Obes Facts 2019;12:78–90

DOI: 10.1159/000495852 © 2019 The Author(s)

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Research Article

The Prevalence of Metabolically

Healthy and Unhealthy Obesity
according to Different Criteria
Chunxiao Liu a Chunxiu Wang a Shaochen Guan a Hongjun Liu a
Xiaoguang Wu a Zhongying Zhang a Xiang Gu a Yanlei Zhang a
Yan Zhao a Lap Ah Tse b Xianghua Fang a
a
Evidence-Based Medical Center, Xuanwu Hospital, Capital Medical University, Beijing,
China; b Jockey Club School of Public Health and Primary Care, The Chinese University of
Hong Kong, Hong Kong, Hong Kong SAR

Keywords
Obesity · Metabolic syndrome · Phenotype · Prevalence

Abstract
Objective: Obesity-related disease risks may vary depending on whether the subject has
metabolically healthy obesity (MHO) or metabolically unhealthy obesity (MUO). At least 5
definitions/criteria of obesity and metabolic disorders have been documented in the litera-
ture, yielding uncertainties in a reliable international comparison of obesity phenotype prev-
alence. This report aims to compare differences in MHO and MUO prevalence according to
the 5 most frequently used definitions. Methods: A random sample of 4,757 adults aged 35
years and older (male 51.1%) was enrolled. Obesity was defined either according to body mass
index or waist circumference, and the definitions of metabolic abnormalities were derived
from 5 different criteria. Results: In MHO, the highest prevalence was obtained when using
the homeostasis model assessment (HOMA) criteria (13.6%), followed by the Chinese Diabetes
Society (11.4%), Adult Treatment Panel III (10.3%), Wildman (5.2%), and Karelis (4.2%) criteria;
however, the MUO prevalence had an opposite trend to MHO prevalence. The magnitude of
differences in the age-specific prevalence of MHO and MUO varied greatly and ranked in dif-
ferent orders. The proportion of insulin resistance for MHO and MUO individuals differed
significantly regardless of which metabolic criterion was used. Conclusion: The prevalence of
MHO and MUO in the Chinese population varies according to different definitions of obesity
and metabolic disorders. © 2019 The Author(s)
Published by S. Karger AG, Basel

L.A.T. and X.F. contributed equally to this work.

Lap Ah Tse Xianghua Fang, PhD

JC School of Public Health and Primary Care, The Chinese University of Evidence-Based Medical Center, Xuanwu Hospital
Hong Kong, 4/F, School of Public Health, Prince of Wales Hospital Capital Medical University, No. 45 Changchun Street
Sha Tin, Hong Kong (Hong Kong SAR) Xicheng District, Beijing 100053 (China)
E-Mail shelly @ cuhk.edu.hk E-Mail fangxianghua @ xwhosp.org
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Liu et al.: The Prevalence of Metabolically Healthy and Unhealthy Obesity according to
Different Criteria

Introduction

The prevalence of obesity is increasing worldwide, and now it has become a major public
health problem in China [1]. Obesity is an identifiable important risk factor for type 2 diabetes,
hypertension, coronary heart disease, stroke, and several types of cancers and is thus linked
to premature death [2, 3]. Additionally, obese individuals are more likely to have osteoar-
thritis, chronic pain, asthma, gallbladder disease, metabolic disorders, and poor quality of life
[4]. Although maintaining a healthy weight to reduce the incidence of these diseases or
adverse health consequences related to obesity has been a global consensus, it is increasingly
recognized that the disease risks may not be uniform among all obese subjects. In an obese
population where metabolic abnormalities are absent (e.g., hypertension, diabetes, dyslip-
idemia, insulin resistance [IR], or inflammatory factors), a better fitness with a 30–50% lower
mortality was observed than in obese peers with these risk factors [5]. This risk difference
indicates that a heterogeneous risk profile might exist among obese subjects. Therefore, a
subset of obesity has been further defined as metabolically healthy obesity (MHO), including
obese subjects who seem to be protected against obesity-related metabolic complications
and lack a set of cardiometabolic abnormalities. Conversely, obesity with metabolic risk
factors is called metabolically unhealthy obesity (MUO) [6]. MHO includes subjects who are
considered as having large quantities of fat mass or body weight but exhibit a healthy meta-
bolic profile; thus, it is referred to as a benign condition [7, 8]. However, a meta-analysis
including 8 longitudinal studies showed that MHO individuals are at increased risk for all-
cause mortality over the long term (≥10 years), which indicates that MHO might be an inter-
mediate stage of MUO [9].
Currently, the prevalence of the MHO phenotype in different populations varies from 1.1
to 28.5%, while this variation might result from the diverse definitions of metabolic abnor-
malities adopted in different studies or from other methodological issues, such as small
sample size or limiting to a special subgroup [7]. Until now, there has been no standard defi-
nition of metabolic abnormality worldwide when defining obesity phenotypes. It also remains
unclear which components of metabolic disorder should be included when defining MHO and
how to identify the detailed cutoffs of the selected metabolic components to differentiate
metabolically healthy from unhealthy subjects. Furthermore, some criteria added IR and
high-sensitivity C-reactive protein (hsCRP) as the basic metabolic components (elevated
blood pressure, dysglycemia, and dyslipidemia) to define obesity phenotypes [10]. Using
different definitions of metabolic disorder to estimate the prevalence of obesity types within
a certain population will diminish or reduce the variation from study design and ensure
internal validity. Therefore, the aims of the current study were to (1) compare the prevalence
of obesity phenotypes using different adiposity measures and criteria of metabolic abnor-
mality; (2) provide evidence if MHO is an intermediate state of MUO; (3) assess if IR and
hsCRP are essential components to define metabolic abnormality in obesity.

