Lipoprotein-Cholesterol Distributions in Selected
North American Populations: The Lipid Research Clinics
Program Prevalence Study
GERARDO HEISS, M.D., ISRAEL TAMIR, M.D., CLARENCE E. DAVIS, PH.D.,
HERMAN A. TYROLER, M.D., BASIL M. RIFKIND, M.D., GUSTAV SCHONFELD, M.D.,
DAVID JACOBS, PH.D., AND IVAN D. FRANTZ, JR., M.D.
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SUMMARY Total plasma lipid and lipoprotein-cholesterol distributions of 4756 white men and women ages
20-59 years are presented. Measurements were obtained during the visit-2 survey of the Lipid Research Clinics
Program Prevalence Study and correspond to a 15% random sample of 35,748 white adults screened during the
LRC visit-1 survey. Standardized examinations were carried out by 10 North American clinics using a common protocol, on diverse target populations chosen to include a range of sociodemographic characteristics.
Age-specific means, medians and selected percentiles are given by sex, with stratification on exogenous sex
hormone use in women.
Plasma lipid and lipoprotein concentrations in men and women vary with age. Differences in lipid and
lipoprotein levels between the study populations are also present and manifest themselves as parallel trends of
age-related changes in the 10 populations examined.
Higher total cholesterol values in men compared with women appear between the ages 20-50 years and
higher LDL cholesterol between the ages 20-55 years. VLDL cholesterol levels are similar in both sexes at
ages 20 and 59 years but higher in men than in women in all intermediate age groups. HDL cholesterol is
higher in women than in men throughout the age range considered.
Women taking sex hormone preparations have higher total cholesterol than women not on hormones
between ages 20-50 years, and higher LDL cholesterol between ages 20-40 years. From the third age decade
onward, HDL cholesterol levels are progressively higher in women taking hormones than in women not taking
sex hormones. Compared with women not taking exogenous sex hormones, women taking hormones have
higher total plasma triglyceride values at all ages from 20-59 years. VLDL cholesterol values are higher in
women on hormones compared with nonusers of hormones younger than 55 years.
THE DATA relating atherosclerotic coronary heart
disease to plasma lipids have grown extensively in this
century. Cumulative confirmatory evidence from
animal experimental, clinical case series, and
epidemiologic population studies have established the
coronary heart disease risk factor status of total
logic investigations. The negative-risk-factor status
of HDL cholesterol (HDL-C) and the positiverisk-factor status of LDL cholesterol (LDL-C) have
been shown in case-control studies,7 cross-sectional
population studies,8 and cohort studies.91' These
studies suggest an independent contribution of the
plasma lipoprotein fractions to the risk of coronary
heart disease; however, additional information regarding quantification of the coronary heart disease risk
among populations with different distributions of
other risk factors, genotypes, and lifestyle attributes is
required.
The Lipid Research Clinics (LRC) Program was
designed to contribute to knowledge of the determinants of plasma lipids and lipoproteins in populations and their cardiovascular sequelae. A series of
studies was initiated that constituted a coronary
primary prevention clinical trial and a program of
population-based surveys. Epidemiologic surveys have
been completed in 13 settings in the U.S., Canada,
Israel, and the USSR; data collection for family
studies and a mortality follow-up are in progress.
In this communication we present a description of
the major characteristics of the lipid and lipoprotein
distributions related to sex, age and sex hormones
utilization by women among the 10 North American
populations studied in the LRC Program. Further
analyses of these data are in progress, and reports will
be issued separately on the effects of genetic and environmental factors, and their relationship to mor-
plasma cholesterol.' Early epidemiologic studies of
plasma lipoproteins resulted in controversy regarding
the information predictive of coronary heart disease
provided by plasma ultracentrifugation in addition to
that derived from total cholesterol measurement.2 S
The further development of concepts of plasma lipid
transport mechanisms and simplified methods for
measurement and classification of lipoprotein abnormalities6 stimulated numerous clinical and epidemioFrom the Departments of Biostatistics and Epidemiology, School
of Public Health, University of North Carolina, Chapel Hill, North
Carolina; Lipid Metabolism Branch, National Heart, Lung, and
Blood Institute, National Institutes of Health, Bethesda, Maryland;
Washington University School of Medicine, St. Louis, Missouri;
and Laboratory of Physiological Hygiene and Department of
Medicine, University of Minnesota, Minneapolis, Minnesota.
Supported by NHLBI contracts N01-HVI-2156-L, NOI-HV12160-L,NO1-HV2-2914-L, Y01-HV3-0010-L, N01-HV2-2913-L,
N01-HVI-2158-L, N01-HVI-2161-L, N01-HV2-2915-L, N01-HV22932-L, N011-HV2-2917-L, N01-HV1-2157-L, N01-HVI-2243-L,
NOI-HVI-2159-L, N01-HV3-2961-L, and N01-HV6-2941-L.
Address for correspondence: Basil M. Rifkind, M.D., Lipid
Metabolism Branch, National Heart, Lung, and Blood Institute,
National Institutes of Health, Bethesda, Maryland 20205.
Received May 3, 1979; revision accepted August 3, 1979.
Circulation 61, No. 2, 1980.
302
PLASMA LIPOPROTEIN-CHOLESTEROL DISTRIBUTIONS/Heiss et al.
bidity and mortality from atherosclerotic vascular disease.
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Methods
The population studies component of the LRC
Program has been described in detail elsewhere.12' 13
Briefly, 10 LRCs in the United States and in Canada
completed a series of population surveys between
1971-1976. The LRCs selected their study populations to ensure wide ethnic, geographic, socioeconomic and age variation; the collaborative LRC
data are not, however, representative of the Canadian
or U.S. populations. All clinics used a common protocol"3 and highly standardized methods.
The Prevalence Study involved a brief visit- 1 screen
to determine plasma cholesterol and triglyceride and
to obtain sociodemographic data and a medication
history. For the second, more extensive examination,
the participating LRCs first recalled a 15% random
sample of visit-1 participants. Subsequently, the remaining visit-1 records were reviewed, and participants with elevated lipid levels or who were taking
lipid-lowering medication were also invited to participate in the visit-2 screen.
Data collected at visit 2 included plasma lipids and
lipoprotein-cholesterol quantification, resting and
graded exercise electrocardiography, detailed dietary
and medication history, nonlipid clinical chemistries,
blood pressure and anthropometric indices.
