European Journal of Nutrition (2022) 61:387–398

https://doi.org/10.1007/s00394-021-02660-7

ORIGINAL CONTRIBUTION

A prospective study of healthful and unhealthful plant‑based diet

and risk of overall and cause‑specific mortality
Hairong Li1,2,3,4 · Xufen Zeng1 · Yingying Wang1 · Zhuang Zhang1 · Yu Zhu1 · Xiude Li1 · Anla Hu1 · Qihong Zhao1 ·
Wanshui Yang1,2,3,4 

Received: 28 April 2021 / Accepted: 4 August 2021 / Published online: 11 August 2021
© Springer-Verlag GmbH Germany, part of Springer Nature 2021

Abstract
Purpose  Although emphasis has recently been placed on the importance of diet high in plant-based foods, the association
between plant-based diet and long-term risk of overall and cause-specific mortality has been less studied. We aimed to
investigate whether plant-based diet was associated with lower death risk.
Methods  This prospective cohort study used data from the US National Health and Nutrition Examination Survey. Diet was
assessed using 24 h dietary recalls. We created three plant-based diet indices including an overall plant-based diet index
(PDI), a healthful plant-based diet index (hPDI), and an unhealthful plant-based diet index (uPDI). Deaths from baseline
until December 31, 2015, were identified. Multivariable-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs)
were calculated using Cox regression.
Results  We documented 4904 deaths among 40,074 participants after a median follow-up of 7.8 years. Greater adherence
to PDI was associated with lower risk of overall (HR comparing extreme quintiles 0.80, 95% CI 0.73, 0.89, ptrend < 0.001)
and cancer-specific (HR = 0.68, 95% CI 0.55, 0.85, ptrend < 0.001) mortality. These inverse associations remained for hPDI
and overall mortality with a HR of 0.86 (95% CI 0.77, 0.95, ptrend = 0.001), but not for cancer or CVD mortality. Conversely,
uPDI was associated with higher risk of total (HR = 1.33, 95% CI 1.19, 1.48, ptrend < 0.001) and CVD-specific (HR = 1.42,
95% CI 1.12, 1.79, ptrend = 0.015) mortality.
Conclusions  Increased intake of a plant-based diet rich in healthier plant foods is associated with lower mortality risk,
whereas a plant-based diet that emphasizes less-healthy plant foods is associated with high mortality risk among US adults.

Keywords  Plant-based diet · Cancer · Mortality · Cardiovascular disease · Cohort study

Introduction

Diet is a major modifiable risk factor for many health out-

* Wanshui Yang
wanshuiyang@gmail.com
1 eases (CVD), and the remainder due to a combination of
Department of Nutrition, School of Public Health, Anhui
Medical University, 81 Meishan Road, Hefei 230032, Anhui,
China
2
Key Laboratory of Population Health Across Life Cycle
(Anhui Medical University), Ministry of Education
of the People’s Republic of China, Hefei, Anhui, China
3
NHC Key Laboratory of Study On Abnormal Gametes
and Reproductive Tract, Hefei, Anhui, China
4
Anhui Provincial Key Laboratory of Population Health
and Aristogenics/Key Laboratory of Environmental
Toxicology of Anhui Higher Education Institutes, Anhui
Medical University, Hefei, Anhui, China
comes. In the United States, poor diet was the first leading
cause of premature death, which accounted for 5,29,299
deaths with 83.9% of these deaths from cardiovascular dis-
cancer and diabetes, and to other diseases in 2016 [1].
A dietary pattern that is higher in plant-based foods and
lower in animal-based foods has been recommended for
chronic disease prevention nowadays [2] and has shown
to be associated with lesser environmental impact than the
current average US dietary intakes [3]. However, most pre-
vious studies [4–9] have defined plant-based diets as ‘veg-
etarian’ diets, which constitute a family of dietary patterns
that exclude some or all animal foods. It would be difficult
for many persons to completely give up some or all animal

