Background Population-wide restriction of dietary sodium has been recommended. However, little evidence directly links sodium intake to morbidity and mortality. The aim of this study was to assess the relation of sodium intake to subsequent all-cause and cardiovascular-disease (CVD) mortality in a general population.
Methods The first National Health and Nutrition Examination Survey established baseline information during 1971-75 in a representative sample of 20729 US adults (aged 25-75). 11348 underwent medical examination and nutritional examination based on 24 h recall. Two had no data on sodium intake available. Vital status at June 30, 1992, was obtained for the 11346 participants through interview, tracing, and searches of the national death index. Mortality was examined in sex-specific quartiles of sodium intake, calorie intake, and sodium/calorie ratio. Multiple regression analyses were done to assess the relations with mortality.
Findings There were 3923 deaths, of which 1970 were due to CVD. All-cause mortality (per 1000 person-years; adjusted for age and sex) was inversely associated with sex-specific quartiles of sodium intake (lowest to highest quartile 23·18 to 19·01, p<0·0001) and total calorie intake (25·03 to 18·40, p<0·0001) and showed a weak positive association with quartiles of sodium/calorie ratio (20·27 to 21·71, p=0·14). The pattern for CVD mortality was similar (sodium 11·80 to 9·60, p<0·0019; calories 12·80 to 8·94, p<0·0002; sodium/calorie ratio 9·73 to 11·35, p=0·017). In Cox multiple regression analysis, sodium intake was inversely associated with all-cause (p=0·0069) and CVD mortality (p=0·086) and sodium/calorie ratio was directly associated with all-cause (p=0·0004) and CVD mortality (p=0·0056). By contrast, calorie intake in the presence of the two measures of sodium intake was not independently associated with mortality (all-cause p=0·86; CVD p=0·74). Analysis restricted to participants with no history of CVD at baseline gave similar results.
Interpretation This observational study does not justify any particular dietary recommendation. Specifically, these results do not support current recommendations for routine reduction of sodium consumption, nor do they justify advice to increase salt intake or to decrease its concentration in the diet.
Lancet 1998; 351: 781-85
Introduction
Ecological, observational, and experimental data largely, but not invariably, support the view that a restricted-sodium diet is associated with, and can induce, lower blood pressure.1-12 Based on these and other associations13 with intermediate physiological variables, some groups recommend restriction of daily sodium intake to 106 mmoles (approximately 2400 mg).14 This recommendation is justified by the expectation that the beneficial changes in intermediate physiological variables outweigh any harmful effects, so that the net effect would be lower cardiovascular morbidity and mortality, or an overall improvement in the quality of life. We could find no empirical data to support these expectations directly.
Although favourable effects on intermediate variables translate into health benefits in many circumstances, this is not always the case.15,16 In previous studies in hypertensive patients, a low-sodium diet was associated with adverse effects on quality of life17 and an increase in cardiovascular morbidity and mortality.18 To find out whether dietary sodium is associated with mortality in a general population, we examined the relation of sodium intake, measured in 1971-75, to all-cause and cardiovascular-disease (CVD) mortality, up to mid-1992, among participants in the first National Health and Nutrition Examination Survey (NHANES I).
Methods
Participants
There were 20729 individuals aged 25-75 years at the time of the NHANES I survey from 1971 to 1975. From the total sample, 14407 (70%) underwent medical examination, and 11348 of these underwent a nutrition investigation based on a 24 h recall. Data on sodium intake were missing for two participants, who were therefore excluded. Vital status was obtained for the remaining 11346 participants through interview, tracing, and searches of the national death index. Deaths and causes of death were confirmed from death certificates. Details on the plan and operation of NHANES I have been published previously.19,20 Since information on mortality was incomplete after June, 1992, the cut-off date for this analysis was June 30, 1992. Participants not reported as dead before this date were presumed to be alive.
The length of follow-up for each individual, expressed as the number of person-years contributed, was calculated from the baseline to the date of death or to the cut-off date.
