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Prevalence of abdominal obesity
and its associated comorbid condition in adult
Yemeni people of Sana'a City
Mohammed Ahmed Bamashmos
Correspondence:
Mohammed
Ahmed Bamashmos (MD),
Associate Professor of Internal Medicine, Faculty
of Medicine,
Sana'a University
Yemen
Email : mohbamashmoos
@yahoo.com
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Abstract
Objective: Abdominal obesity is
a metabolic problem that has become increasingly
common worldwide over the past several
decades. Its prevalence is increased in
both advanced and developing countries
including Yemen. The aim of this cross
sectional study was to investigate the
prevalence of Abdominal obesity in a sample
of Yemeni adult individuals and its association
with other comorbid conditions namely,
hypertension, diabetes, dyslipidemia (high
triglyceride, low high density lipoprotein)
and metabolic syndrome (MS).
Methodology: A sample of 1118 adult
Yemeni people equal to or over 18 years
was randomly chosen to represent the population
living in Sana'a City during a period
of two years from April 2016 to April
2018. All the study group underwent full
clinical history and examination which
included measurement of BP and waist circumference
and the following laboratory investigations
(FBS, serum TG, HDL, and LDL).
Results: The prevalence of abdominal
obesity in this study was 24.5% (7.9%
male and 44.2% female). Central obesity
in this study was significantly correlated
with age and sex. The highest prevalent
comorbidity in patients with abdominal
obesity was high BP (41.3%), followed
by high serum TG (40 %), higher prevalence
of MS (40%), low serum HDL (37.8%) high
LDL (20.1%) raised fasting blood glucose
(22.1%) than those without abdominal obesity
(5.5%, 31.3%, 16.6%, 8.5%, 12.5% and increased
FBS 10% respectively).
Conclusion:
Hypertension, diabetes, dyslipidemia
and MS are strongly correlated with abdominal
obesity.
Key words: central obesity, hypertension,
dyslipidemia, MS
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Obesity is a worldwide epidemic. Beyond the
fat mass per se, the pattern of fat distribution
has a profound influence on cardiometabolic
risk. Visceral abdominal fat (VAF) is metabolically
active and pro-inflammatory and presents a higher
cardiometabolic risk association and calcification
of the coronary arteries than the body mass
index (BMI) and has more impact on health than
subcutaneous fat, presenting a risk factor for
increased incidence of metabolic syndrome (1,
2). Abdominal obesity (AO) is directly associated
with increased VAF, and it is also associated
with endothelial dysfunction, inflammation,
insulin resistance, diabetes mellitus, hypercholesterolemia,
metabolic syndrome [MetS], and cancer (1, 3).
There are several methods available to measure
AO. Waist circumference (WC) provides an indicator
of central adiposity that is the most practical
and easiest method used in large-scale epidemiological
studies (4). It is a good predictor of cardiometabolic
morbidity and mortality, and it has also a positive
association with visceral abdominal fat. However,
WC does not allow us to differentiate between
visceral fat and subcutaneous fat; methods such
as absorptiometry by dual energy X-ray (DEXA),
impedance, or densitometry can be used to handle
this differentiation (5-7). WC measurement requires
correct and standardized procedures, which depend
mainly on training and adequate equipment. A
standardized technique requires that the person
being measured removes bulky or tight garments,
as well as shoes with heels, empties their bladder
then stands in the upright position, with arms
loosely positioned to the side. The tape is
passed around the body and positioned mid-way
between the iliac crest and costal margin of
the lower rib, ensuring that it is Population
Organization Recommended waist circumference
threshold for abdominal obesity Men Women Europid
IDF >94 cm >80 cm Caucasian
WHO >94 cm [increased risk] >102
cm [still higher risk] >80 cm [increased
risk] >88 cm [still higher risk] United
States AHA/NHLBI [ATP III] >102 cm
>88 cm Canada Health Canada >102
cm >88 cm European European cardiovascular
societies >102 cm ?88 cm Asian [including
Japanese] IDF >90 cm >80
cm Asian WHO >90 cm >80
cm Japanese Japanese obesity society >85
cm >90 cm China Cooperative task force
>85 cm >80 cm Middle East,
Mediterranean IDF >94 cm >80
cm Sub-Saharan African IDF >94 cm
>80 cm Ethnic Central and South American
IDF >90 cm >80 cm. Waist
circumference cutoffs are recommended for the
diagnosis of abdominal obesity according to
ethnicity and gender (8,9). In 2009, a method
to standardize the diagnosis of metabolic syndrome
was established, upon discussions held by the
International Diabetes Federation (IDF) and
the American Heart Association/National Heart,
Lung, and Blood Institute. In this context,
it was suggested that ethnicity and gender should
be considered for the diagnosis of AO (9)
In decades past, many clinicians were taught
in medical school that the adipose cell is a
vehicle for energy storage and nothing more.