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388
foods to become vegetarian. Thus, from public health stand-
point, it is important to understand how gradually increasing
plant foods, while decreasing animal foods, affects health. In
addition, most studies of vegetarian diets were also limited
by a lack of differentiation among plant foods and treated
all plant foods equally. Not all plant foods are necessarily
beneficial for health. For example, a higher intake of healthy
plant foods, such as whole grains, nuts, and vegetables has
been associated with lower risk of overall and CVD mor-
tality [10–12], while increased intake of less healthy plant
foods, such as refined grains, potatoes, and sugar-sweetened
beverages (SSBs), has been associated with a higher risk of
cardiometabolic diseases and mortality [13–17].
Recently, Satija et al. [18] developed three plant-based
dietary indices, an overall plant-based diet index (PDI), a
healthful plant-based diet index (hPDI), and an unhealth-
ful plant-based diet index (uPDI). The overall PDI incor-
porates a range of progressively increasing proportions of
plant foods and accompanying reductions in animal foods,
which is similar to the original pro-vegetarian diet [19]. The
hPDI and uPDI overcome the limitation that all plant foods
were treated equally, and distinguish between healthful and
unhealthful plant foods. However, only few prospective stud-
ies [20–22] and a meta-analysis [23] have assessed the long-
term risk of overall or cause-specific death associated with
healthful and unhealthful PDIs. Besides, although previous
studies have suggested a non-linear association between
several dietary patterns and death risk [24–26], it remains
unclear whether there is a non-linear relationship between
PDIs and morality. Therefore, we prospectively examined
the associations between plant-based diet indices and the
risk of overall and cause-specific mortality among US
adults, considering the potential non-linear relationships.
Methods
Study population
Participants in our study were selected from the US National
Health and Nutrition Examination Survey (NHANES).
NHANES is a continuous, nationally representative, cross-
sectional survey conducted since 1999 by the National
Center for Health Statistics (NCHS). The survey examines
a nationally representative sample of about 5000 persons
annually. The NHANES interview includes demographic,
socioeconomic, dietary, and health-related questions. Details
on NHANES study protocol and data collection methods
have been reported previously [27]. Since the mortality data
were derived through 2015, we selected participants at least
completed one 24 h dietary recall during the 8 cycles of
NHANES from 1999 to 2014.
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European Journal of Nutrition (2022) 61:387–398
Participants were excluded if they were younger
than 18  years older (n = 34,735), had missing dietary
data (n = 5,132) or implausible energy intake (< 600
or > 3500 kcal/day for women  and < 800 or  > 4200 kcal/day
for men, n = 2100), or had no linked mortality data (n = 50).
A total of 40,074 participants (20,984 women and 19,090
men) were included in the final analysis (Supplementary
Fig. 1). The participants included in the study were compa-
rable with the excluded participants with regard to a number
of demographics, diet and lifestyle factors (data not shown).
The NCHS approved the NHANES study protocol. All par-
ticipants provided the written informed consent. The Insti-
tutional Review Board at our institute determined that this
analysis used a public dataset, so human subjects’ approval
was waived.
Dietary assessment and the plant‑based diet indices
Dietary data were collected by 24 h recall with the use of the
multiple-pass method to enhance complete and accurate data
collection and decrease respondent burden [28]. Considering
the dietary interview-specific nonresponse and day of the
week for dietary recalls, a multi-stage, unequal probability of
selection design (i.e., dietary sampling weights) was applied
[28, 29]. From 1999 to 2002, a single 24 h dietary recall was
performed in-person in the NHANES Mobile Examination
Center (MEC). After 2003, dietary data were collected using
two 24 h dietary recalls, with a second 24 h dietary interview
of participants being conducted by telephone 3–10 days after
the first recall. we used the method by the National Cancer
Institute (NCI) to reduce measurement error and improve
estimates of usual intake [29]. This method uses informa-
tion from 24 h dietary recall to estimate usual intake of epi-
sodically consumed foods, accounting for the correlation
between the probability of consumption and amount con-
sumed and by incorporating covariate information.
The development of three plant-based dietary indices has
been reported in detail previously [18, 30]. Briefly, we first
created 18 food groups based on nutrients and culinary simi-
larities within the larger categories of healthy plant foods
(whole grains, fruits, vegetables, nuts, legumes, vegetable
oils, and tea/coffee), less healthy plant foods (fruit juices,
SSBs, refined grains, potatoes, and sweets), and animal
foods (animal fats, dairy, egg, fish/seafood, meat, and mis-
cellaneous animal-based foods, Supplementary Table 1).
Of note, fruit juices were considered as less healthy plant-
based foods, due to their high content of natural sugars, with
evidence suggesting that they have similar negative health
effects to those of SSBs [31]. Considering that alcohol drink-
ing has different directions of association for various health
outcomes, and margarine’s fatty acid composition changed
over time from high trans to high unsaturated fats, we did
not include these foods in the indices. Food groups were
European Journal of Nutrition (2022) 61:387–398 389
ranked into quintiles, and given positive scores [i.e., scored
from 1 (lowest quintile) to 5 (highest quintile)] or reverse
scores [i.e., scored from 5 (lowest quintile) to 1 (highest
quintile)] [18, 30]. For overall PDI, foods in both plant food
groups were assigned positive scores and foods in the ani-
mal food group were given reverse scores. For hPDI, foods
in the healthy plant food group were given positive scores
while the less healthy plant and animal food groups received
reverse scores. For uPDI, foods in the less healthy plant food
group were given positive scores, and foods in the healthy
plant and animal food groups received reverse scores. PDI,
hPDI, and uPDI were then derived by summing scores of 18
food groups, ranging from 18 to 90.
Assessments of covariates
Standardized questionnaires were administrated through
household interview to collect demographic and lifestyle
factors, including age, sex, race/ethnicity, educational level,
family income, smoking, and physical activity. Alcohol
intake, body weight, and height were obtained from partici-
pants who received physical examinations in the NHANES
Mobile Examination Center. Body mass index (BMI) was
calculated as weight in kilograms divided by the square of
the height in meters (kg/m2). Economic status was measured
as the ratio of family income to poverty. This ratio divides
family income by the poverty thresholds, which accounts
for family size and annual inflation. Histories of diabetes,
hypertension, other CVDs, and cancer were defined if indi-
viduals reported that they had ever been told by a health
care professional that they had such diseases, or took pre-
scribed medications due to the diseases. Diabetes (a fast-
ing plasma glucose level  ≥ 126 mg/dL) and hypertension
(a systolic blood pressure  ≥ 140 mmHg or a diastolic blood
pressure  ≥ 90 mmHg) were also identified through labora-
tory test or physical examination in the MEC, which was
described elsewhere [32].
Ascertainments of deaths
We identified deaths and causes of death through record
linkage to the National Death Index through December 31,
2015. In this analysis, cause-specific mortality was defined
using the 10th revision of the International Classification
of Diseases (ICD-10). Deaths from major CVDs include
deaths from diseases of heart (ICD-10 codes I00-I09, I11,
I13, I20-I51) and cerebrovascular diseases (I60-169). Death
from cancer was defined as code C00-97.
Statistical analysis
Person-years were calculated from the date of interview
(i.e., date of diet assessment) to the date of death or the
end of the follow-up (December 31, 2015), whichever
came first. We used Cox proportional hazard regression
models to calculate hazard ratios (HRs) and 95% confi-
dence intervals (CIs) of death according to quintiles of
each PDI. Consistent with previous studies of PDI and
death risk [20–22], we also presented the HRs of mortal-
ity per 10-point increase in each PDI. Proportional haz-
ards assumption was tested by including the interaction
term between scores of three PDIs and follow-up time
into the model and found no evidence for violation of this
assumption (all p > 0.05). Model 1 was adjusted for age,
sex, and total energy intake. Model 2 was further adjusted
for race/ethnicity, education, marital status, ratio of fam-
ily income to poverty, physical activity, smoking, alcohol
drinking, BMI, histories of diabetes, hypertension, other
CVDs, and cancer at baseline. Selection of these variables
for adjustment was based on observed baseline incompa-
rability (Table 1) and the previously identified risk fac-
tors for the outcome. Linear trend test was conducted by
assigning medians to each quintile as continuous variable
in the models. To explore if the overall association of PDIs
was driven by a few components, we also evaluated food
groups included in the PDI in relation to the risk of overall
and cause-specific death. We used restricted cubic splines
to test the potential non-linear relationships between three
dietary indices and death risk.
In secondary analysis, to minimize reverse causation
from existing health conditions, we conducted a sensitivity
analysis by excluding participants who died within 3 years
after diet assessment. We used a competitive risk model
when investigating the cause-specific mortality using a pro-
portional subdistributional hazard model weighted for left
truncation and right censoring. We also repeated analyses
after excluding participants with CVD, cancer, or diabetes
at baseline. Besides, we re-analyzed data among individuals
who completed two 24 h dietary recalls. We further excluded
participants who had missing values in any covariates in the
sensitivity analysis.
Subgroup analysis and the potential for effect modifi-
cation were tested for the associations between 3 dietary
indices and death risk by age, sex, race/ethnicity, educa-
tion level, ratio of family income to poverty, marital sta-
tus, smoking, alcohol drinking, physical activity, BMI, and
diabetes. We used Wald test to examine whether the cross-
product terms between these variables and exposures were
statistically significant. All statistical tests were 2-sided
and performed using SAS version 9.4 (SAS Institute Inc,
Cary, NC). Because of many tests being conducted, we
used the Bonferroni correction to define the statistical sig-
nificance as p < 0.005 [0.05/(3 exposures × 3 outcomes)]
for main analysis and p < 0.0005 [0.05/(3 exposures × 3
outcomes × 10 groups)] for subgroup analysis allowing for
multiple comparisons.
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390 European Journal of Nutrition (2022) 61:387–398

Table 1  Age-adjusted characteristics of participants according to PDI, hPDI, uPDI in NHANES (1999–2014)a

Characteristic PDI hPDI uPDI
Quintile 1 Quintile 3 Quintile 5 Quintile 1 Quintile 3 Quintile 5 Quintile 1 Quintile 3 Quintile 5