Subjects and Methods

Study Design and Population

This study included only the Beijing site derived from the China Hypertension Survey, a nation-wide
survey conducted during 2013–2015. The method and design of the survey were described elsewhere, and
the specific protocol was strictly followed at each study site including Beijing [11, 12]. Briefly, a 4-stage strat-
ified random procedure was used to recruit a total of 500,000 permanent residents aged 15 years and older
from 262 urban cities and rural counties over 31 metropolitan/provinces in mainland China. In the 1st-stage
random sampling, we used the probability proportional to size method to randomly select 2–4 cities in urban
areas and 2–4 counties in rural areas from each metropolitan/province. We then used a simple random
sampling method in the 2nd to 3rd stage random procedure to select 2 districts (urban) or townships (rural)
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Liu et al.: The Prevalence of Metabolically Healthy and Unhealthy Obesity according to
Different Criteria

and 3 communities or villages within each district or township, respectively. In the final stage, by using a
simple random sampling method, a given number of participants from each of the 14 gender/age strata
(male/female and aged 15–24, 25–34, 35–44, 45–54, 55–64, 65–74, and ≥75 years) based on the government-
registered data of households were selected. All selected participants were invited to complete a question-
naire and anthropometric measurement. In addition, blood and urine samples were collected from those
aged ≥35 years. Beijing as one of the metropolitan cities in China contributed a total of 13,057 subjects aged
≥15 years to the nationwide survey, and 6,906 subjects were ≥35 years old. The blood and urine samples
were collected from 4,757 participants and used for this analysis.
To ensure the uniformity of the survey, a manual of operations was compiled to standardize the methods
and procedures, including the standard approaches to recruiting subjects, determining the sample size, inter-
viewing the subjects, performing the physical examinations, defining the cardiovascular events, and quality
control. All research staff participating in the survey was required to accept standardized training before the
survey was conducted [11].
The study was approved by the Ethics Committee of both Fuwai Hospital and Xuanwu Hospital (Beijing,
China). A written informed consent was obtained from every subject before data collection.

Data Collection from Questionnaire

All participants answered the standardized questionnaire administered by well-trained investigators,
including information on sociodemographic factors, history of hypertension, diabetes mellitus, dyslipidemia,
cardio- and cerebrovascular diseases, as well as current medications [11]. The medical record was reviewed
carefully.

Measurements of Anthropometric Parameters and Blood Pressure

After the interview, all subjects underwent measurements according to a standardized protocol. Briefly,
body weight was measured in standing position without shoes and in light clothing using an OMRON body
fat and weight measurement device (V-body HBF-371, OMRON, Kyoto, Japan). Height was measured using a
standard right-angle device and a fixed measurement tape (to the nearest 5 mm). Waist circumference (WC)
was defined as mid-way between the lowest rib and iliac crest and measured under steady breaths using a
cloth tape directly on the participant’s skin.
Sitting blood pressure was measured on the right arm 3 times with a 30-s interval with a Professional
Portable Blood Pressure Monitor (OMRON). The average of 3 measurements was used for analysis. Each
subject was asked to empty the bladder and rested at least 20 min before blood pressure was measured.

Biological Data and Laboratory Tests

Ten to twelve milliliters of spot blood samples were taken in the morning after a 12-h fasting from each
eligible participant. All biological samples were sent to the National Center for Cardiovascular Disease of
Fuwai Hospital for analysis. Fasting plasma glucose, total cholesterol, triglycerides, and high-density lipo-
protein cholesterol were determined by routine methods abiding to standards from the National Guide to
Clinical Laboratory Procedures issued by the China Ministry of Health in 2006 [13]. Low-density lipoprotein
cholesterol was calculated using the Friedwald formula. Serum insulin was measured by the immunoassay
method; hsCRP was assessed by high-sensitivity immunonephelometry (German BN ProSpec system). The
sample storage and detection methods were described in detail elsewhere [14].

Definitions of Obesity, Metabolic Abnormality, and Obesity Phenotype

Body mass index (BMI) was calculated as body weight in kilogram divided by the square of height in
meter. Subjects were classified according to BMI as normal weight (18.5–23.9 kg/m2), overweight (24.0–27.9
kg/m2), and obese (≥28.0 kg/m2) according to the Chinese standard [15]. Abdominal obesity was considered
for a waist ≥85 cm for men and ≥80 cm for women in the Chinese population [15]. The homeostasis model
assessment of insulin resistance (HOMA-IR) index was calculated as [fasting serum insulin × (fasting
glucose)/22.5]: insulin concentration is reported in mU/L and glucose in mmol/L. Participants were defined
as IR if their HOMA-IR level was in the top quartile of the distribution among nondiabetic subjects [16, 17].
As systemic inflammation is one component of cardiometabolic abnormalities presented by Wildman et al.
[10], detailed as hsCRP level >90th percentile, we also adopted this cutoff in our study.
The definition of the MHO and MUO phenotypes was obtained based on the joint combination of obesity
markers (BMI or WC) and cardiometabolic abnormalities listed in Table 1. Five sets of cardiometabolic
abnormalities were based on the following definitions: the National Cholesterol Education Program-Adult
Treatment Panel III (ATPIII), Karelis, Wildman, Chinese Diabetes Society (CDS), and the HOMA index [10,
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Liu et al.: The Prevalence of Metabolically Healthy and Unhealthy Obesity according to
Different Criteria

Table 1. Criteria of metabolic abnormality used to define MHO and MUO

Metabolic component ATP III Karelis Wildman CDS HOMA

Central obesity WC >102 cm in men, WC ≥90 cm in

>88 cm in women men, ≥85 cm in
women
Blood pressure, mm Hg SBP ≥130 and/or SBP ≥130 and/or SBP ≥130 or
DBP ≥85 or DBP ≥85 or DBP ≥85 or
treatment treatment treatment
Fasting glucose, mmol/L ≥5.6 or treatment ≥5.6 or ≥6.1 or
treatment treatment
Triglyceride, mmol/L ≥1.7 or treatment ≤1.7 ≥1.7 ≥1.7
HDL-C, mmol/L <1.04 in men, ≥1.3 <1.04 in men, <1.04
<1.29 in women <1.29 in women or
treatment
LDL-C, mmol/L ≤2.6 –
Total cholesterol, mmol/L ≤5.2 –
Insulin sensitivity HOMA-IR HOMA-IR >90th HOMA-IR ≥75th
≤1.95 percentile percentilea
hsCRP, mg/L >90th percentile
Criteria for metabolically ≥3 of the above <2 of the ≥2 of the above ≥3 of the above All
unhealthy above

MUO, individuals with obesity combined with any of the 5 criteria for metabolically unhealthy above; MHO, individuals with
obesity exclusive of MUO; ATPIII, Adult Treatment Panel III; CDS, Chinese Diabetes Society; HOMA, homeostasis model
assessment; WC, waist circumference; SBP, systolic blood pressure; DBP, diastolic blood pressure; HDL-C, high-density
lipoprotein cholesterol; LDL, low-density lipoprotein cholesterol; HOMA-IR, homeostasis model assessment of insulin resistance;
hsCRP, high-sensitivity C-reactive protein. a Among nondiabetic subjects.

18–21]. Thus, subjects were classified into MUO if they belonged to BMI-defined or WC-defined obesity, coex-
isting with a diagnosis of metabolic abnormalities in any of the 5 definitions above. Obese subjects with
absence of metabolic abnormalities were classified as MHO.

