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Dietary Sodium Intake and Incidence of Congestive Heart Failure in Overweight US Men and Women
First National Health and Nutrition Examination Survey Epidemiologic Follow-up Study
Jiang He, MD, PhD;
Lorraine G. Ogden, MS;
Lydia A. Bazzano, PhD;
Suma Vupputuri, MPH, PhD;
Catherine Loria, PhD, MS;
Paul K. Whelton, MD, MSc
Arch Intern Med. 2002;162:1619-1624.
ABSTRACT
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Background Cross-sectional epidemiologic studies suggest that a higher intake of
dietary sodium is associated with an increased risk of left ventricular hypertrophy.
We studied the relationship between dietary sodium intake and incidence of
congestive heart failure (CHF) in the first National Health and Nutrition
Examination Survey Epidemiologic Follow-up Study participants.
Participants and Methods The study sample consisted of 5233 nonoverweight and 5129 overweight
men and women without a history of CHF at their baseline examination. Dietary
sodium and other nutrient intake estimates were obtained by a 24-hour dietary
recall method at the baseline examination, conducted from 1971 to 1975. The
incidence of CHF was assessed using medical records and death certificates
obtained in 1982 to 1984, 1986, 1987, and 1992.
Results During an average of 19 years of follow-up, we documented 413 cases
of CHF in nonoverweight and 679 cases of CHF in overweight participants. After
adjustment for known CHF risk factors, the relative risk of CHF among overweight
participants was 1.43 (95% confidence interval, 1.07-1.91) for those whose
sodium intake was greater than 113.6 mmol/d compared with those whose intake
was less than 50.2 mmol/d. The relative risks of CHF for a 100-mmol/d higher
intake of sodium or per 1743 kcal (average energy intake in the study population)
were 1.26 (95% confidence interval, 1.03-1.53) and 1.21 (95% confidence interval,
1.04-1.40), respectively.
Conclusions A higher intake of dietary sodium is a strong independent risk factor
for CHF in overweight persons. A reduction in sodium intake may play an important
role in the prevention of CHF in overweight individuals and populations.
INTRODUCTION
DESPITE THE dramatic decline in mortality from coronary heart disease
(CHD) and stroke in the US population, mortality from congestive heart failure
(CHF) has been increasing for several decades.1-2
Approximately 4.7 million Americans have CHF and 47 000 die of CHF in
the United States each year.1 The identification
of modifiable risk factors for CHF, which provided a basis for intervention
strategies, has become an important challenge for public health and clinical
medicine.3
Several cross-sectional epidemiologic studies4-7
have suggested a significant and independent association between dietary sodium
intake and left ventricular hypertrophy. In the Treatment of Mild Hypertension
Study,4 dietary sodium intake was estimated
from 2 consecutive overnight urine collections and left ventricular structure
was assessed by M-mode echocardiography in 511 men and 33 women with mild
hypertension. After adjustment for age, sex, race, body mass index, previous
medication, alcohol consumption, cigarette smoking, physical activity, and
systolic blood pressure, a difference of 25 mmol per 8 hours in urinary sodium
excretion was associated with a 41% (95% confidence interval, 22%-63%) increase
in the odds of left ventricular hypertrophy. Messerli and colleagues5 reviewed 9 cross-sectional studies in which the association
between dietary sodium intake and left ventricular mass was assessed. The
correlation coefficients for the relationship varied from 0.22 to 0.61, with P<.05 in each of the studies. Animal studies8-9 also indicate that high sodium intake
is an independent risk factor for the development of cardiac hypertrophy.
However, there are sparse data on the relationship between dietary sodium
intake and the risk of CHF from prospective cohort studies.
We took advantage of the large sample size and prolonged follow-up experience
of participants in the first National Health and Nutrition Examination Survey
(NHANES I) Epidemiologic Follow-up Study (NHEFS) to examine the relationship
between dietary sodium intake and risk of CHF in a nationally representative
sample of the US general population.
PARTICIPANTS AND METHODS
STUDY PARTICIPANTS
In NHANES I, a multistage, stratified, probability sampling design was
used to select a representative sample of the US civilian noninstitutionalized
population aged 1 to 74 years. Details of the study design, sampling methods,
response rate, and data collection have been previously published.10-11 Certain population subgroups, including
those with a low income, women of childbearing age (25-44 years), and persons
65 years or older were oversampled.
