Dietary fat intake and risk of coronary heart disease: the Strong

Heart Study14
Jiaqiong Xu, Sigal Eilat-Adar, Catherine Loria, Uri Goldbourt, Barbara V Howard, Richard R Fabsitz, Ellie M Zephier,
Claudia Mattil, and Elisa T Lee

KEY WORDS
Dietary fat intake, fatty acids, cholesterol, coronary heart disease, mortality, American Indians

INTRODUCTION

The classic diet-heart hypothesis posits that diets high in saturated fatty acids (SFAs) and cholesterol and low in polyunsaturated fatty acids (PUFAs) raise serum total and LDL cholesterol, which in turn increase the risk of coronary heart disease
(CHD) (1). Despite decades of intensive interest and research in
the diet-heart hypothesis, however, investigations of dietary fat
and CHD incidence from prospective epidemiologic studies
have resulted in inconsistent findings. Some studies found a
significantly positive association between total fat intake and
CHD incidence (2 4) and CHD death (5, 6); other studies could
not demonstrate this association (710). SFA intake was found to
be positively associated with CHD incidence (4, 11) and CHD

894

death (5, 6, 12, 13), whereas other studies found no association

between SFAs and CHD death (7, 9, 10, 14). Monounsaturated
fatty acid (MUFA) intake was inversely associated with CHD
incidence in 2 studies (11, 15), whereas other studies reported a
positive association between MUFA intake and CHD incidence
(3, 4) and CHD death (5). An inverse association between PUFA
intake and CHD incidence (10, 15) and CHD death (13, 14) was
found in some studies, but other studies found no association
(25, 79, 16). A positive association between trans fatty acids
(TFAs) and CHD incidence was seen in some studies (9, 10, 15,
17). Age-related differences in the association between dietary
fat and CHD incidence was shown in some studies (35, 10),
which reported that CHD risk differed among age groups. The
inconsistency of the findings from prospective epidemiologic
studies may be partly explained by small sample sizes; use of
different diet assessment methods; incomplete adjustment for
potential confounders, such as energy intake and other types of
fat (13, 15); and effect dilution due to high intraindividual variability (18). To the best of our knowledge, no previous analysis
has been conducted of the association between dietary fat intake
and CHD incidence or CHD death among American Indians.
The Strong Heart Study (SHS), a longitudinal study of cardiovascular disease and its risk factors in American Indian men and
women (19), has shown that CHD incidence is now higher in this
population than in other US populations (20), which suggests that
this populations lifestyle, including diet, has undergone profound changes. The objective of the current analysis was to
1
From the Center for American Indian Health Research, University of
Oklahoma Health Sciences Center, Oklahoma City, OK (JX and ETL); Medstar Research Institute, Hyattsville, MD (SE-A, BVH, and CM); the National
Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD
(CL and RRF); the Indian Health Service, Aberdeen Area Office, Aberdeen,
South Dakota (EMZ); and the Department of Epidemiology and Preventive
Medicine, Sackler Medical Faculty, Tel Aviv University, Tel Aviv, Israel
(UG).
2
The opinions expressed here are those of the authors and do not necessarily reflect the views of the Indian Health Service.
3
Supported by cooperative agreement grants (no. U01HL-41642,
U01HL-41652, and U01HL-41654) from the National Heart, Lung, and
Blood Institute.
4
Address reprint requests to J Xu, Center for American Indian Health
Research, University of Oklahoma Health Sciences Center, College of Public
Health, 801 NE 13th Street, Room 112, Oklahoma City, OK 73190. E-mail:
susan-xu@ouhsc.edu.
Received January 4, 2006.
Accepted for publication May 24, 2006.

Am J Clin Nutr 2006;84:894 902. Printed in USA. 2006 American Society for Nutrition

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ABSTRACT
Background: The results of previous studies on the association
between dietary fat intake and coronary heart disease (CHD) incidence are inconsistent.
Objective: The aim of this study was to examine the association
between dietary fat intake and CHD incidence in American Indians
in the Strong Heart Study.
Design: A total of 2938 participants aged 4779 y and free of CHD
at the second examination (19931995) were examined and followed for CHD, nonfatal CHD, and fatal CHD events to 31 December 2002. Dietary intake was assessed by using a 24-h diet recall and
was calculated as percentages of energy.
Results: Participants were followed for a mean (SD) of 7.2
2.3 y. During follow-up, 436 incident CHD cases (298 nonfatal CHD
and 138 fatal CHD events) were ascertained. Participants aged
4759 y in the highest quartile of intake of total fat, saturated fatty
acids, or monounsaturated fatty acids had higher CHD mortality than
did those in the lowest quartile [hazard ratio (95% CI): 3.57 (1.21,
10.49), 5.17 (1.64, 16.36), and 3.43 (1.17, 10.04), respectively] after
confounders were controlled for. These associations were not observed for those aged 60 79 y.
Conclusions: Total fat, saturated fatty acid, and monounsaturated
fatty acid intake were strong predictors of CHD mortality in American Indians aged 4759 y, independent of other established CHD
risk factors. It may be prudent for American Indians to reduce their
fat intake early in life to reduce the risk of dying from CHD.
Am
J Clin Nutr 2006;84:894 902.

DIETARY FAT INTAKE AND CORONARY HEART DISEASE

examine the association between dietary fat intake and CHD risk
in this population.

