(Stroke. 1995;26:783-789.)
© 1995 American Heart Association, Inc.
Articles |
Dietary Sodium, Potassium, Saturated Fat, Alcohol, and Stroke Mortality
From the Department of Epidemiology, School of Public Health, University of Leuven, Leuven, Belgium (S.S., X.-H.Z., H.K.), and the Department of Health Science, Shiga University of Medical Science, Tsukinowa-cho, Seta, Otsu, Shiga, Japan (S.S.).
Correspondence to Professor H. Kesteloot, Department of Epidemiology, School of Public Health, University of Leuven, Capucijnenvoer 33 B-3000 Leuven, Belgium.
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Abstract |
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Background and Purpose Although positive relationships between blood pressure, dietary sodium, and stroke risk have been reported, studies on the relationship between dietary sodium and stroke mortality are scarce. A significant relationship between dietary saturated fatty acids (SFA) and stroke risk has not been reported in epidemiological studies. The purpose of this study was to examine the relationship between dietary sodium and SFA together with dietary potassium, alcohol, and stroke risk.
Methods The sex- and age-specific stroke mortality rates (log-transformed) for the age classes 45 to 54, 55 to 64, and 65 to 74 years for the period between 1986 and 1988 were obtained from World Health Organization statistics. The 24-hour urinary excretion levels of sodium (U-Na) and of potassium (U-K), dietary SFA intake levels, and alcohol consumption levels were obtained from dietary surveys performed in 17 countries. The relationships between stroke mortality and the dietary variables were examined by Pearson correlation and multiple regression analysis.
Results The highest degree of correlation, both in Pearson correlation and multiple regression analysis, was found between U-Na and log-stroke mortality (P<.01 to P<.001). In multiple regression analysis, U-Na (P<.01 to P<.001), SFA (P<.05 to P<.01), and alcohol (P<.05) independently, significantly, and positively correlated with log-stroke mortality rates, and U-K correlated negatively (P<.05). The exceptions were SFA in both sexes in the age class 45 to 54 years, alcohol in both sexes in the age class 45 to 54 years and in women in the age class 55 to 64 years, and U-K in women in the age class 65 to 74 years.
Conclusions These results suggest that dietary factors, especially sodium and SFA, are of primary importance as determinants of stroke mortality at the population level.
Key Words: alcohol drinking • diet • fatty acids • mortality • sodium • stroke
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Introduction |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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Since the 1950s, mortality from stroke has declined in most developed countries.1 High blood pressure is the major contributor to stroke, as confirmed by several studies.2 But this decline cannot be solely attributed to better treatment of hypertension1 2 3 4 and could be related to a decrease in salt intake in the industrialized world.1 5 Compared with the strong relationship between blood pressure levels and stroke mortality, relationships between dietary factors and stroke mortality are still unclear. Several dietary risk factors such as dietary sodium,5 6 7 potassium,8 and alcohol9 have been suggested as risk factors for stroke. Saturated fatty acids (SFA) have long been hypothesized as a risk factor for ischemic stroke.10 Therefore, using data from 17 countries, we examined the relationship between stroke mortality rates and four dietary factors: sodium, potassium, SFA, and alcohol.
