Journal of Human Hypertension (2001) 15, 299–305
 2001 Nature Publishing Group All rights reserved 0950-9240/01 $15.00
www.nature.com/jhh
ORIGINAL ARTICLE
Apolipoprotein B, ratio of total cholesterol
to HDL-C, and blood pressure in
abdominally obese white and black
American women
IS Okosun1, S Choi1, R Hash2 and GEA Dever1
1
Department of Community Medicine, Mercer University School of Medicine 1550 College Street Macon,
GA, USA; 2Department of Family Medicine, Mercer University School of Medicine 1550 College Street
Macon, GA, USA
Objective: To compare the association of apolipoprotein
B (ApoB) and total cholesterol to high-density lipoprotein cholesterol (TC/HDL) with blood pressure in
abdominally obese white and black American women.
We also sought to determine if there are ethnic differences in blood pressure values that could be explained
by differences in mean values of ApoB and TC/HDL.
Methods: Data (n ⴝ 1844) from the Third US National
Health and Nutrition Examination Survey were used in
this study. Abdominal obesity was defined as waist circumference (WC) of ⭓88 cm or having WC greater than
what was expected as predicted from residuals obtained
from linear regression of WC on BMI. Bi-variate Pearson’s correlation analysis was used to quantify the
degree of association of ApoB and TC/HDL with blood
pressure and other lipids. Multiple linear regression
analysis was used to assess the independent contribution of ApoB and TC/HDL to blood pressure,
adjusting for age, total cholesterol, alcohol intake, and
smoking. To determine ethnic differences in blood
pressure values associated with ApoB or TC/HDL,
dummy variables were used to compare blacks with
whites fitted in multiple regression models, while
adjusting for age, total cholesterol, alcohol intake and
smoking.
Results: Elevated ApoB was positively associated with
diastolic and systolic blood pressure (DBP/SBP) in
blacks and whites, independent of age, total cholesterol,
alcohol intake and smoking (P ⬍ 0.01). Elevated TC/HDL
was also positively associated with increased DBP and
SBP in whites (P ⬍ 0.05). For the same value of ApoB
and TC/HDL whites had higher values of DBP and SBP
than blacks, adjusting for confounding variables.
Conclusions: Compared with TC/HDL, ApoB was more
strongly associated with DBP and SBP in both abdominally obese white and black women. Since ApoB is
associated with hypertension, the combination of elevated ApoB and hypertension may identify a group of
patients with more marked risk of vascular disease,
thus, warranting further investigation.
Journal of Human Hypertension (2001) 15, 299–305
Keywords: blood pressure; abdominal obesity; ApoB; HDL-C; LDL-C, total cholesterol
Introduction
Although a large body of epidemiologic evidence
links abdominal obesity with increased risk of many
cardiovascular diseases (CVD),1–8 the mechanism for
the association is not clear. Elevated total cholesterol and lipoproteins through atherogenic and
thrombotic processes have been hypothesised in the
association of abdominal adiposity with CVD.9,10
Correspondence: Ike S Okosun, PhD, MPH, FRIPHH, Department
of Community Medicine, Mercer University School of Medicine,
1550 College Street Macon, GA, 31207 USA
E-mail: okosunFi얀mercer.edu
Received 15 September 2000; revised 16 November 2000;
accepted 29 November 2000
Among the conventional lipids, the ratio of total
cholesterol to high-density lipoprotein cholesterol
(TC/HDL) is a reliable predictor of CVD often
employed in epidemiologic investigations.
Recent studies suggest apolipoprotein B (ApoB)
may be a better predictor of CVD than TC/HDL.11,12
Indeed, in multiple regression analysis, ApoB was
found to have a much stronger association with
ischaemic heart disease (IHD) than TC/HDL or lipoprotein-cholesterols.12 In a statistical model that
included traditional risk factors such as age, hypertension, smoking, diabetes and family history of
CVD, ApoB was found to be the best metabolic predictor for IHD compared to TC/HDL or lipoprotein-cholesterols.12
Thus, the ability to adequately identify individuals
Atherogenic factors in abdominally obese women
IS Okosun et al
300
at high risk of CVD solely on the basis of TC/HDL
is at variance with evidence showing that up to 50%
of subjects with CVD may have clinically acceptable
values for these lipids.13–17 Data also indicates that
patients undergoing cholesterol-lowering treatments
who achieve a significant decrease in low-density
liproprotein-cholesterol (LDL-C) levels nonetheless
carry risk for CVD.18 Using polyacrylamide gel
electrophoresis, data further suggest that patients
with visceral adiposity often possess greater proportion of small, dense, cholesterol depleted LDL-C
particles than total cholesterol and LDL-C.19 Indeed,
it has been estimated that patients with visceral
obesity have 15–20% higher than normal plasma
ApoB levels despite having normal total cholesterol
and LDL-C.13 Thus, ApoB concentration in abdominally obese subjects could be a more potent atherogenic marker for predicting CVD than conventional
lipids.