Statistical Analysis
The prevalence of MHO and MUO was estimated by age and gender based on the 2010 Beijing municipal
population census; the age- and gender-specific weight-adjusted sample was acquired to estimate the prev-
alence of MHO and MUO. For continuous variables, means ± standard deviations were presented if the data
fitted normal distribution. For continuous variables with a non-normal distribution, medians (interquartile
ranges) were reported, and the differences of medians between groups were assessed by the Kruskal-Wallis
test. The χ2 test was used to determine the differences in the categorical variables. Test for trend was
performed to explore the possible heterogeneities of prevalence of the specific obesity phenotypes over
different age groups.

Results

Among the 4,757 subjects, 1,155 (24.3%) subjects were classified as obese, 1,996 (41.9%)
as overweight, 1,548 (32.5%) as normal weight, and 58 (1.2%) as underweight based on BMI.
Of the 4,757 subjects, 2,994 (62.9%) had abdominal obesity. Compared with men, signifi-
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Liu et al.: The Prevalence of Metabolically Healthy and Unhealthy Obesity according to
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Table 2. Prevalence of MHO/MHAO and MUO/MUAO combined with 5 different metabolic abnormality criteria

Obesity phenotype ATPIII Karelis Wildman CDS HOMA

Total population (n = 4,757), %

MHO 10.3 (7.6–13.0) 4.2 (1.4–7.0) 5.2 (2.4–8.0) 11.4 (8.7–14.1) 13.6 (11.0–16.2)
MUO 14.0 (11.4–16.6) 20.1 (17.6–22.6) 19.1 (16.5–21.7) 12.9 (10.2–15.6) 10.6 (7.9–13.3)
MHAO 35.9 (33.6–38.2) 14.0 (11.4–16.6) 17.6 (15.0–20.2) 36.0 (33.7–38.3) 40.2 (38.0–42.4)
MUAO 27.0 (24.6–29.4) 49.0 (47.0–51.0) 45.3 (43.2–47.4) 26.9 (24.5–29.3) 22.7 (20.2–25.2)

MHO, %
Male (n = 2,433) 11.3 (7.6–15.0)* 2.7 (0–6.6)** 4.0 (0.1–7.9)** 9.0 (5.2–12.8)** 11.6 (7.9–15.3)**
Female (n = 2,324) 9.3 (5.4–13.2) 5.7 (1.8–9.6) 6.5 (2.6–10.4) 13.8 (10.0–17.6) 15.8 (12.1–19.5)

MUO, %
Male (n = 2,433) 11.5 (7.8–15.2)** 20.1 (16.6–23.6) 18.8 (15.2–22.4) 13.8 (10.1–17.5) 11.2 (7.5–14.9)
Female (n = 2,324) 16.6 (12.9–20.3) 20.1 (16.5–23.7) 19.4 (15.7–23.1) 12.0 (8.2–15.8) 10.1 (6.2–14.0)

MHAO, %
Male (n = 2,433) 41.6 (38.6–44.6)** 12.7 (9.0–16.4)* 16.4 (12.8–20.0)* 33.4 (30.2–36.6)** 39.7 (36.6–42.8)
Female (n = 2,324) 29.9 (26.5–33.3) 15.2 (11.5–18.9) 18.9 (15.2–22.6) 38.7 (35.5–41.9) 40.8 (37.7–43.9)

MHUO, %
Male (n = 2,433) 22.7 (19.2–26.2)** 51.6 (48.8–54.4)** 47.9 (45.0–50.8)** 30.9 (27.6–34.2)** 24.7 (21.2–28.2)***
Female (n = 2,324) 31.5 (28.1–34.9) 46.3 (43.3–49.3) 42.6 (39.5–45.7) 22.8 (19.2–26.4) 20.7 (17.1–24.3)

Prevalence of MHO (MHAO) and MUO (MUAO) was estimated by age and gender based on the 2010 Beijing municipal population census. MHO, metabolically
healthy obesity; MUO, metabolically unhealthy obesity; MHAO, metabolically healthy abdominal obesity; MUAO, metabolically unhealthy abdominal obesity; ATPIII,
Adult Treatment Panel III; CDS, Chinese Diabetes Society; HOMA, homeostasis model assessment. * p < 0.05 versus female for the comparison of MHO (MHAO) or
MUO (MUAO) prevalence. ** p < 0.001 versus female for the comparison of MHO (MHAO) or MUO (MUAO) prevalence. *** p < 0.01 versus female for the comparison
of MHO (MHAO) or MUO (MUAO) prevalence.

cantly more women were obese according to BMI (25.9 vs. 22.8%, p = 0.013), but less women
had abdominal obesity (61.5 vs. 64.3%, p = 0.043).
As shown in Table 2, there was a great variation in the prevalence of MHO and MUO
defined by the 5 definitions listed in Table 1. When obesity was classified using BMI, the
highest prevalence of MHO was obtained from HOMA criteria (13.6%, 95% CI 11.0–16.2),
followed by CDS (11.4%, 95% CI 8.7–14.1), ATPIII (10.3%, 95% CI 7.6–13.0), and Wildman
(5.2%, 95% CI 2.4–8.0), whilst the lowest prevalence of MHO was derived from the criteria of
Karelis (4.2%, 95% CI 1.4–7.0). In contrast to MHO, the highest prevalence of MUO was
derived from the criteria of Karelis (20.1%, 95% CI 17.6–22.6), which was 2-fold higher than
the lowest prevalence from HOMA (10.6%, 95% CI 7.9–13.3). The MUO prevalence for
Wildman, ATPIII, and CDS was 19.1% (95% CI 16.5–21.7), 14.0% (95% CI 11.4–16.6), and
12.9% (95% CI 10.2–15.6), respectively. The MHO and MUO prevalence defined by WC was
much higher than that defined by BMI; the prevalence order from high to low was similar to
that of BMI-defined obesity, but the prevalence rates were much higher both for MHO and
MUO in WC-defined obesity than in BMI-defined obesity. The proportion of MHO and MUO or
the ratio of MHO to MUO is demonstrated in online supplementary Figure 1 (for all online
suppl. material, see www.karger.com/doi/10.1159/000495852).
When using BMI to define obesity, a significantly higher prevalence of MHO in females
than in males was observed except for ATPIII criteria, but there was no significant gender
difference in MUO prevalence between the other 4 criteria. In WC-defined MHO, similar
findings of a gender difference were found as for BMI-defined MHO. Moreover, there existed
gender differences in the prevalence of MUO between the 5 definitions of metabolic abnor-
malities (Table 2). A detailed sex constituent ratio of MHO and MUO for different criteria is
shown in online supplementary Figure 1.
In BMI-defined obesity, the prevalence of MHO defined by criteria of ATPIII, Wildman,
CDS, and HOMA increased with age (p for trend <0.05) and reached the peak in those aged 45
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Liu et al.: The Prevalence of Metabolically Healthy and Unhealthy Obesity according to
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a. MHO b.MUO
18.0 30.0

