Hypertension Research (2020) 43:948–955

https://doi.org/10.1038/s41440-020-0439-8

ARTICLE

Association of triglycerides to high-density lipoprotein-cholesterol

ratio with risk of incident hypertension
Dechen Liu1 Li Guan2,3 Yang Zhao1 Yu Liu2,3 Xizhuo Sun2,3 Honghui Li2,3 Zhaoxia Yin2,3 Linlin Li1
● ● ● ● ● ● ● ●

Yongcheng Ren1 Bingyuan Wang1 Cheng Cheng1 Leilei Liu1 Xu Chen1 Qionggui Zhou3 Quanman Li1
● ● ● ● ● ● ●

Chunmei Guo1 Gang Tian1 Ming Zhang3 Dongsheng Hu1 Jie Lu1
● ● ● ●

Received: 7 November 2019 / Revised: 15 March 2020 / Accepted: 17 March 2020 / Published online: 24 April 2020
© The Japanese Society of Hypertension 2020

Abstract
The triglyceride to high-density lipoprotein-cholesterol (TG/HDL-C) ratio is considered a simple surrogate of insulin
resistance. The aim of this study was to explore the association of the TG/HDL-C ratio with the risk of incident hypertension
and whether the TG/HDL-C ratio mediates the obesity–incident hypertension association. The study analyzed 9679
participants from a rural Chinese population. Demographic and anthropometric and laboratory data were collected at
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baseline (2007–2008) and follow-up (2013–2014) examinations. A multivariate logistic regression model was used to
analyze the association of the TG/HDL-C ratio with incident hypertension, estimating odds ratios (ORs) and 95% confidence
intervals (CIs). Mediation analysis was performed to examine the contribution of the TG/HDL-C ratio to obesity-related
incident hypertension. During a median follow-up of 6.00 years, hypertension developed in 1880/9679 participants
(19.42%). The risk of incident hypertension was higher in the highest TG/HDL-C ratio quartile than in the lowest quartile
(OR = 1.21, 95% CI = 1.02–1.42). Subgroup analyses showed that the risk of incident hypertension was increased by 30%,
36%, and 33% among women, participants < 60 years old and those with prehypertension at baseline, respectively. The TG/
HDL-C ratio partially mediated the obesity–incident hypertension association (indirect effect: OR = 1.04, 95% CI:
1.01–1.07; direct effect: OR = 1.36, 95% CI: 1.16–1.62). The TG/HDL-C ratio may be a risk factor for incident
hypertension, especially in women, participants < 60 years old and those with prehypertension. The TG/HDL-C ratio may
also play a mediating role in obesity-related incident hypertension.
Keywords Hypertension Triglycerides High-density lipoprotein cholesterol Obesity
● ● ●