SUBJECTS AND METHODS

Subjects

Data collection
The second examination in the SHS included demographic
data, personal medical history, health habits, family history of
cardiovascular disease and diabetes, blood pressure, body mass
index (BMI), and the collection of fasting blood samples for
measurements of lipids and lipoproteins. Details about the data
collection and laboratory procedures are published elsewhere
(19, 20). Diabetes was defined according to the American Diabetes Association criteria (24), ie, as taking insulin or oral antidiabetic medication or having a fasting glucose concentration
126 mg/dL. Cigarette smoking and alcohol consumption were
determined by questionnaire.
The second examination also included a 24-h dietary recall for
all participants. The interviews were conducted by local field
staff who were trained and supervised by Indian Health Service
dietitians and the principal investigator according to standardized methods (25). Detailed information about staff training,

project supervision, and quality assurance was previously reported (26). Dietary intake data were collected and analyzed by
using the Minnesota Nutrition Data System (NDS version 2.1)
developed by the Nutrition Coordinating Center (NCC), University of Minnesota (Minneapolis, MN; Food Database version 4A;
Nutrient Database version 18; 27, 28). TFA were not available in
NDS version 2.1; therefore, to include them in the nutrient data,
final calculations were completed by using NCC Nutrient Database Version 36 (NDS-R 2005). The NDS-R time-related database updates analytic data while retaining nutrient profiles true to
the version used for data collection (29).
The Indian Health Service, participating institutional review
boards, and the participating tribes approved the SHS. Informed
consent was obtained from all participants.
Ascertainment of endpoints
The primary endpoints for this study were CHD, nonfatal
CHD, and fatal CHD events. CHD events comprised the first nonfatal CHD or fatal CHD event occurring after the second examination but before 31 December 2002. Nonfatal CHD events included
definite MI, definite CHD, and electrocardiogram-evident definite
MI events. Fatal CHD for the purpose of this study was defined as
death from definite fatal MI, definite sudden death due to CHD,
definite fatal CHD, and possible fatal CHD event. Detailed definitions of the nonfatal and fatal events were described previously (30,
31). CHD events that occurred during the follow-up period were
ascertained from the annual mortality and morbidity surveillance or
at the third examination (1998 1999). Medical records were abstracted, and fatal CHD events were ascertained and confirmed by
mortality and morbidity review committees using specific criteria
(32). Records of those who did not participate in the third examination (n 525) were also reviewed. Follow-up for mortality was
99.8% complete.
Statistical analysis
Dietary intake data for all SHS analyses were based on a data
set obtained from NCC Nutrient Database Version 36. To compare dietary intake with that reported in NHANES III, the dietary
intake data for the SHS were obtained from NCC Nutrient Database version 18, which did not include TFA information. Data
are presented as means SDs for the SHS by CHD category and
ages: 4759 y and 60 79 y at the second examination. Previous
studies showed an age-related difference in the association between fat intake and CHD incidence (35, 10). Means and SEMs
are presented for the NHANES III data and were obtained by
using the Proc DESCRIPT procedure in SAS-Callable
SUDAAN (version 9.0; Research Triangle Institute, Research
Triangle Park, NC), which is specifically designed for the analysis of complex survey data. Means or proportions of CHD risk
factors and mean intakes of nutrients were compared by age or
CHD category by using t tests or Wilcoxons rank-sum tests or
chi-square tests whenever appropriate for the SHS, and mean
intakes of nutrients were compared by age by using the
DIFFVAR statement in the Proc DESCRIPT procedure for
NHANES III, in which the sampling weights were provided by
the National Center for Health Statistics. Mean nutrient intakes in
the SHS and NHANES III for the same age group were compared
by t tests.
Time to CHD event or death or censoring for each participant
was calculated from the second examination until the first nonfatal CHD, fatal CHD, or 31 December 2002. Dietary fat intakes

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The SHS is a population-based study of American Indians who

reside in central Arizona, Oklahoma, and North and South Dakota. The SHS cohort consisted of 4549 American Indians aged
4574 y at the baseline examination (1989 1991). We used data
from 3638 participants, who returned to the second SHS examination in 19931995 as the basis for our analysis. Dietary data
were collected from all participants at the second examination at
the Strong Heart clinics by means of a single 24-h dietary recall;
3450 participants completed the second examination and had
complete nutrition data. After excluding adults who had definite
myocardial infarction (MI) or CHD (definite CHD, definite MI,
or definite electrocardiogram-evident MI) before or at the second
examination (n 233), whose total reported energy intake was
600 kcal/d or 8000 kcal/d for men or 6000 kcal/d for women
(n 124), who were under dialysis treatment, or had a kidney
transplant or liver cirrhosis (n 154), and who were older than
79 y (n 1), the final subsample consisted of 2938 participants
aged 4779 y.
To compare the nutrient intakes of the SHS participants with
those of the general US population as obtained in the third National Health and Nutrition Examination Survey (NHANES III)
1988 1994 (21), which occurred at about the same time as the
SHS, a subsample of 6687 persons aged 4779 y was obtained
from the NHANES III data set (22). As in the SHS, total energy
intake was estimated in NHANES III by use of a single 24-h
dietary recall. We excluded those who reported having angina or
a history of MI (n 1099), as described previously (23), and
those whose total reported energy intake was missing or 600
kcal/d or 8000 kcal/d for men or 6000 kcal/d for women
(n 494). Because the SHS participants blood samples were
drawn in the morning, we excluded those in NHANES III who
were assigned to an afternoon or evening session, and plasma
glucose values were obtained after an overnight fast of 9 h
(n 2750). The final subsample included 2344 participants
from NHANES III.

