Arteriosclerosis, Thrombosis, and Vascular Biology. 1999;19:2234-2240
(Arteriosclerosis, Thrombosis, and Vascular Biology. 1999;19:2234-2240.)
© 1999 American Heart Association, Inc.
|
Atherosclerosis and Lipoproteins |
LDL Size in African Americans, Hispanics, and Non-Hispanic Whites
The Insulin Resistance Atherosclerosis Study
Steven M. Haffner;
Ralph D'Agostino, Jr;
David Goff;
Barbara Howard;
Andreas Festa;
Mohammed F. Saad;
Leena Mykkänen
From the Department of Medicine (S.M.H., A.F., L.M.), University of Texas
Health Science Center at San Antonio; the Department of Public Health Sciences
(R.D.A., D.G.), Bowman Gray School of Medicine, Winston-Salem, NC; the
Medlantic Research Institute (B.H.), Washington, DC; and the Department of
Medicine (M.F.S.), UCLA Medical Center, Los Angeles, Calif.
Correspondence and reprint requests to Steven M. Haffner, MD, Department of Medicine, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr, San Antonio, TX 78284-7873.
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Abstract
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AbstractThe prevalence of
cardiovascular disease (CVD)
and
atherosclerosis varies among several minority ethnic
groups
in the United States. Recently, small, dense low density
lipoprotein
(LDL) particle size has been recognized as a risk factor
for
CVD. We examined LDL size as a possible explanation for differences
in
CVD rates in 1571 subjects from the Insulin Resistance
Atherosclerosis
Study (IRAS), a multiethnic study of
insulin resistance and
cardiovascular risk factors. LDL
size (Å) was significantly
different by ethnic group (African
Americans 262.1±0.6,
Hispanics 257.6±0.6, and non-Hispanic whites
259.2±0.4,
P<0.001). Ethnic differences in LDL size
continued to be
statistically significant after adjustment for upper
body adiposity,
insulin resistance, and glucose tolerance status.
However, after
further adjustment for other
cardiovascular risk factors, especially
ethnic
differences in triglyceride and high density lipoprotein
(HDL)
cholesterol levels, the ethnic differences in LDL
size were
markedly attenuated and in general no longer statistically
significant.
The relation of triglyceride, HDL
cholesterol, insulin resistance,
and adiposity to LDL size
in each ethnic group was similar.
LDL size differs by ethnic
group, which is independent of obesity
or insulin resistance. These
ethnic differences appear to be
due to ethnic variations in
dyslipidemia (especially differences
in
triglyceride levels); ethnic differences in LDL size are
not
consistent with previously reported ethnic dissimilarities
in
CVD or atherosclerosis.
Key Words: Hispanics non-Hispanic whites African Americans LDL size coronary heart disease insulin resistance
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Introduction
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Differences in the prevalence of coronary
heart disease (CHD)
and cardiovascular disease (CVD)
have been reported in the United
States between ethnic groups.
Hispanics have been reported to
have rates of CHD
1 2 3 4 5 or
CVD
6 similar to or lower than
those of non-Hispanic
whites, although a few recent reports
have not supported this
position.
7 8 9 African Americans have
increased CVD
relative to non-Hispanic whites.
10 11 12 We have
reported
recently that African Americans have a significantly
greater
intima-media wall thickness than do non-Hispanic whites
in the common
carotid artery in nondiabetic subjects in the
Insulin Resistance
Atherosclerosis Study (IRAS).
13 In the
IRAS,
ethnic differences in the common carotid artery intima-media
wall
thickness could not be explained by conventional
cardiovascular
risk factors. (No ethnic differences
were observed in internal
carotid artery wall thickness in the
IRAS.
13 )
Considerable information has been gathered on
cardiovascular risk factors to explain ethnic
differences in CVD. Hispanics have increased obesity,14
higher triglyceride and lower HDL cholesterol
levels,15 16 and an increased prevalence17 18
and incidence19 of type 2 diabetes. The above ethnic
differences in cardiovascular risk factors suggest a
higher risk of CVD in Hispanics. However, Hispanics have been reported
to have a lower prevalence of hypertension than do non-Hispanic
whites.20 21 The risk of CVD predicted from the Framingham
model is higher in Hispanics than in non-Hispanic
whites.21 African Americans have an increased prevalence
of both hypertension22 and type 2
diabetes23 24 relative to non-Hispanic whites, which might
increase the risk of CVD in the former group. In contrast, African
Americans have lower levels of triglyceride and higher
levels of HDL cholesterol (especially in males) than do
non-Hispanic whites.25 26
Increased levels of small, dense LDL (LDL subgroup pattern B)
have been identified as a risk factor for the
prevalence27 28 29 30 31 and incidence32 33 34 of CHD.