A total of 12,595 white participants of both sexes
were examined during the LRC visit-2 survey. Of
these, 7055 constitute a 15% randomly sampled subset
of LRC visit-i participants and 5540 are visit-i examinees recalled to the second examination on
grounds of hypercholesterolemia or hypertriglyceridemia. The visit-2 survey also examined 1257 nonwhite participants of both sexes; these observations
are not included in this report and are the topic of
separate LRC publications.
The sampling frames and number of study participants for the LRCs are presented in table 1.
Overall participation rates were 74% for visit 1 and
85% for visit 2. The overall response rate for the data
presented in this report, i.e., white visit-1 participants
eligible for visit-2 examination, was 88%, with negligible differences by sex or age.
Laboratory Methods
Blood specimens were obtained from participants
who had fasted for at least 12 hours. Venipuncture was
done with the examinees in a sitting position; a tourniquet was used, but was released before collection of
the blood sample. All samples were immediately
placed on wet ice, and the standardized lipid
laboratory procedures were initiated within 3 hours
after venipuncture.
A detailed description of the laboratory processing
procedures is provided in the LRC Laboratory
Methods Manual.14 Briefly, plasma cholesterol and
triglyceride levels were determined in each LRC core
laboratory by use of Technicon Autoanalyzer I or
303
Autoanalyzer II, adapted by the LRC Program. On
frozen serum pools the AA-I instruments produced
cholesterol values 2.1% higher than the manual AbellKendall target values; the AA-II instruments gave
values 1.3% lower than target values.'5 For plasma
triglyceride concentrations the individual instrument
biases varied from 4.9% below to 1.0% above reference
values. Between-run variability
was
often less than
within-run variability and interlaboratory variation
was considerably less than intralaboratory variation."'
All study determinations were done on fresh samples
and the comparative data indicate differences even less
than the values ascertained for frozen samples.'5 16
Uniform internal quality control and external surveillance systems were used in each LRC lipid
laboratory in order to stabilize performance
throughout the entire project and to achieve comparability of interlaboratory results. Control limits
were established and were used to evaluate each day's
analysis. Cholesterol analyses of nine pools by the
LRC laboratories over 12 months approximated the
reference value (assigned by the CDC Lipid Standardization Laboratory, using the manual Abell-Kendall
method) within 0.2%-2. 1% over a range of 134-343
mg/dl. The overall coefficient of variation ranged
from 3.4% at the lowest concentration to 1.9% at the
highest concentration.17
Lipoproteins were separated by ultracentrifugal
flotation at saline density (d = 1.006 g/ml), to yield a
supernatant fraction containing VLDL cholesterol
(VLDL-C) and an infranatant fraction containing
both LDL-C and HDL-C.
HDL-C was estimated in total plasma after
precipitation of the apo-B-containing lipoproteins by
means of heparin-manganese chloride. After direct
estimation of HDL-C, LDL-C was observed by the
formula: LDL-C = cholesterol in the 1.006 infranatant - HDL-C. VLDL-C was determined by the
formula: VLDL-C = total plasma cholesterol - 1.006
infranatant cholesterol.
In instances of incomplete precipitation of VLDL-C
and LDL-C, the procedure was repeated on the infranatant fraction after ultracentrifugation.'8
To ensure interlaboratory comparability of ultracentrifugal results, 53 unfrozen plasma pools were
distributed quarterly over a 3½/2-year period to each
laboratory. The average coefficients of interclinic
variability in lipoprotein-cholesterol analyses in these
samples were 5% for LDL-C, 10-15% for HDL-C, and
10-40% for VLDL-C.'9
Statistical Methods
The aim of the statistical analysis was to describe
the collaborative data, taking into account any possible differences between the populations surveyed.
Multiple linear regression was used to construct a
model of each lipid and lipoprotein as a function of
age for each of three groups: males, females not taking
hormones, and females taking hormones. The first
step in the analysis was to fit a fifth-degree polynomial
for age. Using a stepwise procedure, we determined
that a linear quadratic equation was adequate for all
CI RCULATION
304
VOL 61, No 2, FEBRUARY 1980
TABLE 1. Number of Eligible and Screened Examinees at Visit 1 and Visit 2 by Participating Lipid Research Clinics Program
Prevalence Study, 1971-1976
Sampling
frame
Clinic
children
Baylor
School
and their parents Cincinnati
Households
Occupational and
Iowa
Johns Hopkins
La Jolla
Minnesota
Oklahoma
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Seattle
industrial groups Stanford
Toronto-McMaster
visit 1
Number
Response
Eligible Screened rate (t o)
64
5,939
3,795
70
10,893
15,571
5,594
5,075
7,791
8,392
9,522
3,918
4,393
6,087
6,046
6,028
11,968
4,999
4,280
8,208
6,750
7,179
Visit 2
Number
Response
Eligible Screened rate (%)
Visit 2,
random
sample,*
whites,
20-59 yrs
902
3,049
637
2,652
71
87
145
388
70
87
78
80
75
1,099
,145
1,644
1,779
1,958
999
1,041
1,459
1,380
1,638
91
91
89
78
84
543
287
315
623
606
83
1,388
1,189
2,182
1,191
1,074
1,781
86
602
483
764
71
69
91
82
4756
85
74
13,852
16,335
60,502
81,926
Total
*Of those screened, the following were excluded from analysis: nonwhite participants (n 12;57), Visit-2 examinees recalled onl
grounds of hyperlipidemia or lipid-lowering treatment (n = 5540); fasting less than 12 hours (n = 24); pregnant womeni (n1 = 13);
ages less than 20 and greater than 59 years (n = 2251); rnissing iniformation on sex hormone usage (n = 11).
lipids and lipoproteins, with the exception of HDL-C
in males, which was best fitted by including a cubic age
term. The second step in the analysis was to determine
if the shape of the lipoprotein-age curve was the same
for all of the participating centers. A separate curve
was fitted for each clinical center and the hypothesis of
homogeneity of the shape of the curves was tested. In
no case could the hypothesis of homogeneity be rejected. Thus, for each of the three groups being compared the association of the lipids and lipoproteins
with age was the same at each clinic and the pooling of
data from all clinics appeared valid. The final step in
the analysis was to perform an analysis of covariance
among the 10 clinics with the appropriate degree
polynomial for age as the covariate. In every case, the
differences among the 10 clinics were statistically
significant (p < 0.05). To produce a single summarizing curve for all of the clinics, the median of the 10
clinic intercepts was used.