The NHEFS is a prospective cohort study of NHANES I participants who
were aged 25 to 74 years when the survey was conducted between 1971 and 1975.12-15 Of
the 14 407 NHEFS participants who were in this age range at their baseline
examination, we excluded 3059 who lacked 24-hour dietary recall information
by study design; 2 who lacked sodium intake information; 176 who had a history
of CHF at their baseline examination, defined as ever having been told by
a physician that they have had heart failure or having used any medication
for a "weak heart" during the 6 months before their baseline interview; and
395 who were consuming a low-salt diet at baseline because of heart disease
or hypertension. Among the remaining participants, 413 (4%) were lost to follow-up.
After these exclusions, experience from 5233 nonoverweight and 5129 overweight
participants was available for analysis. Overweight was defined as a body
mass index (calculated as weight in kilograms divided by the square of height
in meters) of 25.0 or greater for men and women.
MEASUREMENTS
Baseline data collection included a medical history, a standardized
medical examination, a dietary history, laboratory tests, and anthropometric
measurements.10-11 A single 24-hour
dietary recall was conducted by trained NHANES I personnel using a standardized
protocol and 3-dimensional food portion models. Information on frequency,
but not amount, of salt added in the kitchen or at the table was collected.
The dietary recall questionnaires were later coded by interviewers using nutrient
information from the US Department of Agriculture Handbook
No. 8 or other resources. Dietary sodium and caloric intake were calculated
for each participant by the National Center for Health Statistics, Hyattsville,
Md. Frozen serum samples were sent to the Centers for Disease Control and
Prevention, Atlanta, Ga, for measurement of serum total cholesterol levels.
Blood pressure measurements, body weight, and height were obtained using standard
protocols. The baseline questionnaire on medical history included questions
about selected health conditions and medications used for these conditions
during the preceding 6 months. Data on educational level, physical activity,
and alcohol consumption were obtained by interviewer-administered questionnaires.
Baseline information on smoking status was obtained in a random subsample
of 6913 participants who underwent a more detailed evaluation at the time
of their examination.10-11 For
the remaining study participants, information on smoking status at baseline
was derived from responses to questions regarding lifetime smoking history,
which were administered at follow-up interviews conducted from 1982 to 1984
or later.16-17 The validity of
information on smoking status obtained using this approach has been documented.16-17 Baseline diabetes was defined as
ever having been told by a physician that the participant had this condition.
Hypertension was defined as a systolic blood pressure of 160 mm Hg or higher
and/or a diastolic blood pressure of 95 mm Hg or higher and/or use of antihypertensive
medications. Coronary heart disease was defined as ever having been told by
a physician that the participant experienced a heart attack or having a diagnosis
with an International Classification of Diseases, Ninth
Revision (ICD-9), code between 410 and 414. Valvular heart disease
was defined as having a diagnosis with an ICD-9 code
between 394 and 397 or of 424 at the baseline medical examination.
FOLLOW-UP PROCEDURES
Follow-up data were collected between 1982 and 1984 and in 1986, 1987,
and 1992.12-15
Each follow-up examination included tracking a participant or his or her proxy
to a current address; performing an in-depth interview; obtaining hospital
and nursing home records, including pathology reports and electrocardiograms;
and, for decedents, acquiring a death certificate. Incident cardiovascular
disease was based on documentation of an event that met prespecified study
criteria and occurred between the participant's baseline examination and last
follow-up interview. Mortality from cardiovascular disease was based on death
certificate reports. The validity of study outcome data from both sources
has been documented.18
Incident CHF was based on 1 or more hospital and/or nursing home stays
in which the participant had a discharge diagnosis with an ICD-9 code between 428.0 and 428.9 or a death certificate report in
which the underlying cause of death was recorded using an ICD-9 code between 428.0 and 428.9. Incident CHD was based on 1 or
more hospital and/or nursing home stays in which the participant had a discharge
diagnosis with an ICD-9 code between 410 and 414
or a death certificate report in which the underlying cause of death was an ICD-9 code between 410 and 414. The date of record for
incident events was identified as the date of the participant's first hospital
admission with an established study event or the date of death from a study
event in the absence of hospital or nursing home documentation of such an
event.