Median score (IQR) 46 (45–48) 53 (52–54) 60 (59–62) 46 (44–47) 53 (52–54) 61 (60–63) 46 (44–47) 54 (53–55) 62 (61–64)
Age, years 43.1 (19.7) 47.5 (19.5) 51.3 (18.2) 38.3 (17.4) 47.4 (19.1) 56.0 (17.6) 55.6 (17.5) 48.0 (19.0) 36.9 (17.4)
Female, % 49.7 54.5 51.9 39.9 51.8 63.9 54.5 52.6 49.7
Race/ethnicity, %
 Non-Hispanic white 42.4 45.4 50.9 43.2 46.5 49.5 55.8 44.8 38.2
 Non-Hispanic black 27.4 20.5 14.1 28.7 20.0 13.1 10.4 20.7 32.1
 Hispanic 7.1 7.5 6.9 6.8 7.4 7.5 7.0 8.0 6.7
 Other 23.1 26.6 28.2 21.3 26.0 29.9 26.7 26.6 23.0
Education, %
  ≤ 12th grade 36.5 29.3 21.8 30.5 30.8 22.4 17.8 30.5 36.9
 High school graduate 25.4 24.6 19.7 28.0 23.8 18.4 18.4 23.6 26.8
 More than high school 37.9 46.0 58.4 41.4 45.2 59.1 63.7 45.9 36.2
Ratio of family income to poverty
  < 1.3 35.7 29.3 22.7 32.0 30.9 22.6 19.9 29.5 36.9
 1.3–3.5 33.9 34.9 32.9 36.1 33.8 32.1 32.1 34.9 33.9
  ≥ 3.5 21.6 27.9 36.8 24.9 27.0 36.7 40.1 27.3 20.6
Marital status, %
 Married 31.3 25.7 22.4 29.8 25.2 20.9 20.3 24.3 32.6
 Widowed/divorced/sepa- 44.5 52.5 59.9 49.2 53.9 59.0 61.0 53.7 43.5
rated
 Never married 19.4 18.1 15.2 16.6 16.9 17.7 16.6 18.0 19.1
Smoking, %
 Never smoking 50.2 53.9 58.0 45.8 49.7 58.1 56.0 50.7 45.8
 Former smoking 23.5 24.7 27.2 22.6 23.6 26.4 28.5 23.5 19.5
 Current smoking 26.3 21.5 14.7 22.0 20.6 13.2 13.1 20.1 23.7
Drinking, %
 Never drinking 26.5 26.1 25.2 24.2 26.9 28.7 24.0 27.6 27.6
 Low to moderate drinking 22.0 26.1 31.4 24.3 26.5 29.8 31.8 26.0 23.2
 Heavy drinking 37.6 35.7 34.0 38.1 35.4 33.1 36.4 36.0 33.9
Physical activity, METS h/week
  < 8.3 45.8 40.9 35.6 41.3 42.5 35.8 33.6 41.7 47.7
 8.3–16.7 11.4 12.4 13.0 11.7 11.7 12.9 12.8 11.9 11.7
  > 16.7 42.4 46.3 51.1 46.7 45.4 50.8 53.3 46.0 40.3
Total energy, kcal/d 1831 (732) 1988 (718) 2224 (706) 2417 (704) 1951 (690) 1695 (621) 2059 (701) 1979 (730) 1990 (756)
BMI, kg/m2 29.0 (7.2) 28.7 (6.7) 27.9 (6.3) 29.0 (7.0) 28.8 (6.8) 27.7 (6.1) 28.0 (6.2) 28.7 (6.7) 28.8 (7.1)
Diabetes, % 14.5 12.8 10.5 13.1 11.8 12.5 12.5 11.9 11.4
Hypertension, % 37.8 35.7 32.7 34.9 36 34 33.3 35.9 35.9
Other CVDs, % 11.1 10.6 9.5 10.9 11 9.2 8.5 10.7 10.3
Cancer, % 7.4 8.7 9.1 8.4 8.9 9.1 9.9 8.4 7.4

BMI body mass index, CVD cardiovascular diseases, GED general educational development, hPDI healthful plant-based diet index, IQR inter-
quartile range, METS metabolic equivalent tasks, NHANES National Health and Nutrition Examination Survey, PDI plant-based diet index, SD
standard deviation, uPDI unhealthful plant-based diet index
a
 Variables were adjusted for age except for age and PDI index. Continuous variables were expressed as mean (SD) if normally distributed. Cat-
egorical variables were expressed as proportion (%)

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Results Plant‑based diets and mortality

Characteristics of participants As shown in Table  2 and Fig.  1, greater adherence to

Among 40,074 participants aged 18–85 years (mean age,
47.3 years, SD, 19.4 years), we documented 4904 deaths
including 1029 CVD-specific deaths and 1068 cancer-
specific deaths during a median follow-up of 7.8 years.
PDI scores at baseline ranged from a median of 46
(interquartile range, IQR 45–48) in the lowest quintile
to 60 (IQR 59–62) in the highest quintile. As shown in
Table 1 and Supplementary Table 2, participants with
higher scores of PDI or hPDI were more likely to be non-
Hispanic whites, were older, were better educated, had
a higher ratio of family income to poverty, were more
likely to be widowed or divorced or separated, were less
likely to be current smokers, were more physically active,
and had lower BMI; while these trends were reversed for
uPDI. Besides, females tended to have higher scores of
PDI or hPDI.
PDI was associated with a lower risk of total death (HR
comparing extreme quintiles, 0.80, 95% CI 0.73–0.89,
ptrend < 0.001) and death from cancer (HR 0.68, 95% CI
0.55–0.85, ptrend < 0.001), but was not significantly asso-
ciated with CVD mortality (HR 0.84, 95% CI 0.68–1.04,
ptrend = 0.046). We found an inverse association of hPDI
(HR 0.86, 95% CI 0.77–0.95, ptrend = 0.001) with overall
mortality, but not with cancer-specific (HR 0.89, 95% CI
0.71–1.11, ptrend = 0.173) or CVD-specific (HR, 1.09, 95%
CI 0.85–1.40, ptrend = 0.987) mortality. In contrast, greater
adherence to uPDI was associated with higher risk of both
overall (HR 1.33, 95% CI 1.19–1.48, ptrend < 0.001) and
CVD (HR 1.42, 95% CI 1.12–1.79, ptrend = 0.015) mortal-
ity. As shown in Fig. 2, restricted multivariable cubic spline
analyses revealed a linear, decreasing trend for overall PDI,
but a linear increasing trend for uPDI in the risk of overall
mortality. However, multivariable splines for hPDI showed
a non-linear decreasing trend in total mortality risk with
borderline significance (pnonlinearity = 0.079). The decline

Table 2  HRs (95% CIs) for all-cause mortality according to quintiles of the PDI, hPDI, uPDI in NHANES (1999–2014)
HR (95% CI) ptrendc
Quintile 1 Quintile 2 Quintile 3 Quintile 4 Quintile 5 Per 10 point increase

PDI
 No. of deaths/ 989/64243 994/65279 1154/74647 902/61,981 865/59,755
person-years
 ­Model1a 1 (Reference) 1.02 (0.84–1.24) 0.83 (0.76–0.90) 0.73 (0.67–0.80) 0.68 (0.62–0.75) 0.75 (0.71–0.80)  < 0.001
 ­Model2b 1 (Reference) 0.95 (0.87–1.04) 0.89 (0.82–0.97) 0.82 (0.75–0.90) 0.80 (0.73–0.89) 0.85 (0.80–0.90)  < 0.001
hPDI
 No. of deaths/ 622/74109 758/59,449 1013/64886 1338/69784 1173/57678
person-years
 ­Model1a 1 (Reference) 0.95 (0.85–1.06) 0.89 (0.80–0.98) 0.84 (0.76–0.93) 0.72 (0.65–0.80) 0.79 (0.75–0.84)  < 0.001
 ­Model2b 1 (Reference) 1.01 (0.91–1.13) 0.93 (0.84–1.04) 0.94 (0.85–1.04) 0.86 (0.77–0.95) 0.89 (0.84–0.94) 0.001
uPDI
 No. of deaths/ 975/54,019 1270/66,623 1010/62,553 1028/75,903 621/66,808
person-years
 ­Model1a 1 (Reference) 1.25 (1.15–1.36) 1.28 (1.17–1.40) 1.39 (1.27–1.52) 1.60 (1.44–1.78) 1.30 (1.24–1.37)  < 0.001
 ­Model2b 1 (Reference) 1.14 (1.05–1.24) 1.15 (1.05–1.26) 1.19 (1.09–1.30) 1.33 (1.19–1.48) 1.17 (1.11–1.23)  < 0.001