Additional analyses were done on a restricted sample of 9962 participants who, at baseline, reported no pre-existing cardiovascular disorders. Those excluded had a history of circulatory diseases (International Classification of Diseases, 9th Revision, codes 390-450), rheumatic heart disease, or heart operation (ICD-9 procedure codes 29-30).
Measurements
Data on nutrient intake were available from a single 24 h dietary recall. Sodium intake was expressed as mg per day, and total calorie intake as calories per day. Qualitative data on use of table salt were also available from the dietary frequency questionnaire (responses never, sometimes, or always).
As part of the physical examination in NHANES I, one blood-pressure value was recorded. For 33% of participants this value was the mean
of three readings, two with the participant seated and once with him or her supine. In the remaining 67% of participants, one reading was done
with the participant seated. Of the total 11346 participants, 16% had baseline blood-pressure readings in the hypertensive range (systolic 
160 mm Hg, diastolic 95 mm Hg, or both). Both the
actual systolic blood pressure and history of hypertension were included in multivariate analyses as independent variables.
Statistical analysis
Baseline characteristics, including blood pressure, were defined for male and female participants. All statistical tests for continuous (Student's
t test) and categorical variables (
2) were two-tailed. Since distributions of sodium intake for men and women differed significantly, baseline
characteristics were assessed according to sex-specific quartiles of 24 h dietary sodium and calorie intake. The differences between quartiles
were tested for statistical significance by ANOVA. All-cause and CVD death rates (per 1000 person-years), adjusted for age and sex, were
calculated by specific dietary quartiles separately for men and women, standardised by the direct method, with age and sex distribution of the
whole cohort as reference. The differences in mortality rates between the lowest and highest quartiles were tested for statistical significance.
Because sodium intake and total calorie intake were highly correlated (r=0·65), a sodium/calorie ratio (expressed as sodium
per calorie intake per day) was calculated for each participant to reflect the concentration of salt in the diet. Participants were stratified according
to sex-specific quartiles, and all analyses described for sodium and total calorie intake were repeated for sodium/calorie ratio. Cox
proportional-hazards regression models were constructed individually as well as in combination, to assess the association of the three dietary
measures (sodium, total calories, and sodium per calorie) with all-cause and total CVD mortality, with simultaneous control for such available
relevant variables as age at baseline, sex, race, body-mass index, history of CVD and hypertension, and systolic blood pressure. Stepwise
backward regression analysis was done to estimate hazard ratios and 95% CI from a full model. To assess whether models with inclusion of
other dietary measures were better than that with sodium intake as an individual measure, the change in the log-likelihood value was tested for
significance as a 2 statistic with 1 degree of freedom.
All analyses were repeated on the restricted study sample of participants with no reported history of pre-existing CVD at baseline. All statistical analyses were done by means of SPSSWIN (version 7.0).
Results
The 4478 (39·5%) men differed significantly (p<0·05) from the 6868 women in mean age (52·9 vs 46·7 years), weight (76·6 vs 66·1 kg), and blood pressure (138/86 vs 134/82 mm Hg) and frequency of reported history of CVD (15 vs 11%) and hypertension (18 vs 15%). Mean daily sodium intake (2515 vs 1701 mg) and calorie intake (2159 vs 1471 kcal [1 kcal=0·0042 MJ]) were also significantly higher for men than for women. In response to the question on use of table salt more men than women replied "always" (39 vs 24%) and fewer replied "never" (38 vs 53%).
Baseline characteristics of participants by quartile of sodium intake, total calorie intake, and sodium/calorie ratio were analysed for men and women separately. For men and for women, there were significant differences (ANOVA, p<0·05) across the four quartiles of sodium intake in mean age, blood pressure, bodyweight, and body-mass index (women only), use of table salt, and the proportions of black people and individuals with a history of CVD or hypertension (table 1). Mean calorie intake increased from the lowest to the highest sodium-intake quartile, but surprisingly, body-mass index was similar across the quartiles of sodium intake for men. Sodium and calorie intakes were closely correlated (r=0·65). The characteristics of the four quartiles of total calorie intake (not shown) were very similar to those of the quartiles of sodium intake.
