risk factor, accounting for 10·4 million (9·39–11·5) deaths and 218 million (198–237) DALYs, followed by smoking (7·10 million [6·83–7·37] deaths and 182 million [173–193] DALYs), high fasting plasma glucose (6·53 million [5·23–8·23] deaths and 171 million [144–201] DALYs), high body-mass index (BMI; 4·72 million [2·99–6·70] deaths and 148 million [98·6–202] DALYs), and short gestation for birthweight (1·43 million [1·36–1·51] deaths and 139 million [131–147] DALYs). In total, risk-attributable DALYs declined by 4·9% (3·3–6·5) between 2007 and 2017. In the absence of demographic changes (ie, population growth and ageing), changes in risk exposure and risk-deleted DALYs would have led to a 23·5% decline in DALYs during that period. Conversely, in the absence of changes in risk exposure and risk-deleted DALYs, demographic changes would have led to an 18·6% increase in DALYs during that period. The ratios of observed risk exposure levels to exposure levels expected based on SDI (O/E ratios) increased globally for unsafe drinking water and household air pollution between 1990 and 2017. This result suggests that development is occurring more rapidly than are changes in the underlying risk structure in a population. Conversely, nearly universal declines in O/E ratios for smoking and alcohol use indicate that, for a given SDI, exposure to these risks is declining. In 2017, the leading Level 4 risk factor for age-standardised DALY rates was high SBP in four super-regions: central Europe, eastern Europe, and central Asia; north Africa and Middle East; south Asia; and southeast Asia, east Asia, and Oceania. The leading risk factor in the high-income super-region was smoking, in Latin America and Caribbean was high BMI, and in sub-Saharan Africa was unsafe sex. O/E ratios for unsafe sex in sub-Saharan Africa were notably high, and those for alcohol use in north Africa and the Middle East were notably low. Interpretation By quantifying levels and trends in exposures to risk factors and the resulting disease burden, this assessment offers insight into where past policy and programme efforts might have been successful and highlights current priorities for public health action. Decreases in behavioural, environmental, and occupational risks have largely offset the effects of population growth and ageing, in relation to trends in absolute burden. Conversely, the combination of increasing metabolic risks and population ageing will probably continue to drive the increasing trends in non-communicable diseases at the global level, which presents both a public health challenge and opportunity. We see considerable spatiotemporal heterogeneity in levels of risk exposure and risk-attributable burden. Although levels of development underlie some of this heterogeneity, O/E ratios show risks for which countries are overperforming or underperforming relative to their level of development. As such, these ratios provide a benchmarking tool to help to focus local decision making. Our findings reinforce the importance of both risk exposure monitoring and epidemiological research to assess causal connections between risks and health outcomes, and they highlight the usefulness of the GBD study in synthesising data to draw comprehensive and robust conclusions that help to inform good policy and strategic health planning.
Article
Objective: To examine the associations between change in plant-centered diet quality and type 2 diabetes risk and change in body size. Research design and methods: A prospective study conducted in the U.S. enrolled adults ages 18-30 years in 1985-1986 (examination year [Y0]) and followed them through 2015-2016. We analyzed the associations between change in plant-centered diet quality over 20 years (Y0-Y20) and diabetes (Y20-30; n = 2,534) and change (Y0-Y20 and Y20-30) in BMI, waist circumference (WC), and weight (n > 2,434). Plant-centered diet quality was measured using the A Priori Diet Quality Score (APDQS); a higher score favors nutritionally rich plant foods. Cox regression models were used to assess diabetes risk, and linear regression models were used to examine change in body size. Results: During a mean follow-up of 9.3 (± 1.7) years, 206 case subjects with incident diabetes were observed. In multivariable analysis, participants with the largest increase in APDQS over 20 years had a 48% (95% CI 0.31-0.85; P-trend < 0.001) lower risk of diabetes over the subsequent 10 years compared with participants whose score remained stable. Each 1-SD increment in APDQS over 20 years was associated with lower gains in BMI (-0.39 kg/m2; SE 0.14; P = 0.004), WC (-0.90 cm; SE 0.27; P < 0.001), and weight (-1.14 kg; SE 0.33; P < 0.001) during the same period, but not with subsequent changes. Conclusions: Young adults who increased plant-centered diet quality had a lower diabetes risk and gained less weight by middle adulthood.