BMI body mass index, CVD cardiovascular diseases, GED general educational development, hPDI healthful plant-based diet index, IQR inter-
quartile range, METS metabolic equivalent tasks, NHANES National Health and Nutrition Examination Survey, PDI plant-based diet index, SD
standard deviation, uPDI unhealthful plant-based diet index
a
 Model 1 was adjusted for sex (male, female), age (spline variables in the analyses with three knots), and total energy intake (spline variables in
the analyses with three knots)
b
 Model 2 was further adjusted for race/ethnicity (non-Hispanic white, non-Hispanic black, Hispanic or other race), education (≤ 12th grade, high
school graduate/GED or equivalent, or more than high school), marital status (married, widowed/divorced/separated, or never married), ratio of
family income to poverty (< 1.30, 1.30–3.49, or ≥ 3.50), physical activity (< 8.3, 8.3–16.7, or > 16.7 METS h/week), smoking (never smokers,
former smokers, or current smokers), drinking (never drinking, low to moderate drinking, heavy drinking), body mass index (< 18.5, 18.5–24.9,
25.0–29.9, and  ≥ 30.0), diabetes (no, yes), hypertension (no, yes), other CVDs (no, yes), and cancer (no, yes)
c
 Linear trend test was conducted by assigning medians to each quintile as continuous variable in the models, p values lower than Bonferroni-
corrected significance level of 0.005 were highlighted in bold

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392

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Fig. 1  HRs (95% CIs) for cancer mortality and CVD mortality according to quintiles of the PDI, hPDI, uPDI in NHANES (1999–2014)a BMI body mass index, CIs confidence intervals, CVD
cardiovascular diseases, GED general educational development, hPDI healthful plant-based diet index, HRs hazard ratios, METS metabolic equivalent tasks, NHANES National Health and
Nutrition Examination Survey, PDI plant-based diet index, uPDI unhealthful plant-based diet index. aModel was adjusted for sex (male, female), age (spline variables in the analyses with three
knots) and total energy intake (spline variables in the analyses with three knots), race/ethnicity (non-Hispanic white, non-Hispanic black, Hispanic or other race), education (≤ 12th grade, high
school graduate/GED or equivalent, or more than high school), marital status (married, widowed/divorced/separated, or never married), ratio of family income to poverty (< 1.30, 1.30–3.49,
or  ≥ 3.50), physical activity (< 8.3, 8.3–16.7, or > 16.7 METS h/week), smoking (never smokers, former smokers, or current smokers), drinking (never drinking, low to moderate drinking, heavy
drinking), body mass index (< 18.5, 18.5–24.9, 25.0–29.9, and  ≥ 30.0), and diabetes (no, yes), hypertension (no, yes), other CVDs (no, yes), and cancer (no, yes). p values lower than Bonfer-
roni-corrected significance level of 0.005 were highlighted in bold
European Journal of Nutrition (2022) 61:387–398
European Journal of Nutrition (2022) 61:387–398 393
Fig. 2  Dose–response relationship between PDI (A), hPDI (B),
uPDI (C) score and all-cause mortality in NHANES (1999–2014)a
BMI, body mass index, CIs confidence intervals, CVD cardiovascu-
lar diseases, GED general educational development, hPDI healthful
plant-based diet index, HRs hazard ratios, METS metabolic equiva-
lent tasks, NHANES National Health and Nutrition Examination Sur-
vey, PDI Plant-based diet index, uPDI unhealthful plant-based diet
index. aModel was adjusted for sex (male, female), age (spline vari-
ables in the analyses with three knots) and total energy intake(spline
variables in the analyses with three knots), race/ethnicity (non-His-
panic white, non-Hispanic black, Hispanic or other race), education
appeared to occur among those who had hPDI sores of
greater than 56, and became significant when scores were
bigger than 72.
For food groups included in the PDI, we observed a weak
inverse association between two components including nuts
and vegetables and risk of total mortality; while a null or
a non-significant association was found for intake of less
healthy plant foods and some animal foods including SSBs,
potatoes, fruit juices, eggs, and dairy products (Supplemen-
tary Table 3).
Subgroup and sensitivity analyses
In subgroup analysis, we did not find any differential asso-
ciations of PDI, hPDI, and uPDI with risk of total death
(Fig. 3), or death from cancer (Supplementary Fig. 1) or
CVD (Supplementary Fig. 2) according to age, sex, race/
ethnicity, education level, ratio of family income to poverty,
marital status, smoking, alcohol drinking, physical activity,
BMI, and diabetes (all p values for interaction were greater
than Bonferroni-corrected significance level of 0.0005). In
the sensitivity analysis (Supplementary Table 4), the results
were not essentially changed after excluding participants
who had any history of diabetes (n = 636, 1.59%), cancer
(n = 3018, 7.53%), or major CVDs (n = 3156, 7.88%) at
baseline, or excluding individuals (n = 1308, 3.3%) who died
(≤ 12th grade, high school graduate/GED or equivalent, or more
than high school), marital status (married, widowed/divorced/sepa-
rated, or never married), ratio of family income to poverty (< 1.30,
1.30–3.49, or  ≥ 3.50), physical activity (< 8.3, 8.3–16.7, or  > 16.7
METS  h/week), smoking (never smokers, former smokers, or cur-
rent smokers), drinking (never drinking, low to moderate drinking,
heavy drinking), body mass index (< 18.5, 18.5–24.9, 25.0–29.9,
and  ≥ 30.0) and diabetes (no, yes), hypertension (no, yes), other
CVDs (no, yes), and cancer (no, yes). p values lower than Bonferroni-
corrected significance level of 0.005 were highlighted in bold
within 3 years after baseline survey, or excluding individuals
(n = 12,494, 31.38%) with a single 24 h recall, or exclud-
ing any missing data (n = 9862, 24.6%). In competitive risk
models, the associations between each PDI and cause-spe-
cific mortality were similar to those in the main analyses
(Supplementary Table 5).
Discussion
In this large nationally representative cohort study, we found
that greater adherence to overall and a healthful plant-based
diet was significantly associated with lower risk of total mor-
tality. In contrast, individuals who consumed an unhealthful
plant-based diet had an increased risk of both all-cause and
CVD-specific mortality. These results remained after remov-
ing participants who died within 3 years after diet assess-
ment or excluding subjects who had any history of diabetes,
cancer, and major CVDs at baseline, and provide evidence
to support current recommendations to shift to diets rich in
plant-based foods, with lower intake of less healthy plant
foods and animal foods.
Our findings added importantly to and were strongly con-
sistent with the sparse prospective cohort studies examining
pro-vegetarian [19] or plant-based diets [20–22] on mortal-
ity risk. In a population-based cohort study of 12,168 US
13