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XU ET AL

TABLE 1
Coronary heart disease (CHD) risk factors at baseline of 2938 American Indian men and women included in the Strong Heart Study1
4759 y
CHD
(n 185)

No CHD
(n 1474)

CHD
(n 218)

No CHD
(n 1061)

54.5 3.52,3
88 (48)2
128 (70)2
31.8 5.63
38.7 12.32,3
123.8 33.7
192 1242,3
81 (45)2,3
75 (41)3
87 (47)2,3

53.8 3.34
558 (38)4
644 (44)
32.0 6.94
41.1 13.2
119.2 33.8
159 117
494 (34)4
614 (42)4
561 (38)4

67.8 5.1
90 (41)5
141 (65)5
30.5 5.9
39.1 12.55
121.7 36.05
171 1135
58 (27)
49 (23)
136 (62)5

67.2 5.1
315 (30)
472 (45)
30.6 5.9
42.4 13.5
116.6 32.9
146 92
241 (23)
246 (23)
524 (49)

1940 8303

1916 8214

1672 724

1709 670

80.6 43.23
36.9 9.93

77.2 41.24
35.8 9.74

64.4 37.3
33.9 9.7

65.6 33.6
34.1 9.4

27.7 16.03
12.6 4.23

26.1 15.14
12.1 4.04

21.9 13.1
11.5 3.9

22.4 12.2
11.6 3.8

30.8 17.83
14.0 4.33

29.6 16.64
13.7 4.3

25.2 15.6
13.2 4.3

25.0 13.7
13.0 4.2

14.6 8.93
6.8 3.03

14.6 10.04
6.7 3.34

11.2 7.7
5.9 2.5

12.1 7.8
6.3 3.0

5.3 4.33
2.3 1.3
381 2953

5.1 3.8
2.4 1.4
343 276

4.6 3.7
2.5 1.4
336 268

4.6 3.4
2.4 1.3
309 234

All data are x SD for continuous variables and n (%) for categorical variables.
Significantly different from those without CHD among ages 4759 y, P 0.05.
3
Significantly different from those aged 60 79 y among those with CHD, P 0.05.
4
Significantly different from those aged 60 79 y among those without CHD, P 0.05.
5
Significantly different from those without CHD among ages 60 79 y, P 0.05.
1
2

were calculated as a percent of energy and divided into quartiles.

The Cox proportional hazards model (33) was used to study
associations between quartiles of dietary fat intake and CHD,
either nonfatal or fatal CHD event over time separately. The
effect of isocaloric substitution of each dietary fat for carbohydrate was evaluated by multivariate nutrient-density models that
simultaneously included energy intake and percent of energy
from protein (15, 34) and other confounders, including age, sex,
study center (Arizona, Oklahoma, North and South Dakota),
diabetes status (diabetes versus nondiabetes), BMI, HDL cholesterol, LDL cholesterol, total triacylglycerol, smoking status
(current versus past and never), alcohol consumption (current
versus past and never), and hypertension. Triacylglycerol was
log-transformed to stabilize the variance. Interactions were examined in the multivariate-adjusted models for quartiles of dietary fat intake with age group, sex, or diabetes, as well as interaction for age group and all other confounders separately. Tests
for trend were conducted by modeling the median of each
quartile-defined category as a continuous variable in Cox proportional hazards models. The proportionality assumption of the

Cox model was assessed by generating the time-dependent covariate by creating interaction of each covariate and a function of
survival time and including it in the model. There was no evidence for the violation of this assumption for any covariates. We
also repeated the analyses by modeling dietary fat intakes as
continuous variables. All analyses were performed with SAS
version 9.00 (SAS Institute Inc, Cary, NC). All P values were
2-tailed, and statistical significance was defined as P 0.05 for
all tests.
RESULTS

Participants were followed for an average (SD) of 7.2

2.3 y. During follow-up (21 101 person-years), 436 CHD events
were ascertained (298 first nonfatal CHD events and 138 fatal
CHD events). CHD risk factors at baseline are presented by
follow-up CHD category (yes or no) and baseline age group
(4759 and 60 79 y) in Table 1. Within each age group, those
who developed CHD were more likely to be male, diabetic, and
hypertensive and to have lower HDL cholesterol and higher

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CHD risk factors

Age (y)
Male sex [n (%)]
Diabetes [n (%)]
BMI (kg/m2)
HDL (mg/dL)
LDL (mg/dL)
Total triacylglycerol (mg/dL)
Current smokers [n (%)]
Current alcohol consumers [n (%)]
Hypertension [n (%)]
Dietary intake
Energy (kcal)
Total fat
(g)
(% of energy)
Saturated fatty acids
(g)
(% of energy)
Monounsaturated fatty acids
(g)
(% of energy)
Polyunsaturated fatty acids
(g)
(% of energy)
trans Fatty acids
(g)
(% of energy)
Cholesterol (mg)