16.0
25.0

14.0

12.0 20.0
Prevalence (%)

Prevalence (%)
10.0
15.0

8.0

6.0 10.0

4.0
5.0

2.0

0.0 0.0
35- 40- 45- 50- 55- 60- 65- 70- 75- 80- 85- 35- 40- 45- 50- 55- 60- 65- 70- 75- 80- 85-
ATPⅢ 11.3 13.9 15.7 10.0 7.0 7.1 5.6 4.2 4.3 3.2 6.1 ATPⅢ 8.6 8.9 12.7 17.8 17.1 20.0 21.9 18.9 15.8 11.7 12.2
Karelis 4.0 4.6 4.3 4.7 3.5 4.2 3.1 3.4 6.0 3.2 4.1 Karelis 15.9 18.2 24.1 23.1 20.6 22.9 24.6 19.7 14.1 12.6 14.3
Wildman 6.0 7.3 7.6 4.9 3.9 3.4 2.0 1.7 1.6 2.1 2.0 Wildman 13.8 15.5 20.7 22.8 20.1 23.6 25.8 21.3 18.0 13.7 16.0
CDS 11.3 12.8 15.8 13.0 8.6 10.3 7.6 6.7 7.1 5.3 8.3 CDS 8.6 9.9 12.5 14.7 15.6 16.7 20.0 16.7 12.5 10.6 10.4
HOMA 12.1 13.9 16.8 17.1 12.6 13.1 11.7 10.4 10.9 6.4 8.2 HOMA 7.8 8.9 11.5 10.6 11.5 14.0 16.2 12.9 8.7 9.6 10.2

Fig. 1. Age-specific prevalence of obesity phenotypes defined by BMI and different metabolic criteria. a MHO.
b MUO. BMI, body mass index; MUO, metabolically unhealthy obesity; MHO, metabolically healthy obesity;
ATPIII, Adult Treatment Panel III; CDS, Chinese Diabetes Society; HOMA, homeostasis model assessment.

years (Fig. 1a). Then, the prevalence declined with an increment at age 80 years, except for
Wildman criteria. The Wildman-defined MHO prevalence kept on declining after age 45 years.
The trend of age-specific prevalence in Karelis-defined MHO changed differently from the
other 4 definitions. The prevalence remained stable before reaching the peak at age 75 years
and dropped to a minimum at age 80 years. In addition, the Karelis-defined MHO prevalence
was relatively stable across age groups with a narrow variation ranging from 3.1 to 6.0%. The
age-specific prevalence of MHO defined by the other 4 criteria fluctuated greatly across age
groups. The most fluctuating MHO prevalence was found for the ATPIII definition with a wide
variation in prevalence (range 3.2–15.7%), followed by CDS (range 5.3–15.8%), HOMA (range
6.4–16.8%), and Wildman (range 1.6–7.6%).
The age-specific prevalence of BMI-defined MUO increased below age 65 years and then
declined regardless of which criteria were used (Fig. 1b). After age 84 years, the prevalence
defined by CDS criterion kept on declining, but when the criteria of ATPIII, Karelis, Wildman,
and HOMA were used, the prevalence increased slightly. The differences in prevalence
between the maximum and the minimum across all age groups varied greatly as defined by
the 5 criteria. The magnitude of differences in the prevalence was ranked highest for ATPIII
(range 8.6–21.9%), followed by Wildman (range 13.7–25.8%), Karelis (range 12.6–24.6%),
CDS (range 8.6–20.0%), and HOMA (range 7.8–16.2%).
In WC-defined obesity, the age-specific MHO prevalence for different metabolic criteria
showed almost no consistency. HOMA-defined MHO had the highest prevalence in almost all
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Liu et al.: The Prevalence of Metabolically Healthy and Unhealthy Obesity according to
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a. MHAO b. MUAO
60.0 80.0

70.0
50.0

60.0

40.0
50.0

Prevalence (%)
Prevalenve (%)

30.0 40.0

30.0
20.0

20.0

10.0
10.0

0.0 0.0
35- 40- 45- 50- 55- 60- 65- 70- 75- 80- 85- 35- 40- 45- 50- 55- 60- 65- 70- 75- 80- 85-
ATPⅢ 31.5 36.8 39.4 42.5 37.6 31.2 34.0 29.7 31.0 32.6 37.5 ATPⅢ 13.3 13.5 20.9 29.4 34.1 43.7 47.7 46.9 44.0 43.2 41.7
Karelis 10.6 14.4 14.1 16.3 11.6 13.3 13.3 16.8 20.2 15.8 24.5 Karelis 34.3 35.9 46.1 55.6 60.1 61.6 68.4 60.1 54.6 60.0 55.1
Wildman 16.3 22.3 19.8 19.6 17.5 13.0 13.7 13.0 11.4 10.5 16.3 Wildman 28.5 28.0 40.4 52.3 54.2 61.9 68.0 64.0 63.6 65.3 63.3
CDS 29.3 35.0 38.8 43.3 38.5 35.0 33.2 32.8 35.3 32.6 37.5 CDS 15.5 15.3 21.4 28.5 33.2 40.1 48.5 44.1 39.7 43.2 41.7
HOMA 30.6 34.9 39.2 46.8 45.6 44.6 45.4 42.4 47.0 45.3 55.1 HOMA 14.2 15.4 21.1 25.0 26.0 30.3 36.7 34.5 28.4 30.5 24.5

Fig. 2. Age-specific prevalence of obesity phenotypes defined by WC and different metabolic criteria.
a MHAO. b MUAO. WC, waist circumference; MUAO, metabolically unhealthy abdominal obesity; MHAO, meta-
bolically healthy abdominal obesity; ATPIII, Adult Treatment Panel III; CDS, Chinese Diabetes Society; HOMA,
homeostasis model assessment.

