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OPEN Association of different obesity

patterns with hypertension in US
male adults: a cross‑sectional study
Lu Chen 1,5, Jun Zhang 1,5, Nan Zhou 3*, Jia‑Yi Weng 1*, Zheng‑Yang Bao 2* & Li‑Da Wu 4*

Obesity is an important risk factor for hypertension. We aimed to investigate the association between
different obesity patterns and hypertension risk in a large male population in the US. Male participants
from the National Health and Nutrition Examination Survey (NHANES) (2007–2018) were enrolled
in this cross-sectional study. Social demographic information, lifestyle factors, anthropometric
measurements and biochemical measurements were collected. Three obesity patterns were classified
according to the body mass index (BMI) and waist circumference (WC), including overweight and
general obesity, abdominal obesity, and compound obesity. We adopted multivariate logistic
regression to investigate the associations between hypertension and different obesity patterns
after adjusting for cofounding factors. Subgroup analysis, stratified by age, smoking, drinking and
estimated glomerular filtration rate (eGFR), was also conducted to explore the associations between
obesity patterns and hypertension risk among different populations. Moreover, the association
between WC and hypertension among male individuals was also explored using restricted cubic spline
(RCS) analysis. Receiver operating characteristic (ROC) was used to evaluate the discriminatory power
of WC for screening hypertension risk. 13,859 male participants from NHANES survey (2007–2018)
were enrolled. Comparing with the normal-weight group, the odds ratios (ORs) [95% confidence
interval (CI)] for hypertension in individuals with overweight and general obesity, abdominal obesity
and compound obesity were 1.41 [1.17–1.70], 1.97 [1.53–2.54] and 3.28 [2.70–3.99], respectively.
Subgroup analysis showed that the effect of different obesity patterns on hypertension risk was highly
stable among individuals with different clinical conditions. In addition, WC had a positive correlation
with the risk of hypertension (OR: 1.43; 95% CI 1.37–1.52; P < 0.001) in fully adjusted multivariate
logistic regression model. RCS analysis showed that the association between WC and hypertension
risk was in a nonlinear pattern, and WC had a good discriminatory power for hypertension in ROC
analysis. Different patterns of obesity have a great impact on the risk of hypertension among male
individuals. Increment of WC significantly increased the hypertension risk. More attention should
be paid to the prevention of obesity, especially abdominal obesity and compound obesity in male
individuals.

Hypertension refers to a clinical syndrome characterized by elevated arterial blood ­pressure1. The prevalence
rate of hypertension is increasing year by year, with more than 1.3 billion people suffering from hypertension
worldwide at present. One in five adults has hypertension. In addition, the age of onset of hypertension tends to
be younger. Hypertension is particularly harmful to the blood vessels, heart, kidneys and brain, and accounts for
the largest number of deaths from all diseases. The primary treatment goal for patients with hypertension is to
minimize the overall risk of cardiovascular complications and d ­ eath2. Unreasonable life style factors, including
excessive sodium salt, low potassium diet, heavy alcohol consumption, excessive intake of saturated fatty acids can
raise blood pressure. Smoking and heavy alcohol consumption are also risk factors for hypertension. Moreover,
obesity is one of the most important risk factors for hypertension. A better understanding of the relationship
between hypertension and obesity is crucial to prevent h ­ ypertension3.

1
Department of Cardiology, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal
Hospital, Gusu School, Nanjing Medical University, Suzhou 215000, China. 2Department of Internal Medicine,
Wuxi Maternity and Child Health Care Hospital, Women’s Hospital of Jiangnan University, Jiangnan University,
Wuxi 214002, China. 3Health Examination Center, Huadong Sanatorium, Wuxi 214065, China. 4Department of
Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing 210029, China. 5These authors contributed
equally: Lu Chen and Jun Zhang. *email: nanzhouhds@outlook.com; wengjiayi129@126.com; txwdbzy9307@
outlook.com; lidawunjmu@outlook.com