Results
We are reporting the distributions of plasma lipid
and lipoprotein levels for 4756 white participants, ages
20-59 years, who were recalled to visit 2 as part of the
15% random sample. (Table 1 provides additional information on the study populations.) Mean and
selected percentile values for plasma cholesterol and
triglyceride, and lipoprotein-cholesterol fractions are
given by 5-year age groupings in Appendix 1 (tables
1-6); means are also portrayed in figures 1-8. Given
the high prevalence of sex hormone usage and the
demonstrated influences of exogenous sex hormones
on lipid and lipoprotein levels,20-25 data for female
LRC participants are presented by sex hormone
usage, although emphasis in this report is not on the
effect of sex hormone usage. (LRC program
definitions of sex hormone usage differ slightly in
various publications, resulting in minor differences in
the descriptive data.)
Not included in this report are white participants
recalled to visit 2 on grounds of high plasma lipids
(n = 5540);* nonwhite participants (n = 1257);* participants younger than 20 years or older than 59 years
(n = 2251);* participants fasting less than 12 hours
(n 24); and women who were pregnant (n = 13) or
for whom no data on sex hormone usage were
available (n = 1 1).
The main features of multiple regression equations
that best describe the plasma lipid and lipoprotein
levels for the successive birth cohorts in the study population are presented in table 2. Females taking hormones have a linear relationship between their plasma
lipid and lipoprotein levels and age. This is also true
for HDL-C in females not taking hormones, while
curvilinear relationships with age are the characteristic of all other lipid parameters in these females.
Lipid and lipoprotein levels of males are best approximated by a curvilinear fit.
Plots of the best fit of lipid values on age are
presented in figures 1-8 for the subpopulations defined
by sex and hormone usage. The composition of these
figures incorporates additional information in that the
range of interclinic variation of lipid values is
presented in each triplet of estimated curves. A lipidage curve was computed for each of the participating
LRCs; the lipid levels from the highest and the lowest
clinics correspond to the upper and lower curves
shown in the figures as interrupted lines. The middle
curve in turn represents the lipid/lipoprotein levels for
the median clinic.
*Separate reports will be issued for these visit-2 participants.
J
305
PLASMA LIPOPROTEIN-CHOLESTEROL DISTRIBUTIONS/Heiss et al.
Cross-sectional Variation of Plasma Lipid
and Lipoprotein Fractions with Age
240 H
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Plasma Cholesterol and Triglyceride Levels
Figure 1 shows mean plasma cholesterol and
triglyceride levels by age for white male LRC participants ages 20-59 years. Cholesterol values increase
from 162 mg/dl in the age group 20-24 years to a
maximum of 215 mg/dl in the 50-54-year age group.
The slope of the cholesterol increment over successive age cohorts is greatest between 20-34 years;
thereafter, the age-related increase in cholesterol
levels is progressively less pronounced until a plateau
is reached over the age strata 50-59 years. The
triglyceride values of white males rise from 89 mg/dl
in the 20-24-year age group to a peak between the
ages 40-44 years, and decrease subsequently to a
mean value of 134 mg/dl at ages 55-59 years.
Mean plasma cholesterol and triglyceride levels by
age for white females not taking hormones are presented in figure 2. Plasma cholesterol levels show a
curvilinear increase over the successive birth cohorts
examined, from a mean value of 162 mg/dl at ages
20-24 years to 231 mg/dl at ages 55-59 years. Plasma
triglycerides follow a similar pattern of increase with
age, from 68 mg/dl to 132 mg/dl at the youngest and
oldest age groups reported here.
Among white females on exogenous sex hormone
preparations, both cholesterol and triglycerides show
a linear increase with age (fig. 3). The mean
cholesterol level of 20-24-year-olds is 178 mg/dl, and
after a monotonic and linear increase over successive
birth cohorts it reaches 222 mg/dl in the 55-59-yearolds. Fasting plasma triglyceride levels of females can
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AGE IN YEARS
FIGURE 2. Regression estimates of mean plasma lipid
values by age and clinic, white females not taking sex hormones, ages 20-59 years. Lipid Research Clinics Prevalence
Study, Visit 2, random sample.
be seen to increase with age, from 106 mg/dl at ages
20-24 years to 138 mg/dl at ages 55-59 years.
Mean Lipoprotein-Cholesterol Levels
Among white males, LDL-C shows a steep rise
from ages 20-24 years (103 mg/dl) to ages 45-49
240
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",W,9,W,
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A1
20
30
40
50
60
AGE IN YEARS
FIGURE 1. Regression estimates of mean plasma lipid
values by age and clinic, white males, ages 20-59 years.
Lipid Research Clinics Prevalence Study, Visit 2, random
sample.
20
1
1
30
1
I
40
1I
1I
50
I
60
AGE IN YEARS
FIGURE 3. Regression estimates of mean plasma lipid
values by age and clinic, white females taking sex hormones,
ages 20-59 years. Lipid Research Clinics Prevalence Study,
Visit 2, random sample.
306
VOL 61, No 2, FEBRUARY 1980
CIRCULATION
160
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AGE IN YEARS
AGE IN YEARS
FIGURE 4. Regression estimates of mean plasma
lipoprotein-cholesterol values by age and clinic, white males,
ages 20-59 years. Lipid Research Clinics Prevalence Study,
Visit 2, random sample.
FIGURE 5. Regression estimates of mean plasma
lipoprotein-cholesterol values by age and clinic, white
females not taking sex hormones, ages 20-59 years. Lipid
Research Clinics Prevalence Study, Visit 2, random sample.
(144 mg/dl) (fig. 4). Thereafter, the observed in-
figure 6. All three lipoprotein-cholesterol fractions
years
crement with age is less pronounced, and a plateau
appears at ages 50-59 years. HDL-C levels remain at
a stable 44 mg/dl across age strata between the ages
20-54 years but rise to 48 mg/dl in the oldest age
(fig. 4).
VLDL-C levels in white males show a parabolic
relationship to age at 20-59 years. The lowest value is
observed among the 20-40-year-olds (14 mg/dl), an
acme is reached between the ages 40-44 years (26
mg/dl), and is followed by a decrement (22 mg/dl at
ages 55-59 years).