394

13
Fig. 3  Hazard Ratios (HRs) of all-cause mortality per 10 point increase in PDI, hPDI, uPDI score by subgroups in NHANES (1999–2014)a. BMI body mass index, CIs confidence intervals,
GED general educational development, hPDI healthful plant-based diet index, HRs hazard ratios, METS metabolic equivalent tasks, NHANES National Health and Nutrition Examination Sur-
vey, PDI plant-based diet index, uPDI unhealthful plant-based diet index. aCovariates adjusted in the models were the same as those in model 2 in Table 2 (see Table 2 footnote). Of note, vari-
ables examined in this figure were not adjusted. Light physical activity was defined as participants with physical activity less than 8.3 METS h per week, and moderate and vigorous activity was
defined as participants who had physical activity of 8.3 METS h per week or more. The interaction variables consisting of per 10 point increase in PDI, hPDI, uPDI score and subgroup variables
were added in the Cox model to test for an interaction between the PDI, hPDI, uPDI score and subgroup variables
European Journal of Nutrition (2022) 61:387–398
European Journal of Nutrition (2022) 61:387–398 395
adults aged 45–64 years with a median follow-up of 25 years
[20], higher adherence to PDI and hPDI was associated
with 25–11%, and 32–19% (comparing extreme quintiles)
reduced risk of total and CVD mortality, respectively. In the
NHANES III (1988–1994) longitudinal cohort that followed
11,879 participants aged 20–80 years for 19 years, a 10 unit
increase in hPDI was associated with a 5% decreased risk
of overall mortality [21]. Results for the NHANES III also
showed a non-linear relationship between hPDI and mor-
tality risk among participants with hPDI scores above the
median, which was replicated in the current study, and was
in line with previous studies showing non-linear associations
of several dietary pattern indices [24–26] and food groups
including nuts, eggs, dairy products, fruits, and vegetables
[33] with the risk of all-cause and CVD-specific mortality.
In a cohort study of 49,407 nurses and 25,907 male health
professionals aged 30–75 years, a 10-point increase in over-
all PDI or hPDI over a 12-year period was associated with
an approximately 10% lower, whereas uPDI was associ-
ated 7–8% higher risk of both total or CVD mortality [22].
Our observation of an inverse association between PDI and
cancer-specific mortality was in accordance with a recent
meta-analysis pooling 2 cohort studies of pro-vegetarian diet
and cancer mortality [23].
Most previous studies [4–9] have defined plant-based
diets dichotomously as being vegetarian or not, and consist-
ently showed a decreased risk of overall or cause-specific
mortality. They did not differentiate the quality of plant-
based foods. Most of these studies were conducted among
Seventh-day Adventists, a religious group which encourages
a lacto-ovo vegetarian diet. Given only about 3% prevalence
of vegetarianism in the United States [34], it is difficult to
assess the relationship between vegetarianism and disease
outcomes in the general US population. The present study
adds to the evidence base by investigating the association of
gradations of adherence to an overall plant-based diet with
mortality risk. Such an approach has the advantage of being
easily translatable.
Overall PDI, hPDI, and other healthy dietary indices
such as the Healthy Eating Index-2010 (HEI-2010), Alter-
native HEI-2010 (AHEI-2010), Alternate Mediterranean
Diet (AMED), and Dietary Approaches to Stop Hyperten-
sion (DASH), share several common dietary components
including high intake of fruits and vegetables, nuts and
legumes, and whole grains, and low intake of red and pro-
cessed meats, and most indices were generally associated
with lower risk of total, cancer, and CVD mortality [35],
and had a less negative impact on the environment than cur-
rent average dietary intakes [3]. However, there are several
differences across these healthy indices. First, they were
developed with a different set of recommendations in mind
and some as refinements of a previous dietary index [35].
Second, some food components differed across indices. For
example, reduced sodium is recommended in HEI-2010,
AHEI-2010, and DASH, but not in PDIs or AMED. Simi-
larly, low intakes of SSBs and/or fruit juices are included in
overall PDI, uPDI, HEI-2010, and DASH, whereas AMED
did not include fruit juices or SSBs. Alcohol intake is unique
to AHEI-2010 and AMED. Third, the scoring system var-
ied between indices. PDIs, AMED, and DASH utilized the
population’s median or quintiles of intake, whereas AHEI-
2010 used cut-off values based on absolute intakes.
The protective associations between adherence to over-
all PDI or hPDI and lower risk of death are biologically
plausible. The PDI and hPDI recommend several healthy
plant foods such as whole grain, nuts, vegetables, and tea
and coffee. These foods or food groups have been associ-
ated with lower total and CVD mortality [10–12, 36, 37],
which could be partially interpreted by anti-inflammation
and antioxidant effects of dietary fibers, polyphenols, and
unsaturated fatty acids [38–42]. Besides, animal proteins
including protein from eggs and dairy products have been
associated with increased risk of total or cancer mortality
[43–45], and replacement of animal proteins, particularly
proteins from egg, with plant proteins was associated with
lower risk of total and CVD mortality [45]. Plant proteins as
well as vegetarian diet may partly affect health and longevity
through their anti-insulin resistance property by decreasing
insulin-like growth factor 1 (IGF-1) or increasing its binding
proteins [46, 47].
When investigating each food component in the PDIs,
we only found a weak inverse association between two food
components (i.e., nuts and vegetables) and mortality risk in
the study. Compared with the assessment of the effects of a
single food, study on dietary pattern considers the entire diet
and thus captures the complex interaction between dietary
components, which may partly interpret why we observed a
moderate association for plant-based dietary patterns, but a
week or non-significant or null association for several food
components in the dietary pattern.
A non-significant association for the healthy PDI and
CVD mortality was found in the NHANES III study [21]
and was repeated in our study with larger sample size. This
finding was unexpected given that high fiber intake and
decreased saturated fat intake were associated with lower
risk of CVD events including morbidity and mortality [20,
22]. Either there is a null association or the absence of
observing an association could be partly due to inaccuracies
in cause-of-death information on death certificates, particu-
larly for CVD [48, 49]. Another possible explanation is that
participants who were diagnosed with CVDs may change
their dietary habits due to their health conditions.
Strengths of the current study include the use of a nation-
ally representative sample of US adults, large sample size,
prospective cohort design, and data collection utilizing vali-
dated measures. However, our study has several limitations.
13