age groups, which was consistent with BMI-defined MHO. The prevalence kept an ascendant
trend with age increment. The variation in prevalence for both CDS-defined and ATPIII-
defined MHO was large with a similar trend. The top values appeared at age ≥50 years (43.3%
for CDS and 42.5% for ATPIII) and bottom values at age ≥35 years (29.3% for CDS and 31.5%
for ATPIII). The age-specific prevalence of MHO defined by either Wildman or Karelis fluc-
tuated with a narrow variation (from 10 to 20%). The MHO prevalence rose obviously after
age 80 years regardless of which metabolic criteria were used (Fig. 2a). The tendency of the
age-specific prevalence of MUO was similar for the 5 metabolic criteria (Fig. 2b), i.e., it
increased after age 40 years, reached the highest level at age 65 years, and then dropped
slightly.
The proportion of IR was 43.8% (506/1,155) in BMI-defined obesity, which was higher
than in WC-defined abdominal obesity (36.1% [1,080/2,994]). In the case of BMI-defined
obesity, the proportion of IR for MHO and MUO individuals differed significantly regardless
of which metabolic criteria were used (all p values <0.001). The most apparent differences
were observed when Wildman and Karelis criteria were used. In WC-defined obesity, a similar
trend for the presence of IR was found in MHO and MUO. No significant difference was
observed in the proportion of elevated hsCRP between BMI-defined obesity and WC-defined
obesity (11.8% [136/1,155] vs. 10.2% [305/2,994]). Except for the Wildman criterion, which
contained hsCRP as a metabolic component, there appeared no significant difference between
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Liu et al.: The Prevalence of Metabolically Healthy and Unhealthy Obesity according to
Different Criteria

Table 3. Proportion of IR and elevated hsCRP in MHO (MHAO) and MUO (MUAO) defined by 5 metabolic abnormality criteria

Indicator ATPIII p value Karelis p value Wildman p value CDS p value HOMA p value

BMI-defined obesity
IR, %
MHO 30.5 <0.001 16.5 <0.001 22.5 <0.001 30.6 <0.001 0 –
MUO 56.5 54.7 53.0 60.1 100.0
hsCRP abnormal, %
MHO 10.2 0.091 12.5 0.984 0 <0.001 12.1 0.724 12.7 0.895
MUO 13.7 12.6 15.0 12.8 12.4
Abdominal obesity
IR, %
MHAO 25.4 <0.001 16.0 <0.001 17.3 <0.001 25.0 <0.001 0 –
MUAO 51.6 45.4 45.3 53.6 100.0
hsCRP abnormal, %
MHAO 8.9 <0.001 9.6 0.218 1.2 <0.001 9.6 0.021 9.3 <0.001
MUAO 12.7 11.2 13.7 12.1 13.3

Results are expressed as percentages, and statistical analysis was conducted using the χ2 test for categorical variables. MHO,
metabolically healthy obesity; MUO, metabolically unhealthy obesity; MHAO, metabolically healthy abdominal obesity; MUAO,
metabolically unhealthy abdominal obesity; ATPIII, Adult Treatment Panel III; CDS, Chinese Diabetes Society; HOMA, homeostasis
model assessment; BMI, body mass index; IR, insulin resistance; hsCRP, high-sensitivity C-reactive protein.

MHO and MUO in the proportion of elevated hsCRP in BMI-defined obesity. However, in
WC-defined obesity, the proportion of elevated hsCRP was significantly higher in MUO than
in MHO when ATPIII or HOMA criterion was adopted (Table 3).

Discussion

In the present study, we estimated the prevalence of MHO and MUO phenotypes based
on the most up-to-date information from a representative survey of the community-based
population in Beijing, China. After using the Chinese definition of obesity based on BMI and
WC, as well as their combination with 5 criteria of metabolic disorder to define the obesity
phenotypes, we found that the difference in the prevalence of obesity and its phenotypes
varied greatly. The prevalence of MHO varied from 4.2 to 13.6% when obesity was defined by
BMI and from 14.0 to 40.2% when it was defined by WC. MUO prevalence was 10.6–20.1%
and 22.7–49.0%, respectively. No matter which obesity criteria were used, the age-specific
prevalence of MHO defined by HOMA was the highest almost in each age group, followed by
CDS, ATPIII, and Wildman. These findings indicated that the wide variation in the prevalence
of MHO and MUO currently is mainly due to the heterogeneity of both definitions of obesity
and metabolic disorder, which make the results amongst studies not comparable [7].
Therefore, using a standard criterion to define an obesity phenotype is essential.
BMI and WC are the most common indicators to measure obesity in a population. BMI has
been used to define obesity in most obesity phenotype studies, and the cutoffs of BMI for
obesity were generally defined by local guidelines or academic organizations [22, 23]. Hence,
we adopted the BMI cutoffs of obesity from the Guidelines on Prevention and Control of Over-
weight and Obesity in China in the current study. They were issued in 2006 by the Ministry of
Health and Center for Disease Control in China [15]. WC, which is used to measure abdominal
adiposity and whole-body fat, is also an obligatory element in metabolic disorders. For
 Obes Facts 2019;12:78–90 86
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Liu et al.: The Prevalence of Metabolically Healthy and Unhealthy Obesity according to
Different Criteria