The epidemiological correlates of small, dense LDL include increased
triglyceride and decreased HDL cholesterol
levels, male sex, hyperinsulinemia, insulin
resistance, and type 2 diabetes.29 35 36 37 38 39 40 41 42 43 Of these
variables, decreased HDL and especially increased
triglyceride levels are the strongest predictors of small,
dense LDL. We have previously shown that Mexican Americans have
increased small, dense LDL relative to non-Hispanic
whites41 in the San Antonio Heart Study, but these
findings were no longer significant after adjustment for the greater
dyslipidemia in Mexican Americans (increased
triglyceride and decreased HDL cholesterol
levels).
LDL size has not been previously examined in African Americans.
On the basis of previous studies showing increased HDL
cholesterol and decreased triglyceride levels
relative to non-Hispanic whites25 26 in African Americans,
one might expect a larger LDL size (less atherogenic) in the latter
group. However, considering the greater obesity and
diabetes23 24 and increased insulin
resistance44 in African Americans, the effects of which
might decrease LDL size, it is difficult to predict whether LDL size
would be smaller or larger in African Americans compared with
non-Hispanic whites.
In this report, we examine LDL size in a triethnic population (African
Americans, Hispanics, and non-Hispanic whites) in the
IRAS.45 We also examine whether the relation of
traditional correlates of LDL size
(hyperinsulinemia, obesity, and
dyslipidemia) affect LDL size in a similar fashion across
ethnic groups.
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Methods
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A detailed description of the design and methods of the IRAS
has
been published.
45 In brief, this study was conducted at
4
centers: Oakland and Los Angeles, Calif; San Antonio, Tex;
and San Luis
Valley, Colo. Diabetic subjects receiving insulin
were not eligible for
the IRAS. Diabetic subjects with a fasting
glucose level

300 mg/dL
(

16.7 mmol/L) were also excluded.
A total of 1625 individuals participated in the IRAS (56%
women).45 Individuals with normal glucose tolerance
composed the largest segment of the study sample (44%: non-Hispanic
whites, n=291; African Americans, n=187; and Hispanics, n=241),
followed by diabetes (37%: non-Hispanic whites, n=177; African
Americans, n=187; and Hispanics, n=241) and persons with impaired
glucose tolerance (23%: non-Hispanic whites, n=145; African
Americans, n=101; and Hispanics, n=123).
Height, weight, and girths (minimum waist and hips) were measured by
following a standardized protocol. Body mass index (BMI;
weight/height2 [kg/m2])
was used as an estimate of overall adiposity. Waist circumference was
taken as the minimum circumference between the thorax and the hips. The
waist circumference was used as an estimate of body fat
distribution.
The IRAS examination required 2 visits (approximately 1 week apart
[range 2 to 28 days]),45 each lasting
4 hours. An
oral glucose tolerance test and a frequently sampled
intravenous glucose tolerance test (FSIGT) were performed
during the first and second visits, respectively. Glucose tolerance was
classified according to World Health Organization
criteria.46
Insulin sensitivity was assessed by the FSIGT with minimal model
analyses. The protocol has been previously described in
detail.44 45 The FSIGT (insulin modified with 12 time
points) protocol used in the IRAS has been compared with the
hyperinsulinemic euglycemic clamp and shown
to be a valid measure of insulin resistance.47
Plasma glucose was measured with the glucose oxidase technique on an
automated autoanalyzer (Yellow Springs Equipment Co). Insulin
was measured using the dextran-charcoal radioimmunoassay, which has
considerable cross-reactivity with proinsulin.
Plasma lipoprotein measurements were obtained from fasting, single,
fresh plasma samples by using Lipid Research Clinics methods. VLDL was
isolated by preparative ultracentrifugation, and the
VLDL (top) and bottom fractions were measured for
cholesterol and triglyceride concentrations.
HDL cholesterol was measured after precipitation of apo
Bcontaining lipoproteins with MnCl2 and
heparin. The cholesterol content in the supernatant was
measured in a separate autoanalyzer channel set to measure low
cholesterol values. LDL cholesterol was
calculated as the difference between the HDL cholesterol
and the bottom cholesterol. Triglycerides were
measured enzymatically after correction for free glycerol. Direct
measurement of VLDL cholesterol by preparative
ultracentrifugation was done for all subjects.
LDL size distribution (ie, distribution of diameters of the major LDL
peaks for all participants) was determined using the method of Krauss
and Burke.48 Gradient gels were obtained from
Isolab. Measurement of the size of the predominant peak was
calibrated using LDL subfractions whose molecular diameters were
determined by analytical ultracentrifugation (courtesy
of Dr Ronald Krauss, Donner Laboratories, Berkeley, Calif). The LDL
size of the predominant peak for an individual was defined as that
person's LDL size.41 In the IRAS, the coefficient of
variance was 2%.