60 79 y

897

DIETARY FAT INTAKE AND CORONARY HEART DISEASE

TABLE 2
Macronutrient and cholesterol intakes of the Strong Heart Study (SHS) sample and the third National Health and Nutrition Examination Survey (NHANES
III) sample by age1
4759 y

Energy (kcal)
Total fat (% of energy)
SFA (% of energy)
MUFA (% of energy)
PUFA (% of energy)
Cholesterol (mg)

60 79 y

SHS
(n 1659)

NHANES III
(n 934)

SHS
(n 1279)

NHANES III
(n 1410)

1938 830
35.7 9.6
12.2 4.0
14.3 4.3
6.0 2.7
344 272

2061 36.5
34.8 0.6
11.7 0.2
13.4 0.3
7.0 0.1
264 7.4

1711 683
33.9 9.4
11.7 3.9
13.5 4.2
5.6 2.5
310 236

1820 25.6
32.6 0.4
11.1 0.1
12.5 0.2
6.5 0.1
232 6.7

1
All data are x SD for the SHS and x SEM for NHANES III. The dietary intake data set for the SHS was obtained from the University of Minnesota
Nutrition Coordinating Center Nutrient Database version 18. SFA, saturated fatty acids; MUFA, monounsaturated fatty acids; PUFA, polyunsaturated fatty
acids. The difference in dietary intake between the SHS and NHANES III, as well as the difference between age groups in both studies, was significant, P
0.01.

Mean total fat intake, SFA intake, and MUFA intake (all % of
energy) were also higher in the SHS participants, but PUFA
intake was higher in the NHANES III participants, in both age
groups. All differences were significant (P 0.01).
In multivariate analyses, there were no statistically significant
interactions for CHD incidence between quartiles of dietary fat
intake and sex, diabetes, or age group (P values for interactions
varied from 0.11 to 0.98). Intake of total fat and its components
were not associated with CHD incidence after the analysis was
controlled for other confounders (Table 3).
Statistically significant interactions for CHD death were detected between quartiles of dietary fat intake and age group
(Table 4). A higher intake of total fat, SFAs, and MUFAs was
associated with higher CHD mortality among participants aged
4759 y but not among those aged 60 79 y. Participants aged
4759 y in the highest quartile of total fat, SFAs, and MUFAs had
adjusted hazard ratios (HRs) of 3.57 (95% CI: 1.21, 10.49), 5.17
(95% CI: 1.64, 16.36), and 3.43 (95% CI: 1.17, 10.04), respectively. Omitting HDL cholesterol and LDL cholesterol from the
model did not change the results. When evaluating the association between SFAs and MUFAs and CHD death separately, both
SFAs and MUFAs remained significant predictors of CHD death
among persons aged 4759 y [HR for increasing quartiles of
SFAs: 1.00, 3.31 (95% CI: 1.04, 10.55), 1.69 (95% CI: 0.43,
6.60), and 5.65 (95% CI: 1.71, 18.68), P for trend 0.01; for
MUFAs: 1.00, 1.32 (95% CI: 0.38, 4.58), 3.56 (95% CI: 1.07,
11.81), and 5.16 (95% CI: 1.45, 18.32), P for trend 0.01] after
adjustment for the above risk factors as well as PUFAs and TFAs
as a percent of energy. In the similar model including all fat
components simultaneously and adjusted for the above risk factors, SFAs and MUFAs did not predict CHD death independently
of each other in this younger age group [HRs for increasing
quartiles of SFAs: 1.00, 2.52 (95% CI: 0.66, 9.65), 0.98 (95% CI:
0.20, 4.87), and 2.98 (95% CI: 0.66, 13.58), P for trend 0.19;
for MUFAs: 1.00, 0.94 (95% CI: 0.24, 3.67), 2.52 (95% CI: 0.60,
10.64), and 2.88 (95% CI: 0.59, 14.21), P for trend 0.13].
PUFAs, TFAs, and cholesterol intake were not associated with
CHD death (Table 4). There were no statistically significant
interactions for CHD death between quartiles of dietary fat intake
and sex or diabetes. In addition, there were no statistically significant interactions for risk of CHD, either nonfatal or fatal,
between age group and all other confounders.

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triacylglycerol concentrations than those who did not develop