Introduction

Hypertension is a major risk factor for cardiovascular dis-

Supplementary information The online version of this article (https://
doi.org/10.1038/s41440-020-0439-8) contains supplementary
material, which is available to authorized users.
* Jie Lu
Hanyaa800@163.com
1
Department of Epidemiology and Health Statistics, College of
Public Health, Zhengzhou University, Zhengzhou, Henan,
People’s Republic of China
2
The Affiliated Luohu Hospital of Shenzhen University Health
Science Center, Shenzhen, Guangdong, People’s Republic of
China
3 Insulin resistance is associated with hypertension [6, 7].
Department of Epidemiology and Health Statistics, College of
Public Health, Shenzhen University, Shenzhen, Guangdong,
People’s Republic of China
ease and death, and it has become a crucial public health
problem worldwide [1]. The global prevalence of hyper-
tension in adults reached 31.1% in 2010 and is predicted to
increase to 60% in 2025 [2, 3]. At least 7.6 million pre-
mature deaths worldwide were attributed to hypertension,
accounting for 13.5% of all-cause deaths in 2001 [4].
Moreover, hypertension was the leading risk factor con-
tributing to ~211.8 million global disability-adjusted life
years in 2015 [5]. Therefore, due to the negative impact of
hypertension, its related risk factors must be identified as
early as possible to effectively prevent its incidence and
reduce its disease burden.
The hyperinsulinemic euglycemic glucose clamp is the gold
standard method for measuring insulin resistance; however,
Association of triglycerides to high-density lipoprotein-cholesterol ratio with risk of incident. . .
this method is impractical because it is labor- and time-
intensive [8]. Thus, an inexpensive and reliable surrogate
indicator of insulin resistance is urgently needed. Recently,
the ratio of triglycerides to high-density lipoprotein cho-
lesterol (TG/HDL-C ratio) proposed by Gaziano et al. has
been considered a simple surrogate indicator of insulin
resistance [9, 10]. Previous studies have found that the TG/
HDL-C ratio is associated with type 2 diabetes mellitus
[11], cardiovascular events [12], and even death [13].
However, the studies focused on the association of the TG/
HDL-C ratio with hypertension were conducted in Europe
or other countries in Asia [14, 15], and data in rural areas in
China were limited. In addition, previous studies have
demonstrated that obesity is associated with insulin resis-
tance and probably with hypertension [6, 7, 16, 17], so
insulin resistance may be a mediator in obesity-related
incident hypertension.
Thus, we explored the association between the TG/HDL-
C ratio and the risk of incident hypertension in all partici-
pants and in participants grouped by sex, age, and blood
pressure (BP) status at baseline in a rural Chinese popula-
tion. An additional objective was to assess whether the TG/
HDL-C ratio mediated the association between obesity
measured by body mass index (BMI) and incident
hypertension.
Methods
Study population and design
The Rural Chinese Cohort Study enrolled a total of 20,194
adults over 18 years old from the rural area in Luoyang
City, Henan Province, in the middle of China [18]. The
baseline examination was performed from July to August
2007 and July to August 2008. At the baseline examina-
tion, the study participants were free of severe psycho-
logical disorders, physical disabilities, Alzheimer’s
disease, dementia, tuberculosis, AIDS, and other infec-
tious diseases. All participants were invited to participate
in the follow-up examination from July to August 2013
and July to October 2014, and 17,265 participants were
re-investigated (response rate 85.5%; 2929 participants
were lost to follow-up). We excluded participants with
hypertension at baseline (n = 6299), participants who
received lipid-lowering treatment (n = 799), and partici-
pants who had incomplete data for TG, HDL-C, or BMI at
baseline or BP at follow-up (n = 3417). Finally, 9679
eligible participants were included in the present study.
All participants provided informed consent, and the ethics
committee of Zhengzhou University approved the
present study.
949
Data collection
At the baseline examination, questionnaires were adminis-
tered during face-to-face interviews by trained interviewers
to collect data on demographic characteristics (age, sex,
educational level, and marital status) and personal behaviors
(smoking, alcohol consumption, and physical activity).
Smoking was defined as currently smoking and/or smoking
100 cigarettes in one’s life [18]. Participants who had
consumed alcohol at least 12 times during the past year
were considered alcohol consumers [18]. According to the
International Physical Activity Questionnaire, physical
activity was classified as low, moderate, or high [19].
Anthropometric data were collected with participants in
light clothes and barefoot. Body weight and height were
measured twice to the nearest 0.5 kg and 0.1 cm, respec-
tively, by trained investigators according to a standard
protocol. BMI (kg/m2) was calculated as weight (kg) divi-
ded by height (m) squared. According to the Working
Group on Obesity in China, the Chinese standard of general
obesity was defined as follows: BMI < 18.5 kg/m2, under-
weight; 18.5–24 kg/m2, normal weight; 24–28 kg/m2,
overweight; and ≥28 kg/m2, obese [20]. According to the
American Heart Association standardized protocol, BP was
measured three times by trained investigators on the
unclothed right upper arm by using an electronic sphyg-
momanometer (HEM-770AFuzzy, Omron, Japan) at inter-
vals of 30 s, with participants in a seated position after 5 min
of rest [21]. The means of both anthropometric and BP
measurements were used for the analyses. Participants with
systolic BP (SBP) ≥ 140 mmHg or diastolic BP (DBP) ≥ 90
mmHg or current use of antihypertension medication were
considered to have hypertension, and those with SBP ≥ 120
and <140 mmHg and DBP ≥ 80 and <90 mmHg and without
the use of any antihypertension medication were considered