396
First, diet was self-reported using 24 h recalls, which may
cause misclassification of dietary intake, although we used
several methods (i.e., Multiple-Pass method, dietary sam-
pling weights, and the NCI-method) [28, 29] to reduce meas-
urement error and improve estimates of usual intake. Such
misclassification bias in cohort study could be nondifferen-
tial in most situations and is likely to lead to the underesti-
mation of the observed association if exposure data is binary
[50]. While in the present study, the misclassification can
lead to bias in either direction even the misclassification is
nondifferential, given the continuous or polytomous expo-
sure data in the current analysis. Second, although we have
adjusted for a wide range of risk factors such as demograph-
ics, smoking, and physical activity, the possibility of residual
confounding cannot be totally ruled out. Third, given the
observational nature of the study design, we were unable
to determine any causality. Fourth, despite a nationally rep-
resentative sample in the United States in the analysis, the
findings may not be generalizable to other countries.
In summary, we found that following PDI and hPDI was
associated with lower risk of mortality; while a plant-based
diet that emphasized less healthy plant foods was associ-
ated higher risk of mortality among US adults. Guidelines
and interventions highlighting the importance of increasing
intake of plant foods, while decreasing intake of less healthy
plant foods and certain animal foods may therefore promote
health and longevity.
Supplementary Information  The online version contains supplemen-
tary material available at https://d​ oi.o​ rg/1​ 0.1​ 007/s​ 00394-0​ 21-0​ 2660-7.
Acknowledgements  Drs Li and Yang had full access to all the data in
the study and take responsibility for the integrity of the data and the
accuracy of the data analysis. Study concept and design: Yang and Li.
Acquisition, analysis, or interpretation of data: all authors. Drafting of
the manuscript: Li and Yang. Critical revision of the manuscript for
important intellectual content: all authors. Statistical analysis: Li and
Zhu. Obtained funding: Yang. Administrative, technical, or material
support: Yang. Study supervision: Yang.
Author contributions  Hairong Li and Wanshui Yang had full access
to all the data in the study and take responsibility for the integrity
of the data and the accuracy of the data analysis. Study concept and
design: Wanshui Yang and Hairong Li Acquisition, analysis, or inter-
pretation of data: all authors. Drafting of the manuscript: Hairong Li
and Wanshui Yang. Critical revision of the manuscript for important
intellectual content: all authors. Statistical analysis: Hairong Li and Yu
Zhu. Obtained funding: Wanshui Yang. Administrative, technical, or
material support: Wanshui Yang. Study supervision: Wanshui Yang.
Funding  This work was supported by the National Natural Science
Foundation of China (82073651), Anhui Provincial Natural Science
Foundation (2008085MH262), and a grant of the Scientific Research
of BSKY from Anhui Medical University (XJ201935).
Availability of data and material  Data described in the manuscript,
codebook, and analytic code will be made publicly and freely available
without restriction at [https://​www.​cdc.​gov/​nchs/​nhanes/​index.​htm].
13
European Journal of Nutrition (2022) 61:387–398
Code availability  SAS version 9.4.
Declarations 
Conflict of interest  The authors declared that they have no conflict of
interest.
Ethical approval  The National Centers for Health Statistics approved
the NHANES study protocol. The Institutional Review Board at our
institute determined that this analysis used a public dataset, so human
subjects’ approval was waived.
Consent to participate  All participants provided the written informed
consent.
Consent for publication  All of the authors have read and approved the
final version of this manuscript.
References
1. Collaborators USBoD, Mokdad AH, Ballestros K, Echko M,
Glenn S, Olsen HE, Mullany E, Lee A, Khan AR, Ahmadi A, Fer-
rari AJ, Kasaeian A, Werdecker A, Carter A, Zipkin B, Sartorius
B, Serdar B, Sykes BL, Troeger C, Fitzmaurice C, Rehm CD, San-
tomauro D, Kim D, Colombara D, Schwebel DC, Tsoi D, Kolte
D, Nsoesie E, Nichols E, Oren E, Charlson FJ, Patton GC, Roth
GA, Hosgood HD, Whiteford HA, Kyu H, Erskine HE, Huang
H, Martopullo I, Singh JA, Nachega JB, Sanabria JR, Abbas K,
Ong K, Tabb K, Krohn KJ, Cornaby L, Degenhardt L, Moses M,
Farvid M, Griswold M, Criqui M, Bell M, Nguyen M, Wallin M,
Mirarefin M, Qorbani M, Younis M, Fullman N, Liu P, Briant P,
Gona P, Havmoller R, Leung R, Kimokoti R, Bazargan-Hejazi S,
Hay SI, Yadgir S, Biryukov S, Vollset SE, Alam T, Frank T, Farid
T, Miller T, Vos T, Barnighausen T, Gebrehiwot TT, Yano Y, Al-
Aly Z, Mehari A, Handal A, Kandel A, Anderson B, Biroscak B,
Mozaffarian D, Dorsey ER, Ding EL, Park EK, Wagner G, Hu G,
Chen H, Sunshine JE, Khubchandani J, Leasher J, Leung J, Salo-
mon J, Unutzer J, Cahill L, Cooper L, Horino M, Brauer M, Bre-
itborde N, Hotez P, Topor-Madry R, Soneji S, Stranges S, James
S, Amrock S, Jayaraman S, Patel T, Akinyemiju T, Skirbekk V,
Kinfu Y, Bhutta Z, Jonas JB, Murray CJL (2018) The State of US
Health, 1990–2016: burden of diseases, injuries, and risk factors
among US States. JAMA 319(14):1444–1472. https://​doi.​org/​10.​
1001/​jama.​2018.​0158
2. Millen BE, Abrams S, Adams-Campbell L, Anderson CA, Brenna
JT, Campbell WW, Clinton S, Hu F, Nelson M, Neuhouser ML,
Perez-Escamilla R, Siega-Riz AM, Story M, Lichtenstein AH
(2016) The 2015 dietary guidelines advisory committee scientific
report: development and major conclusions. Adv Nutr 7(3):438–
444. https://​doi.​org/​10.​3945/​an.​116.​012120
3. Nelson ME, Hamm MW, Hu FB, Abrams SA, Griffin TS (2016)
Alignment of healthy dietary patterns and environmental sustain-
ability: a systematic review. Adv Nutr 7(6):1005–1025. https://d​ oi.​
org/​10.​3945/​an.​116.​012567
4. Kinlen LJ, Hermon C, Smith PG (1983) A proportionate study
of cancer mortality among members of a vegetarian society. Br J
Cancer 48(3):355–361. https://​doi.​org/​10.​1038/​bjc.​1983.​200
5. Chang-Claude J, Frentzel-Beyme R, Eilber U (1992) Mortality
pattern of German vegetarians after 11 years of follow-up. Epide-
miology 3(5):395–401. https://​doi.​org/​10.​1097/​00001​648-​19920​
9000-​00003
European Journal of Nutrition (2022) 61:387–398 397
6. Key TJ, Thorogood M, Appleby PN, Burr ML (1996) Dietary
habits and mortality in 11,000 vegetarians and health conscious
people: results of a 17 year follow up. BMJ 313(7060):775–779.
https://​doi.​org/​10.​1136/​bmj.​313.​7060.​775
7. Key TJ, Appleby PN, Davey GK, Allen NE, Spencer EA,
Travis RC (2003) Mortality in British vegetarians: review and
preliminary results from EPIC-Oxford. Am J Clin Nutr 78(3
Suppl):533s–538s. https://​doi.​org/​10.​1093/​ajcn/​78.3.​533S
8. Orlich MJ, Singh PN, Sabate J, Jaceldo-Siegl K, Fan J, Knut-
sen S, Beeson WL, Fraser GE (2013) Vegetarian dietary patterns
and mortality in Adventist Health Study 2. JAMA Intern Med