CHD. Participants aged 4759 y who developed CHD were also
older and more frequently smokers than were those who did not
develop CHD. Participants aged 60 79 y who developed CHD
also had higher LDL cholesterol than did those who did not
develop CHD. Comparing those who developed CHD by age
groups, participants aged 4759 y had higher BMI and triacylglycerol and lower HDL and were more likely to be current
smokers and drinkers, but were less likely to be hypertensive,
than were those aged 60 79 y. When comparing those who did
not develop CHD by age group, participants aged 4759 y were
more likely to be male and current smokers and drinkers, were
less likely to be hypertensive, and had higher BMIs than did those
aged 60 79 y.
The mean percentages of energy from dietary fat, SFAs,
MUFAs, PUFAs, and TFAs were 35.1%, 11.9%, 13.4%, 6.5%,
and 2.4%, respectively. Specific types of fat intake were positively correlated with one another, with the highest correlation
between SFAs and MUFAs (r 0.77, P 0.0001). Associations
between TFAs and MUFAs (r 0.46, P 0.0001) were also
high, but those between TFAs and SFAs (r 0.25, P 0.0001)
and between TFAs and PUFAs (r 0.13, P 0.0001) were
lower. Also summarized in Table 1 are dietary intake differences
by CHD category and age group. There was no significant univariate difference in dietary intake between those who developed
CHD and those who did not during follow-up in either age group.
As expected, participants aged 4759 y consumed significantly
more calories and a higher percentage of calories from fat (total,
SFA, MUFA, and PUFA) than did participants aged 60 79 y
regardless of whether they developed CHD during follow-up.
Among those who developed CHD, participants aged 4759 y
consumed significantly more cholesterol than did those aged
60 79 y. There was no significant difference in TFA intake as a
percent of energy between the 2 age groups among either those
who developed CHD or those who did not.
Mean dietary intakes by age group from the SHS and
NHANES III are presented in Table 2. In both the SHS and
NHANES III, dietary intakes followed a similar pattern in each
age group. When comparing mean dietary intake between participants from the SHS and NHANES III, mean energy intake
was lower, but cholesterol intake was higher, in the SHS participants than in the NHANES III participants in both age groups.

898

XU ET AL

TABLE 3
Hazard ratio (HR) and 95% CI of each quartile of dietary fat intake associated with coronary heart disease (CHD) and nonfatal CHD events for all
participants in the Strong Heart Study1
Dietary fat intake quartiles
2

P for trend2

24.0
104
1
74
1

32.3
103
1.04 (0.78, 1.40)
77
1.09 (0.77, 1.54)

38.4
92
0.91 (0.67, 1.23)
66
0.92 (0.64, 1.31)

45.9
104
1.03 (0.77, 1.40)
81
1.12 (0.79, 1.59)

0.97

7.5
99
1
73
1

10.6
95
1.05 (0.78, 1.43)
62
0.90 (0.62, 1.30)

12.9
105
1.12 (0.83, 1.51)
84
1.21 (0.85, 1.71)

16.5
104
1.11 (0.82, 1.51)
79
1.15 (0.81, 1.63)

8.5
97
1
68
1

12.0
101
1.12 (0.82, 1.51)
76
1.18 (0.83, 1.69)

14.7
103
1.01 (0.81, 1.49)
74
1.11 (0.77, 1.59)

18.2
102
1.09 (0.80, 1.48)
80
1.23 (0.86, 1.76)

0.64

3.5
92
1
68
1

5.1
118
1.31 (0.98, 1.76)
86
1.34 (0.94, 1.89)

6.9
105
1.30 (0.96, 1.76)
79
1.40 (0.98, 1.99)

9.9
88
1.12 (0.82, 1.54)
65
1.18 (0.81, 1.71)

0.69

0.9
90
1
62
1

1.8
113
1.17 (0.87, 1.57)
85
1.25 (0.87, 1.78)

2.6
100
1.13 (0.84, 1.54)
74
1.22 (0.85, 1.75)

3.9
100
1.06 (0.78, 1.44)
77
1.21 (0.85, 1.74)

83
91
1
67
1

188
90
0.97 (0.70, 1.34)
63
0.88 (0.60, 1.30)

378
117
1.13 (0.82, 1.55)
87
1.16 (0.80, 1.67)

607
105
1.09 (0.77, 1.54)
81
1.14 (0.76, 1.70)

0.71

0.45
0.24

0.32

0.55

0.88
0.41

0.43
0.23

Multivariate model was adjusted for the variable of interest as a percentage of energy (quartiles), sex, age, study center (South Dakota was the reference
center), diabetes status, BMI, HDL, LDL, triacylglycerol (log-transformed), smoking (current vs ever and never), alcohol consumption (current vs ever and
never), hypertension, percentage of energy from protein, and total energy intake.
2
Tests for trend were conducted by modeling the median of each quartile-defined category as a continuous variable in Cox proportional hazards models.

Shown in Table 5 are the associations of CHD mortality and

dietary fat intake modeled as a continuous variable (% of energy),
adjusted for the risk factors listed above. As with quartiles of
dietary intake, total fat, SFAs, and MUFAs were significantly
associated with CHD death in participants aged 4759 y. Among
these same persons, SFAs and MUFAs, in separate analyses,
remained significant predictors of CHD death independent of
PUFAs and TFAs and the other CHD risk factors listed above
[HR for a 5% increase in energy from SFAs: 0.66 (95% CI: 1.15,
2.42); from MUFAs: 1.68 (95% CI: 1.11, 2.53)]. In analyses
modeling all fat components simultaneously, the associations
between SFAs and MUFAs and CHD death were attenuated, and
SFAs and MUFAs were not independently predictive of CHD
death among those aged 4759 y [HR for a 5% increase in energy
from SFAs: 1.45 (95% CI: 0.84, 2.51); from MUFAs: 1.25 (95%
CI: 0.68, 2.29)]. PUFAs and TFAs were not associated with CHD
death in this younger age group. No association was found between dietary fat and its components and CHD death among

participants aged 60 79 y. To test the robustness of our models,

we repeated our analyses after excluding individuals (n 27)
whose first event occurred within the first 6 mo of follow-up, and
the results did not change.
DISCUSSION