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Materials and Methods |
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Twenty-four-hour urinary excretion levels of sodium and potassium (U-Na and U-K, respectively; millimoles per 24 hours) were collected from 24 published articles concerning dietary surveys performed between the late 1970s and 1980s. To avoid the age-related differences of the excretion levels in a population, studies with populations of a mean age around 40 years were selected. Of 58 surveyed populations, 33 were obtained from the INTERSALT study.11 Sex-specific mean values per country with more than one survey were calculated taking the mean after weighting each survey by the square root of the number of participants. The means of men and women were used as representative values of the country. The weighting was applied to enhance the importance of carefully performed small-scale studies.12 Data were thus available on a total of 17 countries. In addition, 24-hour urinary excretion levels of calcium and magnesium (U-Ca and U-Mg, respectively; millimoles per 24 hours) were collected for 14 countries from the INTERSALT study.11 Intake levels of SFA per country were obtained from 49 dietary surveys performed in 17 countries between 1976 and 1989. The methods of collection and calculation were described in detail elsewhere.12 Briefly, the intake levels of SFA assessed from healthy adult populations, except one dietary survey assessed for breast cancer patients, were collected from published articles. Dietary surveys assessed by either 24-hour recall, dietary record, or dietary history methods were included. Those assessed by food frequency questionnaires, which are usually not designed to obtain the population means of nutrient intake levels,13 were not included; one in Australia that was considered adequate was included. The SFA intake levels were expressed as percentage of total energy including alcohol (%E). This unit was recommended for the comparison between different populations.12 Sex and age were not considered because SFA intake levels were similar in different age classes and in both sexes in most populations when expressed as %E.14 For countries with more than one dietary survey, the mean intake level of SFA per country was calculated after weighting each survey by the square root of the number of participants. Alcohol (ethanol) consumption levels per country were obtained from the food balance sheets of the Food and Agriculture Organization of the United Nations (1979 through 1981).15 The alcohol consumption levels were expressed as %E. These data were considered adequate because alcoholic beverages are used for human consumption only. The dietary data used in the study are listed in Table 1
. Means of age- and sex-specific
stroke (cerebrovascular disease, code 29 in the International
Classification of Diseases [ICD], 9th Revision, or code A85 in the
ICD-8) mortality rates (per 100 000 persons per year) for the period
between 1986 and 1988 for the age classes 45 through 54, 55 through 64,
and 65 through 74 years were obtained from World Health Organization
statistics.16 Mortality rates for stroke in the German
Democratic Republic were underestimated before the unification of
Germany.17 The mortality rates were corrected by
multiplying the reported mortality rates by 1.4.17 The
mortality data used in the study are listed in Table 2.
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Pearson correlation and linear multiple regression analysis were performed including U-Na, U-K, SFA, and alcohol as independent variables. The analysis with the ratio of U-Na to U-K (U-Na/U-K; millimole per millimole) instead of U-Na and U-K was also performed. Independent variables examined were included in the final regression equations regardless of the significance level. When U-Ca and U-Mg were included in the models in addition to U-Na, U-K, SFA, and alcohol, stepwise multiple regression analysis was performed. Mortality rates transformed by natural logarithm were used as dependent variables because the distribution of the mortality rates were positively skewed, and the skewness decreased after log transformation. A log-linear relationship between stroke mortality and blood pressure was reported in several studies.2 The significance level was P<.05.
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Results |
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The Pearson correlation coefficients between log-stroke mortality rates and dietary variables are shown in Table 3
. The
levels of U-Na correlated significantly and positively with all
log-stroke mortality rates examined (r=.64 to
r=.84, P<.01 to P<.001). In both
sexes in the age classes 45-54 and 55-64 years, U-Na/U-K correlated
significantly and positively with log-stroke mortality rates
(r=.55 to r=.71, P<.05 to
P<.01). Alcohol consumption levels correlated significantly
and positively with log-stroke mortality rates in both sexes in the age
class 65-74 years (r=.49 to r=.52,
P<.05). Neither U-K nor SFA intake levels correlated
significantly with log-stroke mortality rates.
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The correlation matrix of the dietary variables is given in Table 4. The intake levels of SFA correlated significantly and
positively with U-K and negatively with U-Na/U-K (P<.05).
The results of the multiple regression analysis of log-stroke
mortality rates with U-Na, U-K, SFA, and alcohol as independent
variables are shown in Table 5. The levels of U-Na
correlated independently, significantly, and positively with all
log-stroke mortality rates examined (P<.01 to
P<.001). The levels of U-K correlated independently,
significantly, and negatively with log-stroke mortality rates
(P<.05) except in women in the age class 65-74 years. The
intake levels of SFA correlated independently, significantly, and
positively with log-stroke mortality rates except in both sexes in the
age class 45-54 years (P<.05 to P<.01). The
consumption levels of alcohol correlated independently, significantly,
and positively with log-stroke mortality rates (P<.05 to
P<.01) except in men in the age class 45-54 years and in
women in the age classes 45-54 and 55-64 years. When U-Na was excluded
from the analysis, SFA did not attain a significance level in any
equation.