173(13):1230–1238. https://d​ oi.o​ rg/1​ 0.1​ 001/j​ amain​ ternm
​ ed.2​ 013.​
6473
9. Appleby PN, Crowe FL, Bradbury KE, Travis RC, Key TJ (2016)
Mortality in vegetarians and comparable nonvegetarians in the
United Kingdom. Am J Clin Nutr 103(1):218–230. https://​doi.​
org/​10.​3945/​ajcn.​115.​119461
10. Bao Y, Han J, Hu FB, Giovannucci EL, Stampfer MJ, Willett
WC, Fuchs CS (2013) Association of nut consumption with total
and cause-specific mortality. N Engl J Med 369(21):2001–2011.
https://​doi.​org/​10.​1056/​NEJMo​a1307​352
11. Aune D, Keum N, Giovannucci E, Fadnes LT, Boffetta P, Green-
wood DC, Tonstad S, Vatten LJ, Riboli E, Norat T (2016) Whole
grain consumption and risk of cardiovascular disease, cancer, and
all cause and cause specific mortality: systematic review and dose-
response meta-analysis of prospective studies. BMJ 353:i2716.
https://​doi.​org/​10.​1136/​bmj.​i2716
12. Wang X, Ouyang Y, Liu J, Zhu M, Zhao G, Bao W, Hu FB
(2014) Fruit and vegetable consumption and mortality from all
causes, cardiovascular disease, and cancer: systematic review and
dose-response meta-analysis of prospective cohort studies. BMJ
349:g4490. https://​doi.​org/​10.​1136/​bmj.​g4490
13. Muraki I, Rimm EB, Willett WC, Manson JE, Hu FB, Sun Q
(2016) Potato consumption and risk of type 2 diabetes: results
from three prospective cohort studies. Diabetes Care 39(3):376–
384. https://​doi.​org/​10.​2337/​dc15-​0547
14. Yang Q, Zhang Z, Gregg EW, Flanders WD, Merritt R, Hu FB
(2014) Added sugar intake and cardiovascular diseases mortality
among US adults. JAMA Intern Med 174(4):516–524. https://d​ oi.​
org/​10.​1001/​jamai​ntern​med.​2013.​13563
15. Veronese N, Stubbs B, Noale M, Solmi M, Vaona A, Demur-
tas J, Nicetto D, Crepaldi G, Schofield P, Koyanagi A, Maggi S,
Fontana L (2017) Fried potato consumption is associated with
elevated mortality: an 8 y longitudinal cohort study. Am J Clin
Nutr 106(1):162–167. https://​doi.​org/​10.​3945/​ajcn.​117.​154872
16. Malik VS, Li Y, Pan A, De Koning L, Schernhammer E, Willett
WC, Hu FB (2019) Long-term consumption of sugar-sweetened
and artificially sweetened beverages and risk of mortality in US
Adults. Circulation 139(18):2113–2125. https://​doi.​org/​10.​1161/​
CIRCU​LATIO​NAHA.​118.​037401
17. Steffen LM, Jacobs DR Jr, Stevens J, Shahar E, Carithers T, Fol-
som AR (2003) Associations of whole-grain, refined-grain, and
fruit and vegetable consumption with risks of all-cause mortal-
ity and incident coronary artery disease and ischemic stroke: the
atherosclerosis risk in communities (ARIC) Study. Am J Clin Nutr
78(3):383–390. https://​doi.​org/​10.​1093/​ajcn/​78.3.​383
18. Satija A, Bhupathiraju SN, Rimm EB, Spiegelman D, Chiuve SE,
Borgi L, Willett WC, Manson JE, Sun Q, Hu FB (2016) Plant-
based dietary patterns and incidence of type 2 diabetes in us men
and women: results from three prospective cohort studies. PLoS
Med. https://​doi.​org/​10.​1371/​journ​al.​pmed.​10020​39
19. Martinez-Gonzalez MA, Sanchez-Tainta A, Corella D, Salas-
Salvado J, Ros E, Aros F, Gomez-Gracia E, Fiol M, Lamuela-
Raventos RM, Schroder H, Lapetra J, Serra-Majem L, Pinto X,
Ruiz-Gutierrez V, Estruch R, Group P (2014) A provegetarian
food pattern and reduction in total mortality in the Prevencion
con Dieta Mediterranea (PREDIMED) study. Am J Clin Nutr
100(Suppl 1):320S-328S. https:// ​ d oi. ​ o rg/ ​ 1 0. ​ 3 945/ ​ ajcn.​ 1 13.​
071431
20. Kim H, Caulfield LE, Garcia-Larsen V, Steffen LM, Coresh J,
Rebholz CM (2019) Plant-based diets are associated with a lower
risk of incident cardiovascular disease, cardiovascular disease
mortality, and all-cause mortality in a general population of mid-
dle-aged adults. J Am Heart Assoc. https://​doi.​org/​10.​1161/​jaha.​
119.​012865
21. Kim H, Caulfield LE, Rebholz CM (2018) Healthy plant-based
diets are associated with lower risk of all-cause mortality in US
adults. J Nutr 148(4):624–631. https://​doi.​org/​10.​1093/​jn/​nxy019
22. Baden MY, Liu G, Satija A, Li Y, Sun Q, Fung TT, Rimm EB,
Willett WC, Hu FB, Bhupathiraju SN (2019) Changes in plant-
based diet quality and total and cause-specific mortality. Circula-
tion 140(12):979–991. https://d​ oi.o​ rg/1​ 0.1​ 161/c​ ircul​ ation​ aha.1​ 19.​
041014
23. Molina-Montes E, Salamanca-Fernández E, Garcia-Villanova B,
Sánchez MJ (2020) The impact of plant-based dietary patterns
on cancer-related outcomes: a rapid review and meta-analysis.
Nutrients. https://​doi.​org/​10.​3390/​nu120​72010
24. Kant AK, Graubard BI, Schatzkin A (2004) Dietary patterns pre-
dict mortality in a national cohort: the National Health Interview
Surveys, 1987 and 1992. J Nutr 134(7):1793–1799. https://​doi.​
org/​10.​1093/​jn/​134.7.​1793
25. Heidemann C, Schulze MB, Franco OH, van Dam RM, Mantzoros
CS, Hu FB (2008) Dietary patterns and risk of mortality from car-
diovascular disease, cancer, and all causes in a prospective cohort
of women. Circulation 118(3):230–237. https://​doi.​org/​10.​1161/​
CIRCU​LATIO​NAHA.​108.​771881
26. Stewart RA, Wallentin L, Benatar J, Danchin N, Hagstrom E, Held
C, Husted S, Lonn E, Stebbins A, Chiswell K, Vedin O, Watson
D, White HD, Investigators S (2016) Dietary patterns and the
risk of major adverse cardiovascular events in a global study of
high-risk patients with stable coronary heart disease. Eur Heart J
37(25):1993–2001. https://​doi.​org/​10.​1093/​eurhe​artj/​ehw125
27. Centers for Disease Control and Prevention. National Health
and Nutrition Examination Survey (NHANES) (2017) About the
National Health and Nutrition Examination Survey. https://​www.​
cdc.​gov/​nchs/​nhanes/​about_​nhanes.​htm. Accessed on 11 March
2021
28. Ahluwalia N, Dwyer J, Terry A, Moshfegh A, Johnson C (2016)
Update on NHANES dietary data: focus on collection, release,
analytical considerations, and uses to inform public policy. Adv
Nutr 7(1):121–134. https://​doi.​org/​10.​3945/​an.​115.​009258
29. Tooze JA, Midthune D, Dodd KW, Freedman LS, Krebs-Smith
SM, Subar AF, Guenther PM, Carroll RJ, Kipnis V (2006) A new
statistical method for estimating the usual intake of episodically
consumed foods with application to their distribution. J Am Diet
Assoc 106(10):1575–1587. https://​doi.​org/​10.​1016/j.​jada.​2006.​
07.​003
30. Satija A, Bhupathiraju SN, Spiegelman D, Chiuve SE, Manson
JE, Willett W, Rexrode KM, Rimm EB, Hu FB (2017) Healthful
and unhealthful plant based diets and the risk of coronary heart
disease in U. S. Adults. J Am Coll Cardiol. https://​doi.​org/​10.​
1016/j.​jacc.​2017.​05.​047
31. Guasch-Ferre M, Hu FB (2019) Are fruit juices just as unhealthy
as sugar-sweetened beverages? JAMA Netw Open 2(5):e193109.
https://​doi.​org/​10.​1001/​jaman​etwor​kopen.​2019.​3109
32. Centers for Disease Control and Prevention. National Health and
Nutrition Examination Survey (NHANES) (2021) NHANES Lab-
oratory Data. https://w ​ wwn.c​ dc.g​ ov/n​ chs/n​ hanes/s​ earch/d​ atapa​ ge.​
aspx?​Compo​nent=​Labor​atory. Accessed on 11 March 2021
33. Schwingshackl L, Schwedhelm C, Hoffmann G, Lampousi AM,
Knuppel S, Iqbal K, Bechthold A, Schlesinger S, Boeing H
(2017) Food groups and risk of all-cause mortality: a systematic
13

