Journal of Human Hypertension

https://doi.org/10.1038/s41371-017-0007-0

REVIEW ARTICLE

Coffee consumption and risk of hypertension: a systematic review

and dose–response meta-analysis of cohort studies
Chen Xie1 Lingling Cui1 Jicun Zhu1 Kehui Wang2 Nan Sun3 Changqing Sun1
● ● ● ● ●

Received: 9 June 2017 / Revised: 20 July 2017 / Accepted: 13 September 2017

© Macmillan Publishers Limited, part of Springer Nature 2017

Abstract
Some debates exist regarding the association of coffee consumption with hypertension risk. We performed a meta-analysis
including dose–response analysis aimed to derive a more quantitatively precise estimation of this association. PubMed and
Embase were searched for cohort studies published up to 18 July 2017. Fixed-effects generalized least-squares regression
models were used to assess the quantitative association between coffee consumption and hypertension risk across studies.
Restricted cubic spline was used to model the dose–response association. We identified eight articles (10 studies)
investigating the risk of hypertension with the level of coffee consumption, including 243,869 individuals and 58,094
1234567890

incident cases of hypertension. We found no evidence of a nonlinear dose–response association of coffee consumption and
hypertension (Pnonlinearity = 0.243). The risk of hypertension was reduced by 2% (relative risk (RR) = 0.98, 95% confidence
interval (CI) 0.98–0.99) with each one cup/day increment of coffee consumption. With the linear cubic spline model, the
RRs of hypertension risk were 0.97 (95% CI 0.95–0.99), 0.95 (95% CI 0.91–0.99), 0.92 (95% CI 0.87–0.98), and 0.90 (95%
CI 0.83–0.97) for 2, 4, 6, and 8 cups/day, respectively, compared with individuals with no coffee intakes. This meta-analysis
provides quantitative evidence that consumption of coffee was inversely associated with the risk of hypertension in a
dose–response manner.

Introduction burden, the importance of preventing hypertension by

Hypertension, a key risk factor for cardiovascular diseases,
is also the leading cause of premature death and the third
cause of disability. It affects one billion people worldwide,
leading to heart attacks, strokes, and renal failure [1–4]. The
total number of people with hypertension is expected to
increase to 1.56 billion by 2025 [5]. Given its significant
Electronic Supplementary Material The online version of this article
(https://doi.org/10.1038/s41371-017-0007-0) contains supplementary
material, which is available to authorized users
* Changqing Sun
suncq126@126.com
1 therefore performed a systematic review and dose–response
Department of Epidemiology and Health Statistics, College of
Public Health, Zhengzhou University, 100 Kexue Avenue,
Zhengzhou, Henan 450001, China
2
The First Affiliated Hospital of Henan University of Traditional
Chinese Medicine, People’s Road, Henan, China
3
Terry College of Business, University of Georgia, Athens, GA,
USA
adopting a healthy lifestyle is imperative and undoubted.
Coffee is one of the most widely consumed beverages in
the world, with a global consumption of 500 billion cups
per year [6]. Because of the wide consumption of coffee, its
effects on hypertension could have considerable public
health and clinical implications. Since early 1930s, coffee
consumption has attracted interest as a potential risk factor
because of an acute pressor effect of caffeine on blood
pressure (BP), but the long-term effect on hypertension risk
remains controversial in a number of randomized controlled
trials and cohort studies [7–16]. Two previous meta-
analyses of coffee consumption and risk of hypertension
have been published [17, 18]. s and incident hypertension.
Given the different definitions of coffee exposure among
studies, the association between coffee consumption and
risk of hypertension could not be analyzed precisely. We
meta-analysis of all available data of cohort studies on the
association of coffee consumption with the risk of
hypertension.