example, both the International Diabetes Federation and the American Heart Association/
National Heart, Lung, and Blood Institute regard WC as one of the basic components of meta-
bolic syndrome [24]. However, WC is not a necessary element in the definition of metabolic
disorder in the criteria of Karelis, Wildman, and HOMA in the studies of obesity phenotypes
[10, 19, 21]. A study by Velho et al. [25] showed that obesity defined by WC would obtain a
higher MHO prevalence than when defined by BMI, and this finding was consistent with the
present study (62.9 vs. 24.3%). Therefore, we concluded that the prevalence of WC-defined
MHO and MUO was much higher than that defined by BMI, accordingly.
Although dozens of criteria for the diagnosis of metabolic disorder were used in studies
concerning obesity phenotypes, only few studies focused on the diversity in obesity phenotype
prevalence derived from criteria. Phillips et al. [26] adopted BMI ≥30 kg/m2 to define obesity
in Irish to estimate the prevalence of MHO and MUO, using criteria of Karelis, Wildman, ATPIII,
HOMA, and Aguilar-Salinas to define metabolic disorder. The ranking of MHO and MUO prev-
alence from high to low was similar to that in our study. In the current study, we adopted
criteria of ATPIII, Wildman, Karelis, CDS, and HOMA for the following reasons. The ATPIII was
the most frequently used criterion in obesity phenotype studies, and the majority of the
reports from China also adopted it to define metabolic subtypes in obesity when estimating
prevalence [27–29]. Thus, the adoption of ATPIII will make our results comparable to previous
studies both from China and other countries. As previous studies in China used the expert
consensus to define metabolic abnormality issued by the CDS in 2013 [30], in which the meta-
bolic components included and their cutoff points might be more appropriate for Chinese, we
chose CDS criterion in our study.
Considering that the pathological mechanisms of metabolic disorder and obesity are both
associated with IR, the criteria of Wildman and Karelis incorporated IR as a component of
metabolic abnormality [10, 19, 31]. In an Italian study [32], the estimated IR calculated by
HOMA-IR was the only indicator to define metabolic disorder, despite the presence of other
metabolic factors, such as hypertension, hyperlipidemia, and hyperglycemia. So, we adopted
Wildman, Karelis, and HOMA criteria as well. However, whether IR is an essential indicator
to define metabolic disorder is a controversial issue. A study by Bertoni et al. [33] suggested
that HOMA-IR is not especially useful in addition to ATPIII criterion for metabolic syndrome
in assessing coronary or carotid subclinical disease. Also, insulin does not belong to the
clinical routine laboratory indexes. Moreover, the cutoff value of HOMA-IR varied greatly
between the Karelis, Wildman, and HOMA criteria. In the current study, the presence of IR
was defined as above the upper quartile of the distribution of the calculated HOMA index
among nondiabetic subjects. The definition was also widely used in most studies focusing on
IR and diabetes [34, 35]. In our study, the proportions of IR in MHO defined by BMI in combi-
nation with ATPIII, Karelis, Wildman, or CDS were 30.5, 16.5, 22.5, and 30.6%, respectively.
The corresponding proportions of IR in MUO were approximately 2-fold higher than those of
MHO (range 53.0–60.1%). Moreover, the presence of IR was much higher in MHO than in MUO
according to the definitions of ATPIII and CDS. Similar findings were generated in WC-defined
obesity. These findings suggested that IR might not be an essential component to define the
MHO and MUO phenotype.
Apart from IR, the Wildman criterion also involved hsCRP, an inflammatory marker, as
one of the metabolic components [36]. There was no significant difference in elevated hsCRP
between MHO and MUO when using BMI-defined obesity in the current study, which indi-
cated that hsCRP might not be a necessary component in defining metabolic status. However,
the elevated hsCRP was significantly higher in MUO than in MHO when we used WC combined
with ATPIII and HOMA (p < 0.001). Further study is needed to clarify the role of hsCRP in
obesity phenotype classification.
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Different Criteria

Using BMI to define obesity, several epidemiologic studies from America showed that the
prevalence of MHO ranged from 4.0 to 9.7% and that of MUO from 9.0 to 28.5% [5, 10, 21, 37,
38]. The prevalence of MHO in Europe varied from 1.1 to 6.6% and that of MUO from 7.2 to
21.4% [32, 39–41]. Compared to a European population, Americans had a higher prevalence
of MHO, and this was consistent with a meta-analysis [42] focusing on the prevalence of MHO
in adults. Studies in Korea showed that the prevalence of MHO varied from 5.7 to 25.8% and
the prevalence of MUO from 13.6 to 25.9%, and most studies used ATPIII to define metabolic
abnormality [22, 29, 43–45]. Our study revealed that the MHO prevalence was 4.2–11.4% and
MUO prevalence was 12.9–20.1% when we adopted ATPIII, CDS, Wildman, and Karelis criteria
to define metabolic status. These figures showed a good agreement with the previously
published data in China (MHO: 1.0–9.2%, MUO: 4.0–30.4%) [27, 28, 46, 47]. However, a
broader spectrum of age groups from 20 to 90 years was used in previous studies. As the
prevalence of both obesity and metabolic disorder would vary greatly with age, the impact of
age on the heterogeneity of the obesity phonotype prevalence between studies cannot be
ruled out and makes comparisons between studies difficult.
Few studies have reported on the age-specific prevalence of obesity phenotypes, and
thus, the relevant data are limited. The prevalence of obesity phenotypes varied considerably
with age in the current study. This was not in agreement with a study focusing on middle-aged
men from Yoo et al. [48]. One explanation for this inconsistency might be the age difference.
The participants’ age ranges in Yoo et al.’s study were relatively narrow and young, with the
majority of the participants being in their 30s to 40s.
Several studies proposed that MHO is a transient state, and it may turn into MUO in a later
life stage. A follow-up study from England [49] showed that 44.5% of MHO individuals had
transited into an unhealthy metabolic state within 8 years. In the present study, when using
WC to define obesity, the age-specific prevalence of the 2 obesity phenotypes supported the
hypothesis that MHO is the intermediate state of MUO. For example, after 65 years of age, the
prevalence of HOMA-defined MHO increased, but MUO had an opposite trend. The prevalence
of BMI-defined MHO decreased with age after 45 years, and the prevalence of MUO increased
with age during 45–65 years, which supported that both MHO and MUO were in an unstable
state. However, the prevalence of BMI-defined MHO and MUO both obviously decreased after
age 65 years, which implied that a number of obese people transformed into a nonobese state.
The BMI- and WC-defined age-specific prevalence of total obesity could explain the diversity
of the above findings (online suppl. Fig. 2). The prevalence of WC-defined obesity remained
increased with aging, whilst the age-specific prevalence of BMI-defined obesity remained
stable before age 65 years and then decreased gradually afterward, and this was similar to
the findings of Xu et al. [50] in China.
As there is no standard definition, different indicators, inclusion criteria, and/or
cutoffs have been used to define metabolic obesity phenotypes, thus making comparisons
between studies difficult. Moreover, the obesity and metabolic status varied for popu-
lation and ethnicity. Using 1 population to estimate the impact of diverse definitions of
obesity phenotypes could be a novel approach. To our knowledge, the current study is the
first community-based epidemiological study to provide the whole picture comparing the
MHO and MUO phenotypes between different obesity and metabolic disorder criteria in a
large-scale population. The sample was well representative of the general population. The
biomarkers collected in the current study were comprehensive and making it possible to
define obesity phenotypes with different criteria. The large sample size allowed us to
perform a subgroup analysis to obtain age- and gender-specific prevalence. However,
because of the nature of a cross-sectional study, we could not tell which criterion of obesity
and metabolic health would be best to predict adverse health outcomes, which poses the
major limitation to the present study. In addition, the differences in obesity phenotype
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Liu et al.: The Prevalence of Metabolically Healthy and Unhealthy Obesity according to
Different Criteria

prevalence by different criteria may not be directly extrapolated to other populations

because of the possible differences in the genetic and environmental background between
populations.

Conclusion

In summary, our study demonstrated that the prevalence of MHO and MUO varies consid-
erably according to criteria/definitions of both obesity and metabolic abnormalities. MHO
might be an intermediate state of MUO, and further study is needed to clarify this issue.

Acknowledgements

This study was supported by grants from the Beijing Municipal Science and Technology Commission
(D121100004912002) and by the National Science and Technology Support Program (2011BA/11B01).