Today, there is a different perception of the
adipose cell; specifically, it is an active
endocrine organ that communicates with gut hormones
and a master regulator in the brain to control
appetite and satiety. It also exerts pathologic
effects on other organs and critical metabolic
and immunologic processes .Four major hormones-ghrelin,
insulin, peptide YY (PYY) from the gut, and
leptin from fat tissue-participate in appetite
and satiety regulation in communication with
each other and the central control of energy
balance, the arcuate nucleus in the hypothalamus.
Ghrelin is a short-term appetite hormone, the
"hunger hormone", that brings on feelings
of hunger at mealtimes. Secreted in the gastric
fundus, ghrelin rises immediately before meals
and falls as insulin levels rise in response
to the meal(10,11). It also increases during
weight loss, which may be a factor in making
successful weight loss so difficult. However,
ghrelin levels decrease in persons who have
had gastric bypass surgery, which may aid in
maintaining weight loss (10). Insulin, in addition
to its multiple other metabolic functions, acts
as a satiety signal to the brain, causing feelings
of fullness. PYY, secreted in the distal small
intestine in response to food, signals satiety
to the hypothalamus to counteract the influence
of ghrelin. Levels of PYY are significantly
lower in obese versus normal-weight persons,(8)
but are elevated after gastric bypass(11). Leptin
was the original "satiety factor,"
discovered to much excitement by Friedman and
coworkers in 1994(12). This hormone is produced
in adipose tissue in proportion to body fat;
the more fat present, the more leptin secreted.
Initially, it was hoped that exogenous leptin
administration would be a "magic bullet"
for curing obesity and establishing the condition
as a metabolic disorder instead of a personal
failing(9). Despite its effectiveness in mice
with a genetic defect in the leptin molecule,
exogenous leptin does not produce meaningful
weight loss in obese humans, apparently because
the brain becomes resistant to it. However,
leptin is one of many neuro hormonal pathways
that have evolved genetically to prevent starvation
and ensure survival. In addition, the hypothalamus
contains neurons that can either stimulate or
inhibit food intake, and many of the gut hormones
exert actions on both sides of the equation(13).
The possibilities for routes to intervention
among this wealth of pathways remain promising
and rational in the search for weight control
treatments. Current thinking now holds that
fat tissue is an active participant in weight
regulation. In one current theory, it is the
basis of adiposopathy, defined by Bays and colleagues
as pathogenic adipose tissue whose toxicity
may be worsened by fat accumulation and a sedentary
lifestyle in genetically susceptible individuals(14).
This dysfunctional tissue releases increased
amounts of free fatty acids (FFAs) and abnormal
amounts of inflammatory factors such as cytokines
from macrophages. Such changes can promote insulin
resistance in skeletal muscle and the liver,
increased insulin secretion, dyslipidemia, hypertension,
and type 2 diabetes, all components of the metabolic
syndrome, which increases the risk of atherosclerosis
(14-16). Muscle biopsies in obese patients show
that deposits of fat are stored in liver when
fat can no longer be stored subcutaneously,
with some cases resulting in steatohepatitis
and eventually fibrosis. Excess fat may be associated
with androgen elevations in women (or decreases
in men); increases in plasminogen-activator
inhibitor 1, which encourages thrombosis; and
asthma, as a consequence of pro inflammatory
changes. Even osteoarthritis may be an outcome
of increased inflammation, although it is also
mediated by the mechanical load of excess weight
on the joints(17,18). Not everyone who is obese
has metabolic syndrome or type 2 diabetes-although
these are perhaps the most prevalent complications
of obesity. Genetic susceptibility is yet another
confounding component of obesity. The ability
to differentiate genetically susceptible humans
is not yet within reach. Better predictors of
who will and will not respond to adiposity with
endocrine and other consequences are still needed.