In this large longitudinal study, higher intakes of total fat,

SFAs, and MUFAs at baseline were associated with higher CHD
mortality among American Indians aged 4759 y but not among
those aged 60 79 y. There was no association between total fat
intake or its components and nonfatal CHD events in this population. Additionally, we found no association between PUFAs,
TFAs, and cholesterol intake and total CHD incidence (fatal or
nonfatal event). Our findings were consistent regardless of how we
categorized macronutrient intake, either as quartiles or as continuous intake. American Indians aged 4759 y who were in the highest
quartile of intake from total fat (42.6% of energy), SFAs (14.6%

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Total fat
Median intake (% of energy)
CHD event (n)
HR (95% CI)
Nonfatal CHD (n)
HR (95% CI)
Saturated fatty acids
Median intake (% of energy)
CHD event (n)
HR (95% CI)
Nonfatal CHD (n)
HR (95% CI)
Monounsaturated fatty acids
Median intake (% of energy)
CHD event (n)
HR (95% CI)
Nonfatal CHD (n)
HR (95% CI)
Polyunsaturated fatty acids
Median intake (% of energy)
CHD event (n)
HR (95% CI)
Nonfatal CHD (n)
HR (95% CI)
trans Fatty acids
Median intake (% of energy)
CHD event (n)
HR (95% CI)
Nonfatal CHD (n)
HR (95% CI)
Cholesterol
Median intake (mg)
CHD event (n)
HR (95% CI)
Nonfatal CHD (n)
HR (95% CI)

899

DIETARY FAT INTAKE AND CORONARY HEART DISEASE

TABLE 4
Hazard ratio (HR) and 95% CI of each quartile of dietary fat intake associated with coronary heart disease (CHD) death by age group in the Strong Heart
Study1
Dietary fat intake quartiles
1

24.8
23.0
7
27
1
1

33.0
31.2
8
22
1.44 (0.45, 4.58)
1.20 (0.67, 2.17)
0.37

39.1
37.3
13
21
2.42 (0.83, 7.06)
0.73 (0.38, 1.40)
0.11

46.6
44.7
18
22
3.57 (1.21, 10.49)
0.77 (0.41, 1.45)
0.01

7.8
7.2
6
23
1
1

10.8
10.2
14
32
3.23 (1.03, 10.14)
1.59 (0.89, 2.83)
0.30

13.1
12.7
6
18
1.58 (0.42, 6.04)
0.81 (0.41, 1.63)
0.40

16.7
16.1
20
19
5.17 (1.64, 16.36)
0.80 (0.41, 1.54)
0.02

8.7
8.2
7
27
1
1

12.3
11.7
8
25
1.13 (0.34, 3.74)
1.05 (0.58, 1.91)
0.90

15.1
14.3
14
22
2.55 (0.88, 7.43)
0.89 (0.49, 1.65)
0.16

18.6
17.7
17
18
3.43 (1.17, 10.04)
0.54 (0.27, 1.06)
0.01

3.5
3.4
8
24
1
1

5.3
4.8
16
25
1.78 (0.71, 4.47)
1.03 (0.57, 1.86)
0.31

7.2
6.6
10
27
1.02 (0.36, 2.84)
1.11 (0.61, 2.01)
0.24

10.4
9.5
12
16
1.47 (0.55, 3.96)
0.69 (0.35, 1.36)
0.07

0.9
1.0
14
20
1
1

1.8
1.8
8
27
0.84 (0.32, 2.18)
1.33 (0.72, 2.46)
0.60

2.6
2.6
9
25
0.84 (0.33, 2.18)
1.43 (0.76, 2.67)
0.55

4.0
3.9
15
20
1.15 (0.49, 2.68)
0.83 (0.42, 1.66)
0.38

85
79
5
27
1
1

197
170
10
22
1.90 (0.60, 6.04)
0.93 (0.49, 1.77)
0.38

396
357
20
21
2.64 (0.88, 7.88)
0.81 (0.42, 1.56)
0.05

641
587
11
22
1.53 (0.46, 5.13)
0.76 (0.38, 1.54)
0.19

P for trend2

0.01
0.24

0.01
0.22

0.01
0.07

0.78
0.30

0.66
0.54

0.77
0.41

Multivariate model was adjusted for the variable of interest as a percentage of energy (quartiles), sex, age, study center (South Dakota was the reference
center), diabetes status, BMI, HDL, LDL, triacylglycerol (log-transformed), smoking (current vs ever and never), alcohol consumption (current vs ever and
never), hypertension, percentage of energy from protein, and total energy intake.
2
Tests for trend were conducted by modeling the median of each quartile-defined category as a continuous variable in Cox proportional hazards models.
3
For participants aged 4759 y.
4
For participants aged 60 79 y.
5
P for interaction between dietary fat and age group (4759 or 60 79 y).

of energy), or MUFAs (16.6% of energy) had a higher risk of

dying from CHD than did those in the lowest quartile. Substituting
5% of energy from either MUFAs or SFAs with the same amount of
energy from carbohydrate was associated with 62 68% higher

CHD mortality. However, the relations of CHD death to SFAs and

MUFAs were not independent of each other.
The inconsistencies in epidemiologic studies of the association between dietary fat and CHD incidence are summarized in