Mean values of the cardiovascular risk factors
were compared according to ethnic group by ANCOVA (SAS
version 6.08, SAS Institute). Logarithmic transformations (for
statistical testing) were used for triglyceride values.
Further adjustment was made for variables previously shown to
affect LDL size (Table 3
). Because waist circumference and BMI
were highly correlated (r=0.82), they were not included in
the same regression model. Spearman correlations were used to describe
the relationship of LDL size to possible confounding variables
separately in the ethnic groups (Table 2
). The LDL size by
ethnic group is also shown stratified by possible confounding
variables (the Figure
) by using
ANCOVA. Because the non-Hispanic whites were sampled at all 4
locations, whereas African Americans and Hispanics were sampled at only
2 areas, we examined whether the reference group (non-Hispanic whites)
was similar in all 4 areas with respect to key variables
(triglyceride, HDL cholesterol, and LDL size).
Non-Hispanic whites were similar with respect to these variables,
and therefore, we compared the ethnic groups by adjusting for clinic
location.
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Results
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Table 1

shows the clinical and
biochemical characteristics of
the population. Obesity (BMI) was
greater in Hispanics and African
Americans than in non-Hispanic whites.
Insulin concentrations
were higher and insulin sensitivity lower in
Hispanics and African
Americans relative to non-Hispanic whites.
African Americans
had the highest blood pressure, and Hispanics had the
lowest
blood pressure. The proportion of subjects on lipid-lowering
medications
was very low in all ethnic groups (8.0%) and did not
differ
by ethnic group. Because the results for subsequent
analyses
were similar with and without these subjects (on lipid
treatment),
we report data including these subjects. As might be
expected
from previous studies, African Americans had lower
triglyceride
and higher HDL cholesterol levels
than did non-Hispanic whites.
Hispanics had the opposite pattern, with
higher triglyceride
and lower HDL cholesterol
levels than non-Hispanic whites. LDL
size (Å) differed significantly
(
P<0.001) by ethnic
group (African Americans 262.1±0.6,
Hispanics 257.6±0.6,
and non-Hispanic whites 259.2±0.4). In pairwise
comparisons,
African Americans had a significantly greater LDL size
than
did non-Hispanic whites (
P<0.001) or Hispanics
(
P<0.001).
Hispanics had a slightly smaller LDL size than
did non-Hispanic
whites (
P=0.039).
Table 2
shows the correlations
between LDL size and selected variables. In the overall population,
LDL size was significantly correlated with obesity (BMI)
(r=-0.09), waist circumference (r=-0.19),
fasting glucose (r=-0.17), 2-hour glucose
(r=-0.20), fasting insulin (r=-0.18),
insulin sensitivity (SI) (r=0.21), HDL
cholesterol (r=0.38), and
triglyceride (r=-0.47). However, LDL size was
not significantly related to systolic (r=-0.01) or
diastolic (r=0.04) blood pressure. These
associations were similar in each ethnic group. After further
adjustment for diabetic status (data not shown), LDL size continued to
be significantly related to triglyceride, HDL
cholesterol, and insulin sensitivity, although the
magnitude of the association was somewhat attenuated.
The Figure
shows LDL size by ethnic group stratified by
selected variables by use of a 2-wayANOVA. Male sex, type 2
diabetes, high triglyceride levels, and low HDL
cholesterol levels were associated with smaller LDL size.
African Americans continued to have a higher LDL size after adjustment
for sex or diabetic status compared with non-Hispanic whites. Hispanics
had a smaller LDL size than did non-Hispanic whites after adjustment
for sex or diabetic status. However, after adjustment for
triglyceride or HDL levels, the ethnic differences in LDL
size were attenuated, especially in the groups with low
triglyceride or high HDL cholesterol
values.
Table 3
shows ethnic differences in LDL
size after sequential adjustment in possible confounding variables.
Ethnic differences in LDL size remained statistically significant after
further adjustment for demographic variables or the following
variables: obesity, body fat distribution, glucose levels, or
insulin sensitivity. However, adjustment for triglyceride
and HDL cholesterol attenuated the ethnic differences in
LDL size, although there remained modestly lower LDL size in Hispanics
than in African Americans (model 5 or 6).
 |
Discussion
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We have confirmed earlier data that African Americans have
decreased
triglyceride and increased HDL
cholesterol levels compared with
non-Hispanic
whites.
25 26 In this report, for the first time,
we have
shown that LDL size is significantly higher in African
Americans than
in non-Hispanic whites. These differences are
not the result of the
greater adiposity, diabetes, or insulin
resistance in African
Americans. However, after controlling
for the lower
triglyceride and higher HDL cholesterol levels
in
African Americans, the ethnic differences in LDL size are no
longer
significant, except for possibly a smaller LDL size in
Hispanics than
in African Americans (Table 3

, models 5 and 6).