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Obesity has already become a serious public health problem and associated with numerous complications,
including hyperlipidemia, hypertension, arteriosclerosis and other chronic d ­ iseases4. In addition, patients with
obesity are more likely to have diabetes, gout and some tumor-related ­diseases5–7. Obesity is due to high fat food
intake or small amount of activity, leading to the accumulation of fat in the body. Obesity causes thickening
of subcutaneous fat, resulting in increased blood volume, and eventually leading to hypertension and even left
ventricular ­hypertrophy8. There are three main patterns of obesity at present, including overweight and general
obesity, abdominal obesity and compound ­obesity9. Both of abdominal obesity and hypertension are important
components of metabolic syndrome, and their common pathogenesis includes insulin resistance, secondary
hyperinsulinemia and inflammatory reaction, which can cause damage to heart, kidney and other organs. The
main harm of abdominal obesity is that it can lead to diabetes, hyperlipidemia, hypertension, and visceral dam-
age, which is prone to fatty liver and heart disease. In women, it can also lead to breast and cervical cancer. Waist
circumference (WC) often serves as an index for abdominal obesity, and body mass index (BMI) is the most used
indicator to evaluate the status of general o­ besity10.
Few studies have examined the level of hypertension risk associated with different patterns of obesity. In
addition, current studies believe that the prevalence of hypertension in male population is higher than that
in female population, and the influence of obesity on hypertension in male population is greater than that in
female ­population11. To the best of our knowledge, we firstly focus on the influence of different obesity patterns
on hypertension particularly in male population. We conducted a cross-sectional study to further explore the
association between different obesity patterns and the hypertension risk in male individuals. Subgroup analyses
were also performed to assess the effect of different obesity patterns on the hypertension risk of in male individu-
als with different clinical conditions.

Methods
Study population. National Health and Nutrition Examination Survey (NHANES) is a research program
­ S12. A mass of data in NHANES
designed to assess the health and nutrition status of adults and children in the U
database have been analyzed extensively, which is of great help in finding the etiologies, understanding the
epidemiology, and searching for novel biomarkers of different ­diseases13–15. To ensure that the samples were
representative, the method of stratified multistage probability sampling was used to screen out participants in
NHANES survey. In our study, five continuous cycles of the NHANES (2007–2008, 2009–2010, 2011–2012,
2013–2014, 2015–2016, and 2017–2018) were adopted. Male participants with complete demographic data,
standard physical measurements, biochemical indicators, and lifestyle information were included in the pre-
sent study. The exclusion criteria were as follows: (1) age < 18 or ≥ 80 years, (2) estimated glomerular filtration
rate (eGFR) < 60 ml/min/1.73 ­m2, (3) participants without key clinical records, including BMI, WC and blood
pressure records. This is an observational study performed according to the STROBE Checklist (https://​www.​
strobe-​state​ment.​org/​check​lists/).

Anthropometric measurements. Experienced examiners measured weight, height, and WC of partici-

pants using standardized techniques and equipment. WC, an index for abdominal obesity, was measured at
the superior border of the iliac crests and categorized into quartiles. BMI is an indicator of general obesity. The
formula of dividing weight (Kg) by the square of height (m) was adopted to calculate BMI (Kg/m2)16. Detailed
procedures for all anthropometric measurements are available on the NHANES website.

Different obesity patterns. According to the standards of International Diabetes Federation (IDF),
normal weight was defined as 18.5 kg/m2 ≤ BMI < 23.9 kg/m2; BMI ≥ 24.0 kg/m2 was regarded as overweight;
general obesity was defined as BMI ≥ 28.0 kg/m2 without an abnormal WC; abdominal obesity was defined as
WC ≥ 102 cm for men and WC ≥ 80 cm for women, with normal BMI at the same time; the coexistence of both
general and abdominal obesity was regarded as compound ­obesity17.

Definition of hypertension. According to the protocol of blood pressure measurement released by the
American Heart Association, the blood pressure was recorded by a trained examiner. The average systolic/
diastolic blood pressure of three consecutive measurements was obtained and reported. It is the same as the
previous published researches on the analysis of NHANES database, hypertension was defined as (1) average
SBP ≥ 140 mmHg, (2) average DBP ≥ 90 mmHg, (3) self-reported hypertension; (4) individuals with prescribed
antihypertensive medications. The criteria of 140/90 mmHg refers to the guideline of International Society of
­Hypertension18.

Covariates. We selected covariates according to the previously published ­studies19–21. Age, race/ethnicity,
and education level were obtained from the demographic questionnaire. Diabetes history, alcohol consump-
tion and smoking status were adopted from the health questionnaire. After at least 8 h of an overnight fast,
blood samples were collected and used to examine the levels of triglyceride (TG), total cholesterol (TC), low-
density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), red blood cell (RBC),
white blood cell (WBC), blood platelet (PLT), neutrophil (NE), lymphocyte (LY), hemoglobin, Hemoglobi-
nA1c (HbA1c), fast blood glucose (FBG), aspartate aminotransferase (ALT) and aspartate transaminase (AST).
NHANES website provided the detailed procedures in collecting biochemical measurements.