Although the mechanism of action of TC/HDL and
ApoB is not well understood, some investigators
have postulated the action of these lipoprotein
phenotypes in CVD is linked to visceral or abdominal adiposity by atherogenic and thrombotic mechanisms.9,10,20,21 ApoB is the protein moiety of LDL-C
that provides estimates of circulating LDL-C particle
numbers. Total plasma ApoB concentration also
accounts for the number of triglyceride-rich lipoproteins (very low-density lipoprotein and intermediate-density lipoproteins).11 TC/HDL has been speculated to be linked to CVD by its thrombotic action,
while ApoB facilitates the delivery of cholesterol to
peripheral tissue.22
Despite differences in rates of abdominal obesity
and risks for hypertension, the association of ApoB
and TC/HDL with blood pressure in white and black
American women has been studied minimally. In
this study we aimed to compare the association of
ApoB and TC/HDL with blood pressure in abdominally obese white and black American women. We
also sought to determine if there are ethnic differences in blood pressure values that could be
explained by differences in mean values of ApoB
and TC/HDL.
Materials and methods
Data source
Data from the Third US National Health and
Nutrition Examination Survey (NHANES III), as provided by the National Center for Health Statistics,
were used in this investigation. The sampling and
measurement procedures have been described in
detail by other investigators.23,24 Briefly, NHANES
III is a multistage probability sample of non-institutionalised US population groups defined and
examined in two phases between 1988 and 1994.
Only abdominally obese subjects identified as nonHispanic white and non-Hispanic black women who
had no prior histories of hypertension or diabetes
were eligible for this investigation.
Journal of Human Hypertension
This study was further confined to individuals
aged 17–90 years for whom the variables, weight,
height, waist, diastolic (DBP) and systolic (SBP)
blood pressure, HDL-C, LDL-C, total cholesterol and
ApoB were obtained. Weight was measured at a
standing position using a Toledo self-zeroing weight
scale. Height was measured at an upright position
with a standiometer. Waist measurement was made
at the natural waist midpoint between the bottom of
the rib cage and above the top of the iliac crest, and
to the nearest 0.1 cm.
Detailed methods used in measuring serum cholesterol, HDL-C and LDL-C have been described elsewhere.25,26 Cholesterol was measured enzymatically
in serum or plasma in a series of coupled reactions
that hydrolysed cholesterol ester and triglyceride to
cholesterol and glycerol, respectively. ApoB was
measured by radial immunodiffusion in the first
8.2% of the specimens and by rate immunonephelometry for the remaining.27
Three blood pressure measurements were
obtained from each subject using a standard mercury sphygmomanometer at a 60-second interval
between inflation cuffs. The average of the three
readings was utilised for this analysis. Smoking and
alcohol intake were assessed by self-report. Current
smoking was defined as having had at least one cigarette in the last 5 days and categorised as 1 and 0,
for current smokers and non-smokers, respectively.
Alcohol use was defined as drinking 1 or more
alcoholic drinks in a day, and was also graded
dichotomously.
Definition of terms
Abdominal obesity: Abdominal obesity was defined
as waist circumference (WC) of 88 cm or greater.28,29
Due to the degree of correlation between body mass
index (BMI) and WC, it is often difficult to differentiate the roles of these obesity phenotypes without
imaging techniques such as magnetic resonance or
computerised tomography. Imaging techniques are,
however, impractical in large-scale field epidemiology because they are arduous and expensive, and
their use carries risk of radiation. In this study BMI
adjusted abdominal obesity was defined as WC
larger than expected from BMI predicted WC value
(measured WC minus circumference predicted from
their BMI).30 Predicted WC values were derived
from linear regression of WC on BMI.30 The
residuals were obtained from WC = 2.31*BMI +
30.60, r2 = 0.73. Thus, subjects having positive
residual values were also classified as abdominally
obese.