Materials and methods
Literature search strategy
We searched the electronic databases PubMed and Embase
for all articles of cohort studies investigating the association
between coffee consumption and hypertension that were
published up to 18 July 2017. Our search included both
free-text and Medical Subject Heading (MeSH) terms, such
as “coffee [MeSH]”, “caffeine [MeSH]”, “coffee”, “caffein*”,
“hypertension [MeSH]”, “cardiovascular diseases [MeSH]”,
“high blood pressure*”, OR “cardiovascular disease”,
“hypertens*”, “HBP”, and “CVD”. Details of the wide search
terms are shown in Supplementary Table 1. The reference
lists of all retrieved articles [9–16] and previous systematic
reviews [17–19] were manually searched for additional
relevant studies. We restricted the search to studies on
humans and written in English. The meta-analysis was
conducted and reported in accordance with the Meta-
analysis of Observational Studies in Epidemiology guide-
lines [20].
Study selection
Studies included in this meta-analysis met the following
criteria: (1) the study design was cohort; (2) the articles
were published in English; (3) reported relative risks (RRs),
odds ratios (ORs), or hazard ratios (HRs) with 95% con-
fidence intervals (CIs) or data to calculate them; (4) the
exposure was coffee consumption; (5) the outcome was risk
of hypertension; and (6) provide the frequency and amount
of coffee consumption, number of cases, exposed person-
years, or participant numbers for the dose–response analy-
sis. Abstract of only publications, comment, or conference
articles were excluded. A search for unpublished literature
was not performed.
Data extraction and quality assessment
Data were extracted by using a pre-designed extraction
form. The following information was collected: the first
author; publication year; country where the study was
conducted; study name; study design; follow-up period;
number of incident MetS cases and total population; mean
or median age of the study population at baseline; coffee
consumption ranges or median or mean categories at
baseline; RRs, HRs, ORs, and 95% CIs for the association;
definition for hypertension; and covariates on which the
analyses were adjusted. When the required data were not
reported in the original articles, we emailed authors to
obtain further details. If a study only reported caffeinated
coffee consumption instead of total coffee consumption,
caffeinated coffee consumption was also included in the
C. Xie et al.
total coffee consumption analysis. If the numbers of cases in
each category were unavailable, these data were inferred on
the basis of the number of total cases, level-specific exposed
participant numbers, and the reported effect size. If the
exposed participant numbers were not reported in each
category, group sizes were assumed to be approximately
equal [21]. Cohort study quality was assessed by the
Newcastle–Ottawa Scale, which allows for a total score of
up to nine points summarizing eight aspects of each study
the scale gives a maximum of 9 stars [22]. All retrieved
articles were screened by two independent reviewers (C.X.
and L.C.). Data extraction and quality assessment were
done by C.X. and checked by L.C. Any disagreements were
discussed until agreement was reached.
Statistical methods
To analyze the trend of coffee consumption and risk of
hypertension, we used both semiparametric and parametric
methods. For the semiparametric method, four coffee con-
sumption groups were generated: lowest, third highest,
second highest, and highest. For each included study, the
lowest and the highest coffee consumption categories cor-
responded to the lowest and highest groups, respectively.
For studies with four exposure categories, the second and
third categories corresponded to the second and third
highest groups, respectively. For studies with three expo-
sure categories, the middle category corresponded to either
the second or the third highest group, whichever median
coffee consumption amount was most similar. If the study
had more than four exposure categories, two consumption
groups, other than the lowest and highest, were chosen on
the basis of their similarity of the amount of coffee con-
sumption in that category to the second and third highest
groups. For studies reporting HRs or ORs for hypertension,
we assumed that the HRs and ORs were approximately RRs
[23]. A fixed-effects model [24] was used to calculate the
summary RR estimates.
For the parametric method, generalized least-squares
(GLS) regression was used to estimate study-specific
dose–response association. GLS regression model esti-
mates the linear dose–response coefficient, taking into
account the covariance for each exposure category within
each study, because they are estimated relative to a common
referent PA exposure category [25, 26]. A fixed-effects
model was used to pool the study-specific dose–response
RR estimates [24]. First, a linear association was assumed;
study-specific RR estimates were calculated per one cup/
day of coffee consumption increment and then pooled. In
addition, we examined possible nonlinear associations by
modeling coffee consumption using a restricted cubic spline
with three knots located at the 25th, 50th, and 75th per-
centiles of the distribution [27].
Fig. 1 Flowchart of study
selection for the meta-analysis
To perform the dose–response meta-analysis, we assigned
the median or mean coffee consumption in each category of
consumption to the corresponding RR for each study. If the
mean or median consumption per category was not reported,
the midpoint of the upper and lower boundaries in each
category was assigned as the mean consumption. If the
highest or lowest category was open-ended, the width of the
interval was assumed to be the same as in the closest category
[28]. Only studies reporting risk estimates for at least three
coffee consumption exposure levels for risk of hypertension
were included in this analysis. The P value for nonlinearity
was calculated by testing the null hypothesis that the coeffi-
cient of the second spline is equal to zero.
Heterogeneity was tested by Cochran Q and I2 statistics
[29]. For the Q statistic, P < 0.1 was considered statistically
significant; and for the I2 statistic, I2 values of ~25%, 50%,
and 75% are considered to reflect low, moderate, and high
heterogeneity, respectively. Subgroup analyses were con-
ducted to investigate potential sources of heterogeneity,
including study design, gender, age, region, diagnostic
criteria number of cases, and the covariates adjusted in the
analysis (age, smoking, alcohol consumption, physical
activity, family history of hypertension, education, intake of
sodium, and body mass index). We performed a sensitivity
analysis by excluding one study at a time to assess the
stability of results and potential sources of heterogeneity.
Table 1 Basic characteristics of cohort studies investigating the association of coffee consumption and incident hypertension
First author Region Gender (M/W) Follow-up period (years) Age (mean) BMI (kg/m2) Participants (case) Coffee category (cup/day) OR/RR/HR