Statistical analysis. Continuous variables were presented as the mean ± standard deviation (SD) (normal
distribution), or the median (interquartile range) (skewed distribution). We adopted Kolmogorov–Smirnov test

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to assess the normality. Categorical variables were presented as the number (percentage). We compared baseline
characteristics among individuals with different obesity patterns based on Chi-square test for categorical vari-
ables and one-way ANOVA test (normal distribution) or Shapiro–Wilk test (skewed distribution) for continuous
variables. Kernel density estimation was used to illustrate distributions of WC in individuals with and without
hypertension. To evaluate the associations between different obesity patterns and WC with hypertension risk,
multiple logistic regression analysis was performed after adjusting for confounding factors selected by the step-
wise backward selection method (age, race/ethnicity, education, smoking, drinking, diabetes, TG, TC, LDL-C,
HDL-C, RBC, hemoglobin and eGFR). Individuals with normal-weight were the reference and the odds ratios
(ORs) with 95% confidence intervals (CIs) were calculated. Considering overweight is a risk factor for hyper-
tension, the overweight and general obesity populations were merged into a single group as previous studies.
Subgroup analyses stratified by age, smoking, drinking and eGFR were performed to further assess the associa-
tions between different obesity patterns and hypertension. Restricted cubic spline analysis (RCS) (with three
piecewise points) was used to evaluate the nonlinear associations between WC and the risk of hypertension, the
median value of WC was used as a reference. Receiver operating characteristic (ROC) curve was used to evaluate
the discriminative power of WC in identifying individuals with hypertension. A P value < 0.05 was considered
significant. All statistical analyses were conducted using R software (R Core Team, 2022; version 4.1.6) and SPSS
25.0 software (SPSS Institute, Chicago).

Ethics approval and consent to participate. The new ethic statement as follows: The NCHS Ethics
Review Board protects the rights and welfare of NHANES participants. The NHANES protocol complies with the
U.S. Department of Health and Human Services Policy for the Protection of Human Research Subjects. NCHS
IRB/ERC Protocol number: 2011–17. Ethical review and approval were waived for this study as it solely used
publicly available data for research and publication. Informed consent was obtained from all subjects involved
in the NHANES. This study was deemed exempt from review by the Ethics Committee of Huadong Sanatorium.

Results
Characteristics of the study population. 13,859 male participants from NHANES (2007–2018) was
enrolled in the present study. The proportions of compound obesity, abdominal obesity and overweight and
general obesity were 4,366 (31.5%), 1,460 (10.5%) and 4090 (29.5%), respectively. The prevalence of hyperten-
sion among compound obesity, abdominal obesity, overweight and general obesity and normal weight groups
were 2800 (64.1%), 916 (62.7%), 1643 (40.2%) and 1269 (32.0%). A significant difference was observed in the
prevalence of hypertension among age ≥ 60 years group and age < 60 years in the normal weight, overweight and
general obesity, abdominal obesity and compound obesity groups (p < 0.05) (Fig. 1). Significant differences in
demographic characteristics, blood biochemical indexes and life style factors were observed among the different
obesity patterns (Table 1).

Association between different obesity patterns and hypertension. In the non-adjusted model,
compound obesity (OR, 3.81; 95% CI, 3.48–4.17, P < 0.001), abdominal obesity (OR, 3.59; 95% CI, 3.16–4.07,
P < 0.001) and overweight and general obesity (OR, 1.43; 95% CI, 1.31–1.57, P < 0.001) were all strongly associ-
ated with hypertension risk. In the minimally adjusted model, after adjusting for confounding factors, the asso-
ciations between different obesity patterns and hypertension risk decreased. However, all of these three obesity
patterns were still independent factors associated with increased hypertension risk. After adjusting for age, race/
ethnicity, education, smoking, drinking, diabetes, TG, TC, LDL-C, HDL-C, RBC, hemoglobin and eGFR, indi-

Figure 1.  Comparison of the prevalence rate of hypertension between individuals ≥ 60 years and
individuals < 60 years among different obesity patterns (n = 13,859).