STATISTICAL ANALYSES
Because a statistically significant interaction between dietary sodium
intake and overweight status on CHF was detected, all analyses were stratified
by overweight status. The quartiles of dietary sodium intake were calculated
using the total sample (nonoverweight and overweight participants). For each
baseline characteristic, the mean value or corresponding percentage of study
participants was calculated by overweight status. The cumulative incidence
of CHF by quartile of sodium intake was calculated using the Kaplan-Meier
method, and differences in cumulative rates were examined by the log-rank
test for trend.19-20 Cox proportional
hazards models were used to explore the relationship between dietary sodium
intake and cardiovascular disease risk.21 History
of CHD was modeled as a time-dependent variable in Cox proportional hazards
models. Age was used as the time scale for all time-to-event analyses.22 Cox proportional hazards models were stratified by
birth cohort using 10-year intervals to control for calendar period and cohort
effects.22 Sodium intake was assessed as a
categorical (quartile) and a continuous variable. Methods to estimate variances
that take into account sample clustering and stratification of the NHANES
I sample were used in Cox proportional hazards models.22
Sex differences in the relationships between sodium-calorie ratio and cardiovascular
diseases and all-cause mortality were tested using interaction terms in Cox
proportional hazards models. Because there were no significant differences,
men and women were pooled in the main analysis.
RESULTS
Table 1 shows the baseline
characteristics of the study participants by weight status. Compared with
the nonoverweight study participants, those who were overweight were older;
were more likely to be men, African American, and have a high school education;
had a higher mean systolic blood pressure and serum total cholesterol level;
had a higher prevalence of hypertension, diabetes mellitus, and CHD; were
less likely to engage in recreational physical activity; and had a lower prevalence
of current cigarette smoking and alcohol consumption. In addition, dietary
intake of sodium, potassium, calcium, and total calories (energy) was lower
in the overweight compared with the nonoverweight participants.
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Table 1. Baseline Characteristics of 10 362 Study Participants
According to Body Weight: NHANES I Epidemiologic Follow-up Study*
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During 85 035 person-years of follow-up from 1971 through 1992,
413 CHF events were documented in the nonoverweight participants. The cumulative
incidence of CHF was not significantly associated with baseline sodium intake
in the nonoverweight participants. For example, the cumulative incidence of
CHF at age 90 years, adjusted for total calorie intake, was 35.6%, 42.9%,
37.4%, and 47.4% among patients within the first, second, third, and fourth
quartiles of dietary sodium intake, respectively (P
= .48 for trend). During a total of 80 265 person-years of follow-up
in the overweight participants, 679 CHF events were documented. The cumulative
incidence of CHF at age 90 years, adjusted for total calorie intake, was 44.0%,
43.6%, 53.6%, and 63.1% among overweight participants within the first, second,
third, and fourth quartiles of dietary sodium intake, respectively (P = .02 for trend).
Relative risks and 95% confidence intervals for CHF according to baseline
quartiles of dietary sodium intake in the nonoverweight and overweight participants
are presented in Table 2. Dietary
sodium intake was not significantly associated with risk of CHF in the nonoverweight
study participants. In contrast, dietary sodium intake was significantly associated
with risk of CHF among overweight individuals. In age-, race-, sex-, and total
calorie intake–adjusted analyses, CHF incidence was positively and significantly
associated with the corresponding trend in dietary sodium intake in the 5129
participants who were classified as overweight. After additional adjustment
for educational level, physical activity, cigarette smoking, alcohol consumption,
systolic blood pressure, serum total cholesterol level, history of diabetes
mellitus and valvular heart disease, and time-dependent history of CHD, the
association remained largely unchanged and statistically significant. Likewise,
additional adjustment for dietary intake of potassium and calcium did not
materially change the results. Similar findings were obtained when quartile
of sodium-calorie ratio was used as the independent variable and when history
of hypertension was used as an adjustment variable instead of systolic blood
pressure (data not shown).