Mean levels of lipoprotein-cholesterol fractions by
age for females not on hormones are shown in figure 5.
LDL-C values rise with age, and have larger increments among middle-aged females compared with
the slope of LDL-C increase among younger females.
Mean LDL-C among 20-24-year-old females is 98
mg/dl and 150 mg/dl among the 55-59-year-olds.
HDL-C changes with age among females not on sex
hormones are depicted in figure 5 as a moderate,
linear increase from a low of 52 mg/dl (ages 20-24
years) to 60 mg/dl among the 55-59-year-olds.
VLDL-C shows little change with age in the younger
5-year birth cohorts presented. A gradually steeper
upward trend of VLDL-C levels with age is seen subsequently, leading to a mean of 21 mg/dl among the
50-59-year-olds.
Lipoprotein-cholesterol levels by age for females
taking sex hormone preparations are presented in
show a linear rise with age from ages 20-59 years.
LDL-C levels increase from 108 mg/dl to 133 mg/dl,
HDL-C from 55 mg/dl to 71 mg/dl, and VLDL-C
from 15 mg/dl to 19 mg/dl.
group
Comparisons by Age, Sex, and Hormone Use
In figure 7 cholesterol and triglyceride levels by age
presented for males and for females identified by
of exogenous sex hormones.
The 20-24-year-old males and females not taking
sex hormones have comparable mean cholesterol
values; the age-dependent increase of plasma
cholesterol levels occurs predominantly between ages
20-45 years in males, and in females it takes place also
during middle age. Consequently, a crossover of
plasma cholesterol levels of males and females takes
place at approximately age 50 years.
The cholesterol levels of females taking hormones
are higher than those of females not taking sex hormone preparations at all ages below the age stratum
50-54 years. A reversal occurs at this point, and
females not on hormones have higher cholesterol
levels in the older age groups.
The age distribution of plasma triglyceride levels
shows marked differences among the three groups
compared. Males and females not on hormones show
inconspicuous differences in triglyceride levels at age
20 years; the plasma triglyceride of females follows an
almost linear incremental tendency over the age strata
are
use
307
PLASMA LIPOPROTEIN-CHOLESTEROL DISTRIBUTIONS/Heiss et al.
160 1
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FIGURE 6. Regression estimates of mean plasma
lipoprotein-cholesterol values by age and clinic, white
females taking sex hormones, ages 20-59 years. Lipid
Research Clinics Prevalence Study, Visit 2, random sample.
240
I
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50
1
30
40
1,
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50
60
AGE IN YEARS
FIGURE 8. Regression estimates of mean plasma
lipoprotein-cholesterol values by age for males, females not
taking sex hormones and females on sex hormone
preparations. Lipid Research Clinics Prevalence Study,
Visit 2, random sample.
considered, while the males reflect a more rapid increase of plasma triglyceride levels during young
adulthood and a decrease during middle age. Thus,
*'°
D
o...o Females Not on Hormones
0
20
n
60
Regression estimates of mean plasma lipid
values by age for males, females not taking sex hormones
and femiales taking sex hormone preparations. Lipid
Research Clinics Prevalence Study, Visit 2, random sample.
differences in plasma levels of triglyceride between
males and females not taking hormones are maximal
over the ages 35-44 years and minimal at both extremes of the age range presented. Females on hormone compounds have consistently, and markedly,
higher total triglyceride levels than females not taking
hormones at all ages.
Figure 8 summarizes the changes of lipoproteincholesterol levels by age, contrasting sex and hormone
usage subgroups. The LDL-C of males and females
not taking hormones increase with age, with the
by sex already described. The
differentialof slope
LDL-C levels for the sexes occurs in the
crossover
age group 50-54 years and leads to higher LDL-C
values in -females not taking hormones than in males
in the age group 55-59 years.
In young females up to the age group 35-39 years,
plasma LDL-C is higher among females characterized
by use of exogenous sex hormones than in females not
taking hormones. A reversal of this pattern is seen in
females beyond age 40: higher LDL-C values are now
characteristic of females not on hormones. This
difference in LDL-C levels between females not on
hormones and those taking hormones increases with
increasing age.
VOL 61, No 2, FEBRUARY 1980
CI RCULATION
308
TABLE, 2. 11 altipic Lincar i?eqresszon Analysis of P)lasma Lipi(ls and ILpoprotein-cholesterol Fractions on Age,
by Sex and 1 {,s of Exoyg nloei.s 8I ormtones. Lipid R?escarch Clinics Visit-2 Random Sample, Ages 20-59 Years
Intercept
Cholesterol
Triglyceride
LDL cholesterol
HDL cholesterol
VLDL cholesterol
Downloaded from http://circ.ahajournals.org/ by guest on June 14, 2017
Cholesterol
Triglyceride
LDL cholesterol
HDL cholesterol
VLDL cholesterol
Cholesterol
Triglyceride
LDL cholesterol
HDL cholesterol
VLDL cholesterol
*Shown are coefficients with
71.0
65.9
34.2
47.2
21.9
Estimated coefficielet (d)*
Age
(years)
Age'
Age3
Males (n = 2458)
5.17
9.24
4.12
0.23
2.03
-0.060
-0.097
-0.042
-0.015
-0.022
0.001
Females not taking horntones (n
0.32
144.3
0.024
1.42
27.6
0.006
0.61
75.7
0.014
5)4.0
0.15
0.61
0.012
18.4
174.3
110.4
112.8
53.1
8.6
Females taking hormones (n
0.59
0.21
0.28
0.14
0.17
=
M\Iultiple
It2
F
0.17
0.05
0.14
0.08
0.04
16.84
4.59
13.30
5.57
3.66
0.28
0.16
0.21
0.10
0.11
22.0
10.5
15.1
9.9
7.1
0.16
0.07
0.08
0.21
0.10
6.1
2.4
2.9
8.5
3.6
1652)
646)
partial F of p < 0.05.
The plasma levels of HDL-C are seen to be lower in
males than in females at all ages between 20-59 years.
In all age groups beyond age 30 years, females taking
hormones have higher HDL-C levels than females not
taking hormones, with an increasing difference over
successively older examinees.