to have prehypertension [22].
Overnight fasting blood samples were collected into
vacuum tubes to assess fasting plasma glucose (FPG), total
cholesterol (TC), TG, and HDL-C. FPG, TC, TG, and
HDL-C were measured by using a HITACHI automatic
clinical analyzer (Model 7060, Tokyo). The TG/HDL-C
ratio was calculated as TG divided by HDL-C (both
expressed in milligrams/deciliter) [10]. Details about the
storage and measurement methods were published pre-
viously [18].
Follow-up data were collected from July to August 2013
and July to October 2014. For the baseline examination,
follow-up data were collected by questionnaires and
anthropometric and laboratory measurements. New-onset
hypertension was diagnosed according to both SBP and
DBP and current use of antihypertension medication at
follow-up.
950
Statistical analyses
Continuous data are presented as the median (interquartile
range [IQR]), and categorical data are presented as the
number (percentage) by quartiles of the TG/HDL-C ratio.
Participants were classified into four groups based on four
quartiles of baseline TG/HDL-C ratio: quartile 1 (<1.69),
quartile 2 (1.69–2.53), quartile 3 (2.53–3.93), and quartile 4
(≥3.93). The linear trend for baseline characteristics was
calculated by linear regression for continuous variables and
logistic regression for categorical variables. Participants
were also classified as having normal or new-onset hyper-
tension. The Wilcoxon rank sum test or chi-square test was
used to test differences in baseline characteristics between
normal and new-onset hypertension participants.
Because of the lack of data on hypertension onset, a
multivariate logistic regression model was used to estimate
odds ratios (ORs) and 95% confidence intervals (CIs) of
developing hypertension for each quartile of the TG/HDL-C
ratio in all participants and by sex, age, and BP status at
baseline, with quartile 1 considered the reference group. In
addition to the unadjusted model (model 1), two other
models were fitted: model 2 was adjusted for sex, age,
educational level, marital status, smoking, alcohol con-
sumption, and physical activity, and model 3 was adjusted
for variables included in model 2 plus obesity, SBP and
FPG and TC. The linear trends across TG/HDL-C ratio
categories were evaluated by using the median TG/HDL-C
ratio value within each quartile as a continuous variable.
Tests for the interaction between the TG/HDL-C ratio and
age, BP status at baseline and effects on the risk of incident
hypertension involved multivariate logistic regression
models adjusted for the same covariates as those listed for
model 3 above. In addition, previous epidemiologic studies
have conventionally taken sex differences into account
[23, 24], so we explored sex differences in the association
between the TG/HDL-C ratio and the risk of incident
hypertension.
Mediation analysis involved using the PROCESS pro-
cedure in SAS v9.4 [25]. Baseline obesity status was the
independent variable (X), incident hypertension was the
dependent variable (Y), and the baseline TG/HDL-C ratio
was the mediator variable (M). The associations among the
three variables are shown in Fig. 1: (1) the total effect of the
exposure (obesity) on the outcome (incident hypertension)
(path c); (2) the effect of the exposure variable (obesity) on
the changes in the mediator (baseline TG/HDL-C ratio)
(path a); (3) the association between the mediator (baseline
TG/HDL-C ratio) and the outcome (incident hypertension)
(path b); and (4) the direct effect of the exposure (obesity)
on the outcome (incident hypertension), keeping the effect
of the baseline TG/HDL-C ratio constant (path c′). Struc-
tural equation modeling was used to conduct mediation
D. Liu et al.
Fig. 1 The simple multiple mediator model of the association between
obesity, the ratio of triglycerides to high-density lipoprotein choles-
terol (TG/HDL-C ratio), and incident hypertension. Path c reflects the
total effect, path c′ reflects the direct effect and path ab reflects the
indirect effect
analysis to explore whether obesity-related incident hyper-
tension was explained by the TG/HDL-C ratio. The med-
iation analysis was adjusted for the same covariates as those
adjusted in the multivariable logistic regression model.
Complete mediation indicated a statistically significant
indirect effect and a nonsignificant direct effect between
obesity and hypertension; partial mediation indicated sta-
tistically significant direct and indirect effects, which sig-
nifies that multiple mediating factors are involved [26].
All statistical analyses were performed using SAS v9.4
(SAS Institute, Cary, NC). All P-values were two-sided,
with P < 0.05 considered statistically significant.
Results
A total of 9679 participants were enrolled for the baseline
examination (5813 women). The median (IQR) TG/HDL-C
ratio was 2.53 (1.69–3.93). The baseline characteristics of
all participants by quartiles of the TG/HDL-C ratio are
presented in Table 1. Age, SBP, DBP, FPG, TC and TG
levels increased and HDL-C decreased with quartiles of the
TG/HDL-C ratio (all Ptrend < 0.05). Compared with partici-
pants in quartile 1 of the TG/HDL-C ratio, those in higher
quartiles more frequently smoked, consumed alcohol, were
married/cohabiting and were obese. Participants with new-
onset hypertension were more frequently older, female, and
less educated; had low HDL-C levels but high SBP, DBP,
and FPG, TC, and TG levels; and were less frequently
married/cohabitating than those with normal BP (all P <
0.05) (Supplementary Table 1).
During a median follow-up of 6.00 years, 1880/9679
(1109/5813 women) participants developed hypertension.
Compared with the reference quartile, the highest TG/HDL-C
ratio quartile (≥3.93) was positively associated with the risk
of incident hypertension (OR 1.21, 95% CI 1.02–1.42)
(Table 2). As the TG/HDL-C ratio quartiles increased, the
Association of triglycerides to high-density lipoprotein-cholesterol ratio with risk of incident. . . 951