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Variables Normal weight (n = 3943) Overweight and general obesity (n = 4090) Abdominal obesity (n = 1460) Compound Obesity (n = 4366) P values
Age, years 38 (24, 56) 41 (30, 54) 58 (46, 67) 48 (35, 61) < 0.001
WC, cm 84.0 (78.7, 89.3) 95.6 (91.9, 98.9) 105.2 (103.3, 107.9) 115.5 (109.1, 124.2) < 0.001
BMI, kg/m2 22.8 (21.3, 23.9) 27.1 (26.0, 28.5) 28.6 (27.5, 29.7) 34.1 (31.8, 37.6) < 0.001
SBP, mmHg 118.3 (110.1, 128.7) 113.1 (106.2, 130.9) 125.3 (116.6, 135.3) 125.1 (116.9, 136.2) < 0.001
DBP, mmHg 70.2 (62.3, 77.1) 72.1 (65.6, 79.8) 73.6 (65.2, 80.3) 75.1 (67.2, 83.1) < 0.001
Race/ethnicity, % < 0.001
Non-Hispanic White 1457 (37.0%) 1272 (31.1%) 785 (53.8%) 1851 (42.4%)
Non-Hispanic Black 930 (23.6%) 871 (21.3%) 206 (14.1%) 996 (22.8%)
Mexican American 440 (11.2%) 834 (20.4%) 206 (14.1%) 816 (18.7%)
Other Hispanic 300 (7.6%) 525 (12.8%) 153 (10.5%) 416 (9.5%)
Other races 816 (20.7%) 588 (14.4%) 110 (7.5%) 287 (6.6%)
Education levels, % < 0.001
Below high school 311 (7.9%) 459 (11.2%) 165 (11.3%) 384 (8.8%)
High school 1712 (43.5%) 1578 (38.6%) 566 (38.8%) 1766 (40.5%)
Above high school 1916 (48.6%) 2051 (50.2%) 728 (49.9%) 2212 (50.7%)
Diabetes, % 309 (7.8%) 474 (11.6%) 341 (23.4%) 1178 (27.0%) < 0.001
Smoking, % 1946 (52.4%) 1879 (47.6%) 899 (61.9%) 2226 (51.7%) < 0.01
Drinking, % 1318 (49.4%) 1508 (51.7%) 458 (44.6%) 1538 (50.1%) < 0.001
eGFR, ml/min/1.73m2 103.6 (89.7, 117.5) 99.0 (86.3, 111.9) 90.4 (78.2, 101.6) 96.8 (83.5, 110.5) < 0.001
TG, mmol/L 0.94 (0.67, 1.37) 1.19 (0.82, 1.73) 1.24 (0.93, 1.88) 1.41 (0.99, 2.01) < 0.001
TC, mmol/L 4.63 (3.98, 5.30) 4.89 (4.19, 5.56) 4.89 (4.19, 5.60) 4.86 (4.16, 5.56) < 0.001
LDL-C, mmol/L 2.66 (2.17, 3.28) 2.97 (2.41, 3.60) 2.92 (2.38, 3.57) 2.97 (2.38, 3.62) < 0.001
HDL-C, mmol/L 1.37 (1.16, 1.63) 1.22 (1.03, 1.42) 1.19 (1.01, 1.40) 1.11 (0.96, 1.29) < 0.001
RBC, × ­109/L 4.90 (4.62, 5.17) 4.99 (4.73, 5.26) 4.91 (4.62, 5.18) 5.02 (4.74, 5.28) < 0.001
WBC, × ­109/L 6.42 (5.31, 7.82) 6.63 (5.61, 8.03) 7.12 (5.93, 8.40) 7.42 (6.11, 8.82) < 0.001
PLT, × ­106/L 22.3 (19.2, 25.8) 22.6 (19.5, 26.3) 22.3 (18.8, 25.9) 23.0 (19.5, 26.7) < 0.001
NE, × ­109/L 3.62 (2.81, 4.73) 3.71 (2.92, 4.71) 4.10 (3.22, 5.12) 4.31 (3.43, 5.46) < 0.001
LY, × ­109/L 1.92 (1.63, 2.42) 2.03 (1.72, 2.61) 2.02 (1.62, 2.41) 2.13 (1.69, 2.56) < 0.001
Hemoglobin, g/L 15.0 (14.3, 15.7) 15.1 (14.5, 15.9) 15.0 (14.3, 15.9) 15.1 (14.4, 15.9) < 0.001
HbA1c, % 5.4 (5.1, 5.7) 5.5 (5.2, 5.8) 5.6 (5.3, 6.0) 6.2 (5.7, 7.4) < 0.001
FBG, mmol/L 5.4 (5.1, 5.9) 5.6 (5.3, 6.1) 5.8 (5.4, 6.5) 5.9 (5.5, 6.8) < 0.001
ALT, u/L 20.0 (16.0, 27.0) 25.0 (20.0, 34.0) 24.0 (19.0, 33.0) 28.0 (22.0, 39.0) < 0.001
AST, u/L 23.0 (20.0, 28.0) 25.0 (21.0, 30.0) 24.0 (21.0, 30.0) 24.0 (21.0, 29.0) < 0.001