VLDL-C in females taking hormones is higher than
in females not taking hormones among the LRC participants less than 50 years old. Females in their sixth
age decade show little difference in VLDL-C levels by
hormone use, and thereafter a reversal seems to take
place in that females not on hormones show higher
plasma levels of VLDL-C. Males approximate the
female values of VLDL-C in the youngest and oldest
age strata, and have higher VLDL-C levels in the intermediate age groups.
Discussion
The results presented, based on cross-sectional
data, indicate that plasma lipid and lipoprotein levels
vary with age in males, in females not taking hormones, and to a lesser degree in females who take sex
hormones. The patterns of total plasma cholesterol
and triglyceride by age, sex, and hormone use
replicate the findings published by the LRC Program
on visit-l prevalence study participants.12 Based on
48,502 examinees, the latter findings provide descriptive data on total plasma lipids in 10 North American
communities, but do not contain lipoprotein-fraction
measurements. This study provides a comparable
baseline of lipoprotein-cholesterol distributions in the
10 North American populations examined by the
LRC Population Studies.
That lipoproteins have a role in atherogenesis has
been recognized for many years. Recent clinical,
laboratory and epidemiologic studies have gathered
evidence suggestive of an independent contribution of
the plasma lipoprotein fractions to atherogenesis and
atherosclerotic cardiovascular disease. Most important, the risk of atherosclerotic heart disease increases
with increasing levels of LDL-C;8' 26-28 conversely, it
decreases with increasing levels of HDL-C.7 9-l 27
At a time of increased interest in lipoprotein
metabolism it is relevant to describe population levels
of the lipoprotein-cholesterol fractions, and to examine the determinants of their distributional
patterns. Such data can add to comparison between
populations, monitoring of secular trends, clinical
decision making, and formulation of public-health
policies.
The age- and sex-related changes in LDL-C levels
documented in this study closely resemble those for
total plasma cholesterol. This is not surprising,
because almost 70% of total cholesterol is transported
by lipoprotein in the ultracentrifugal low-density
range. The male-female differences, however, are of
greater magnitude for LDL-C.
The well-known higher HDL-C levels in females
compared with males7' 29-34 can be observed across the
PLASMA LIPOPROTEIN-CHOLESTEROL DISTRIBUTIONS/Heiss et al.
full age span covered in this report. Mean HDL-C
values greater than 55 mg/dl are seen in most age
strata of the females, contrasted to values of 45 mg/dl
in age-comparable males. The HDL-C differences by
sex increase over successive birth cohorts through
middle age, by virtue of a small linear increment of
HDL with age in females, while no changes with age
are detectable on HDL-C values in males until the
sixth age decade.
Exogenous estrogen increases HDL-C concentrations in women29' 31, 35 and in men;28 progestins
appear to modify the response to estrogen and either
decrease HDL-C concentrations35 or increase the
heavier HDL3 subclass.29 In contrast to estrogen, androgens appear to decrease HDL-C levels.36-38
Downloaded from http://circ.ahajournals.org/ by guest on June 14, 2017
Between 50-59 years of age, males have a tendency for
HDL-C to increase with age. This characteristic has
not been described before in population studies. On a
speculative basis, age-related changes in gonadal hormone levels39' 40 and selective survival may explain this
phenomenon.
Women taking hormones compared with women
not taking hormones have higher LDL-C levels
between ages 20-40 years, higher HDL-C between
ages 30-59 years, and higher VLDL-C between the
ages 20-55 years. The differential effects of hormone
usage on the lipoprotein-cholesterol fractions by age
presumably reflect age-related changes in the type of
exogenous sex hormone used. Sex hormones taken
before menopause are likely to be oral contraceptive
preparations, while estrogen replacement will be
represented predominantly among the postmenopausal hormone users. The changes in lipoproteincholesterol levels associated with oral contraceptive
and estrogen use in the LRC populations are presented in detail by Wallace et al.25
Several population-based studies on lipoprotein distributions have been reported, although from a less extensive data base than the LRC Prevalence Study. A
small sample of Swedish men and women was examined by Carlson and Ericsson to ascertain referent
control values for their study on lipoproteins in coronary heart disease patients.32 Bang et al. studied lipid
and lipoprotein subfraction levels in: 1) Eskimos in
Greenland, 2) Eskimos in Denmark and 3)
Causcasians in Denmark, and found differences by
place of residence and by ethnicity.4' 42 Tyroler and
co-workers described systematic differences between
black and white adult residents of Evans County,
Georgia.33 Similar black-white differences in children
ages 5-14 years were noted by Srinivasan et al. in the
Bogalusa Louisiana Study.43 Stanhope et al. described
lower serum HDL-C levels in Maori compared with
non-Maori New Zealand adolescents.44 They found
that boys had lower HDL-C levels than girls.
Slack and co-workers45 reported on serum cholesterol and triglyceride and electrophoretically determined lipoproteins in residents of northwest London.
The age trends by sex of total serum cholesterol and
triglyceride presented by Slack et al. are similar to
those we describe. The measurements reported by
309
these authors for serum lipoprotein concentrations are
also similar; however, the absolute values are not
directly comparable because of differences in methods
of lipoprotein quantification.
The age trends in LDL-C observed in the
Cooperative Lipoprotein Phenotyping Study varied
considerably from one population to another.34 No
well-defined age trends were observed for HDL-C in
the men and women ages 40 years and older.
Interlaboratory variability may be partially responsible for these differences.
The Four City Study46 compared serum lipid and
lipoprotein levels in four apparently healthy European
populations ages 20-69 years. The sampling frames
considered working populations in Geneva, London
and Naples; in Uppsala a random sample was drawn
from the population register. Considerable interpopulation differences were found in total serum lipid
levels, with parallel trends for total cholesterol and
triglycerides. Differences between the four populations
in the total serum lipids were mostly accounted for by
differences in LDL-C and VLDL-C concentrations.
Little or no interpopulation differences in HDL-C
were apparent.
Similarly, the 10 study populations surveyed by the
North American LRCs reveal differences in their
mean and median levels of total plasma lipids and
lipoprotein-cholesterol fractions. These differences are
statistically significant and are maintained as parallel
trends across the age groups examined. The rigorous
quality control of the LRC protocol makes it unlikely
that interlaboratory variability is a source of this
diversity among populations. The characteristics of
the LRC study populations are being examined to
ascertain the determinants of lipid and lipoprotein
levels and the observed differences among population
groups.