Table 1 Baseline characteristics of study population based on quartiles of triglycerides to high-density lipoprotein cholesterol ratio
(TG/HDL-C ratio)
Baseline characteristic TG/HDL-C ratio quartiles Ptrend
Quartile 1 (<1.69) Quartile 2 (1.69–2.53) Quartile 3 (2.53–3.93) Quartile 4 (≥3.93)

n 2418 2423 2418 2420

Age (years) 44.00 (37.00–55.00) 46.00 (39.00–57.00) 49.00 (41.00–57.00) 49.00 (41.00–57.00) <0.001
Men 840 (34.74) 935 (38.59) 1009 (41.73) 1082 (44.71) <0.001
High school or above 275 (11.37) 256 (10.57) 270 (11.17) 271 (11.20) 0.978
Married/cohabiting 2214 (91.56) 2248 (92.78) 2260 (93.58) 2264 (93.55) 0.004
Smoking 576 (23.82) 669 (27.61) 735 (30.40) 798 (32.98) <0.001
Alcohol consumption 260 (10.75) 271 (11.18) 315 (13.03) 371 (15.33) <0.001
Physical activity 0.475
Low 635 (26.26) 641 (26.45) 582 (24.07) 640 (26.45)
Moderate 508 (21.01) 498 (20.55) 541 (22.37) 555 (22.93)
High 1275 (52.73) 1284 (52.99) 1295 (53.56) 1225 (50.62)
Obesity 89 (3.68) 187 (7.72) 282 (11.66) 432 (17.85) <0.001
SBP (mmHg) 112.67 (105.33–121.67) 115.33 (107.67–123.67) 116.67 (108.67–125.33) 118.33 (109.67–126.00) <0.001
DBP (mmHg) 71.67 (66.33–77.00) 73.33 (68.00–78.67) 74.33 (69.00–79.67) 75.67 (70.33–80.67) <0.001
FPG (mmol/L) 5.18 (4.85–5.52) 5.23 (4.90–5.60) 5.30 (4.98–5.69) 5.43 (5.11–5.93) <0.001
TC (mmol/L) 4.05 (3.56–4.63) 4.20 (3.69–4.80) 4.35 (3.82–4.91) 4.55 (3.94–5.18) <0.001
TG (mmol/L) 0.74 (0.62–0.87) 1.08 (0.95–1.24) 1.49 (1.30–1.70) 2.39 (1.97–3.13) <0.001
HDL-C (mmol/L) 1.36 (1.21–1.55) 1.20 (1.06–1.35) 1.09 (0.97–1.22) 0.97 (0.86–1.09) <0.001
Data are number (percentage) or median (interquartile range)
SBP systolic blood pressure, DBP diastolic blood pressure, FPG fasting plasma glucose, TC total cholesterol, TG triglycerides, HDL-C high-
density lipoprotein cholesterol