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Total fat
Median intake (% of energy)3
Median intake (% of energy)4
CHD death (n)3
CHD death (n)4
HR (95% CI)3
HR (95% CI)4
P for interaction5
Saturated fatty acids
Median intake (% of energy)3
Median intake (% of energy)4
CHD death (n)3
CHD death (n)4
HR (95% CI)3
HR (95% CI)4
P for interaction
Monounsaturated fatty acids
Median intake (% of energy)3
Median intake (% of energy)4
CHD death (n)3
CHD death (n)4
HR (95% CI)3
HR (95% CI)4
P for interaction
Polyunsaturated fatty acids
Median intake (% of energy)3
Median intake (% of energy)4
CHD death (n)3
CHD death (n)4
HR (95% CI)3
HR (95% CI)4
P for interaction
trans Fatty acids
Median intake (% of energy)3
Median intake (% of energy)4
CHD death (n)3
CHD death (n)4
HR (95% CI)3
HR (95% CI)4
P for interaction
Cholesterol
Median intake (mg)3
Median intake (mg)4
CHD death (n)3
CHD death (n)4
HR (95% CI)3
HR (95% CI)4
P for interaction

900

XU ET AL

TABLE 5
Hazard ratio (95% CI) associated with coronary heart disease death per macronutrient intake (5% increment in percentage of energy as a continuous
variable) in the Strong Heart Study1

Total fat
Saturated fatty acids
Monounsaturated fatty acids
Polyunsaturated fatty acids
trans Fatty acids

4759 y

60 79 y

P for interaction2

1.28 (1.08, 1.52)

1.68 (1.17, 2.41)
1.62 (1.14, 2.30)
1.25 (0.76, 2.06)
1.73 (0.57, 5.25)

0.91 (0.81, 1.02)

0.82 (0.62, 1.10)
0.82 (0.63, 1.07)
0.78 (0.52, 1.16)
1.34 (0.48, 2.46)

0.01
0.01
0.01
0.10
0.89

1
Multivariate model was adjusted for the variable of interest as a percentage of energy, sex, age, study center (South Dakota was the reference center),
diabetes status, BMI, HDL, LDL, triacylglycerol (log-transformed), smoking (current vs ever and never), alcohol consumption (current vs ever and never),
hypertension, percentage of energy from protein, and total energy intake.
2
P for interaction between dietary fat and age group (4759 or 60 79 y).

group given that many older cohort members were excluded

because of existing CHD. In addition, older cohort members
who did not have preexisting CHD may have been more likely
than younger cohort members to have one or more CHD risk
factors, such as diabetes, and may have changed their diets as
a consequence.
Our positive findings for CHD death and lack of findings for
CHD incidence are supported by data from the -Tocopherol,
-Carotene Cancer Prevention Study (13), which showed that
TFA intake was associated with CHD death but not with CHD
incidence. This may be due to the difficulty in collecting complete event data, because participants may not report it and hospital records could not be located, which may lead to a possible
misclassification and lower risk estimates. In contrast, death data
are usually more complete.
Our results support the hypothesis that a high intake of dietary
fat is associated with CHD death among middle-aged American
Indian adults. The strengths of the present study include a large
sample size and adjustment for energy intake and protein
intake in addition to other established CHD risk factors. To the
best of our knowledge, this is the first study to quantify the
association between dietary fat intake and CHD incidence in
American Indians.
The current study had several limitations: a single-days diet is
a poor descriptor of an individuals usual intake because of intraindividual variability. However, we found similar results
when using intake as a continuous measure or categorized into
quartiles, which assumes that bias was of a relatively constant
magnitude. Multiple 24-h recalls or some other assessment
method that measures usual intake would reduce random error
and further increase the strength of the associations reported here
(5, 41). In addition, we only included diet at the second SHS
examination in our models, and diet may have changed during the
follow-up period. Because this is an epidemiologic analysis, we
cannot determine a causal association between fat intake and
CHD incidence. It is possible that individuals at high CHD risk,
for whatever reason, tend to consume more fat in their diet.
Consumption of a diet lower in fat and SFAs might reflect high
compliance to medications or lifestyle modification, which
would improve general health in these persons. Thus, dietary
intake alone may not be the sole factor underlying lower CHD
incidence.
In conclusion, the results of this epidemiologic study suggest that
CHD death, in middle-aged but not elderly American Indians, is
related to both the quantity and the quality of dietary fats. A higher

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Table 6. Our findings of positive associations between total fat,