Statistical analysis
Statistical programmes available in SPSS for Windows were utilised for this analysis.31 Because of the
complex sampling method used for NHANES III,
variance estimates were obtained using WesVarPC
Atherogenic factors in abdominally obese women
IS Okosun et al
statistical programme.32 Ethnic differences for continuous and categorical variables were assessed with
the Student’s t-test and ␹2 statistics, respectively.
Pearson’s correlation analysis was used to quantify
the degree of linear correlation of ApoB and TC/HDL
with blood pressure and other lipids. To investigate
ethnic differences in blood pressure values attributable to ApoB or TC/HDL, dummy variables were
used to compare blacks with whites fitted in multiple regression models, adjusting for age, total cholesterol, alcohol intake and smoking. Multiple linear
regression analysis was used to assess the independent contribution of ApoB and TC/HDL to blood
pressures, among individuals with abdominal obesity defined as WC ⭓88 cm (Model I) and among subjects meeting abdominal obesity criteria of WC
larger than expected (Model II). In both models,
adjustment were made for age, total cholesterol,
alcohol intake and smoking. The traditional P ⬍
0.05 was used to indicate statistical significance.
Results
The basic anthropometric and clinical characteristics of the 1844 eligible abdominally obese subjects as defined by WC ⭓88 cm are shown in Table
1. As expected, mean values for total cholesterol and
LDL-C in these abdominally obese women were
higher than clinically acceptable values. The mean
values of TC/HDL were also above the clinically
acceptable value of less than 3.5 mg/dl. There were
significant ethnic differences for most anthropometric and clinical variables. White women tended
Table 1 Characteristics of studied sample of abdominally obese
American women
n (%)
Age (yrs)
Weight (kg)
Waist girth (cm)
BMI (kg/m2)
Total cholesterol
(TC) (mg/dl)
HDL-cholesterol
(mg/dl)
LDL-cholesterol
(mg/dl)
ApoB (mg/dl)
TC/HDL
Diastolic BP
(mm Hg)
Systolic BP
(mm Hg)
Hypertension (%)
Alcohol intake
(%)
Smoking (%)
White
Black
P-value
1250 (67.8)
54.0 ± 19.6
81.1 ± 13.9
99.9 ± 8.9
27.6 ± 4.2
594 (32.2)
41.8 ± 16.3
86.3 ± 17.0
100.5 ± 10.9
30.0 ± 5.8
⬍0.001
⬍0.001
0.224
⬍0.001
285.4 ± 224.9
307.9 ± 262.4
⬍0.057
47.2 ± 14.2
52.4 ± 15.3
⬍0.001
138.5 ± 37.5
113.0 ± 26.0
6.6 ± 5.8
129.1 ± 39.1
103.9 ± 26.1
6.5 ± 6.3
0.001
⬍0.001
0.606
73.5 ± 9.7
73.5 ± 11.3
0.979
122.3 ± 17.8
16.5
124.5 ± 16.3
19.4
0.006
0.080
54.2
26.6
45.5
35.3
⬍0.001
⬍0.001
Abdominal obesity was defined as waist circumference of 88 cm
or greater; TC/HDL, ratio of total cholesterol to HDL-cholesterol;
Hypertension was defined as diastolic blood pressure (DBP) ⭓90
mm Hg and systolic blood pressure (SBP) ⭓140 mm Hg.
to be older and presented with significantly higher
values of LDL-C and ApoB (P ⬍ 0.001). Black
women were heavier as determined by weight and
BMI (P ⬍ 0.001). Black women also had significantly
higher HDL-C concentration and SBP values compared to white women (P ⬍ 0.01). There were statistically significant differences in the prevalence of
alcohol use and smoking (P ⬍ 0.01). The prevalences of alcohol intake and smoking were 54.2%
and 26.6%, and 45.5% and 35.3%, in whites and
blacks, respectively. There was no statistically significant difference with respect to the prevalence of
hypertension, as defined by SBP ⭓140 mm Hg or
DBP ⭓90 mm Hg in the two groups.