The difficulties in choosing normal cutoff values for
use in clinical and public-health practice are well
known. A corollary to the cross-sectional trends in
total plasma lipid and lipoprotein-cholesterol concentrations presented in this report is the necessity to take
into account differences by age, sex and idiosyncratic
population characteristics when conventional limits
are used.
Several factors other than sex, age and ethnicity
have been found to influence the levels of lipoproteincholesterol fractions in human groups, although few of
these associations are convincingly established. No
attempt is made in this study to report on the correlates of the population distributions of lipid and
lipoprotein-cholesterol fractions presented. Instead,
this report represents a descriptive reference document for the forthcoming analytic studies of the LRC
Population Studies.
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CI RCULATION
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Gonadal hormones, blood lipids and ischemic heart disease.
Prog Biochem Pharmacol 4: 334, 1968
21. Dyerberg J, Horne H: Plasma lipid and lipoprotein levels in a
Danish population. Acta Med Scand 191: 413, 1972
22. Wynn V, Doar JWH, Mills GL, Stokes D: Fasting serum
triglyceride, cholesterol, and lipoprotein levels during oral contraceptive therapy. Lancet 2: 756, 1969
23. Rossner S, Larsson-Cohn Y, Carlson LA, Boberg J: Effects of
an oral contraceptive agent on plasma lipids, plasma
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lipase activity. Acta Med Scand 190: 301, 1971
24. Wallace RB, Hoover J, Sandler D, Rifkind BM, Tyroler HA:
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25. Wallace R, Hoover J, Barrett-Connor E, Hunninghake D,
Mackenthun A, Wahl P: Lipid and lipoprotein alterations
associated with oral contraceptive and estrogen use - the LRC
Program. Lancet 2:111, 1979
26. Gofman JW, Lindgren F, Elliott H, Mantz W, Hewitt J,
Strisower B, Herring V, Lyon TP: The role of lipids and
lipoproteins in atherosclerosis. Science 111: 166, 1950
27. Carlson LA, Ericsson M: Quantitative and qualitative serum
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28. Stamler J, Katz LN, Pick R, Lewis LA, Page IH, Pick A,
Kaplan BM, Berkson DM, Century D: Effects of long-term estrogen therapy on serum cholesterol-lipid-lipoprotein levels and
on mortality in middle-aged men with previous myocardial infarction. In Drugs Affecting Lipid Metabolism, edited by
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311
PLASMA LIPOPROTEIN-CHOLESTEROL DISTRIBUTIONS/Heiss et al.
APPENDIX 1
TABLE Al. Mean and Percentile Values of Plasma Cholesterol and Triglyceride (mg/dl) by Age-White
Males 20-59 Years, Visit 2 Random Sample
Percentiles
Age
Downloaded from http://circ.ahajournals.org/ by guest on June 14, 2017
(years)
n
Mean
SEM
20-24
25-29
30-34
35-39
40-44
45-49
50-54
55-59
Total
118
253
403
371
383
326
339
260
2453
162.2
178.7
193.1
200.6
205.2
213.4
213.3
214.6
2.5
2.1
1.8
1.9
1.9
1.9
1.9
2.2
20-24
25-29
30-34
35-39
40-44
45-49
50-54
55-59
118
253
403
372
385
327
339
260
2457
89.3
104.2
122.1
140.8
152.4
143.4
153.5
134.1
5
Cholesterol
118
130
142
147
150
163
156
161
10
50
90
95
126
137
152
157
161
171
168
172
159
176
190
195
204
210
211
214
197
223
237
248
251
258
263
259
212
234
258
267
260
275
274
276
50
51
57
58
69
65
75
70
78
88
102
109
123
119
128
117
146
171
214
250
252
218
244
210
165
204
253
316
318
279
313
262
Triglyceride
3.7
4.2
3.7
5.5
6.9
5.9
5.5
4.2
44
45
46
52
56
56
63
60
Total
Missing values: cholesterol = 5; triglyceride = 1; inconsistent reporting of gonadal hormone use = 1.
Minimum cell size for display of percentiles: 5th and 95th > 100; 10th and 90th > 75; 50th > 40.
TABLE A2. Mean and Percentile Values of Plasma Cholesterol and Triglyceride (mg/dl) by Age-White Females
20-59 Years, No Hormones*, Visit-2 Random Sample
Percentiles
Age
5
10
SEM
n
Mean
50
90
95
(years)
Cholesterol
124
3.4
161
162.1
96
202
20-24
2.2
129
140
172
173.6
181
213
222
25-29
131
1.9
137
173
234
174.3
211
220
30-34
139
148
184
2.2
230
251
188.3
248
35-39
2.1
147
159
191
196.2
238
253
40-44
253
147
160
2.3
199
254
267
204.6
257
45-49
163
3.0
173
221.5
217
269
292
187
50-54
183
2.8
175
231
278
296
230.8
55-59
190
1646
Total
Triglyceride
100
37
65
3.4
68.2
96
64
43
40
108
128
2.1
71.0
181
42
38
63
111
138
3.0
74.1
235
149
38
78
45
174
3.0
88.6
250
179
151
50
80
2.7
44
91.8
255
91
44
165
192
53
3.6
105.4
257
214
183
56
98
52
4.0
111.5
187
246
280
110
65
57
5.6
131.6
190
1651
Total
Missing values: cholesterol = 6; triglyceride = 1.
Minimum cell size for display of percentiles: 5th and 95th > 100; 10th and 90th > 75; 50th > 40.
*Defined as congruent reporting of gonadal hormone usage during the previous 2 weeks.