Chei et al. [16] Singapore M/W 9.5 54.9 22.72 38,592 (13 658) 1 1
2 0.98 (0.94, 1.02)
3.5 0.93 (0.86, 1.00)
Rhee et al. [15] America W 3 62.5 25.97 29,985 (5566) 0 1
1 1.00 (0.93, 1.08)
2–3 0.95 (0.89, 1.02)
≥4 0.99 (0.90, 1.08)
Grosso et al. [14] Poland M/W 5 56.2/55.2 26.6/26.3 2725 (1735) <1 1
1–2 0.86 (0.68, 1.07)
3–4 0.75 (0.58, 0.95)
>4 1.58 (0.85, 3.64)
Uiterwaal et al. [11] Netherlands M 11 40.7 25.34 2297 (493) 0–3 1
3–6 1.08 (0.79, 1.47)
>6 1.03 (0.72, 1.46)
Uiterwaal et al. [11] Netherlands W 11 40.1 24.63 2892 (463) 0–3 1
3–6 0.83 (0.64, 1.07)
>6 0.67 (0.46, 0.98)
Hu et al. [13] Finland M/W 13.2 43.56 25.84 24,710 (2505) 0–1 1
2–3 1.27 (1.07, 1.51)
4–5 1.20 (1.01, 1.42)
6–7 1.21 (1.01, 1.44)
≥8 1.13 (0.94, 1.36)
Palatini et al. [12, 36] Italy M/W 6.4 33.3 (8.4) 25.4 (3.4) 1107 (561) 0 1
1–3 1.27 (1.04–1.56)
≥4 1.24 (0.94–1.66)
Winkelmayer et al. [10] America W 12 55.4 24.8 53,175 (19,364) <1 1
1 1.06 (1.01–1.10)
2–3 1.00 (0.97–1.04)
4–5 0.93 (0.88–0.99)
≥6 0.88 (0.80–0.98)
Winkelmayer et al. (2002) America W 12 36 24.3 87,369 (13 468) <1 1
1 1.06 (1.01–1.13)
2–3 1.00 (0.95–1.04)
4–5 0.91 (0.84–0.98)
C. Xie et al.
 Potential publication bias was evaluated by the Egger’s test

0.91 (0.80–1.04)

1.24 (0.87–1.77)
1.49 (1.01–2.20)
1.07 (0.67–1.69)
OR/RR/HR [30] and results were considered to indicate publication bias
at P < 0.10. All analyses involved use of Stata 12.1 (Stata

1
Corp, College Station, TX, USA).
Coffee category (cup/day)

Results

Characteristics of studies
1–2
3–4
≥6

≥5
0

We identified eight articles of 10 cohort studies in PubMed

and Embase for the meta-analysis (Fig. 1). In total, the
review included 243,869 individuals and 58,094 incident
cases of hypertension. The main characteristics of each
Participants (case)

study are presented in Table 1.