We examined the bi-variate relationships of ApoB
and TC/HDL with age, weight, BMI, blood pressure,
and other lipids (Table 2). A statistically significant
positive correlation existed between ApoB and LDLC, age, BMI, DBP and SBP, while a negative correlation existed between ApoB and HDL in both white
and black women (P ⬍ 0.05). A positive correlation
between TC/HDL and total cholesterol, weight and
DBP, and an inverse relationship with HDL and age
was observed in whites and blacks. The degree of
correlation of ApoB and TC/HDL with DBP and SBP
tended to be higher for blacks than whites.
In order to determine whether ethnicity was associated with higher values of ApoB and TC/HDL,
independent of other factors, ethnicity, blood pressure, age, total cholesterol, alcohol intake, and smoking were tested in multiple linear regression models
using ApoB and TC/HDL as dependent variables.
We also compared model I and model II, representing abdominal obesity defined as WC ⭓88 cm
and as WC larger than expected, respectively (Table
3). Dummy variables were used to compare blacks
with whites. In both models that included DBP and
SBP, blacks were negatively associated with ApoB,
independent of other factors (P ⬍ 0.05). A similar
inverse association of blacks with higher TC/HDL
values, relative to whites, was also observed (P ⬍
0.01).
The results of regression model I showed that
black ethnicity accounted for total variations in
ApoB that ranged from 6.8% to 7.4% in models that
adjusted for DBP or SBP. The corresponding values
for model II ranged from 1.3% to 4.5%. The total
variation in TC/HDL due to black ethnicity was
approximately 80% adjusting for DBP or SBP.
Multiple linear regression models (Table 4) were
computed to determine whether differences in ApoB
or TC/HDL were associated with ethnic differences
in blood pressure after also controlling for age, cholesterol, alcohol intake and smoking. For model I, in
both whites and blacks, ApoB was positively associated with increased values for DBP and SBP (P ⬍
0.01). Model II also indicated a positive association
of ApoB with increased DBP and SBP (P ⬍ 0.01).
Among whites in model I, an approximately
0.5 mg/dl increase in ApoB was associated with a
1 mm Hg increase in DBP and SBP in whites. The
301
Journal of Human Hypertension
Atherogenic factors in abdominally obese women
IS Okosun et al
302
Table 2 Correlation of ApoB and total cholesterol/HDL with blood pressure and other variables in abdominally obese American women
Black women
ApoB
ApoB
TC/HDL
HDL-C
LDL-C
White TC
women Age
Weight
BMI
DBP
SBP
TC/HDL
0.039
0.010
−0.170**
0.858**
−0.044
0.159**
−0.022
0.059*
0.101**
0.142**
−0.339**
−0.005
0.903**
−0.170**
0.232**
0.040
0.089**
−0.053
HDL-C
LDL-C
−0.159**
−0.329**
0.850**
0.010
−0.106
−0.092*
−0.027
0.112**
−0.271**
−0.116**
−0.068*
0.064*
−0.025
0.120**
−0.084*
0.012
0.69
0.102*
TC
Age
0.015
0.918**
−0.078
−0.030
−0.153**
0.173**
0.010
0.059*
−0.050
0.257**
−0.085*
0.051
0.308**
−0.083*
−0.352**
−0.206**
−0.074**
0.487**
Weight
0.050
0.159**
−0.283**
−0.016
0.111**
−0.194**
0.750**
0.243**
−0.085**
BMI
0.027
0.021
−0.226**
−0.007
−0.020
−0.177**
0.834**
0.149**
−0.023
DBP
0.123**
0.096
−0.019
0.009
0.070
0.168**
0.144**
0.013
SBP
0.201**
0.034
0.027
0.153*
0.051
0.465**
0.059
−0.011
0.503**
0.346**
Abdominal obesity was defined as waist circumference of 88 cm or greater; values are Pearson’s regression coefficients; HDL-C, highdensity lipoprotein-cholesterol; LDL-C, low-density lipoprotein cholesterol; TC, total cholesterol; TC/HDL, ratio of total cholesterol to
HDL-cholesterol; BMI, body mass index; DBP, diastolic blood pressure; SBP, systolic blood pressure; **P ⬍ 0.01; *P ⬍ 0.05 level.