Table 1.  Comparison of patients’ characteristics among different obesity patterns (n = 13,859). Normally
distributed continuous variables are presented as the mean ± standard deviation; Non-normally distributed
continuous variables are presented as the mean (interquartile range); Categorical variables are presented as
the number (percentage). WC waist circumference, BMI body mass index, SBP systolic blood pressure, DBP
diastolic blood pressure, eGFR estimated glomerular filtration rate, TG triglycerides, TC total cholesterol, LDL-
C low-density lipoprotein cholesterol, HDL-c high-density lipoprotein cholesterol, RBC red blood cells, WBC
white blood cells, PLT platelets, NE neutrophils, LY lymphocytes, HbA1c glycated hemoglobin, FBG fasting
blood glucose, ALT alanine aminotransferase, AST glutamic transaminase.

viduals in the compound obesity group had more than three-fold increase in the odds of developing hyperten-
sion (OR: 3.28; 95% CI 2.70–3.99; P < 0.001) compared with individuals with normal weight in the fully adjusted
model. People with abdominal obesity were nearly twice as likely of developing hypertension (OR:1.97, 95% CI
1.53–2.54; P < 0.001). Overweight and general obesity also associated with the hypertension risk (OR:1.41, 95%
CI 1.17–1.70; P < 0.001) (Table 2).

Subgroup analysis of different obesity patterns and the risk of hypertension. We also carried
out subgroup analyses stratified by age, smoking, drinking and eGFR, after adjusting for age, race/ethnicity,
education, smoking, drinking, diabetes, TG, TC, LDL-C, HDL-C, RBC, hemoglobin, and eGFR. In Figs. 2, 3,
4, compared with normal weight at baseline, the risk of hypertension was found to increase in all three obesity
patterns. Our results showed that the effects of different obesity patterns on hypertension risk was highly stable.
In each subgroup, individuals with compound obesity were all associated with a high-risk value of developing
hypertension (Fig. 3). Nevertheless, abdominal obesity and overweight and general obesity were not associated
with the increased prevalence rate of hypertension in the population of age more than 60 years group (Figs. 2,
3). We also found that, across subgroups, the risk of hypertension was increased in individuals with overweight

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Non-adjusted model Minimally adjusted model Fully adjusted model

Hypertension
Obesity Patterns Total (n, %) OR [95% CI] P-value OR [95% CI] P-value OR [95% CI] P-value
Normal weight 3943 1260 (32.0%) Reference – Reference – Reference –
Overweight and
4090 1643 (40.2%) 1.43 [1.31, 1.57] P < 0.001 1.37 [1.21, 1.54] P < 0.001 1.41 [1.17, 1.70] P < 0.001
general obesity
Abdominal
1460 916 (62.7%) 3.59 [3.16, 4.07] P < 0.001 1.86 [1.58, 2.19] P < 0.001 1.97 [1.53, 2.54] P < 0.001
obesity
Compound
4366 2800 (64.1%) 3.81 [3.48, 4.17] P < 0.001 3.23 [2.86, 3.64] P < 0.001 3.28 [2.70, 3.99] P < 0.001
obesity

Table 2.  Multivariate logistic regression model of associations between different patterns of obesity and
hypertension Risk (n = 13,859). Minimally adjusted model, we adjusted for age, race/ethnicity, education,
smoking, drinking. Fully adjusted model, we adjusted for age, race/ethnicity, education, smoking, drinking,
diabetes, TG, TC, LDL-C, HDL-C, RBC, hemoglobin, and eGFR. TG triglycerides, TC total cholesterol, LDL-C
low-density lipoprotein cholesterol, HDL-C high-density lipoprotein cholesterol, RBC red blood cells, eGFR
estimated glomerular filtration rate.