Statement of Ethics

The study protocol was approved by the research institute’s committee on human research.

Disclosure Statement

The authors have no conflicts of interest to declare.

References
1 Wang Y, Mi J, Shan XY, Wang QJ, Ge KY. Is China facing an obesity epidemic and the consequences? The trends
in obesity and chronic disease in China. Int J Obes. 2007 Jan;31(1):177–88.
2 Mokdad AH, Ford ES, Bowman BA, Dietz WH, Vinicor F, Bales VS, et al. Prevalence of obesity, diabetes, and
obesity-related health risk factors, 2001. JAMA. 2003 Jan;289(1):76–9.
3 Van Gaal LF, Mertens IL, De Block CE. Mechanisms linking obesity with cardiovascular disease. Nature. 2006
Dec;444(7121):875–80.
4 Guh DP, Zhang W, Bansback N, Amarsi Z, Birmingham CL, Anis AH. The incidence of co-morbidities related to
obesity and overweight: a systematic review and meta-analysis. BMC Public Health. 2009 Mar;9(1):88.
5 Ortega FB, Lee DC, Katzmarzyk PT, Ruiz JR, Sui X, Church TS, et al. The intriguing metabolically healthy but
obese phenotype: cardiovascular prognosis and role of fitness. Eur Heart J. 2013 Feb;34(5):389–97.
6 Primeau V, Coderre L, Karelis AD, Brochu M, Lavoie ME, Messier V, et al. Characterizing the profile of obese
patients who are metabolically healthy. Int J Obes. 2011 Jul;35(7):971–81.
7 Phillips CM. Metabolically healthy obesity: definitions, determinants and clinical implications. Rev Endocr
Metab Disord. 2013 Sep;14(3):219–27.
8 Stefan N, Kantartzis K, Machann J, Schick F, Thamer C, Rittig K, et al. Identification and characterization of
metabolically benign obesity in humans. Arch Intern Med. 2008 Aug;168(15):1609–16.
9 Kramer CK, Zinman B, Retnakaran R. Are metabolically healthy overweight and obesity benign conditions?: A
systematic review and meta-analysis. Ann Intern Med. 2013 Dec;159(11):758–69.
10 Wildman RP, Muntner P, Reynolds K, McGinn AP, Rajpathak S, Wylie-Rosett J, et al. The obese without cardio-
metabolic risk factor clustering and the normal weight with cardiometabolic risk factor clustering: prevalence
and correlates of 2 phenotypes among the US population (NHANES 1999-2004). Arch Intern Med. 2008 Aug;
168(15):1617–24.
11 Wang Z, Chen Z, Zhang L, Wang X, Hao G, Zhang Z, et al.; China Hypertension Survey Investigators. Status of
hypertension in China: results from the China Hypertension Study. Circulation. 2018 May;137(22):2344–56.
12 Wang Z, Zhang L, Chen Z, Wang X, Shao L, Guo M, et al.; China Hypertension Survey Group. Survey on preva-
lence of hypertension in China: background, aim, method and design. Int J Cardiol. 2014 Jul;174(3):721–3.
13 Ye Y, Wang Y, Shen Z. National Guide to Clinical Laboratory Procedures. 3rd ed. Nanjing, China: Southeast
University Press; 2006.
 Obes Facts 2019;12:78–90 89
DOI: 10.1159/000495852 © 2019 The Author(s). Published by S. Karger AG, Basel
www.karger.com/ofa

Liu et al.: The Prevalence of Metabolically Healthy and Unhealthy Obesity according to
Different Criteria

14 Fang X, Wang Z, Wang C, Wu J, Yang Y, Li F, et al. Cardiovascular and Cognitive Health Study in Middle-Aged
and Elderly Residents of Beijing (CCHS-Beijing): design and Rationale. Neuroepidemiology. 2016;46(3):182–
90.
15 Chen C, Kong L. Guidelines on prevention and control of overweight and obesity in China. Beijing, China:
People’s Medical Publishing House; 2006.
16 Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment:
insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man.
Diabetologia. 1985 Jul;28(7):412–9.
17 Balkau B, Charles MA; European Group for the Study of Insulin Resistance (EGIR). Comment on the provisional
report from the WHO consultation. Diabet Med. 1999 May;16(5):442–3.
18 Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive Summary
of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evalu-
ation, And Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III). JAMA. 2001 May;
285(19):2486–97.
19 Karelis AD, Brochu M, Rabasa-Lhoret R. Can we identify metabolically healthy but obese individuals (MHO)?
Diabetes Metab. 2004 Dec;30(6):569–72.
20 Chinese Diabetes Society. China T2DM prevention and treatment guideline (2013). Chin J Diabetes Mellitus.
2014;6:447–498.
21 Meigs JB, Wilson PW, Fox CS, Vasan RS, Nathan DM, Sullivan LM, et al. Body mass index, metabolic syndrome,
and risk of type 2 diabetes or cardiovascular disease. J Clin Endocrinol Metab. 2006 Aug;91(8):2906–12.
22 Chang Y, Ryu S, Suh BS, Yun KE, Kim CW, Cho SI. Impact of BMI on the incidence of metabolic abnormalities in
metabolically healthy men. Int J Obes. 2012 Sep;36(9):1187–94.
23 Guo F, Garvey WT. Cardiometabolic disease risk in metabolically healthy and unhealthy obesity: stability of
metabolic health status in adults. Obesity (Silver Spring). 2016 Feb;24(2):516–25.
24 Alberti KG, Eckel RH, Grundy SM, Zimmet PZ, Cleeman JI, Donato KA, et al.; International Diabetes Federation
Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Asso-
ciation; World Heart Federation; International Atherosclerosis Society; International Association for the
Study of Obesity. Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes
Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American
Heart Association; World Heart Federation; International Atherosclerosis Society; and International Associ-
ation for the Study of Obesity. Circulation. 2009 Oct;120(16):1640–5.
25 Velho S, Paccaud F, Waeber G, Vollenweider P, Marques-Vidal P. Metabolically healthy obesity: different prev-
alences using different criteria. Eur J Clin Nutr. 2010 Oct;64(10):1043–51.
26 Phillips CM, Dillon C, Harrington JM, McCarthy VJ, Kearney PM, Fitzgerald AP, et al. Defining metabolically
healthy obesity: role of dietary and lifestyle factors. PLoS One. 2013 Oct;8(10):e76188.
27 Chen Y, Zhang N, Sun G, Guo X, Yu S, Yang H, et al. Metabolically healthy obesity also has risk for hyperuricemia
among Chinese general population: A cross-sectional study. Obes Res Clin Pract. 2016 Sep;10 Suppl 1:S84–95.
28 Cao X, Zhou J, Yuan H, Wu L, Chen Z. Chronic kidney disease among overweight and obesity with and without
metabolic syndrome in an urban Chinese cohort. BMC Nephrol. 2015 Jun;16(1):85.
29 Yang Y, Herting JR, Choi J. Obesity, metabolic abnormality, and health-related quality of life by gender: a cross-
sectional study in Korean adults. Qual Life Res. 2016 Jun;25(6):1537–48.
30 Luo D, Liu F, Li X, Yin D, Lin Z, Liu H, et al. Comparison of the effect of ‘metabolically healthy but obese’ and
‘metabolically abnormal but not obese’ phenotypes on development of diabetes and cardiovascular disease in
Chinese. Endocrine. 2015 May;49(1):130–8.
31 Cani PD, Amar J, Iglesias MA, Poggi M, Knauf C, Bastelica D, et al. Metabolic endotoxemia initiates obesity and
insulin resistance. Diabetes. 2007 Jul;56(7):1761–72.
32 Calori G, Lattuada G, Piemonti L, Garancini MP, Ragogna F, Villa M, et al. Prevalence, metabolic features, and
prognosis of metabolically healthy obese Italian individuals: the Cremona Study. Diabetes Care. 2011 Jan;
34(1):210–5.
33 Bertoni AG, Wong ND, Shea S, Ma S, Liu K, Preethi S, et al. Insulin resistance, metabolic syndrome, and
subclinical atherosclerosis: the Multi-Ethnic Study of Atherosclerosis (MESA). Diabetes Care. 2007 Nov;
30(11):2951–6.
34 Jennings CL, Lambert EV, Collins M, Joffe Y, Levitt NS, Goedecke JH. Determinants of insulin-resistant pheno-
types in normal-weight and obese Black African women. Obesity (Silver Spring). 2008 Jul;16(7):1602–9.
35 Pimentel AC, Scorsatto M, de Oliveira GM, Rosa G, Luiz RR. Characterization of metabolically healthy obese
Brazilians and cardiovascular risk prediction. Nutrition. 2015 Jun;31(6):827–33.
36 Santaniemi M, Ukkola O, Malo E, Bloigu R, Kesäniemi YA. Metabolic syndrome in the prediction of cardiovas-
cular events: the potential additive role of hsCRP and adiponectin. Eur J Prev Cardiol. 2014 Oct;21(10):1242–8.
37 Hankinson AL, Daviglus ML, Van Horn L, Chan Q, Brown I, Holmes E, et al. Diet composition and activity level
of at risk and metabolically healthy obese American adults. Obesity (Silver Spring). 2013 Mar;21(3):637–43.
38 Kanagasabai T, Thakkar NA, Kuk JL, Churilla JR, Ardern CI. Differences in physical activity domains, guideline
adherence, and weight history between metabolically healthy and metabolically abnormal obese adults: a
cross-sectional study. Int J Behav Nutr Phys Act. 2015 May;12(1):64.
 Obes Facts 2019;12:78–90 90
DOI: 10.1159/000495852 © 2019 The Author(s). Published by S. Karger AG, Basel
www.karger.com/ofa