| Characteristic* | Men | Women | ||||||
| Q1 (n=1120) | Q2 (n=1118) | Q3 (n=1120) | Q4 (n=1120) | Q1 (n=1717) | Q2 (n=1721) | Q3 (n=1713) | Q4 (n=1717) | |
| Demographic characteristics | ||||||||
| Age (years) | 56·9 (14·3) | 54·4 (15·5) | 51·7 (15·5) | 48·6 (15·1) | 49·8 (16·0) | 49·2 (16·0) | 47·8 (15·9) | 43·9 (14·9) |
| Black race | 24·4% | 17·0% | 13·3% | 8·8% | 26·0% | 18·3% | 15·4% | 11·5% |
| History | ||||||||
| CVD | 17·6% | 15·4% | 14·5% | 11·3% | 11·5% | 12·0% | 9·4% | 9·6% |
| Hypertension | 21·6% | 18·1% | 15·5% | 14·9% | 16·8% | 15·0% | 14·2% | 12·6% |
| Anthropometric characteristics | ||||||||
| Body-mass index (kg/m2) | 25·7 (4·3) | 25·4 (4·0) | 25·2 (4·2) | 25·5 (4·1) | 26·6 (6·0) | 25·6 (5·7) | 25·3 (5·5) | 24·6 (5·5) |
| Bodyweight (kg) | 76·0 (14·5) | 76·4 (13·4) | 76·4 (14·2) | 77·7 (13·7) | 68·4 (16·3) | 66·3 (15·2) | 65·6 (14·3) | 64·3 (14·9) |
| Blood pressure (mm Hg) | ||||||||
| Systolic | 142·4 (24·9) | 138·8 (33·2) | 136·0 (22·3) | 134·4 (20·6) | 136·7 (26·8) | 134·9 (26·1) | 133·7 (26·2) | 129·5 (24·5) |
| Diastolic | 87·3 (14·0) | 85·8 (13·0) | 84·5 (12·1) | 84·6 (11·8) | 83·5 (13·7) | 82·6 (13·8) | 81·8 (13·1) | 80·2 (12·8) |
| 24 h dietary recall | ||||||||
| Sodium intake (mg) | 1041 (322) | 1832 (195) | 2647 (282) | 4538 (1489) | 678 (229) | 1232 (138) | 1791 (196) | 3105 (1002) |
| Calorie intake (kcal) | 1473 (638) | 1930 (708) | 2297 (732) | 2937 (1050) | 989 (408) | 1331 (434) | 1589 (518) | 1976 (682) |
| Sodium/calorie (mg/kcal) | 0·80 (0·35) | 1·07 (0·42) | 1·27 (0·44) | 1·67 (0·61) | 0·76 (0·35) | 1·02 (0·35) | 1·25 (0·48) | 1·70 (0·66) |
| Use of table salt | ||||||||
| Always | 33·9% | 39·2% | 37·2% | 45·9% | 20·4% | 21·5% | 24·5% | 30·0% |
| Never | 46·2% | 35·5% | 36·4% | 31·9% | 57·4% | 57·0% | 52·5% | 46·9% |
| *Data presented as mean (SD) or as % of participants. | ||||||||
| Table 1: Baseline characteristics by quartile (Q) of sodium intake from 24 h recall | ||||||||
Baseline characteristics generally differed (ANOVA, p<0·05), for men and for women, across quartiles of sodium/calorie ratio, with the exceptions of systolic blood pressure in men; weight, body-mass index, and use of table salt always in women; and diastolic blood pressure, history of hypertension, history of CVD, and use of table salt "never" in both sexes (table 2).