Figure 2.  Subgroup analyses for the risks of developing hypertension in the overweight and general obesity
group compared with the normal-weight group.

Figure 3.  Subgroup analyses for the risks of developing hypertension in the abdominal obesity group compared
with the normal-weight group.

and general obesity than with normal weight, but higher in individuals with abdominal obesity, individuals with
compound obesity having the highest risk.

Association between WC and hypertension. Considering individuals with abdominal obesity and
compound obesity had a larger WC and a significantly higher prevalence rate of hypertension, we explored the
relationship between WC and hypertension. The distribution of WC stratified by hypertension is provided in

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Figure 4.  Subgroup analyses for the risks of developing hypertension in the compound obesity group compared
with the normal-weight group.

Figs. 5. Increased WC (per 10 cm) had a positive correlation with the prevalence rate of hypertension in non-
adjusted model (OR: 1.58; 95% CI 1.54–1.62; P < 0.001), minimally adjusted model (OR: 1.42; 95% CI 1.38–1.47;
P < 0.001) and fully adjusted model (OR: 1.43; 95% CI 1.37–1.52; P < 0.001) (Table 3). When fully adjusting for
age, race/ethnicity, education, smoking, drinking, diabetes, TG, TC, LDL-C, HDL-C, RBC, hemoglobin and
eGFR, individuals in the second to the fourth quartile of WC still had a higher risk for hypertension. Results of
RCS analysis also demonstrated that WC were positively corelated with the increased prevalence rate of hyper-
tension, and in a nonlinear pattern. The hypertension risk increased rapidly with the increase of WC, especial
in the upper quantile (Fig. 6A). ROC analysis showed that WC had a well discriminatory power for screening
hypertension risk, and the AUC of WC is 0.691 (95% CI 0.682–0.699; optimal cutoff value: 98.2) (Fig. 6B).

Discussion
In the present cross-sectional study, we included 13, 859 male participants from NHANES (2007–2018) to
explore the association between the hypertension risk and different obesity patterns in male population. BMI
and WC were used as indicators for general obesity and abdominal obesity, respectively. The prevalence rate of
hypertension among male individuals with compound obesity (64.1%), abdominal obesity (62.7%), overweight
and general obesity (40.2%) and normal weight (32.0%) was evaluated in detail. Moreover, after adjusting for
covariates, we carried out multivariable regression analysis to further investigate the increased risk of hyperten-
sion in male individuals with different obesity patterns compared with individuals with normal weight. Results
of multivariable regression analysis showed that different obesity patterns were independent risk factors for
hypertension in male population. The risk of hypertension in individuals with abdominal obesity and compound
obesity was higher than individuals with overweight and general obesity. Therefore, different obesity patterns

Figure 5.  The overall distribution of WC and distribution of WC in individuals with hypertension and
individuals without hypertension.

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Non-adjusted model Minimally adjusted model Fully adjusted model

Obesity Patterns Total Hypertension (n, %) OR [95% CI] P-value OR [95% CI] P-value OR [95% CI] P-value
Waist circumference
13,859 6619 (47.8%) 1.58 [1.54, 1.62] P < 0.001 1.42 [1.38, 1.47] P < 0.001 1.43 [1.37, 1.52] P < 0.001
(per 10 cm)
Categories
Q1 3482 883 (25.4%) Reference – Reference – Reference –
Q2 3459 1462 (42.3%) 2.16 [1.95, 2.39] P < 0.001 1.40 [1.23, 1.60] P < 0.001 1.51 [1.23, 1.87] P < 0.001
Q3 3459 1924 (55.6%) 3.69 [3.33, 4.08] P < 0.001 2.18 [1.91, 2.49] P < 0.001 2.37 [1.91, 2.95] P < 0.001
Q4 3459 2350 (67.9%) 6.24 [5.62, 6.92] P < 0.001 3.92 [3.42, 4.50] P < 0.001 4.10 [3.26, 5.16] P < 0.001

Table 3.  Multivariate logistic regression model of associations between waist circumference and hypertension
risk (n = 13,859). Minimally adjusted model, we adjusted for age, race/ethnicity, education, smoking, drinking.
Fully adjusted model, we adjusted for age, race/ethnicity, education, smoking, drinking, diabetes, TG, TC,
LDL-C, HDL-C, RBC, Hemoglobin, and eGFR. TG triglycerides, TC total cholesterol, LDL-C low-density
lipoprotein cholesterol, HDL-C high-density lipoprotein cholesterol, RBC red blood cells, eGFR estimated
glomerular filtration rate.