In the meantime, ongoing research on appetite
and satiety regulation has made it clear that
obesity is a disease largely beyond an individual's
control(19) rather than a function of inadequate
willpower. The development and availability
of medications and procedures that address the
underlying pathobiology of obesity heralds a
new approach to stemming the tide of the obesity
epidemic.
This
was
a
cross
sectional
population
based
study
conducted
in
Sana'a
city
for
a
period
of
2
years
between
April
2017
and
April
2018.
A
sample
of
1,118
adult
Yemeni
people
(508
male
and
610
aged
This
was
a
cross
sectional
population
based
study
conducted
in
Sana'a
city
for
a
period
of
2
years
between
April
2017
and
April
2018.
A
sample
of
1,118
adult
Yemeni
people
(508
male
and
610
aged
This
was
a
cross
sectional
population
based
study
conducted
in
Sana'a
city
for
a
period
of
2
years
between
April
2017
and
April
2018.
A
sample
of
1,118
adult
Yemeni
people
(508
male
and
610
aged
>18
years)
was
randomly
selected.
The
data
collection
was
from
those
attending
Al-Kuwait
University
Hospital
and
Consultation
Clinic.
All
the
participants
in
this
study
underwent
complete
clinical
history
(regarding
their
age,
occupation,
habits,
any
history
of
hypertension,
diabetes
mellitus,
dyslipidemia
and
medication).
Anthropometric
measurements
included
measurement
of
waist
circumference
and
systolic
and
diastolic
blood
pressure.
Waist
circumference
was
manually
measured
on
standing
subjects
with
soft
tape
midway
between
the
lowest
rib
and
the
iliac
crest.
WC
was
divided
into
abdominal
overweight
(85-95
cm
in
males
and
80-90
cm
in
females)
and
abdominal
obesity
groups
(WC
>
95
cm
in
males
and
>90
cm
in
females)
(20,21
).
WC
>85
cm
in
males
and
>80
cm
in
females
were
defined
as
elevated
WC.
Two
blood
pressure
recordings
were
obtained
from
the
right
arm
of
patients
with
standard
mercury
sphygmomanometer
in
a
sitting
position
after
10
minutes
of
rest;
measurements
were
taken
in
3-5
minute
intervals
and
the
mean
values
were
calculated.
Blood
pressure
was
classified
as
normotensive
(SBP
<
120
mmHg
and
DBP
<
80
mmHg),
pre-hypertensive
(SBP:
120-139
mmHg
and/or
DBP:
80-89
mmHg)
and
hypertensive
(SBP
>140
mmHg
and/or
DBP
?
90
mmHg)
by
the
Seventh
Report
of
the
Joint
National
Committee
on
the
Prevention,
Detection,
Evaluation,
and
Treatment
of
High
Blood
Pressure
(22,23);
fasting
blood
glucose,
total
cholesterol,
triglyceride,
LDL
and
HDL
cholesterol
were
measured.
The
American
Diabetes
Association
criteria
was
used
to
classify
FBG
as
normal
glucose
(FBG
<
5.6
mmol/L),
impaired
fasting
glucose
(IFG)
(FBG
>5.6
mmol/L
<FBG
<
7.0
mmol/L),
and
diabetic
(FBG
>7.0
mmol/L).
Type
2
diabetes
mellitus
was
defined
according
to
the
American
Diabetes
Association
(24)
A1C
>6.5%.
The
test
should
be
performed
in
a
laboratory
using
a
method
that
is
NGSP
certified
and
standardized
to
the
DCCT
assay
or
FPG
>126
mg/dl
(7.0
mmol/l).
Fasting
is
defined
as
no
caloric
intake
for
at
least
8
hours.
In
the
absence
of
unequivocal
hyperglycemia,
result
should
be
confirmed
by
repeat
testing
or
2-hour
plasma
glucose
>
200
mg/dl
(11.1mmol/l)
during
an
OGTT.