| Characteristic* | Men | Women | ||||||
| Q1 (n=1118) | Q2 (n=1120) | Q3 (n=1120) | Q4 (n=1119) | Q1 (n=1716) | Q2 (n=1717) | Q3 (n=1717) | Q4 (n=1717) | |
| Demographic characteristics | ||||||||
| Age (years) | 50·3 (15·9) | 52·9 (15·3) | 54·0 (15·2) | 54·5 (15·0) | 46·1 (15·5) | 48·1 (16·0) | 48·7 (16·0) | 47·9 (15·9) |
| Black race | 20·1% | 14·8% | 17·0% | 11·6% | 23·2% | 17·4% | 16·8% | 13·8% |
| History | ||||||||
| CVD | 12·5% | 14·6% | 15·4% | 16·0% | 9·3% | 10·4% | 11·7% | 11·1% |
| Hypertension | 17·1% | 15·6% | 18·4% | 19·0% | 13·9% | 14·2% | 14·6% | 16·0% |
| Anthropometric characteristics | ||||||||
| Body-mass index (kg/m2) | 25·7 (4·2) | 25·4 (4·1) | 25·2 (4·2) | 25·4 (4·1) | 25·6 (5·9) | 25·5 (5·5) | 25·4 (5·9) | 25·6 (5·6) |
| Bodyweight (kg) | 77·7 (14·3) | 76·4 (13·7) | 76·0 (14·1) | 76·2 (13·7) | 66·4 (15·9) | 66·2 (14·9) | 65·7 (15·5) | 66·1 (14·7) |
| Blood pressure (mm Hg) | ||||||||
| Systolic | 137·0 (22·8) | 137·0 (22·9) | 138·8 (22·6) | 138·8 (23·7) | 131·6 (25·5) | 133·7 (25·8) | 134·9 (26·4) | 134·5 (26·4) |
| Diastolic | 85·7 (12·8) | 85·1 (12·8) | 85·9 (12·8) | 85·6 (12·9) | 81·7 (13·7) | 82·1 (13·3) | 82·3 (13·1) | 82·0 (13·4) |
| 24 h dietary recall | ||||||||
| Sodium intake (mg) | 1436 (730) | 2134 (904) | 2663 (1177) | 3827 (1845) | 920 (483) | 1408 (579) | 1815 (767) | 2662 (1254) |
| Calorie intake (kcal) | 2330 (1069) | 2208 (916) | 2098 (922) | 2003 (898) | 1520 (706) | 1506 (609) | 1467 (604) | 1391 (604) |
| Sodium/calorie (mg/kcal) | 0·62 (0·16) | 0·97 (0·82) | 1·27 (0·10) | 1·95 (0·52) | 0·60 (0·16) | 0·94 (0·08) | 1·24 (0·11) | 1·96 (0·58) |
| Use of table salt | ||||||||
| Always | 45·5% | 37·8% | 37·8% | 35·3% | 23·7% | 25·4% | 23·9% | 23·5% |
| Never | 35·5% | 36·8% | 37·8% | 39·9% | 53·9% | 52·2% | 53·5% | 54·0% |
| *Data presented as mean (SD) or as % of participants. | ||||||||
| Table 2: Baseline characteristics by quartile (Q) of sodium per calorie intake from 24 h recall | ||||||||
Dietary intake and mortality
Of the 11346 participants, 7423 were presumed alive and 3923 had died (1970 from CVD) by June 30, 1992. All-cause mortality rates adjusted for age and sex (figure) were inversely and significantly related to sodium intake per day (lowest to highest quartile 23·18 to 19·01 per 1000 person-years; p<0·0001) and total calorie intake per day (25·03 to 18·40 per 1000 person-years; p<0·0001). A similar inverse relation was seen for CVD mortality rates from lowest to highest quartile of sodium intake (11·80 to 9·60 per 1000 person-years; p<0·0019) and calorie intake (12·80 to 8·94 per 1000 person-years; p<0·0002). The results were similar for the analysis limited to participants with no reported history of CVD at baseline (not shown).
|
For sodium/calorie ratio, there was a weak direct relation to all-cause mortality (lowest to highest quartile 20·27 to 21·71 per 1000 person-years; p=0·14) and a significant direct relation to CVD mortality (9·73 to 11·35 per 1000 person-years; p=0·017). When the analysis was restricted to participants with no reported history of CVD at baseline (not shown), both all-cause and CVD mortality were directly related to sodium/calorie ratio, but the relation did not achieve statistical significance.