Table 3 Multiple linear regression analysis of ethnicity with blood pressure, ApoB and TC/HDL abdominally obese American women
Independent variables
Dependent variables
ApoB
TC/HDL
Model I
Model II
Model I
Model II
DBP (mm Hg)
Blacks
Age (yrs)
Total cholesterol (mg/dl)
Alcohol intake
Smoking
Adjusted R2
0.278**
−2.269**
0.262**
−0.001
−1.781
2.809*
0.074
0.216**
−1.724**
0.247**
0.001
−2.887*
1.105
0.045
0.188**
−0.836**
−0.089**
0.226**
−0.448**
0.480**
0.829
0.242**
−0.910**
−0.064
0.218**
−0.456**
0.294**
0.800
SBP (mm Hg)
Blacks
Age (yrs)
Total cholesterol (mg/dl)
Alcohol intake
Smoking
Adjusted R2
0.134**
−6.663**
0.206**
−0.001
−1.508
2.579
0.068
0.108**
−1.711**
0.200**
0.013
−2.576
0.866
0.013
0.016
−0.839**
−0.095**
0.023**
−0.422**
0.454*
0.828
0.023
−0.873**
−0.072**
0.219**
−0.415**
0.265**
0.799
Values are linear regression coefficients; TC/HDL, ratio of total cholesterol to HDL-cholesterol; Abdominal obesity was defined as having
waist circumference (WC) ⭓88 cm (model I), and as WC larger than expected (model II) as defined from standardised regression residuals
from linear regression analysis between WC and BMI (WC = 2.31* BMI + 30.60); **P ⬍ 0.01; *P ⬍ 0.05.
corresponding value in blacks was approximately
0.4 mg/dl for 1 mm Hg in blood pressure. In model
II, 苲0.4 mg/dl and 苲0.2 mg/dl increases in ApoB
were associated with a 1 mm Hg increase in DBP
and SBP in whites, respectively. The corresponding
values for TC/HDL were 10.4 mg/dl in whites.
Among blacks, increases associated with DBP and
SBP due to TC/HDL did not attain statistical significance.
The results of the regression models showed that
ApoB accounted for a higher total variation in SBP
in both whites and blacks compared to DBP. The
values for model I were 24.2% and 23.8% for blacks
and whites, respectively, and for model II 24.3%
and 23.1% for blacks and whites, respectively. A
similar higher total variation was observed in
TC/HDL for SBP. The respective values for whites
Journal of Human Hypertension
and blacks were 23.8% and 23.4%, and 23.6% and
23%, for model I and model II, respectively.
Discussion
Ideally, abdominal obesity is best assessed with
imaging techniques. In this study, WC was
employed as the anthropometric surrogate of visceral adiposity. We chose to use WC because of its
much stronger correlation with visceral adiposity
rather than waist-to-hip ratio or BMI.33
Visceral adiposity is the component of body composition that is most highly associated with many
metabolic abnormalities such as hypertension, glucose intolerance, hyperinsulinaemia, hypercholesterolaemia, hypertriglyceridaemia, and high levels
of low-density lipoprotein cholesterol.34–38 The WC
Atherogenic factors in abdominally obese women
IS Okosun et al
Table 4 Ethnic-specific linear regression analysis of ApoB and Total cholesterol to HDL-lipoprotein-cholesterol ratio (TC/HDL) with
diastolic (DBP) and systolic (SBP) blood pressure in abdominally obese American women
Independent
variable
DBP
White
SBP
Black
White
DBP
Black
White
SBP
Black
Model I
ApoB
Age
Total cholesterol
Alcohol intake
Smoking
Adjusted R2
TC/HDL
Age
Total cholesterol
Alcohol intake
Smoking
Adjusted R2
0.455**
−0.052**
0.023
0.342
−2.266**
0.316**
0.111**
0.023
3.528**
−1.387
0.452**
0.400**
0.025
−0.521
−2.860**
0.003
0.062
0.242
0.360**
−0.391*
0.061*
0.408
−2.362**
0.206
0.124**
−0.022
3.604**
−1.389
0.162*
0.421**
−0.013
−0.506
−2.880
0.024
0.059
0.238
303
White
Black
0.468**
0.425**
0.014
−0.341
−1.644
0.160
0.486**
−0.018
4.047*
3.044
Model II
0.419**
0.455**
0.036
3.895**
0.279
0.238
0.111
0.476**
0.062
3.890**
0.252
0.234
0.439**
−.208
0.017
1.040
−2.199**
0.019
0.495
0.021
4.155**
0.813
0.023
0.052
0.243
0.231
0.426**
−0.064
−0.773**
1.105
−2.261**
0.226
0.484
−0.273
4.027**
0.802
0.148**
0.438**
−0.016
0.359
−1.666
−0.842
0.491**
0.001
4.012*
3.016
0.022
0.055
0.236
0.230
Values are linear regression coefficients; Abdominal obesity was defined as having waist circumference (WC) ⭓88 cm (model I), and
as WC larger than expected (model II) as defined from standardised regression residuals from linear regression analysis between WC
and BMI (WC = 2.31 *BMI + 30.60); **P ⬍ 0.01; *P ⬍ 0.05.