Liu et al.: The Prevalence of Metabolically Healthy and Unhealthy Obesity according to
Different Criteria

39 Popa S, Moţa M, Popa A, Moţa E, Serafinceanu C, Guja C, et al. Prevalence of overweight/obesity, abdominal
obesity and metabolic syndrome and atypical cardiometabolic phenotypes in the adult Romanian population:
PREDATORR study. J Endocrinol Invest. 2016 Sep;39(9):1045–53.
40 Mørkedal B, Vatten LJ, Romundstad PR, Laugsand LE, Janszky I. Risk of myocardial infarction and heart failure
among metabolically healthy but obese individuals: HUNT (Nord-Trøndelag Health Study), Norway. J Am Coll
Cardiol. 2014 Mar;63(11):1071–8.
41 Arnlöv J, Ingelsson E, Sundström J, Lind L. Impact of body mass index and the metabolic syndrome on the risk
of cardiovascular disease and death in middle-aged men. Circulation. 2010 Jan;121(2):230–6.
42 Wang B, Zhuang R, Luo X, Yin L, Pang C, Feng T, et al. Prevalence of Metabolically Healthy Obese and Meta-
bolically Obese but Normal Weight in Adults Worldwide: A Meta-Analysis. Horm Metab Res. 2015 Oct;47(11):
839–45.
43 Choi KM, Cho HJ, Choi HY, Yang SJ, Yoo HJ, Seo JA, et al. Higher mortality in metabolically obese normal-weight
people than in metabolically healthy obese subjects in elderly Koreans. Clin Endocrinol (Oxf). 2013 Sep;79(3):
364–70.
44 Lee SK, Kim SH, Cho GY, Baik I, Lim HE, Park CG, et al. Obesity phenotype and incident hypertension: a
prospective community-based cohort study. J Hypertens. 2013 Jan;31(1):145–51.
45 Jung CH, Lee MJ, Kang YM, Jang JE, Leem J, Hwang JY, et al. The risk of incident type 2 diabetes in a Korean
metabolically healthy obese population: the role of systemic inflammation. J Clin Endocrinol Metab. 2015 Mar;
100(3):934–41.
46 Zhang N, Chen Y, Guo X, Sun G, Dai D, Sun Y. Metabolic Abnormalities, But Not Metabolically Healthy Obesity,
Are Associated with Left Ventricular Hypertrophy. Heart Lung Circ. 2017 Mar;26(3):251–7.
47 Du T, Zhang J, Yuan G, Zhang M, Zhou X, Liu Z, et al. Nontraditional risk factors for cardiovascular disease and
visceral adiposity index among different body size phenotypes. Nutr Metab Cardiovasc Dis. 2015 Jan; 25(1):
100–7.
48 Yoo HK, Choi EY, Park EW, Cheong YS, Bae RA. Comparison of Metabolic Characteristics of Metabolically
Healthy but Obese (MHO) Middle-Aged Men According to Different Criteria. Korean J Fam Med. 2013 Jan;
34(1):19–26.
49 Hamer M, Bell JA, Sabia S, Batty GD, Kivimäki M. Stability of metabolically healthy obesity over 8 years: the
English Longitudinal Study of Ageing. Eur J Endocrinol. 2015 Nov;173(5):703–8.
50 Xu W, Zhang H, Paillard-Borg S, Zhu H, Qi X, Rizzuto D. Prevalence of Overweight and Obesity among Chinese
Adults: Role of Adiposity Indicators and Age. Obes Facts. 2016;9(1):17–28.