Multivariate analysis
Because sodium intake, total calorie intake, and sodium/calorie ratio were all associated with all-cause and CVD mortality, we undertook stepwise Cox proportional-hazards regression analysis with all three dietary measures in the model (table 3). Models were constructed separately for all-cause and CVD mortality as dependent variables. These models had significantly better likelihood values (p<0·001) than models limited to one dietary measure. In these single-measure analyses, sodium intake had a significant inverse association with both all-cause and CVD mortality. Sodium/calorie ratio showed a significant positive relation to both all-cause and CVD mortality. However, in the model with both measures of sodium intake, total calorie intake no longer had an independent relation to mortality. The relation of sodium intake to all-cause mortality, although significant (p=0·0069), was small. For example, an increase in dietary sodium of 1000 mg was associated with a 10% reduction in mortality. When potassium intake, alcohol use, family income, and education of head of household were each added to the models, the results for sodium intake and sodium/calorie ratio did not change substantially. Both potassium intake and alcohol use were removed from the all-cause and CVD models during backwards stepwise elimination. The results were similar when these analyses were restricted to the participants with no history of CVD at baseline.
| Variable* | All-cause mortality | CVD mortality | ||||
| ß | p | Hazard ratio (95% CI) |
ß | p | Hazard ratio (95% CI) | |
| Male | -0·6286 | <0·0001 | 1·88 (1·75-2·01) | -0·6361 | <0·0001 | 1·89 (1·71-2·09) |
| Black race | -0·1585 | <0·0001 | 1·17 (1·08-1·27) | -0·0465 | <0·4347 | 1·05 (0·93-1·18) |
| History of CVD | -0·4033 | <0·0001 | 1·50 (1·39-1·62) | -0·4859 | <0·0001 | 1·63 (1·46-1·80) |
| History of hypertension | -0·1000 | <0·0241 | 1·11 (1·01-1·21) | -0·0834 | <0·1668 | 1·09 (0·97-1·22) |
| Age (years) | -0·0810 | <0·0001 | 3·62 (3·44-3·82) | -0·0922 | <0·0001 | 4·33 (3·98-4·71) |
| Body-mass index (kg/m2) | -0·0047 | <0·1932 | 0·98 (0·94-1·01) | -0·0081 | <0·1000 | 1·04 (0·99-1·10) |
| Systolic blood pressure (mm Hg) | -0·0057 | <0·0001 | 1·15 (1·11-1·20) | -0·0103 | <0·0001 | 1·29 (1·23-1·36) |
| Sodium (mg) | -0·0001 | <0·0069 | 0·88 (0·80-0·96) | -0·00009 | <0·0864 | 0·89 (0·77-1·02) |
| Calories (kcal) | -0·00001 | <0·8562 | 0·99 (0·91-1·08) | -0·00002 | <0·7394 | 0·98 (0·87-1·11) |
| Sodium/calories (mg/kcal) | -0·1955 | <0·0004 | 1·12 (1·05-1·19) | -0·2159 | <0·0056 | 1·13 (1·04-1·24) |
| Table salt use (always) | -0·0741 | <0·1201 | 1·08 (0·98-1·18) | -0·0130 | <0·8510 | 0·99 (0·86-1·13) |
| Table salt use (never) | -0·0057 | <0·8889 | 1·01 (0·93-1·09) | -0·0012 | <0·9825 | 1·00 (0·89-1·12) |
| *For categorical variables, yes=1. For table salt use variables, reference=sometimes. | ||||||
| For continuous variables, hazard ratios are for 1 SD change. SDs: age=15·9 years, body-mass index=5·15
kg/m2, systolic blood pressure=24·98 mm Hg, sodium=1313 mg, calories=849 kcal, sodium/calorie=0·5787
mg/kcal. | ||||||
| Table 3: Variables associated with risk of all-cause and CVD mortality in Cox proportional-hazards regression (full model) | ||||||
All analyses were repeated with stratification for age (<65 and 65 years). For the older age-group, the relation of sodium intake, sodium/calorie ratio, and calorie
intake to all-cause and CVD mortality were similar to those observed for the whole study population and were statistically significant. Trends
for the younger group were similar, but did not achieve significance.