SFAs, and MUFAs and CHD death are consistent with some
studies (5, 6, 12). Although some animal studies suggest that
MUFAs may induce atherosclerosis (35), it is also very likely that
our finding for MUFAs is confounded with SFA intake. In our
study population, the main sources of MUFAs were meat, poultry, and fish (46%) and these same food groups provided almost
the same contributions of SFAs (45%). These mutual food
sources for both fatty acids may explain the high correlation
between SFAs and MUFAs and the lack of independent associations of them with CHD death. For most previous studies that
found MUFAs to be associated with lower CHD death, the main
MUFA source was olive oil (1), whereas in our study, olive oil
and olives contributed only 0.3% of MUFA intake. This suggests
that in other studies, the beneficial effects may have been related
to other components in the olive oil rather than MUFAs, and that
the source of MUFAs may be important in determining CHD
risk. The higher intake of total fat, SFAs, and MUFAs and lower
intake of PUFAs in the SHS than in the US population suggests
a less healthy eating pattern among American Indians that contributed to higher CHD death.
Although several studies have reported a relation between
TFA intake and CHD incidence (9, 10, 15, 17), there was no
association between TFA intake and incident CHD, either nonfatal or fatal, in our study. The mean TFA intake in our study was
similar to that calculated by using a 24-h recall and a 2-d food
record in the Continuing Survey of Food Intakes by Individuals
(36). Another study in middle-aged men and women reported
lower percentages of TFA intake: in UK men and women, 1.6%
and 1.3% of energy, respectively, and in US men and women,
2.0% and 1.9% of energy, respectively (37). The lack of association in our study merits further investigation, including the
examination of the contributions of naturally occurring versus
hydrogenated vegetable oil sources on CHD incidence, because
TFAs from the 2 sources might be differentially associated with
risk factors or progression of heart disease (38, 39).
Epidemiologic studies on age-related differences in the association between dietary fat intake and CHD incidence are sparse.
As far as we are aware, only 4 prospective studies examined
differences by age (35, 10). Our findings are consistent with
their findings that CHD death increases with higher intakes of
total fat, SFAs, and MUFAs among participants aged 4759 y but
not among participants aged 60 79 y. This may arise from differences in baseline risk, because the magnitude of baseline risk
determines the magnitude of the relative effect (40). Another
possibility is that participants aged 60 79 y comprise a selected

901

DIETARY FAT INTAKE AND CORONARY HEART DISEASE

TABLE 6
Major prospective studies of dietary fat intake and risk of coronary heart disease (CHD)1
No. of subjects
and sex

Honolulu Heart Program (2)

8006 men

4568

10

24-h recall

Framingham Study (3)

859 men

4565

16

24-h recall

Denmark (4)

3686 men and

women

3071

16

7-d food record

Lipid Research Clinics Prevalence

Follow-up Study (5)

4546 men and

women

3079

12

24-h recall

Health and Lifestyle Survey (6)

2676 men and

women

4075

16

FFQ

Puerto Rico Heart Health Program (7)

Health Professionals Follow-up Study (8)
Alpha-Tocopherol, Beta-Carotene Cancer
Prevention Study (9)
Nurses Health Study (10)

8218 men
43 757 men
21 930 men

4564
4075
5069

6
6
6

78 778 women

3055

20

FFQ

Seven Countries Study (11)

11 579 men

4059

15

7-d food record

Ireland-Boston Diet-Heart Study (12)

1001 men

3069

20

FFQ

Israeli Ischemic Heart Disease Study (13)

10 059 men

40 and over

23

FFQ

Western Electric Study (14)

1900 men

4055

20

FFQ

Nurses Health Study (15)

80 082 women

3055

14

FFQ

Zutphen Study (16)

Zutphen Elderly Study (17)

871 men
667 men

4059
6484

10
10

FFQ
FFQ

Age

Follow-up

Dietary assessment
method

24-h recall
FFQ
FFQ

Association

Positive association between total fat

and CHD incidence
Positive association between total fat
and MUFA and CHD incidence
among 4555-y-olds
Positive association between total
fat, SFA, MUFA, and CHD
incidence among women aged
60 y
Positive association between total
fat, SFA, MUFA, and CHD death
among 3059-y-olds
Positive association between total fat
and SFA and CHD death in
women
No association
No association
Positive association between TFA
and CHD death
Inverse association between PUFA
and CHD incidence, positive
association between TFA and
CHD incidence, more evident
among women aged 65 y
Positive association between SFA,
inverse association between
MUFA and CHD incidence
Positive association between SFA
and CHD death
Positive association between SFA
and CHD death, inverse
association between PUFA and
CHD death
Inverse association between PUFA
and CHD death
Inverse association between MUFA
and PUFA, positive association
between TFA and CHD incidence
No association
Positive association between TFA
and CHD incidence

FFQ, food-frequency questionnaire; SFA, saturated fatty acids; MUFA, monounsaturated fatty acids; PUFA, polyunsaturated fatty acids; TFA, trans fatty

acids.

fat intake as a percent of energy from SFAs and MUFAs is associated with increased CHD mortality in this population subgroup. It
may be prudent for American Indians to reduce their fat intake early
in life to reduce the risk of dying from CHD.
We acknowledge the assistance and cooperation of the Ak-Chin Tohono
OOdham (Papago)/Pima, Gila River, and Salt River Pima/Maricopa communities in Arizona; the Apache, Caddo, Comanche, Deleware, Fort Sill
Apache, Kiowa, and Wichita communities in Oklahoma; and the Oglala
Sioux, Cheyenne River Sioux, and Spirit Lake communities in North and
South Dakota, without whose support this study would not have been possible. We also thank the Indian Health Service hospitals and clinics at each
center; the directors of the Strong Heart Study clinics, Betty Jarvis, Tauqeer
Ali, Alan Crawford, and Marcia OLeary, and their staffs; and the physicians
who performed the mortality and morbidity reviews.

All authors were responsible for the critical revision of the manuscript for
important intellectual content. Additionally, JX and SE-A were responsible
for the hypothesis, the analysis concept, the data analysis and interpretation,
and drafting of the manuscript. CL and UG assisted with the analysis and
interpretation of data. BVH, RRF, EMZ, and ETL were responsible for the
study design and data collection. None of the authors had a conflict of interest.

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