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When U-Ca and U-Mg were included in the analysis together with U-Na, U-K, SFA, and alcohol in stepwise regression analysis (n=14), the independent and significant relationship between U-Na and stroke mortality rates was consistent (P<.01 to P<.001). The levels of U-Ca correlated independently, significantly, and negatively with log-stroke mortality rates in men in the age classes 45-54 and 55-64 years and in women in the age classes 55-64 and 65-74 years (P<.05). The intake levels of SFA (P<.01) and alcohol (P<.05) correlated independently, significantly, and positively with log-stroke mortality rates only in women in the age class 65-74 years. Neither U-K nor U-Mg were selected in any final equation.
The results of the multiple regression analysis with SFA, alcohol,
and U-Na/U-K are shown in Table 6. All three independent
variables correlated independently, significantly, and positively with
log-stroke mortality rates (P<.05 to P<.001)
except alcohol in women in the age class 45-54 years. The levels of
significance of SFA and of alcohol were in general higher in the older
age class (Tables 5
and 6). The levels of R2
(multiple determination coefficient) observed in the above two analyses
were higher than 0.7 (P<.002) except in women in the age
class 45-54 years.
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Discussion |
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In the present study, significant positive correlations were obtained between U-Na, U-Na/U-K, SFA, and alcohol, and negative ones were obtained between U-K and stroke mortality rates.
Of all dietary factors analyzed, the highest degree of correlation both
in Pearson correlation and multiple regression analysis was found
between U-Na and stroke mortality (P<.01 to
P<.001) (Tables 3, 5, and 6). The 24-hour U-Na and U-K are
considered to be valid reflections of respective dietary
intake.18 A positive relationship between dietary sodium
and stroke mortality has been reported previously.5
Ecological studies with similar data sets show a significantly positive
relationship between U-Na and stroke mortality independent of blood
pressure.6 7 A direct relationship between dietary sodium
levels and stroke mortality without a change in blood pressure levels
has also been observed in animal experiments.19 Another
ecological study performed in Japan reported a significantly positive
relationship between regional salt consumption levels and stroke
mortality in women (P<.05) but not in men.20
In within-population studies, one prospective21 and one
case-control22 study reported a significantly positive
relationship between preference for salty food and stroke risk in
Chinese populations but not in western populations.23 A
similar discrepancy in the results between within- and
between-population studies has been observed in the relationship
between intake levels of sodium and blood pressure
levels.24 In developed countries, a negative relationship
between U-Na and blood pressure levels was also
observed.25 It was explained partly because hypertensive
persons were likely to reduce their salt intake levels more than those
who were normotensive.25 Moreover, a degree of
intraindividual variability of sodium intake is much greater than the
interindividual differences in industrialized
populations.26 This could result in the negative or
nonsignificant relationship between intake levels of sodium and blood
pressure levels observed in some within-population
studies.24
The negative relationship between U-K and stroke mortality is in agreement with findings of a previous prospective study.8 A negative relationship between dietary potassium and blood pressure levels was also reported.27 A direct relationship between dietary potassium intake levels and stroke mortality without a change in blood pressure levels was observed in animal experiments.28
A positive relationship between alcohol consumption and stroke risk has been reported in several within-population studies.9 One ecological study showed a significantly positive relationship,7 but this was not confirmed in another study.29 The latter study did not adjust for other possible risk factors such as sodium intake levels. A linear or a J-shaped relationship between alcohol consumption and hemorrhagic and ischemic stroke risk has been proposed.9 In western populations, 70% to 85% of stroke mortality is due to ischemic stroke.30 31 In Japan, however, only 49% of stroke mortality was attributed to cerebral infarction in the age-standardized mortality rates (45 through 74 years old) in 1985.32 Alcohol is generally consumed predominantly by men11 and in middle-aged populations.11 The more consistent relationship between alcohol and stroke mortality in men compared with women observed in this study could be explained partly by the sex difference in alcohol consumption. Alcohol might contribute to stroke mortality in several ways, promoting hemorrhagic stroke and decreasing thrombotic stroke.33 The age-related differences between alcohol consumption and stroke mortality observed in this study should be further examined.