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Table 2. Relative Risk of Congestive Heart Failure According to Quartile
of Dietary Sodium Intake: NHANES I Epidemiologic Follow-up Study*
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Table 3 presents multivariate
relative risks of CHF associated with a 100-mmol/d or per 1743 kcal increase
in sodium intake by overweight status, where sodium intake (100 mmol/d) and
sodium-calorie ratio (100 mmol per 1743 kcal, average energy intake in the
study population) were treated as continuous variables. There were borderline
statistically significant interactions between sodium intake and overweight
status on CHF. Dietary sodium intake was significantly associated with an
increased risk of CHF incidence in overweight, but not in nonoverweight, persons.
Furthermore, the relative risks were similar when either sodium-calorie ratio
or absolute sodium intake was used as the independent variable.
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Table 3. Multivariate Relative Risk of Congestive Heart Failure Associated
With a 100-mmol Increase in Dietary Sodium Intake Among Nonoverweight and
Overweight Participants*
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COMMENT
To the best of our knowledge, the present study is the first prospective
investigation to document a strong and independent relationship between dietary
intake of sodium and increased risk of CHF among overweight persons. Previous
information on dietary sodium intake and CHF has come from cross-sectional
epidemiologic studies and animal experiments.4-9
Among those studies, a positive association between dietary sodium intake
and measures of left ventricular structure was a consistent observation.
The findings from the present study have important public health and
clinical implications. The incidence of and mortality from CHF have been increasing
relentlessly in the US population during recent decades.1-2
With an increasingly older population and progressive improvements in survival
following acute myocardial infarction, it is almost inevitable that CHF will
continue to be an important public health challenge in the foreseeable future.
Because of the high mortality associated with CHF, it is important to identify
modifiable risk factors and develop effective strategies for the prevention
of CHF in the general population. We previously reported that cigarette smoking,
overweight status, physical inactivity, and a history of hypertension, diabetes
mellitus, and CHD were important modifiable risk factors for CHF in the study
population.3 The present findings suggest that
a high dietary intake of sodium is an independent risk factor for CHF and
that a reduced sodium intake may play an important role in the prevention
of CHF in the community.
A moderately low intake of dietary sodium (<2400 mg/d) has been recommended
for all Americans by several organizations and government agencies.23 The beneficial effect of a moderately low intake
of dietary sodium includes decreasing the risk of hypertension and cardiovascular
disease.24 Observational epidemiologic studies25-26 have documented that a high intake
of dietary sodium is associated with an elevated blood pressure and an increased
risk of hypertension. Randomized controlled trials27-28
have also demonstrated that a reduced dietary intake of sodium lowers blood
pressure in hypertensive and normotensive persons. Several prospective cohort
studies29-30 have indicated that
a high dietary intake of sodium increases the risk of stroke and CHD. Our
study findings provide additional information to support recommendation for
a moderately low intake of dietary sodium in the US population.
Our study indicates that the increased risk of CHF associated with high
dietary sodium intake presented in overweight persons only. It has been suggested
that overweight persons may be more sodium sensitive because of enhancing
renal tubular sodium reabsorption and sodium retention.31-32
In a study of 60 obese and 18 nonobese adolescents, Rocchini et al33 found that blood pressure was more sensitive to dietary
sodium intake in overweight than nonoverweight adolescents and that this increased
sodium sensitivity was reduced after weight loss. Increased sodium sensitivity
in overweight persons may explain why we identified an independent positive
relationship between dietary sodium intake and risk of CHF. Several previous
epidemiologic studies29-30 also
indicated that the association between dietary sodium intake and risk of cardiovascular
disease was much stronger in overweight compared with nonoverweight persons.
Overweight is a common and important risk factor for CHF.3
According to data from the third NHANES, conducted from 1988 to 1991, 54.5%
of US adults 20 years or older were overweight, as defined by a body mass
index of 25 or higher.31 Particularly troublesome,
the prevalence of obesity has increased progressively during recent decades
in all race and sex groups in the United States.34
To reduce the CHF risk in overweight patients, weight loss and sodium reduction
should be recommended. For persons with difficulty losing body weight, greater
attention to reductions in sodium intake may be appropriate.