Table 2 Risk of incident hypertension by TG/HDL-C ratio in all participants

Quartiles of TG/HDL-C ratio Total Hypertension cases Incidence (%) OR (95% CI)
Model 1a Model 2b Model 3c

Q1 (<1.69) 2418 365 15.10 1.00 1.00 1.00

Q2 (1.69–2.53) 2423 448 18.49 1.28 (1.10–1.48) 1.22 (1.04–1.42) 1.07 (0.91–1.27)
Q3 (2.53–3.93) 2418 507 20.97 1.49 (1.29–1.73) 1.38 (1.18–1.60) 1.11 (0.95–1.31)
Q4 (≥3.93) 2420 560 23.14 1.69 (1.46–1.96) 1.59 (1.37–1.84) 1.21 (1.02–1.42)
P for trend <0.001 <0.001 0.024
Per unit increase 1.06 (1.04–1.08) 1.06 (1.04–1.08) 1.03 (1.01–1.05)
Data are odds ratios (OR) and 95% confidence intervals (CI)
a
No adjusted variable
b
Adjusted for sex, age, marital status, educational level, smoking, alcohol consumption, and physical activity
c
Adjusted for variables inb as well as obesity, systolic blood pressure, fasting plasma glucose, and total cholesterol

risk of incident hypertension increased substantially for all
participants (Ptrend = 0.024).
Tests for multiplicative interaction demonstrated that age
and BP status at baseline modified the association of the
TG/HDL-C ratio with the risk of incident hypertension
(P = 0.019 and P < 0.001). Therefore, we performed sub-
group analyses by age, sex, and BP status at baseline.
Figure 2 shows the association of the TG/HDL-C ratio with
incident hypertension by sex, age, and BP status at baseline.
Among women, participants < 60 years old and those with
prehypertension, compared with the reference quartile, the
highest TG/HDL-C ratio quartile was associated with a
30%, 36%, and 33% increased risk of incident hyperten-
sion, respectively. No appreciable association was found
among men, participants ≥ 60 years old or those with
normal BP.
Table 3 presents the results of the mediating role of the
TG/HDL-C ratio in the obesity–incident hypertension
952 D. Liu et al.

Fig. 2 Association of the TG/HDL-C ratio with incident hypertension status, educational level, smoking, alcohol consumption, physical
by sex, age and status of blood pressure at the baseline examination. activity, obesity, systolic blood pressure, fasting plasma glucose, and
The superscripted a indicates that no variables were adjusted. The total cholesterol at baseline
superscripted b means the model was adjusted for sex, age, marital