20-24
25-29
30-34
35-39
40-44
45-49
50-54
55-59
CIRCULATION
312
VOL 61, No 2, FEBRUARY 1980
TABLJE A3. Mean and Percentile Values of Plasma Cholesterol and Triglyceride (mg/dl) by Age-White Females
20-59 Years, on Hormones*, Visit-2 Random Sanple
Age
(years)
n
Mean
SEM
101
132
97
50
63
71
70
60
644
178.0
187.2
190.7
195.6
202.9
211.8
205.9
222.4
3.4
2.6
3.3
6.1
5.0
4.2
3.5
4.9
3
10
Percentiles
30
90
93
170
184
188
196
201
212
224
224
231
247
236
207
-
Cholesterol
20-24
25-29
30-34
35-39
40-44
45-49
50-54
55-59
Total
132
138
-
140
131
-
-
150
-
214
-
-
Triglyceride
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20-24
62
101
105.6
4.0
161
176
54
99
201
25-29
96
161
132
109.4
5.3
a2
59
30-34
97
60
104
114.6
5.3
176
35-39
146.3
123
50
10.2
40-44
63
123.6
6.1
109
45-49
72
137.7
8.3
131
50-54
70
127.8
6.4
114
55-59
60
138.2
9.9
117
Total
645
Missing values: cholesterol = 2; triglyceride = 1.
Minimum cell size for display of percentiles: 5th and 95th > 100; 10th and 90th > 75; 50th > 40.
*Defined as congruent reporting of gonadal hormone usage during the previous 2 weeks.
TABLE A4. Mean and Percentile Values of LDL, HDL, and VLDL Cholesterol (mg/dl) by Age- White Males
20-59 Years, Visit-2 Random Sample
Age
(years)
n
Mean
SEM
20-24
25-29
30-34
35-39
40-44
45-49
30-54
55-59
Total
118
253
403
371
385
325
339
260
2454
103.3
116.7
126.4
133.2
135.6
143.8
142.4
145.4
2.4
1.9
1.6
1.7
1.6
1.8
1.7
2.1
20-24
25-29
30-34
35-39
40-44
118
252
403
45.4
44.7
45.5
43.4
44.3
1.0
5
10
Percentiles
50
90
95
147
165
185
135
138
157
166
176
173
189
186
141
143
145
186
185
190
202
197
202
45
44
45
43
43
45
44
46
57
58
63
63
63
62
67
64
63
71
LDL cholesterol
45-49
50-54
55-59
Total
371
383
325
339
260
2452
43.4
44.1
47.7
0.7
0.6
0.6
0.6
0.6
0.6
0.9
66
70
78
81
87
98
89
88
73
73
88
92
98
106
102
103
HDL cholesterol
30
32
31
32
28
29
27
30
28
28
32
31
31
33
31
31
101
116
124
131
59
58
60
60
58
64
313
PLASMA LIPOPROTEIN-CHOLESTEROL DISTRIBUTIONS/Heiss et al.
TABLE A-4 Continued
Percentiles
Age
(years)
n
Mean
SEM
5
10
VLDL cholesterol
1
5
3
6
5
8
3
7
5
8
5
8
8
10
3
6
50
90
95
20-24
118
13.7
0.8
12
24
28
25-29
253
17.4
0.9
15
31
36
30-34
403
21.3
0.9
18
36
48
35-39
372
24.1
1.0
19
46
56
40-44
384
25.5
1.2
21
43
56
45-49
326
24.4
1.1
20
40
51
50-54
339
26.8
1.2
23
49
62
18
55-59
260
21.6
1.1
39
49
Total
2455
Missing values: LDL = 4; HIDL 6; VLDL = 3; inconsistent reporting of gonadal hormone use = 1.
Minimum cell size for display of percentiles: 5th and 95th > 100; 10th and 90th > 75; 50th > 40.
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TABLE, A5. Mean and Percentile Values of LDL, HDL, and VLDI, Cholesterol (mg/dl) by Age-White Females
20-59 Years, No Horm7ones*, Visit-2 Random Sample
Percentiles
Age
n
Mean
SEM
5
10
50
90
95
(years)
LDL cholesterol
136
98
62
2.8
96
98.1
20-24
141
151
103
2.0
70
73
106.0
181
25-29
141
148
109
77
68
1.7
108.9
232
30-34
173
161
117
81
76
2.1
118.8
249
35-39
174
122
163
89
76
1.9
254
125.1
40-44
188
90
173
127
81
2.1
130.0
255
45-49
214
191
140
102
90
2.8
186
145.0
50-54
212
148
202
101
93
2.7
150.4
189
55-59
1642
Total
HDL cholesterol
20-24
25-29
30-34
35-39
40-44
45-49
50-54
55-59
Total
96
181
233
248
254
257
186
189
a2.2
55.9
55.4
54.5
57.0
57.7
60.0
59.5
1.5
1.0
0.8
0.9
1.0
1.1
1.1
1.2
37
38
34
34
33
37
36
37
39
40
38
39
39
40
39
50
55
55
52
55
56
58
58
68
73
71
74
78
78
77
82
3
4
2
3
5
4
4
4
10
22
11
212
9
13
12
14
14
19
26
26
32
81
75
82
87
86
89
86
1644
VLDL cholesterol
20-24
25-29
30-34
35-39
40-44
45-49
50-54
55-59
Total
96
181
233
247
254
255
186
189
1641
11.9
12.0
10.5
14.4
14.1
16.9
16.6
21.3
0.7
0.6
0.5
0.7
0.5
0.8
1.2
0.9
2
0
1
3
2
0
2
18
33
39
Missing values: LDI = 10; HDL = 8; VLDL = 11.
Minimum cell size for display of percentiles: 5th and 95th > 100; 10th and 90th > 75; 50th > 40.
*Defined as congruent reporting of gonadal hormone usage during the previous 2 weeks.
24
24
35
29
40
37
49
314
CI RCULATION
VOL 61, No 2, FEBRUARY 1980
TABLE A6. Mean and Percentile Values of LDL, HDL, and VLDL Cholesterol (mgldl) by Age-White Females
20-59 Years, on Hormones*, Visit-2 Randomn Sample
Age
(years)
Percentiles
Downloaded from http://circ.ahajournals.org/ by guest on June 14, 2017
n
Mean
SEM
20-24
25-29
30-34
35-39
40-44
45-49
50-54
55-59
Total
101
132
95
50
63
108.3
113.9
117.4
118.9
124.8
127.3
119.7
132.5
3.3
2.5
3.1
20-24
25-29
30-34
35-39
40-44
45-49
50-54
55-59
Total
101
55.0
56.1
1.4
1.3
58.0
57.0
61.1
65.6
67.6
70.8
1.7
2.2
2.5
2.1
2.1
2.3
15.2
15.3
15.6
20.4
17.2
19.0
18.7
19.2
0.9
1.0
0.9
2.0
1.5
1.4
1.1
71
70
60
642
132
97
50
63
71
70
60
644
5.4
4.7
4.0
3.3
4.7
5
10
a0
90
95
LDL cholesterol
62
66
72
s8
106
149
157
155
163
169
74
75
77
79
83
27
28
24
30
36
-
80
-
-
HDL cholesterol
34
35
38
38
36
1ll
110
114
124
127
120
129
53
a4
57
57
57
6a65
-
-
68
71
VLDL cholesterol
20-24
25-29
30-34
35-39
40-44
45-49
50-54
55-59
Total
101
132
95
1
2
4
3
5
14
13
15
15
16
17
50
63
72
70
18
60
1.9
17
643
Missing values: LDL 4; HDL = 2; VLDL = 3.