An excess dietary intake of sodium might induce sodium and water retention,
especially in persons who are more sensitive to sodium intake, such as obese
patients.31-32 Sodium and water
retention plays an important role in the pathogenesis of hypertension and
CHF.35-36 A high dietary intake
of sodium might originate CHF by increasing blood pressure (pressure overload)
or extracellular fluid (volume overload).
There are several potential limitations of the present study. The dietary
sodium intake was estimated by a single 24-hour dietary recall. This may result
in misclassification of usual sodium intake at the individual level. In addition,
the dietary recall method used in NHANES I may have underestimated sodium
intake because it did not include quantitative data on discretionary use of
salt in cooking or at the table settings, which account for about 15% to 30%
of the sodium intake in Western societies.37-38
Likewise, NHEFS participants might have underreported their dietary total
caloric intake, which further underestimated sodium intake.39
In addition, repeated measurements of dietary sodium intake during the follow-up
period are not available from the NHEFS. These measurement errors would tend
to bias our relative risk estimates toward 1 (effect to 0) in univariate models.
Besides a possibly lower sensitivity to sodium intake in nonoverweight compared
with overweight persons, our finding of a null association in nonoverweight
persons may have been attributed to the measurement errors in sodium intake.
Another limitation of our study was the fact that study participants were
followed up in a passive rather than an active fashion. Because CHF status
was identified by information obtained from hospital discharge diagnoses or
death certificates, the cumulative incidence of CHF may be underestimated.
However, there is no reason to believe that CHF outcome measurements would
differ by baseline dietary intake of sodium. Because of the nature of the
passive follow-up, echocardiographic or electrocardiographic data were not
available and left ventricular dysfunction could not be studied.
Our study has several important strengths. The findings can be generalized
to overweight persons in the US general population because the NHEFS cohort
is a random sample of this population. In addition, temporal relationships
can be established with confidence because dietary sodium intake was measured
at baseline and subsequent incidence of CHF was assessed over an average duration
of 19 years. The fact that follow-up experience was available for more than
96% of study participants further enhances the validity of our findings.
In conclusion, our study results suggest that a high dietary intake
of sodium is an independent risk factor for CHF. Furthermore, these findings
suggest that sodium reduction may play an important role in the prevention
of CHF in the US general population. Future prospective cohort studies with
better measurements of usual dietary sodium intake (ie, multiple measurements
of 24-hour urinary excretion of sodium at baseline and during follow-up visits)
and CHF outcome are needed to confirm our findings.
AUTHOR INFORMATION
Accepted for publication November 20, 2001.
This study was supported by grant R03 HL61954, and in part by grant
R01 HL60300, from the National Heart, Lung, and Blood Institute, Bethesda,
Md. The NHANES I NHEFS has been developed and funded by the National Center
for Health Statistics, Hyattsville, Md; the National Institute on Aging, Bethesda;
the National Cancer Institute, Bethesda; the National Institute of Child Health
and Human Development, Bethesda; the National Heart, Lung, and Blood Institute,
Bethesda; the National Institute of Mental Health, Rockville, Md; the National
Institute of Diabetes and Digestive and Kidney Diseases, Bethesda; the National
Institute of Arthritis and Musculoskeletal and Skin Diseases, Bethesda; the
National Institute of Allergy and Infectious Diseases, Bethesda; the National
Institute of Neurological and Communicative Disorders and Stroke, Bethesda;
the Centers for Disease Control and Prevention, Atlanta, Ga; and the US Department
of Agriculture, Washington, DC.
Corresponding author and reprints: Jiang He, MD, PhD, Department
of Epidemiology, Tulane University School of Public Health and Tropical Medicine,
1430 Tulane Ave, Mail Box SL18, New Orleans, LA 70112 (e-mail: jhe{at}tulane.edu).
From the Departments of Epidemiology (Drs He, Bazzano, Vupputuri, and
Whelton) and Biostatistics (Ms Ogden), Tulane University School of Public
Health and Tropical Medicine, New Orleans, La; the Department of Medicine,
Tulane University School of Medicine, New Orleans (Drs He and Whelton); and
the National Heart, Lung, and Blood Institute, Bethesda, Md (Dr Loria).
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