association. The total effect of obesity on incident hyper- Table 3 Mediation analysis to determine the association between
tension was significant (OR = 1.42, 95% CI = 1.20–1.67). obesity and incident hypertension via TG/HDL-C ratio in all
participants
The TG/HDL ratio partially mediated the association
between obesity and incident hypertension, with a sig- Parameter estimate OR (95% CI)
(95% CI)a
nificant indirect effect (OR = 1.04, 95% CI = 1.01–1.07)
and direct effect (OR = 1.36, 95% CI = 1.15–1.62); 11.43% Direct effect—path c′ 0.31 (0.14–0.48) 1.36 (1.15–1.62)
of the total effect was explained by the specified mediator. Path a 1.23 (1.06–1.40) –
Path b 0.03 (0.01–0.05) 1.03 (1.01–1.05)
Indirect effect—path ab 0.04 (0.01–0.07) 1.04 (1.01–1.07)
Discussion Total effect—path c 0.35 (0.18–0.51) 1.42 (1.20–1.67)
Proportion mediated, % 11.43 (5.56–13.73)
Our study demonstrated that the TG/HDL-C ratio was (95% CI)b
positively associated with incident hypertension, especially
Path a: the exposure variable (obesity) affects changes in the
in women, participants < 60 years old and those with pre- hypothesized mediator (baseline TG/HDL-C ratio); Path b: the
hypertension at baseline, and it partially mediated the association between the mediator (baseline TG/HDL-C ratio) and the
association between obesity and incident hypertension. outcome (incident hypertension); Path c: the total effect of exposure
(obesity) on the outcome (incident hypertension); Path c′: the direct
The results of the association between the TG/HDL-C
effect of exposure variable (obesity) on the outcome (incident
ratio and hypertension are not consistent [14, 15, 27, 28]. In hypertension), holding the effect of baseline TG/HDL-C ratio constant
European populations, a Spanish cohort study and an a
Adjusted for sex, age, marital status, educational level, smoking,
Eastern Finnish cohort study both showed similar results for alcohol consumption, physical activity, systolic blood pressure, fasting
the association. The Spanish cohort study with a mean 8.49- plasma glucose, and total cholesterol
b
year follow-up reported that the TG/HDL-C ratio was Proportion mediated was calculated by [In (indirect effect)/In (total
associated with hypertension only in men; in the fifth effect)]
quintile of the TG/HDL-C ratio, the risk of hypertension
increased by ~90% [14]. The Eastern Finnish cohort study, with incident hypertension; with a one-standard deviation
focusing on middle-aged men with a 7-year follow-up, also change, the risk of hypertension increased by ~52% [28].
showed that the TG/HDL-C ratio was positively associated For Asian populations, a cohort study of Middle Eastern
Association of triglycerides to high-density lipoprotein-cholesterol ratio with risk of incident. . .
women with a median 6.4-year follow-up found that in the
fourth quartile of the TG/HDL-C ratio, the risk of hyper-
tension increased by ~71%, which was similar to our
findings [15]. Only one cross-sectional study of Korean
male adults showed that the TG/HDL-C ratio was not
associated with hypertension [27]. The different results
between European and Asian studies may be due to the
ethnicity of participants because the association of the TG/
HDL-C ratio with the risk of incident hypertension may
vary according to ethnicity [29].
The association of insulin resistance with hypertension
may be explained by the following mechanism. Insulin
resistance has a certain inhibitory effect on the synthesis
of nitric oxide in endothelial cells, blocking capillary
recruitment, reducing blood flow, and decreasing the
uptake of glucose and fatty acids [30, 31]. In addition,
with insulin resistance, adipose tissue compensates for
increased insulin secretion to ensure glucose and fatty
acid intake [32]; however, excess insulin in the blood may
further stimulate the activity of the renin-angiotensin-
aldosterone system (RAAS), causing sympathetic activa-
tion, promoting the indirect absorption of H2O and Na+,
impairing sodium excretion from the kidney, leading to
water sodium retention, and increasing the vascular
activity of noradrenaline and AT-II to finally cause
hypertension [33–37].
A previous study demonstrated sex differences in the
association of increased interleukin six levels with the risk
of developing insulin resistance, as well as an increased risk
of hypertension in individuals with elevated C-reactive
protein levels; both associations were found only in women,