We have also shown that Hispanics have a smaller LDL size than do
non-Hispanic whites, as has been reported previously from the San
Antonio Heart Study.41 As in that report, Hispanics and
non-Hispanic whites had similar LDL size after adjustment for
dyslipidemia and lipoproteins. In the current report,
Hispanics had lower HDL cholesterol and higher
triglyceride levels than did non-Hispanic whites, which is
consistent with a number of previous
studies.15 16
In previous articles, LDL size was associated with increased
triglyceride levels, decreased HDL cholesterol
levels, hyperinsulinemia, insulin resistance,
obesity, and an unfavorable body fat
distribution.29 35 36 37 38 39 40 41 42 43 With the exception of a few
studies,41 43 those studies were done in predominantly
white (ie, non-Hispanic white) populations. The current report
demonstrates that these relations also occur in African Americans and
Hispanics. (Because of the large number of subjects, relatively weak
associations such as BMI (r=-0.09; Table 2
) may be
statistically significant. The correlations, however, of LDL size with
triglyceride and HDL were strong as in other studies.)
Although it might be expected that similar relations between LDL size
and other variables among different ethnic groups might exist, this
is not always true of all associations. In the IRAS, insulin resistance
was related to atherosclerosis in Hispanics and
non-Hispanic whites but not in African Americans.49
Insulin resistance has been related to blood pressure in whites but not
in African Americans in 1 study50 ; however, in another
study, insulin resistance was related to blood pressure in African
Americans.51
Previous studies have suggested increased CVD in African
Americans.10 11 12 Because our data suggest that LDL size is
actually higher in African Americans than in non-Hispanic whites, this
observation cannot explain the ethnic difference in CVD rates.
Hispanics were initially reported to have lower CVD rates than
non-Hispanic whites,1 2 3 4 5 6 although recent findings have
shown higher rates of CVD in Hispanics.7 8 9 52 In the
IRAS, common carotid artery intima-media wall thickness was highest in
African Americans and lowest in Hispanics,13 which is the
opposite pattern observed for LDL size in this respect.
The reason for the higher LDL size in African Americans is not well
understood. Cohen et al53 have suggested that the human
hepatic lipase gene is a major determinant of HDL
cholesterol levels, although Mahaney et al,54
in a Mexican-American population, have found a major gene linked to HDL
cholesterol and apoA1 but excluded the possibility
of linkage to the human hepatic lipase locus. African Americans have
been found to have a high frequency of the A allele at
the human hepatic lipase locus,55 56 which is
associated with lower hepatic triglyceride lipase levels
and thus, could be an explanation for the higher LDL size in this
ethnic group, although further work is needed in this area.
We have shown that LDL size is greater in African Americans than in
non-Hispanic whites or Hispanics after adjustment for upper body
adiposity, fasting glucose, and insulin resistance (Table 3
,
model 4). After further adjustment for triglyceride or HDL
cholesterol (models 5 and 6), the higher LDL size in
African Americans was markedly attenuated. However, adjustment for
triglyceride or HDL cholesterol in regression
models in which LDL size is a dependent variable can be
problematic because of the strong correlations (possible
"statistical issue" of multicolinearity) and because
triglyceride and HDL levels are major determinants of LDL
size ("physiological issue"). Austin and
colleagues57 have introduced the combination of LDL size,
triglyceride, and HDL cholesterol, which they
have named the atherogenic lipoprotein phenotype. With the use
of factor analysis, the atherogenic lipoprotein
phenotype has been associated with insulin
resistance58 and is increased in prediabetic subjects who
are insulin resistant.59 Interestingly, Lamarche
et al60 have recently shown that "nontraditional risk
factors" (LDL size, apo B, and insulin levels) strongly predict the
development of ischemic heart disease in men.
In conclusion, we have found an ethnic difference in the LDL size
distribution, with African Americans having the highest LDL size
("less atherogenic") and Hispanics having the lowest LDL size;
these ethnic differences in LDL size, however, appear to be primarily
due to differences in triglyceride and HDL
cholesterol among the ethnic groups. Similar variables
(triglyceride, HDL cholesterol, insulin
resistance, etc) appear to be related to LDL size in these ethnic
groups. Last, ethnic differences in LDL size are not consistent
with previously reported differences in their risk of CVD or
atherosclerosis; in fact, the ethnic differences in LDL
size may be opposite the CVD risk differences by ethnic group.
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Acknowledgments
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|---|
This work was supported by the National Heart, Lung, and Blood
Institute,
Bethesda, Md (grants HL47887, HL47889, HL47890, HL47892, and
HL47902),
and the General Clinic Research Centers Program (grants NCRR
GCRC,
MO1 RR431, and MO1 RR01346) (to S.M.H. and
M.F.S.).
Received November 23, 1998;
accepted January 25, 1999.
 |
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