Figure 6.  RCS analysis between WC and the risk of hypertension and the ROC curve. (A) RCS analysis for the
association between WC and the risk of hypertension; (B) ROC curve of WC for discriminating hypertension
risk.

have a great impact on the prevalence of hypertension in male population. Multivariable regression analysis was
also performed to investigate the association between WC and hypertension, which showed that increased WC
was also an independent risk factor for h ­ ypertension22.
Back in the 1960s, the Framingham heart study found that obesity significantly increased the risk of
­hypertension23. In recent years, the prevalence of hypertension and obesity has increased significantly
­worldwide24. The research on the pathogenesis of obesity-related hypertension is helpful to find out reasonable
treatment methods. Obesity can be mainly divided into overweight and general obesity, abdominal obesity and
compound obesity. Many studies have explored the effects of different obesity patterns on different diseases. Lu
et al. performed a retrospective study and found that different types of obesity had significant effects on the risk
of Hashimoto’s thyroiditis, and compound obesity was an independent risk f­ actor17. Barcelar et al. also demon-
strated that obesity, particularly the abdominal obesity, was associated with respiratory system alterations, and
severe abdominal obesity could eventually lead to respiratory ­dysfunction25. In addition, abdominal obesity is
also closely associated with nonalcoholic fatty liver disease, diabetes, coronary heart disease and other chronic
­diseases26. In the present cross-sectional study, we firstly investigated the effects of different obesity patterns on
the risk of hypertension based on data from NHANES database. Our results showed that obesity patterns had
significant effects on the prevalence rate of hypertension in male population. Male population are more prone to
metabolic disorders, which may explain why different obesity patterns had a greater impact on the prevalence of
hypertension in male population. In addition, we also conducted a detailed subgroup analysis stratified by age,
smoking, drinking, and eGFR, the effect of different obesity patterns on hypertension was highly stable. Results
of subgroup analysis demonstrated that, among individuals older than 60 years, only compound obesity was the