Discussion
Our main findings are that dietary sodium intake is inversely associated with all-cause and CVD mortality, and that dietary sodium/calorie ratio is directly associated with both mortality rates. These associations, although small, are significant and independent, both of each other and of other factors known to influence mortality.
The inverse association of salt intake with mortality is consistent with the findings of a similar observational study of 3000 participants in a systematic programme to control hypertension.18 In both studies, baseline sodium intake was assessed and related (with control for known confounders) to subsequent morbidity or mortality. Different ways of estimating sodium intake--dietary recall and 24 h urinary measurement--produced similar results in the two studies. NHANES I baseline data, unlike the study in hypertensive patients, included information on other dietary factors. Since there was a strong correlation of sodium intake with total energy consumption, we explored the relation of calorie intake to mortality, both as an isolated variable and in relation to its sodium content. We found that both sodium alone and the sodium concentration in the diet helped to explain, in opposite directions, variations in all-cause and cardiovascular mortality.
These findings suggest that, although there may be a specific relation of sodium to survival, it is not likely to be simple; at the very least, it must be considered in the total dietary context. Moreover, given the genetic, behavioural, environmental, and dietary heterogeneity in most industrialised societies, different individuals may have different optimum sodium intakes. Other research supports the concept that the diet as a whole may be a more important determinant of health outcome than an individual component.21 The high degree of correlation between most dietary components and total calorie consumption suggests that there may be important interaction with other individual dietary components.
The available data do not provide an explanation for the observations. A favourable effect of sodium restriction on various intermediate physiological variables has been shown, particularly, but not exclusively, for blood pressure and other haemodynamic characteristics. In addition to the single outcome study suggesting increased morbidity in treated patients on a low-sodium diet,18 there is convincing evidence of adverse effects of a low-sodium diet on important physiological characteristics, including the sympathetic system and the renin-angiotensin system in particular.22-26 The ultimate health outcome of any intervention is the sum of all its biological effects. For a low-sodium diet, harm may outweigh benefit.
An important limitation of this study is the reliability of the dietary measures. Assessment of the exposure (dietary sodium and calories) was made only once, at baseline, and by recall rather than objective measurement. The dietary recall of sodium and calorie intake is probably an underestimation, as NHANES III, using new methods, suggests.27 Memory can be faulty, estimates of portion size can be mistaken, and diet can change from day to day. However, to the extent that such variation was random, it would tend to mute the relation of exposure (sodium and sodium/calories) to outcome (death). Although a bias is possible, there is no inherent reason to suspect one. Also, we have no information about dietary patterns after the baseline examination. However, other studies have shown that middle-aged people are likely to have a stable nutrient intake over many years.28,29 Nevertheless, no valid inferences can be made about the effect of usual, long-term dietary patterns. The substantial limitations of the dietary measures should be seen in the context that these data are the best available for a large, long-term population study in which mortality outcomes are also available. These data have been used for other studies linking nutrients to outcome.30-32.
The outcome data are more reliable, since all-cause mortality is an unequivocal endpoint; ascertainment was unbiased and complete. Confidence in less precise disease-specific mortality must be guarded.
All research, especially that with non-experimental designs, is prey to confounding. Ecological studies of sodium in populations are the most susceptible to confounding, but observational studies of individuals, such as ours, are not exempt. There can be control for some known confounders, but not for all. The problem arises when an unrecognised factor, or a factor for which insufficient data are available, confounds the observed associations by being associated with both exposure and outcome. Smokers, among whom we expect the mortality rate to be higher, might also have different dietary intake, but we did not have data to address this issue here. However, in a previous study, data on smoking were available, and smoking did not affect the inverse sodium to mortality relation.18
Another difficulty is that people with CVD, who are therefore at higher risk of mortality, might be more likely to adopt a low-sodium diet. To address this issue, we undertook stratified analysis that excluded participants with pre-existing CVD, as well as multiple regression analysis. In both cases, the relation of sodium to mortality persisted. Nevertheless, confounding by indication, despite efforts to control for it, cannot be entirely excluded as a possible contributor to these results.