which may explain the sex difference in the association
between insulin resistance and the risk of hypertension [38].
The aging of the body results in a variety of physiological
changes, especially in the cardiovascular system, such as the
loss of elastin fibers and the accumulation of stiffer collagen
fibers [39, 40], and the effect of this change on the devel-
opment of hypertension may outweigh the effect of insulin
resistance. For participants with different BP statuses, one
possible explanation is that participants with prehyperten-
sion had a higher TG/HDL-C ratio than those with normal
BP at baseline in our study, so the association of the TG/
HDL-C ratio with incident hypertension may be more sig-
nificant in participants with prehypertension than in those
with normal BP.
Our results showed that obesity could increase the TG/
HDL-C ratio in rural Chinese individuals. Studies have
shown that obesity leads to insulin resistance, a process that
involves a complex interplay of genetic and environmental
factors [16, 17, 41]. Our study found that the TG/HDL-C
ratio was significantly associated with the risk of incident
hypertension. The partial mediation of the TG/HDL-C ratio
on the obesity–incident hypertension association suggests
953
that the mechanism remains unclear. The mechanism of
obesity-induced hypertension is complex; in addition to
insulin resistance, other mechanisms are involved: (1)
changes in the leptin pathway, (2) microvascular dysfunc-
tion, (3) activation of the RAAS and sympathetic nervous
system, (4) dysfunction of the central nervous system, (5)
kidney damage, and (6) immune and inflammatory
mechanisms, genetic factors, and fat afferent reflex [42–46].
Although insulin resistance is considered a key link
between obesity and hypertension, it could only be one
pathway mediating this association because of the complex
mechanism [47].
The TG/HDL-C ratio is a risk factor for hypertension. To
our knowledge, this is the first large cohort study examining
the association of obesity with incident hypertension
mediated by the TG/HDL-C ratio in rural Chinese people.
In addition, compared with traditional methods with normal
distribution assumed in the sampling, bootstrapping has
advantages in evaluating the indirect or direct effect of 95%
CIs [48].
However, the present study has some limitations. First,
participants were recruited from only one county in the
middle of China; therefore, the results cannot be generalized
to other populations with certainty. Second, dietary factors
may lead to the occurrence of dyslipidemia, but the study
did not analyze the effect of this factor because of insuffi-
cient dietary data [49]. Third, leptin or other metabolic
factors associated with obesity-induced hypertension should
be considered in future studies [50]. Fourth, selection bias
seemed unavoidable in this study.
In conclusion, the TG/HDL-C ratio was positively
associated with the risk of incident hypertension in a rural
Chinese population, especially in women, participants < 60
years old and those with prehypertension at the baseline
examination. The TG/HDL-C ratio may help identify peo-
ple at early risk of future hypertension independent of other
risk factors, and more attention should be given to
those with a higher TG/HDL-C ratio. In addition, the
obesity–incident hypertension association is partially
explained by a high TG/HDL-C ratio, which could provide
epidemiological evidence of a cause of the association.
Acknowledgements DL, JL, and DH substantially contributed to the
design and drafting of the study and the analysis and interpretation of
the data. LG, YZ, YL, XS, HL, ZY, LiL, YR, BW, CC, LeL, XC, QZ,
QL, CG, GT, and MZ revised the paper critically for important
intellectual content. The investigators are grateful to the dedicated
participants and all research staff involved in the study. All authors
were involved in the collection of data and approved the final version
of the paper.
Funding This study was supported by the National Natural Science
Foundation of China (grant nos. 81373074, 81402752, and 81673260)
and the Natural Science Foundation of Guangdong Province (grant no.
2017A030313452).
954
Compliance with ethical standards
Conflict of interest The authors declare that they have no conflict of
interest.
Publisher’s note Springer Nature remains neutral with regard to
jurisdictional claims in published maps and institutional affiliations.
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