Article
Importance The 2015-2020 Dietary Guidelines for Americans recommend multiple healthy eating patterns. However, few studies have examined the associations of adherence to different dietary patterns with long-term risk of cardiovascular disease (CVD). Objective To examine the associations of dietary scores for 4 healthy eating patterns with risk of incident CVD. Design, Setting, and Participants Prospective cohort study of initially healthy women from the Nurses’ Health Study (NHS) (1984-2016) and the NHS II (1991-2017) and men from the Health Professionals Follow-up Study (HPFS) (1986-2012). The dates of analysis were July 25 to December 4, 2019. Exposures Healthy Eating Index–2015 (HEI-2015), Alternate Mediterranean Diet Score (AMED), Healthful Plant-Based Diet Index (HPDI), and Alternate Healthy Eating Index (AHEI). Main Outcomes and Measures Cardiovascular disease events, including fatal and nonfatal coronary heart disease (CHD) and stroke. Results The final study sample included 74 930 women in the NHS (mean [SD] baseline age, 50.2 [7.2] years), 90 864 women in the NHS II (mean [SD] baseline age, 36.1 [4.7] years), and 43 339 men in the HPFS (mean [SD] baseline age, 53.2 [9.6] years). During a total of 5 257 190 person-years of follow-up, 23 366 incident CVD cases were documented (18 092 CHD and 5687 stroke) (some individuals were diagnosed as having both CHD and stroke). Comparing the highest with the lowest quintiles, the pooled multivariable-adjusted hazard ratios (HRs) of CVD were 0.83 (95% CI, 0.79-0.86) for the HEI-2015, 0.83 (95% CI, 0.79-0.86) for the AMED, 0.86 (95% CI, 0.82-0.89) for the HPDI, and 0.79 (95% CI, 0.75-0.82) for the AHEI (P for trend <.001 for all). In addition, a 25-percentile higher dietary score was associated with 10% to 20% lower risk of CVD (pooled HR, 0.80 [95% CI, 0.77-0.83] for the HEI-2015; 0.90 [95% CI, 0.87-0.92] for the AMED; 0.86 [95% CI, 0.82-0.89] for the HPDI; and 0.81 [95% CI, 0.78-0.84] for the AHEI). These dietary scores were statistically significantly associated with lower risk of both CHD and stroke. In analyses stratified by race/ethnicity and other potential risk factors for CVD, the inverse associations between these scores and risk of CVD were consistent in most subgroups. Conclusions and Relevance In 3 large prospective cohorts with up to 32 years of follow-up, greater adherence to various healthy eating patterns was consistently associated with lower risk of CVD. These findings support the recommendations of the 2015-2020 Dietary Guidelines for Americans that multiple healthy eating patterns can be adapted to individual food traditions and preferences.
Article
Importance Although the associations between processed meat intake and cardiovascular disease (CVD) and all-cause mortality have been established, the associations of unprocessed red meat, poultry, or fish consumption with CVD and all-cause mortality are still uncertain. Objective To identify the associations of processed meat, unprocessed red meat, poultry, or fish intake with incident CVD and all-cause mortality. Design, Setting, and Participants This cohort study analyzed individual-level data of adult participants in 6 prospective cohort studies in the United States. Baseline diet data from 1985 to 2002 were collected. Participants were followed up until August 31, 2016. Data analyses were performed from March 25, 2019, to November 17, 2019. Exposures Processed meat, unprocessed red meat, poultry, or fish intake as continuous variables. Main Outcomes and Measures Hazard ratio (HR) and 30-year absolute risk difference (ARD) for incident CVD (composite end point of coronary heart disease, stroke, heart failure, and CVD deaths) and all-cause mortality, based on each additional intake of 2 servings per week for monotonic associations or 2 vs 0 servings per week for nonmonotonic associations. Results Among the 29 682 participants (mean [SD] age at baseline, 53.7 [15.7] years; 13 168 [44.4%] men; and 9101 [30.7%] self-identified as non-white), 6963 incident CVD events and 8875 all-cause deaths were adjudicated during a median (interquartile