Minimum cell size for display of percentiles: 5th and 95th > 100; 10th and 90th > 75; 50th > 40.
*Defined as congruent reporting of gonadal hormone usage during the previous 2 weeks.
Appendix 2
Lipid Research Clinics
North American Clinics
Baylor College of Medicine, Houston, Texas
Director: William Insull, M.D.
Past Director: Antonio Gotto, M.D.
*George Washington University, Washington, D.C.
Director: John LaRosa, M.D.
Johns Hopkins University, Baltimore, Maryland
Director: Peter Kwiterovich, M.D.
Oklahoma Medical Research Foundation, Oklahoma City,
Oklahoma
Director: Reagan Bradford, M.D.
Stanford University, Palo Alto, California
Director: John Farquhar, M.D.
University of California at San Diego, La Jolla, California
Director: Fred Mattson, Ph.D.
Co-director: Daniel Steinberg, M.D.
Past Director: Virgil Brown, M.D.
University of Cincinnati, Cincinnati, Ohio
Director: Charles Glueck, M.D.
University of Iowa, Iowa City, Iowa
Director: Francois Abboud, M.D.
Past Director: William Connor, M.D.
University of Minnesota, Minneapolis, Minnesota
Director: Ivan D. Frantz, Jr., M.D.
University of Toronto/McMaster University at Hamilton, Ontario,
Canada
PLASMA LIPOPROTEIN-CHOLESTEROL DISTRIBUTIONS/Heiss et al.
Director: Alick Little, M.D.
Co-Directors: Maurice Mishkel, M.D. and George Steiner, M.D.
University of Washington, Seattle, Washington
Director: Robert Knopp, M.D.
Past Directors: Edward Bierman, M.D., William Hazzard, M.D.
*Washington University, St. Louis, Missouri
*Drug
Supply
and Distribution Center
Mead Johnson, Evansville, Indiana
Director: John Boenigk, Ph.D.
Lipid
Standardization
Laboratory
Center for Disease Control, Atlanta,
Director: Gerald
Nutrition
Director: Gustav Schonfeld, M.D.
Past Director: Robert Shank, M.D.
315
Coding
University
Georgia
Cooper, M.D., Ph.D.
Center
of Minnesota,
Director: P.
Victor
Minneapolis,
Minnesota
Grambsch
USSR Clinics
All Union
Cardiologic Institute,
Program Office
Moscow
Director: Elena Gerasimova, M.D.
Institute of
Lipid Metabolism Stranch,
Experimental Medicine, Leningrad
Director: Anatoli Klimov, M.D.
National
Heart, Lung, and Blood
Institute
Chief: Basil
Past
Chief:
Rifkind, M.D.
Robert Levy,
M.D.
Israeli Clinic
Hadassah Medical School and Hebrew
University, Jerusalem
Director: Yechezkiel Stein, M.D.
Downloaded from http://circ.ahajournals.org/ by guest on June 14, 2017
Anderson, Ph.D.; Elizabeth Barrett-Connor, M.D.; Mary
Brockway, Ph.D.; Gary Chase, Ph.D.; Bobbe Christensen, Ph.D.;
Michael Criqui, M.D.; Michael Davies, M.D.;
Deev,
Ph.D.; Ido deGroot, M.P.H.; Marian Fisher, Ph.D.; Elena
Glasunov, M.D.; Gaetan Godin, MS.;
M.D.;
S. T.
M.D.; Robin Harris, M.P.H.; William Haskell,
Paul
Support Agencies
Central Clinical
LRC Epidemiology Committee
Chairperson: H. A. Tyroler, M.D.
Alexander
Chemistry Laboratory
Bio-Science Laboratories, Van Nuys, California
Director: Frank Ibbott, Ph.D.
Past Director: Donald Wybenga, B.M.
Gerasimova,
Halfon,
lgor
Ph.D.; Gerardo Heiss, M.D., Ph.D.; David Hewitt, M.A.; Judith
Central
Electrocardiographic Laboratory
University of Alabama, Birmingham, Alabama
Director: L. Thomas Sheffield, M.D.
Central Patient
Registry
and
Coordinating
Center
Hill, MrS.; Joanne Hoover, M.D.; David Jacobs, Ph.D.; Kathe
Kelly, MAS.; Anatoli Klimov, M.D.; Alick Little, M.D.; Arden
MP S.; Richard Mowery,
Mackenthun, Ph.D.; Irma Mebane,
M.S.P.H.; John Morrison, Ph.D.; Basil Rifkind, M.D.; Dimitri
University of North Carolina, Chapel Hill, North Carolina
Director: 0. Dale Williams, Ph.D.
Past Director: James E. Grizzle, Ph.D.
Shestov,
*Did not participate in the LRC Prevalence Study.
*Did not participate in the LRC Prevalence Study.
Van
M.D.; Israel Tamir, M.D.; Henry Taylor, Ph.D.; Pearl
0. Dale Williams,
Ph.D.; Robert Wallace,
M.D.;
Natta,
Ph.D.; Andrei
Zadoja,
M.D.
Lipoprotein-cholesterol distributions in selected North American populations: the lipid
research clinics program prevalence study.
G Heiss, I Tamir, C E Davis, H A Tyroler, B M Rifkand, G Schonfeld, D Jacobs and I D
Frantz, Jr
Downloaded from http://circ.ahajournals.org/ by guest on June 14, 2017
Circulation. 1980;61:302-315
doi: 10.1161/01.CIR.61.2.302
Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright © 1980 American Heart Association, Inc. All rights reserved.
Print ISSN: 0009-7322. Online ISSN: 1524-4539
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