cut-point utilised for abdominal obesity is in line
with the recommendation by the National Institute
of Health (NIH) expert panels and others for identifying increased relative risk for obesity related comorbidities for most adults.28,29
Elevated ApoB is the most prevalent dyslipidaemia, accounting for 45% of patients who developed
IHD in the Quebec Cardiovascular Study.39 Comparing the various lipoprotein phenotypes in a prospective study, Kwiterovich et al,40 reported hyperapobetalipoproteinemia to be the most prevalent
condition associated with CVD. In a study by Lamarche et al,39 subjects with hyperapobetalipoprotein
dyslipidaemia with or without elevated triglycerides
had a three-fold increased risk for IHD, compared
with controls. Controlling for triglycerides, HDL
cholesterol, or TC/HDL did not eliminate the
relationship between ApoB levels and IHD.39
In this report we used the US national survey to
examine the association between ApoB and TC/HDL
with blood pressure in abdominally obese women.
Elevated ApoB was found to be positively associated
with increasing DBP and SBP in blacks and whites.
This finding was independent of age, total cholesterol, alcohol intake and smoking. Elevated TC/HDL
was also found to be associated with DBP and SBP
in white abdominally obese women. In this group of
abdominally obese women, whites were found to
have higher values of DBP and SBP at the same
value of ApoB and TC/HDL than blacks, adjusting
for confounding variables.
Our finding suggesting that ApoB is more strongly
associated with elevated blood pressure than
TC/HDL is supported by the results from the Quebec
Cardiovascular Study.41 In the Quebec Cardiovascu-
lar Study, Lamarche et al11,12,39,41 found ApoB to be
better in assessing IHD risk than conventional lipids
such as, LDL, HDL and TC/HDL. Thus, because it
may provide information that would not be obtained
from the conventional lipid-lipoprotein profile,
ApoB may prove to be regarded as a more useful tool
in the assessment of CVD risk.
The NHANES III data used for this study represents the best available data since the sampling
scheme was national representative in scope. The
training programme and quality control measures
instituted in NHANES III give added credence to the
data. However, some limitations must be taken into
account in the interpretation of results from this
study. First, bias due to survey non-response and
missing values for some variables cannot be ruled
out. However, previous studies of National Health
and Nutrition Examination Surveys have shown
little bias due to non-response.42 Second, because of
the high correlation between WC and BMI it was
impossible to adjust for BMI using traditional
regression techniques. Hence, alternate approach
using regression residuals derived from regression
of WC on BMI,30 was also used to define abdominal
obesity. In cross-sectional studies, residuals provide
a reasonably simple method for evaluating independent contributions of highly correlated parameters.30 The validity and reliability of this measure
against imaging techniques such as MRI warrants
further investigation. Third, this study did not consider physical activity factors. There is large body of
evidence demonstrating that ApoB and other lipoproteins level can be altered by physical activity.43,44
Fourth, although some evidence suggest ApoA1,
which coats for HDL-C, to be a better predictor of
Journal of Human Hypertension
Atherogenic factors in abdominally obese women
IS Okosun et al
304
CVD than HDL-C,45 we did not assess the correlation
between ApoA1 and hypertension in this study.
Further study assessing the correlation of ApoA1,
and especially ApoB/ApoA1 ratio with hypertension is warranted.
In conclusion, although epidemiological evidence
provides credence for association between TC/HDL
and CVD, results from this study indicate ApoB to
be a stronger risk factor in abdominally obese
women. Since ApoB is associated with hypertension, the combination of elevated ApoB and hypertension may identify a group of patients with more
marked risk of CVD, thus, warranting further investigation.
14
15
16
17
Acknowledgement
Data from the NHANES III were obtained from the
US National Center for Health Statistics.