A positive relationship between dietary fat intake, especially of SFA,
and stroke risk has been proposed as a hypothesis.10 A
significant positive relationship between SFA intake levels and stroke
risk has never been reported as far as we know except in a study of our
group using similar data sets.34 However, serum
cholesterol levels correlated significantly and positively with
nonhemorrhagic stroke mortality in the Multiple Risk Factor
Intervention Trial (MRFIT) cohort (P<.001)35
and with thromboembolic stroke incidence in Hawaiian Japanese men
(P<.01).36 A positive relationship between
serum cholesterol and blood pressure has also been reported in large
population studies.37 38 The change in stroke mortality
rates correlated significantly and positively with the change in
coronary heart disease mortality rates in 29 countries between 1968 and
1987 (r=.74 to r=.84,
P<.001).39 Fish intake levels correlated
significantly, but marginally, and negatively with stroke
incidence40 as well as with coronary heart disease
mortality41 in an elderly Dutch cohort. This evidence
suggests the presence of common risk factors for ischemic stroke and
coronary heart disease. A positive relationship between SFA intake
levels and blood pressure was also demonstrated.38 We
analyzed the relationship excluding Japan (n=16), where ischemic stroke
was not predominant.32 The levels of significance of SFA
in general remained unchanged. The intake levels of SFA did not attain
a significance level when U-Na was not included in the multiple
regression analysis. The relationship between SFA intake levels and
stroke mortality rates was not significant in Pearson correlation
analysis (Table 3). A negative but not significant correlation
between SFA intake levels and U-Na was observed (Table 4). Therefore,
an adjustment for U-Na or sodium intake levels is necessary to examine
the relationship between SFA intake levels and stroke risk. The lack of
a significant relationship between SFA, or total fat, intake levels and
stroke mortality in previous studies can be explained partly by a lack
of adjustment for sodium intake levels.
To examine a relative importance among risk factors, standardized
regression coefficients were calculated (Tables 5 and 6). The
standardized regression coefficient of U-Na was the highest among four
independent variables in all equations (Table 5). For example, in
elderly Belgians U-Na decreased by 77 mmol/24 h in men between 1967 and
1986.5 A 58% decrease in stroke mortality rates in men in
the age class 65-74 years can be calculated from the multiple
regression equation shown in Table 5. On the other hand, the change in
U-K was less marked during the same period.5 The intake
levels of SFA decreased by 2.6%E between 1960 and 1980 through
1984,42 and alcohol consumption levels increased by 0.5%E
between 1965 and 1987 in Belgium.43 From these changes, a
13% decrease and a 6% increase in stroke mortality rates in men in
the age class 65-74 years can be calculated from the multiple
regression equation shown in Table 5. Therefore, the observed decrease
in stroke mortality in Belgium, 50% in men in the age class 70-74
years between 1969 and 1987,1 could be attributed mainly
to a decrease in sodium intake levels and to some extent to a decrease
in SFA intake levels in this population. The contribution of the
alcohol consumption levels to stroke mortality is markedly smaller than
that of the sodium intake levels.
A lowering of blood pressure has been suggested to be an effect of dietary calcium.44 However, the relationship between blood pressure and dietary calcium is controversial.45 When U-Ca was included in the analysis, U-Ca correlated significantly and negatively with log-stroke mortality rates. Over 55% and 43% of dietary calcium is derived from dairy products in western populations.46 Dairy products are major sources of animal protein.47 Experimental studies have demonstrated a protective effect of animal protein on stroke mortality.48 One ecological study reported a significantly negative relationship between stroke mortality rates and 24-hour urinary excretion levels of creatinine.6 Urinary creatinine is an indicator of the level of protein intake.49 Moreover, U-Ca is only an imperfect indicator of calcium intake.50 The number of countries included was smaller and the levels of R2 in general were lower than those in the models with U-Na, U-K, SFA, and alcohol. Therefore, the observed negative relationship between stroke mortality rates and U-Ca may not suggest the direct relationship between them. The relationship between dietary magnesium and blood pressure is also of interest.51 However, no significant relationship between U-Mg and stroke mortality rates was observed in this study.