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independent factor. This may be due to a significant increase in the prevalence rate of hypertension due to the
hardening of blood vessels with increasing age.
Using multivariable regression analysis, we found that the prevalence of hypertension was significantly higher
in individuals with either type of obesity patterns than individuals with normal weight. However, individuals with
abdominal obesity or compound obesity had a higher risk of hypertension than individuals with overweight and
general obesity. Abdominal obesity is a kind of abnormal phenotypes of fat distribution, and is associated with
insulin resistance and chronic inflammation, which can lead to hypertension through multiple m ­ echanisms27. In
abdominal obesity, the levels of RAAS components such as renin, angiotensin, and aldosterone are significantly
increased, and the elevated levels of aldosterone exceed the renin activity. In addition to renal RAAS activation,
RAAS of cardiac system, RAAS of vascular system, RAAS of adipose system and RAAS of central nervous system
are also significantly activated, eventually leading to h ­ ypertension28. Vascular dysfunction in abdominal obe-
sity includes changes in vascular structure, endothelial dysfunction and increased vascular stiffness. Abnormal
endothelial function and increased vascular stiffness are the main changes in the early stage of obesity-induced
hypertension, and insulin resistance is an important mechanism to initiate this ­process29. Increased body volume
load and impaired renal function are important clinical features of obesity. In recent years, researchers found that
impaired renal function may occur before obesity-induced hypertension h ­ appens30. The activation of sympathetic
nervous system caused by obesity is also an important mechanism of obesity related hypertension. Moreover,
leptin levels are elevated in most individuals with obesity, suggesting leptin resistance. Hyperleptinemia can
promote norepinephrine conversion and increase sympathetic activity, leading to elevated blood p ­ ressure31.
Most studies used BMI as the main criterion for assessing obesity at present, however, BMI does not accurately
reflect the distribution of body ­fat32. WC is one of the most commonly used indicators of anthropometry and
widely used for the diagnosis of abdominal obesity. According to the guidelines recommended by the IDF, it is
necessary to combine BMI and WC in the assessment of obesity, which is helpful for the relationship between
different forms of obesity and different ­diseases33. Several studies have already investigated associations between
WC and clinical outcomes in patients with type 2 d ­ iabetes34. A recent prospective case–control study examined
the associations between circulating levels of inflammation factors and demonstrated that WC is associated with
an increased coronary heart disease (CHD) risk independent of other underlying risk factors such as physical
­ MI35,36. Another systematic review and meta-analysis suggest that regular aerobic exercise
activity levels and B
can moderately reduce WC and visceral adipose tissue accumulation, and reduce the risk of cardiovascular and
cerebrovascular diseases, while high-intensity exercise may benefit patients without underlying chronic diseases
more than moderate intensity e­ xercise37. We also investigated the exact relationship between WC and the hyper-
tension risk, and our results also showed that increased WC could be an independent risk factor for hypertension.
Elevated WC can lead to the secretion of interleukin (IL) -6 and tumor necrosis factor (TNF) -α from white
adipose cells in the body, leading to the infiltration of macrophages, and eventually chronic ­inflammation38. The
function of infiltrated islet cells is affected and insulin resistance eventually occurs. On the other hand, inflam-
matory factors can affect the normal secretion and regulation function of vascular endothelial cells, resulting
in the loss of normal function of endothelial ­cells39. Besides, we found that the association between WC and
hypertension was in a nonlinear pattern, the risk of hypertension increased significantly with the increment of
WC, especially in the upper quantile. Controlling of WC and abdominal obesity is very important for the control
of ­hypertension40. Moreover, WC can be also adopted to screen out the risk of hypertension in male individuals.
Although we conducted a detailed analysis of the effects of different obesity patterns on the prevalence of
hypertension, there are still some limitations to be noted in this study. First, this study used only a nationally
representative sample from the US, but there are large ethnic differences in diet, physical activity, genetic vari-
ants, lipid metabolism, and susceptibility to cardiovascular disease, and the generality of our conclusions to other
populations is unclear. Second, due to the inherent nature of cross-sectional studies, it is difficult to determine
the causal relationship between different modes of obesity and h ­ ypertension41. More prospective studies are
needed to determine the exact relationship between different forms of obesity and hypertension. Third, although
we adjusted for multiple covariates, we could not completely exclude the influence of other confounding factors
on our results.

Conclusions
In conclusion, we investigated the association of different obesity patterns with hypertension and found that
abdominal obesity and compound obesity were strongly associated with increased risk of hypertension. With
the increasing burden of hypertension and its resulting cardiovascular and cerebrovascular diseases worldwide,
the management of obesity, especially abdominal obesity, should be strengthened to prevent hypertension.

Data availability
Publicly available datasets were analyzed in this study. All the raw data used in this study are derived from the
public NHANES data portal (https://​wwwn.​cdc.​gov/​nchs/​nhanes/​analy​ticgu​ideli​nes.​aspx).

Received: 20 January 2023; Accepted: 20 June 2023

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Acknowledgements
We acknowledge NHANES database for providing their platforms and contributors for uploading their meaning-
ful datasets. And we thank all participants included in our present study.

Author contributions
L.-DaW. and N.Z. were involved in the experiment design. L.-DaW. and J.-Y.W. performed the data analysis. J.-
Y.W. and N.Z. wrote the manuscript. J.Z. reviewed the manuscript and provided critical suggestions. L.C. revised
the manuscript according to the comments by editors and reviewers and provided valuable suggestions for the
article’s revisions, especially for statistics section. L.C. also polished the overall language, greatly improving the
English quality of the article. Similarly, Z.-Y.B. offered valuable suggestions during the article revision process
and will bear a portion of the publication fee, which is crucial for expanding the dissemination of our article’s
findings and conclusions. All authors approved the final manuscript.

Funding
This research was funded by the National Natural Science Foundation of China (Grant No. 82100360) and the
tutorial system of Suzhou (Grant No. Qngg2022021).

Competing interests
The authors declare no competing interests.

Additional information
Supplementary Information The online version contains supplementary material available at https://​doi.​org/​
10.​1038/​s41598-​023-​37302-x.
Correspondence and requests for materials should be addressed to N.Z., J.-Y.W., Z.-Y.B. or L.-D.W.
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