18
19
References
1 Brochu M et al. Coronary risk profiles in men with coronary artery disease; effects of body composition, fat
distribution, age and fitness. Coron Artery Dis 2000;
11: 137–144.
2 Okosun IS, Prewitt TE, Cooper RS. Abdominal obesity
in the United States: prevalence and attributable risk
of hypertension. J Hum Hypertens 1999; 13: 425– 430.
3 Okosun IS et al. Association of waist circumference
with risk of hypertension and type 2 diabetes in Nigerians, Jamaicans, and African-Americans. Diabetes Care
1998; 21: 1836–1842.
4 Despres JP. Abdominal obesity as important component of insulin-resistance syndrome. Nutrition 1993; 9:
452– 459.
5 Dowling HJ, Pi-Sunyer FX. Race-dependent health
risks of upper body obesity. Diabetes 1993; 42: 537–
543.
6 Bjorntorp P. Abdominal fat distribution and disease:
an overview of epidemiological data. Ann Med 1992;
24: 15–18.
7 Van Gaal LF, Vansant GA, De Leeuw IH. Upper body
adiposity and the risk for atherosclerosis. J Am Coll
Nutr 1989; 8: 504 –514.
8 Carey DG et al. Abdominal fat and insulin resistance in
normal and overweight women: Direct measurements
reveal a strong relationship in subjects at both low and
high risk of NIDDM. Diabetes 1996; 45: 633–638.
9 Johnson WL et al. The Bidirectional efflux of intracellular sterol from cholesterol between cells and lipoprotein. J Biol Chem 1986; 261: 5766–5776.
10 Hokland BM, Slotte JP, Bierman EL, Oram JF. Cyclic
AMP stimulates efflux of intracellular sterol from cholesterol loaded cells. J Biol Chem 1993; 268: 25343–
25349.
11 Lamarche B et al. Fasting insulin and apolipoprotein B
levels and low-density lipoprotein partice size as risk
factors for ischemic heart disease. JAMA 1999; 279:
1955–1961.
12 Lamarche B et al. Apolipoprotein A-I and B levels and
the risk of ischemic heart disease during a five-year
follow-up of men in the Quebec Cardiovascular Study.
Circulation 1996; 94: 273–278.
13 Despres J-P et al. The insulin resistance-dyslipedemic
Journal of Human Hypertension
20
21
22
23
24
25
26
27
28
29
30
syndrome: Contribution of visceral obesity and therapeutic implications. Int J Obes 1995; 19: S76–S86.
Genest JJ et al. Lipoprotein cholesterol, apolipoprotein
A-I and B and lipoprotein (a) abnormality in men with
premature coronary heart disease. J Am Coll Cardiol
1992; 19: 792–802.
Ginsburg GS, Safran C, Pasternak RC. Frequency of
low serum high-density lipoprotein cholesterol levels
in hospitalized patients with desirable total cholesterol levels. Am Coll Cardiol 1991; 68: 187–192.
Sniderman AD et al. Association of hyperapobetalipoprotenemia with endogenous hypertriglyceridemia
and arteriosclerosis. Ann Intern Med 1982; 97: 833–
839.
Sniderman A et al. Association of coronary arteriosclerosis with hyperapobetalipoprotenemia (increased
protein but normal cholesterol levels in human low
density lipoproteins). Proc Natl ACVD Sci USA 1980;
77: 604 –608.
Superko HR. Beyond LDL-cholesterol reduction. Circulation 1996; 94: 2351–2354.
Tchernof A et al. The dense LDL phenotype: association with plasma levels, visceral obesity, and hyperinsulinemia in men. Diabetes Care 1996; 19: 629–637.
Kamboh MI et al. Plasma apolipoprotein A-I, apolipoprotein B, lipoprotein(a) concentrations in normoglycemic Hispanic and Non-Hispanic Whites from San
Luis valley, Colorado. Am J Epidemiol 1997; 146:
1011–1018.
Hokland BM, Slotte JP, Bierman EL, Oram JF. Cyclic
AMP stimulates efflux of intracellular sterol from cholesterol loaded cells. J Biol Chem 1993; 268: 25343–
25349.
Kottke BA et al. Apolipoproteins and coronary heart
disease. Mayo Clin Proc 1986; 61: 313–320.