Because of the controversy that surrounds the issue of appropriate sodium intake, these new data are valuable. Much research links dietary sodium and its variation to intermediate biological characteristics, but this study adds to the smaller body of information relating sodium intake to ultimate morbidity and mortality. The information derives from a methodologically sound study carried out in a probability sample of the US population. During follow-up of more than two decades, 3923 deaths occurred.
Even if the association is valid, and confirmed elsewhere, it does not sustain any claim of causality. Even if the association is significant, dose-related, and independent, it may be a marker for some other dietary or non-dietary factor and therefore not causally related. In addition, the observational data here provide no insight into what might occur if consumption were artificially altered to modify absolute sodium intake or its dietary concentration. A manipulated sodium intake would not inevitably yield the outcomes that occur in individuals naturally consuming that amount of salt. In other words, these data provide no support for a recommendation to increase (or decrease) intake of salt or to decrease its concentration in the diet.
Contributors
All three investigators contributed to design, analysis, and the writing of the paper.
Acknowledgments
The NHANES I Epidemiologic Followup study was developed and funded by the National Center for Health Statistics of the Centers for Disease Control and Prevention, the National Institute on Aging, the National Cancer Institute, and other institutes of the National Institutes of Health.
This study was partly supported by the Hermione Foundation.
References
1 Gleiberman L. Blood pressure and dietary salt in human populations. Ecol Food Nutr 1973; 2: 143-56.
2 Jackson FLC. An evolutionary perspective on salt, hypertension, and human genetic variability. Hypertension 1991; 17 (suppl I): I-129-32.
3 Elliott P. Observational studies of salt and blood pressure. Hypertension 1991; 17 (suppl I): 3-8.
4 Law MR, Frost CD, Wald NJ. By how much does dietary salt reduction lower blood pressure? I: analysis of observational data among populations. BMJ 1991; 302: 811-15.
5 Frost CD, Law MR, Wald NJ. By how much does dietary salt reduction lower blood pressure? II: analysis of observational data within populations. BMJ 1991; 302: 815-18.
6 Cutler J, Follman D, Elliott P, Suh I. An overview of randomised trials of sodium reduction and blood pressure. Hypertension 1991; 17 (suppl I): I-27-33.
7 Intersalt Cooperative Research Group. The Intersalt study. J Hum Hypertens 1989; 3: 279-331.
8 Folkow B, Ely DL. Cardiovascular and sympathetic effects of 240-fold salt intake variations: studies in rats, with comparisons to man. Acta Physiol Scand 1989; 136 (suppl 583): 89-96.
9 Dahl LK, Love RM. Evidence of relationship between sodium (chloride) intake and human hypertension. Arch Intern Med 1954; 94: 525-31.
10 Hollenberg NK, Martinez G, McCullough M, et al. Aging, aculturation, salt intake, and hypertension in the Kuna of Panama. Hypertension 1997; 29: 171-76.
11 McCarron DA, Morris CD, Henry HJ, Stanton JL. Blood pressure and nutrient intake in the United States. Science 1984; 224: 1392-98.
12 Midgley JP, Matthew AG, Greenwood CMT, Logan AG. Effect of reduced dietary sodium on blood pressure: a meta-analysis of randomized controlled trials. JAMA 1996; 275: 1590-97.
13 MacGregor GA, Sever PS. Salt--overwhelming evidence but still no action: can a consensus be reached with the food industry? CASH (Consensus Action on Salt and Hypertension). BMJ 1996; 312: 1287-89.
14 Dietary Guidelines Advisory Committee. Report of the Dietary Guidelines Advisory Committee on the Dietary Guidelines for the Americans, 1995. Washington, DC: US Dept of Agriculture, US Dept of Health and Human Services.