Overall, four studies were conducted in the United
1017 (281)

States, one in Asia, and five in Europe. In all, four articles

did not distinguish between gender, one article described
stratified analyses by gender, and three described analysis of
only men or women. Of these, five articles defined hyper-
BMI (kg/m2)

tension as systolic BP ≥140 mm Hg or/and diastolic BP

23.1 (2.5)

≥90 mm Hg or use of antihypertensive medication and three

defined as self-reported hypertension. Results of cohort
study quality assessment (score 0–9) yielded an average
score of 7.78 (Supplementary Table 2).
Age (mean)

26.3 (2.4)

High vs. low coffee consumption analysis

OR odd ratio, RR relative risk, HR hazard ratio, CI confidence interval, M men, W women

The pooled results of different levels of coffee consumption

Follow-up period (years)

categories compared with the lowest category are shown in

Fig. 2. Compared with the lowest category (median con-
sumption 0 cups/day), the pooled RR for incident hyper-
33

tension was 0.95 (95% CI 0.91–0.99, I2 = 44.0%,

Pheterogeneity = 0.066) for individuals in the highest category
of consumption (6.2 cups/day), 0.96 (95% CI 0.89–1.03,
I2 = 61.8%, Pheterogeneity = 0.011) for individuals in the
second highest category of consumption (4.5 cups/day),
Gender (M/W)

1.02 (95% CI 0.97–1.06, I2 = 58.9%, Pheterogeneity = 0.017)

M

for individuals in the third highest category of consumption

(1.5 cups/day). In the sensitivity analyses, removing one
study at a time did not change the pooled risk substantially
in any of the three coffee consumption levels. We found no
America
Region

evidence of publication bias for the highest (P = 0.305), for

the second highest (P = 0.393), and for the third highest
level of coffee consumption (P = 0.154) vs. the lowest
consumption by Egger’s test.

Dose–response analysis of coffee consumption with

Table 1 (continued)

risk of hypertension
Klag et al. [9]
First author

Data from 10 cohort studies were included in the linear

dose–response analysis of coffee consumption with risk of
hypertension. The risk of hypertension was reduced by 2%
 C. Xie et al.

Fig. 2 Forest plot of relative risks (RRs) and 95% CIs for the asso- cups/day), the pooled RR for incident hypertension was 0.95 (95% CI
ciation between coffee consumption and hypertension risk in cohort 0.91–0.99, I2 = 44.0%) for the highest category of consumption, 0.96
studies. Compared with the lowest category (median consumption 0 (0.89–1.03, I2 = 61.8%) for the second highest, and 1.02 (0.97–1.06,
I2 = 58.9%) for the third highest category of coffee consumption
Fig. 3 Risk of incident
hypertension for each 1cup/day
increment in coffee
consumption. RR relative risk,
CI confidence interval, M men,
W women
(RR = 0.98, 95% CI 0.98–0.99) with each one cup/day
increment of consumption (Fig. 3).
We found no evidence of nonlinear association between
coffee consumption and hypertension risk (Pnonlinearity =
0.243); therefore, restricted cubic spline was adopted to
model the linear dose–response association. We found a
linear negative correlation between coffee consumption and
risk of hypertension (Fig. 4). Compared to those with no
coffee consumption, the RR estimated directly from the
cubic spline model was 0.97 (95% CI 0.95–0.99) for two
cups/day, 0.95 (95% CI 0.91–0.99) for four cups/day, 0.92
(95% CI 0.87–0.98) for six cups/day, and 0.90 (95% CI
0.83–0.97) for eight cups/day.
Subgroup, sensitivity analyses, and publication bias
To explore the sources of heterogeneity, we performed
subgroup analyses by study design, gender, age, region,
diagnostic criteria, number of cases, the covariates (age,
smoking, alcohol consumption, physical activity, family
Fig. 4 Linear dose–response association between coffee consumption
and hypertension modeled by using restricted cubic spline
history of hypertension, education, intake of sodium, and
BMI) adjusted in the analysis (Table 2). In general, the
association was consistent in most analyses. The hetero-
geneity appeared to be lower in Americans, age >50 years
old and number of case ≥1000 populations, with I2 reduced
to 0.0%, 12.7%, and 28.3%, respectively. No significant
changes of heterogeneity occurred in other subgroup
analyses.
When performing sensitivity analyses by removing one
study at a time, none of the individual studies changed the
pooled risk substantially. No publication bias was detected
by Egger’s test (P = 0.618).
Discussion
The findings from this systematic review and meta-analysis,
based on 247,659 participants and 54,639 incident cases of
hypertension, demonstrate an inverse association between
risk of hypertension and coffee consumption, with a
reduction of 2% per one cup/day increment of coffee con-
sumption. With the linear cubic spline model, the RRs of
hypertension risk were 0.97 (95% CI 0.95–0.99), 0.95 (95%
CI 0.91–0.99), 0.92 (95% CI 0.87–0.98), and 0.90 (95% CI
0.83–0.97) for 2, 4, 6, and 8 cups/day, respectively, com-
pared with individuals with no coffee intakes.
Controversy exists in the current studies investigating the
effects of coffee intake on hypertension risk. In a meta-
analysis of five cohort studies, Zhang et al. found an inverse
J-shaped association between caffeinated coffee intake and
hypertension risk, with the risk increasing with up to three
cups coffee/day compared with less than one cup/day and
then decreasing at higher intakes [18]. On the basis of the
same original studies, Steffen et al. reported opposite find-
ings, suggesting no statistically significant effect of coffee
 C. Xie et al.