The
test
should
be
performed
as
described
by
the
World
Health
Organization,
using
a
glucose
load
containing
the
equivalent
of
75
g
anhydrous
glucose
dissolved
in
water.
In
the
absence
of
unequivocal
hyperglycemia,
result
should
be
confirmed
by
repeat
testing
or
in
a
patient
with
classic
symptoms
of
hyperglycemia
or
hyperglycemic
crisis,
a
random
plasma
glucose
200
mg/dl
(11.1mmol
|
l).
Dyslipidemia
was
classified
according
to
ATP
III,
TG:
Normal
<
1.69
mmol/L,
Borderline
high
1.69-2.26
mmol/L,
High
2.26-5.65
mmol/L,
Very
high
>5.65
mmol/L;
TC:
Desirable
<
5.17
mmol/L,
Borderline
high
5.17-6.24
mmol/L,
High
>6.24
mmol/L;
HDL-C:
High
1.56
mmol/L,
Optimal
1.03-1.56
mmol/L,
Low
<l.03
mmol/L;
LDL-C:
Optimal
<2.59
mmol/L,
Near
optimal
2.59-3.38
mmol/L,
Borderline
high
3.38-4.16
mmol/L,
High
4.16-4.94
mmol/L,
Very
high
>4.94
mmol/L.(25).
Metabolic
syndrome
was
diagnosed
by
the
presence
of
three
or
more
of
the
following
criteria
(26).
•
Fasting
glucose
?100
mg/dL
(or
receiving
drug
therapy
for
hyperglycemia)
•
Blood
pressure
?130/85
mm
Hg
(or
receiving
drug
therapy
for
hypertension)
•
Triglycerides
?150
mg/dL
(or
receiving
drug
therapy
for
hypertriglyceridemia)
•
HDL-C
<
40
mg/dL
in
men
or
<
50
mg/dL
in
women
(or
receiving
drug
therapy
for
reduced
HDL-C)
•
Waist
circumference
>102
cm
(40
in)
in
men
or
>88
cm
(35
in)
in
women;
if
Asian
American,
>90
cm
(35
in)
in
men
or
>80
cm
(32
in)
in
women
(The
international
diabetes
federation
[IDF]
criteria
allow
the
use
of
a
body
mass
index
[BMI]
>30
kg/m2
in
lieu
of
the
waist
circumference
criterion.)
Statistical
analysis
was
undertaken
using
the
Statistical
Package
for
the
Social
Sciences
(Windows
version
13.0;
SPSS,
Chicago
IL
USA).
Differences
between
groups
were
tested
statistically
using
the
Chi
square
test
for
categorical
and
T
test
for
numerical
variables.
Data
were
considered
statistically
significant
when
the
p-value
was
<
0.05.
A
study
sample
included
1,118
persons
aged
between
18-83;
of
them
508
(45.4%)
were
male
and
610
(54.6%)
were
female
.
The
Mean
age
±
SD
was
47.4
±10.2
years,
with
an
age
range
of
30-77
years
with
no
significant
age
difference
between
men
and
women.
The
prevalence
of
abdominal
obesity
according
to
WC
was
24.5%.
The
physical
and
metabolic
characteristic
of
the
study
population
by
gender
are
shown
in
Table
1.
Women
have
significantly
higher
prevalence
of
abdominal
obesity,
systolic
and
diastolic
BP,
high
serum
TG,
high
LDL,
low
serum
HDL
as
well
as
high
prevalence
of
MS.
Table
1:
shows
the
clinical
and
laboratory
characteristics
of
the
study
group
Table
2:
The
prevalence
of
both
clinical
and
laboratory
characteristics
between
obese
and
non-obese
The
highest
prevalent
comorbidity
in
patients
with
abdominal
obesity
was
high
BP
(41.3%),
followed
by
high
serum
TG
(40
%),
high
prevalence
of
MS
(40%),
low
serum
HDL
(37.8%)
high
LDL
(
20.1%
)
raised
fasting
blood
glucose
(22.1%)
than
those
without
abdominal
obesity
(5.5%,
31.3%,
16.6%,
8.5%,
12.5%
and
increased
FBS
10%
respectively).
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