Ezzati TM et al. Sample design: Third National Health
and Nutrition Examination Survey. Vital Helath Stat
2 1992; 113: 1–35.
National Center for Health Statistics. National Health
and Nutrition Examination Survey III: Data collection
forms. National Center for Health Statistics: Hyattsville, MD, 1991.
Johnson CL et al. Declining serum total cholesterol levels among US adults. The National Health and
Nutrition Examination Surveys. JAMA 1993; 269:
3002–3008.
Ernst ND, Sempos CT, Briefel RR, Clark MB. Consistency between US dietary fat intake and serum total
cholesterol concentrations: the National Health and
Nutrition Examination Surveys. Am J Clin Nutr 1997
(Suppl 4): 965S–972S.
Bachorik PS, Lovejoy KL, Carroll MD, Johnson CL.
Apolipoprotein B and AI distributions in the United
States, 1988–1991: Results of the National Health and
Nutrition Examination Survey III (NHANES III). Clin
Chem 1997; 43: 2364 –2378.
Lean ME, Han TS, Morrison CE. Waist circumference
as a measure for indicating need for weight management. BMJ 1995; 311: 158–161.
National Institute of Health/National Heart Lungs and
Blood Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in
Adults. The Evidence Report. Obesity Res 1998; 6:
51S–209S.
Han TS, Bijnen FCH, Lean MEJ, Seidell JC. Separate
association of waist and hip circumference with lifestyle factors. Int J Epidemiol 1998; 27: 422– 430.
Atherogenic factors in abdominally obese women
IS Okosun et al
31 Norusis MJ. SPSS for Windows Release 10.0. SPSS Inc.
Chicago, 1999.
32 WesVarPC. A User’s guide to WesVarPC version 2.1.
Westat Inc. Rockville, MD, 1997.
33 Molarius A, Seidell JC. Selection of anthropometric
indicators for classification of abdominal fatness – a
critical review. Int J Obes Relat Metab Disord 1998; 22:
719–727.
34 Ko GT et al. Simple anthropometric indexes and cardiovascular risk factors in Chinese. Int J Obes Relat
Metab Disord 1997; 21: 995–1001.
35 Sattar N et al. Associations of indices of adiposity with
atherogenic lipoprotein subfractions. Int J Obes Relat
Metab Disord 1998; 22: 432– 439.
36 Lemieux S et al. Anthropometric correlates to changes
in visceral adipose tissue over 7 years in women. Int
J Obes Relat Metab Disord 1996; 20: 618–624.
37 Haffner SM et al. Prospective analysis of the insulinresistance syndrome (syndrome X). Diabetes 1992; 41:
715–722.
38 Despres J-P. The insulin resistance-dyslipidemic syndrome of visceral obesity: effect on patients’ risk.
Obesity Res 1998; 6: 8S–17S.
39 Lamarche B et al. Prevalence of dyslipidemic phenotypes in ischemic heart disease. Am J Cardiol 1995; 75:
1189–1195.
40 Kwiterovich PO, Coresh J, Bachorik PS. Prevalence of
hyperapobetalipoprotenemia and other lipoprotein
phenotypes in men. (⭐50 years) and women (⭐60
years) with coronary artery disease. Am J Cardiol 1993;
71: 631–639.
41 Lamarche B et al. Small, dense low-density lipoprotein particles as a predictor of the risk of ishemic heart
disease in men. Prospective results from the Quebec
cardiovascular study. Circulation 1997; 95: 69–75.
42 Landis JR, Lepkowski JM, Eklund SA, Stehouwer SA.
A statistical methodology for analyzing data from a
complex survey: the first National health and Nutrition
Examination Survey. Vital Health Stat 2 1982; 92: 1–
52.
43 Despres J-P, Larmache B. Effects of diet and physical
activity on adiposity and body fat distribution: implications for the prevention of cardiovascular disease.
Nutr Res Rev 1993; 6: 137–159.
44 Williams PT, Krauss RM, Vranizan KM, Wood PD.
Changes in lipoprotein subfractions during dietinduced and exercise-induced weight loss in moderately overweight men. Circulation 1990; 81: 1293–
1304.
45 Garfagnini A et al. Relationship between HDL-cholesterol and apolipoprotein A1 and the severity of coronary artery disease. Eur Heart J 1995; 16: 465– 470.
305
Journal of Human Hypertension