398
review and meta-analysis of prospective studies. Am J Clin Nutr
105(6):1462–1473. https://​doi.​org/​10.​3945/​ajcn.​117.​153148
34. Ruby MB (2012) Vegetarianism A blossoming field of study.
Appetite 58(1):141–150. https://​doi.​org/​10.​1016/j.​appet.​2011.​
09.​019
35. Liese AD, Krebs-Smith SM, Subar AF, George SM, Harmon BE,
Neuhouser ML, Boushey CJ, Schap TE, Reedy J (2015) The die-
tary patterns methods project: synthesis of findings across cohorts
and relevance to dietary guidance. J Nutr 145(3):393–402. https://​
doi.​org/​10.​3945/​jn.​114.​205336
36. Gardener H, Rundek T, Wright CB, Elkind MS, Sacco RL (2013)
Coffee and tea consumption are inversely associated with mortal-
ity in a multiethnic urban population. J Nutr 143(8):1299–1308.
https://​doi.​org/​10.​3945/​jn.​112.​173807
37. Ding M, Satija A, Bhupathiraju SN, Hu Y, Sun Q, Han J, Lopez-
Garcia E, Willett W, van Dam RM, Hu FB (2015) Association of
coffee consumption with total and cause-specific mortality in 3
large prospective cohorts. Circulation 132(24):2305–2315. https://​
doi.​org/​10.​1161/​circu​latio​naha.​115.​017341
38. Ma Y, Hebert JR, Li W, Bertone-Johnson ER, Olendzki B, Pagoto
SL, Tinker L, Rosal MC, Ockene IS, Ockene JK, Griffith JA, Liu S
(2008) Association between dietary fiber and markers of systemic
inflammation in the Women’s Health Initiative Observational
Study. Nutrition 24(10):941–949. https://​doi.​org/​10.​1016/j.​nut.​
2008.​04.​005
39. Cassidy A, Rogers G, Peterson JJ, Dwyer JT, Lin H, Jacques PF
(2015) Higher dietary anthocyanin and flavonol intakes are associ-
ated with anti-inflammatory effects in a population of US adults.
Am J Clin Nutr 102(1):172–181. https://d​ oi.o​ rg/1​ 0.3​ 945/a​ jcn.1​ 15.​
108555
40. Ishikawa T, Suzukawa M, Ito T, Yoshida H, Ayaori M, Nishiwaki
M, Yonemura A, Hara Y, Nakamura H (1997) Effect of tea flavo-
noid supplementation on the susceptibility of low-density lipo-
protein to oxidative modification. Am J Clin Nutr 66(2):261–266.
https://​doi.​org/​10.​1093/​ajcn/​66.2.​261
41. Mozaffarian D, Wu JH (2011) Omega-3 fatty acids and cardio-
vascular disease: effects on risk factors, molecular pathways, and
clinical events. J Am Coll Cardiol 58(20):2047–2067. https://​doi.​
org/​10.​1016/j.​jacc.​2011.​06.​063
13
European Journal of Nutrition (2022) 61:387–398
42. van Dam RM, Hu FB (2005) Coffee consumption and risk of type
2 diabetes: a systematic review. JAMA 294(1):97–104. https://d​ oi.​
org/​10.​1001/​jama.​294.1.​97
43. Kroenke CH, Kwan ML, Sweeney C, Castillo A, Caan BJ (2013)
High- and low-fat dairy intake, recurrence, and mortality after
breast cancer diagnosis. J Natl Cancer Inst 105(9):616–623.
https://​doi.​org/​10.​1093/​jnci/​djt027
44. Lu W, Chen H, Niu Y, Wu H, Xia D, Wu Y (2016) Dairy products
intake and cancer mortality risk: a meta-analysis of 11 population-
based cohort studies. Nutr J 15(1):91. https://​doi.​org/​10.​1186/​
s12937-​016-​0210-9
45. Huang J, Liao LM, Weinstein SJ, Sinha R, Graubard BI, Albanes
D (2020) Association between plant and animal protein intake
and overall and cause-specific mortality. JAMA Intern Med
180(9):1173–1184. https://​doi.​org/​10.​1001/​jamai​ntern​med.​2020.​
2790
46. Holmes MD, Pollak MN, Willett WC, Hankinson SE (2002) Die-
tary correlates of plasma insulin-like growth factor I and insulin-
like growth factor binding protein 3 concentrations. Cancer Epi-
demiol Biomarkers Prev 11(9):852–861
47. Allen NE, Appleby PN, Davey GK, Kaaks R, Rinaldi S, Key TJ
(2002) The associations of diet with serum insulin-like growth
factor I and its main binding proteins in 292 women meat-eaters,
vegetarians, and vegans. Cancer Epidemiol Biomarkers Prev
11(11):1441–1448. https://​doi.​org/​10.​1001/​jamai​ntern​med.​2013.​
6473
48. Smith CJ, Scott SM, Wagner BM (1998) The necessary role
of the autopsy in cardiovascular epidemiology. Hum Pathol
29(12):1469–1479. https://​d oi.​o rg/​1 0.​1 016/​s 0046-​8 177(98)​
90018-1
49. Pagidipati NJ, Gaziano TA (2013) Estimating deaths from cardio-
vascular disease: a review of global methodologies of mortality
measurement. Circulation 127(6):749–756. https://​doi.​org/​10.​
1161/​CIRCU​LATIO​NAHA.​112.​128413
50. Jurek AM, Greenland S, Maldonado G, Church TR (2005) Proper
interpretation of non-differential misclassification effects: expec-
tations vs observations. Int J Epidemiol 34(3):680–687. https://​
doi.​org/​10.​1093/​ije/​dyi060
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