15 Echt DS, Liebson PR, Mitchell LB, et al. Mortality and morbidity in patients receiving encainide, flecainide, or placebo: the Cardiac Arrhythmia Suppression Trial. N Engl J Med 1991; 324: 781-88.
16 Packer M, Carver JR, Rodeheffer RJ, et al. Effect of oral milrinone on mortality in severe chronic heart failure. N Engl J Med 1991; 325: 1468-75.
17 Wassertheil-Smoller S, Blaufox MD, Oberman A, et al. Effect of antihypertensives on sexual function and quality of life: the TAIM Study. Ann Intern Med 1991; 114: 613-20.
18 Alderman MH, Madhavan S, Cohen H, Sealey JE, Laragh JH. Low urinary sodium is associated with greater risk of myocardial infarction among treated hypertensive men. Hypertension 1995; 25: 1144-52.
19 Cox CS, Rothwell ST, Madans JH, et al. Plan and operation of the NHANES I Epidemiologic Follow-up Study, 1987. National Center for Health Statistics. Vital Health Stat 1992; 1: 1-190.
20 Public use data tape documentation. NHANES I epidemiologic followup study, 1992 vital and tracing status. US Department of Health and Human Services, Public Health Service, Center for Disease Control and Prevention, National Center for Health Statistics, 1996.
21 Huijbregts P, Feskens E, Rasanen L, et al. Dietary pattern and 20 year mortality in elderly men in Finland, Italy, and the Netherlands: longitudinal cohort study. BMJ 1997; 315: 13-17.
22 Engstrom AM, Tobelmann RC. Nutritional consequences of reducing sodium intake. Ann Intern Med 1983; 98: 870-72.
23 Luft FC, Rankin LI, Bloch R, et al. Cardiovascular and humoral responses to extremes of sodium intake in normal black and white men. Circulation 1979; 60: 697-706.
24 De Simone G, Devereux RB, Chien S, Alderman MH, Atlas SA, Laragh JH. Relation of blood viscosity to demographic and physiologic variables and to cardiovascular risk factors in apparently normal adults. Circulation 1990; 81: 107-17.
25 Gracia G, Cattaneo BM, Seravalle G, Lanfranchi A, Bolla G, Mancia G. Baroreflex impairment by low sodium diet in mild or moderate essential hypertension. Hypertension 1997; 29: 802-07.
26 Alderman MH, Madhavan S, Ooi WL, Cohen H, Sealey JE, Laragh JH. Association of the renin-sodium profile with the risk of myocardial infarction in patients with hypertension. N Engl J Med 1991; 324: 1098-104.
27 Alaimo K, McDowell MA, Briefel RR, et al. Dietary intake of vitamins, minerals, and fiber of persons aged 2 months and over in the United States: third National Health and Nutrition Examination Survey, Phase 1, 1988-91. Advance Data. Washington, DC: Department of Health and Human Services, 1994; 258: 1-28.
28 Jensen OM, Wahrendorf J, Rosenquist A, Geser A. The reliability of questionnaire-derived historical dietary information and temporal stability of food habits in individuals. Am J Epidemiol 1984; 120: 281-90.
29 James GD, Sealey JE, Alderman MH, Laragh JH. Year to year stability of urine sodium, potassium, aldosterone and PRA in normotensive men and women. Am J Hypertens 1993; 6: 86A-90A.
30 Kim I, Williamson DF, Byers T, Koplan JP. Vitamin and mineral supplement use and mortality in a US cohort. Am J Public Health 1993; 83: 546-50.
31 Dwyer JT, Madans JH, Turnbull B, et al. Diet, indicators of kidney disease, and later mortality among older persons in the NHANES I Epidemiologic Follow-Up Study. Am J Public Health 1994; 84: 1299-303.
32 Kant AK, Graubard BI, Schatzkin A, Ballard-Barbash R. Proportion of energy intake from fat and subsequent weight change in the NHANES I Epidemiologic Follow-up Study. Am J Clin Nutr 1995; 61: 11-17.