range) follow-up of 19.0 (14.1-23.7) years. The associations of processed meat, unprocessed red meat, poultry, or fish intake with incident CVD and all-cause mortality were monotonic (P for nonlinearity ≥ .25), except for the nonmonotonic association between processed meat intake and incident CVD (P for nonlinearity = .006). Intake of processed meat (adjusted HR, 1.07 [95% CI, 1.04-1.11]; adjusted ARD, 1.74% [95% CI, 0.85%-2.63%]), unprocessed red meat (adjusted HR, 1.03 [95% CI, 1.01-1.06]; adjusted ARD, 0.62% [95% CI, 0.07%-1.16%]), or poultry (adjusted HR, 1.04 [95% CI, 1.01-1.06]; adjusted ARD, 1.03% [95% CI, 0.36%-1.70%]) was significantly associated with incident CVD. Fish intake was not significantly associated with incident CVD (adjusted HR, 1.00 [95% CI, 0.98-1.02]; adjusted ARD, 0.12% [95% CI, −0.40% to 0.65%]). Intake of processed meat (adjusted HR, 1.03 [95% CI, 1.02-1.05]; adjusted ARD, 0.90% [95% CI, 0.43%-1.38%]) or unprocessed red meat (adjusted HR, 1.03 [95% CI, 1.01-1.05]; adjusted ARD, 0.76% [95% CI, 0.19%-1.33%]) was significantly associated with all-cause mortality. Intake of poultry (adjusted HR, 0.99 [95% CI, 0.97-1.02]; adjusted ARD, −0.28% [95% CI, −1.00% to 0.44%]) or fish (adjusted HR, 0.99 [95% CI, 0.97-1.01]; adjusted ARD, −0.34% [95% CI, −0.88% to 0.20%]) was not significantly associated with all-cause mortality. Conclusions and Relevance These findings suggest that, among US adults, higher intake of processed meat, unprocessed red meat, or poultry, but not fish, was significantly associated with a small increased risk of incident CVD, whereas higher intake of processed meat or unprocessed red meat, but not poultry or fish, was significantly associated with a small increased risk of all-cause mortality. These findings have important public health implications and should warrant further investigations.
Article
Background: Plant-based diets have been associated with lower risk of type 2 diabetes and cardiovascular disease (CVD) and are recommended for both health and environmental benefits. However, the association between changes in plant-based diet quality and mortality remains unclear. Methods: We investigated the associations between 12-year changes (from 1986 to 1998) in plant-based diet quality assessed by three plant-based diet indices (score range: 18 to 90)-an overall plant-based diet index (PDI), a healthful plant-based diet index (hPDI), and an unhealthful plant-based diet index (uPDI)-and subsequent total and cause-specific mortality (from 1998 to 2014). Participants were 49,407 women in the Nurses' Health Study (NHS) and 25,907 men in the Health Professionals Follow-Up Study (HPFS) who were free from CVD and cancer at 1998. Multivariable-adjusted Cox proportional-hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). Results: We documented 10,686 deaths including 2,046 CVD deaths and 3,091 cancer deaths in the NHS over 725,316 person-years of follow-up, and 6,490 deaths including 1,872 CVD deaths and 1,772 cancer deaths in the HPFS over 371,322 person-years of follow-up. Compared with participants whose indices remained stable, among those with the greatest increases in diet scores (highest quintile), the pooled multivariable-adjusted HRs for total mortality were 0.95 (95% CI, 0.90-1.00) for PDI, 0.90 (95% CI, 0.85-0.95) for hPDI, and 1.12 (95% CI, 1.07-1.18) for uPDI. Among participants with the greatest decrease (lowest quintile), the multivariable-adjusted HRs were 1.09 (95% CI, 1.04-1.15) for PDI, 1.10 (95% CI, 1.05-1.15) for hPDI, and 0.93 (95% CI, 0.88-0.98) for uPDI. For CVD mortality, the risk associated with a 10-point increase in each plant-based diet index was 7% lower (95% CI, 1-12%) for PDI, 9% lower (95% CI, 4-14%) for hPDI, and 8% higher (95% CI, 2-14%) for uPDI. There were no consistent associations between changes in plant-based diet indices and cancer mortality. Conclusions: Improving plant-based diet quality over a 12-year period was associated with a lower risk of total and CVD mortality, whereas increased consumption of an unhealthful plantbased diet was associated with a higher risk of total and CVD mortality.