Table 2 Dose–response subgroup analysis of risk of hypertension with coffee consumption

Subgroups No. of studies Coffee consumption, per one cup/day
RR (95% CI) P-valuea I2 (%)

All studies 10 0.98 (0.98–0.99) 0.072 42.9

Sex
Men 2 1.01 (0.96–1.05) 0.671 0.0
Women 4 0.98 (0.97–0.99) 0.413 0.0
Both 4 0.99 (0.96–1.02) 0.018 70.3
Age
≤50 6 0.99 (0.97–1.01) 0.042 56.6
>50 4 0.98 (0.97–0.99) 0.329 12.7
Region
America 4 0.98 (0.97–0.99) 0.587 0.0
Europe 5 0.99 (0.95–1.02) 0.035 61.3
Asia 1 0.97 (0.95–1.00) – –
Diagnostic criteria
Objective evaluationb 5 0.99 (0.97–1.00) 0.195 34.0
Self-reported 3 0.98 (0.97–0.99) 0.752 0.0
No. of cases
N < 1000 4 1.00 (0.97–1.03) 0.063 59.0
N ≥ 1000 6 0.98 (0.98–0.99) 0.222 28.3
Adjustment
Age
Yes 9 0.98 (0.98–0.99) 0.064 45.8
No 1 1.02 (0.95–1.10) – –
Smoking
Yes 10 0.98 (0.98–0.99) 0.072 42.9
No 0 – – –
Alcohol consumption
Yes 10 0.98 (0.98–0.99) 0.072 42.9
No 0 – – –
Physical activity
Yes 8 0.98 (0.98–0.99) 0.003 46.9
No 2 0.97 (0.91–1.03) 0.132 56.0
Family history of hypertension
Yes 4 0.98 (0.98–0.99) 0.087 54.4
No 6 0.99 (0.97–1.00) 0.121 42.6
Education
Yes 5 0.98 (0.97–1.00) 0.075 52.9
No 5 0.98 (0.98–0.99) 0.125 44.5
Intake of sodium
Yes 3 0.98 (0.96–1.00) 0.179 41.8
No 7 0.98 (0.98–0.99) 0.058 50.7
BMI
Yes 8 0.98 (0.98–0.99) 0.003 46.9
No 2 0.97 (0.91–1.03) 0.132 56.0
RR relative risk, CI confident interval, SBP systolic blood pressure.
a
Estimated by the Cochran’s Q test
b
Hypertension was defined as SBP ≥ 140 mm Hg or/and DBP ≥ 90 mm Hg or use of antihypertensive medication
consumption on the risk of hypertension [17]. Given that
three additional articles have been published since the
previous two meta-analyses and the inconsistent results
between them, a more precise method is needed to access
the association of coffee consumption with hypertension
risk.
The linear inverse association between coffee consump-
tion and hypertension risk might be true based on plausible
biological mechanisms. First, coffee is rich in BP-lowering
minerals (that is, vitamin E, niacin, potassium, and mag-
nesium) and antioxidant compounds (polyphenols) that may
have the antihypertensive effects of caffeine [31, 32]. Sec-
ond, coffee consumption lowers the risk of type 2 diabetes
(the consequences of hyperinsulinemia and insulin resis-
tance) [33]; moreover, hyperinsulinemia and insulin resis-
tance may contribute to hypertension via the effects of
insulin on the retention of sodium increasing sympathetic
nervous system activity and vascular smooth muscle pro-
liferation [34], for another possible mechanism of the
antihypertensive effect of coffee.
Except for the mechanisms mentioned above, genetics,
smoking, alcohol consumption, and other aspects of the diet
may modify the effects of coffee intakes on hypertension
[35].There have been several studies certifying that the
background characteristics, such as smoking and alcohol
use, influence the effect of coffee on hypertension risk [14,
36, 37]. Almost all the included studies have adjusted the
confounding factors, and the pooled results remained to be
significantly negative correlation, indicating the consistency
of the findings. Previous reports have suggested that
obvious inter-individual differences in the sensitivity of the
coffee effect were mainly due to the variants of caffeine
metabolism-related gene [35, 38–40]. Given that only a few
studies investigated the role of genes in the association of
coffee consumption with hypertension risk, further resear-
ches based on genetic aspects are warranted.
To discover potential sources of heterogeneity, we per-
formed various analyses, and the results generally supported
our overall finding. We found that the presence of hetero-
geneity among studies may be related to geographical area.
A slight reduction of hypertension risk and no heterogeneity
were observed among studies conducted in Americans
rather than Europeans, perhaps because of varied coffee
composition, different types of coffee powder, and serving
size across countries. In addition, different genotypes and
gene–environment interactions may partially explain the
discrepancy across regions. Results from studies stratified
by sex were more consistent and robust than from studies of
mixed gender, indicating an interaction with hypertension
risk of coffee intake between men and women (such as the
different habits of coffee consumption and body constitu-
tions), which suggest us to separate them while analyzing
the relationship in the future [11].
Our meta-analysis contains several strengths. Primarily,
the meta-analysis included 10 high-quality cohort studies
and a large number of participants, minimizing the potential
sampling error and providing sufficient power to detect the
association. Also, a dose–response analysis was also per-
formed to clarify the quantitative estimation of the asso-
ciation between hypertension risk and coffee consumption,
which provided a comprehensive description of the shape of
the relationship. What’s more, the large number of studies
enabled us to conduct subgroup analyses based on study
design, sex, age, region, BMI, diagnostic criteria, number of
cases, the covariates' adjustment, and sensitivity analyses to
clarify the consistency and robustness of the results.
However, the limitations of the study should also be
considered. All of the studies were observational, of which
the inherent residual confounding may affect them to reach
more plausible conclusion. Nevertheless, because of the
observational nature of the studies, a causal relationship
cannot be established with these data alone. Moreover,
almost all of the exposures of coffee intakes were measured
by self-reporting questionnaires, which is inevitable to
introduce the misclassification of exposure. However,
results from validation studies indicated that self-reported
questionnaires can assess the coffee consumption with
relatively high validity [41, 42]. Furthermore, information
on the type of coffee (such as caffeinated and decaffeinated
coffee) and the size of standard coffee cups was limited.
Whether caffeinated and decaffeinated coffee have different
effects on BP and hypertension risk is not clear till now [10,
43]. Also, the different size of coffee cups can distort the
real relationship. Finally, we included only English lan-
guage publications because of resource constraints. How-
ever, small study bias (including publication bias) was
investigated by the funnel plot and Egger’s test, with no
such bias detected.
Conclusion
In conclusion, this meta-analysis provides quantitative evi-
dence that consumption of coffee was inversely associated
with the risk of hypertension in a dose–response manner.
Longer-term randomized controlled trials are needed to
establish causality and testify the true association.
Summary
What is known about this topic?
● Coffee consumption has attracted interest as a potential
risk factor due to an acute pressor effect of caffeine on
blood pressure, but the long-term effect on hypertension
risk remains controversial.

● Given the different definitions of coffee exposure among
studies, the association between coffee consumption and
risk of hypertension could not be analyzed precisely.
What this study adds?
● The risk of hypertension was reduced by 2% (RR=0.98,
95% CI: 0.98-0.99) with each 1 cup/day increment of
coffee consumption.
● Compared with individuals with no coffee intakes, the
RRs of hypertension risk were 0.97 (95% CI: 0.95-0.99),
0.95 (95% CI: 0.91-0.99), 0.92 (95% CI: 0.87-0.98), and
0.90 (95% CI: 0.83-0.97) for 2, 4, 6 and 8 cups/day,
respectively.
Acknowledgments This research was supported by the National
Social Science Foundation of China (Grant number 15BSH043). This
research was supported by the National Social Science Foundation of
China (Grant number 15BSH043). The National Social Science
Foundation of China had no role in the design/conduct of the study,
collection/analysis interpretation of the data, and preparation/review
approval of the manuscript.
Compliance with Ethical Standards
Conflict of interest The authors declare that they have no competing
financial interest.
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