It should be noted that the data sources used in this study are not optimal. However, the reliability and usefulness of the SFA intake levels used in the study were examined previously, and the data were considered useful in epidemiological studies.12 The data on alcohol concerned consumption levels, not intake levels. However, alcoholic beverages are used by human subjects only. Moreover, alcohol intake levels assessed by dietary surveys in eastern European countries such as Hungary11 are much lower than the corresponding consumption levels obtained from the food balance sheets.15 Alcohol intake levels in these countries appear to be underestimated. A significant positive relationship (r=.67 to r=.74, P<.001) was observed between the alcohol consumption levels used in this study and chronic liver disease mortality rates, both in men and women, in 26 countries.34 Therefore, the alcohol consumption levels obtained from the food balance sheets were considered useful in epidemiological studies. The data on U-Na and U-K are not optimal either. The results of two studies on the relationship between stroke mortality rates and 24-hour urinary excretion levels of cations and consumption levels of alcohol obtained from the INTERSALT study were similar to those in the present study, although the countries included were different among the three studies.6 7
Several other possible risk factors, such as smoking,35 52 obesity,53 protein intake levels,6 48 and fish intake levels,40 were not included in the study and could confound the issue. Even more important, the level of pharmacological treatment of hypertension has not been included. Many studies have irrefutably shown that pharmacological treatment decreases stroke risk,54 but doubt has been expressed whether these results, obtained in carefully planned and conducted studies, can be extrapolated to the population at large.1 4 55 An ecological approach cannot confirm the causality of any relationship between mortality rates and possible risk factors.56 The data used in this study are far from optimal but are the best available. There is a great need for adequate data characterizing the nutritional habits of populations. The strength of the findings, however, suggests that dietary factors, especially dietary sodium and SFA, are of primary importance as determinants of stroke mortality at the population level.
Received August 17, 1994; revision received February 3, 1995; accepted February 3, 1995.
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N. R Cook, J. A Cutler, E. Obarzanek, J. E Buring, K. M Rexrode, S. K Kumanyika, L. J Appel, and P. K Whelton Long term effects of dietary sodium reduction on cardiovascular disease outcomes: observational follow-up of the trials of hypertension prevention (TOHP) BMJ, April 28, 2007; 334(7599): 885 - 885. [Abstract] [Full Text] [PDF]
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M. H. Alderman Evidence relating dietary sodium to cardiovascular disease. J. Am. Coll. Nutr., June 1, 2006; 25(3 Suppl): 256S - 261S. [Abstract] [Full Text] [PDF]
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K. He, A. Merchant, E. B Rimm, B. A Rosner, M. J Stampfer, W. C Willett, and A. Ascherio Dietary fat intake and risk of stroke in male US healthcare professionals: 14 year prospective cohort study BMJ, October 4, 2003; 327(7418): 777 - 782. [Abstract] [Full Text] [PDF]
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L. A. Bazzano, J. He, L. G. Ogden, C. Loria, S. Vupputuri, L. Myers, and P. K. Whelton Legume Consumption and Risk of Coronary Heart Disease in US Men and Women: NHANES I Epidemiologic Follow-up Study Arch Intern Med, November 26, 2001; 161(21): 2573 - 2578. [Abstract] [Full Text] [PDF]
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J. Fang, S. Madhavan, and M. H. Alderman Dietary Potassium Intake and Stroke Mortality Stroke, July 1, 2000; 31(7): 1532 - 1537. [Abstract] [Full Text] [PDF]
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N. M Kaplan The dietary guideline for sodium: should we shake it up? No Am. J. Clinical Nutrition, May 1, 2000; 71(5): 1020 - 1026. [Abstract] [Full Text] [PDF]
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A. E. Kunst, M. del Rios, F. Groenhof, and J. P. Mackenbach Socioeconomic Inequalities in Stroke Mortality Among Middle-Aged Men : An International Overview Stroke, November 1, 1998; 29(11): 2285 - 2291. [Abstract] [Full Text] [PDF]
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F. R. Artalejo, P. Guallar-Castillon, J. R. B. Banegas, B. d. A. Manzano, and J. d. R. Calero Consumption of Fruit and Wine and the Decline in Cerebrovascular Disease Mortality in Spain (1975–1993) Stroke, August 1, 1998; 29(8): 1556 - 1561. [Abstract] [Full Text] [PDF]
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F. R. Artalejo, P. Guallar-Castillon, J. L. Gutierrez-Fisac, J. R. Banegas, and J. d. R. Calero Socioeconomic Level, Sedentary Lifestyle, and Wine Consumption as Possible Explanations for Geographic Distribution of Cerebrovascular Disease Mortality in Spain Stroke, May 1, 1997; 28(5): 922 - 928. [Abstract] [Full Text]
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J. He, M. J. Klag, Z. Wu, and P. K. Whelton Stroke in the People's Republic of China : I. Geographic Variations in Incidence and Risk Factors Stroke, December 1, 1995; 26(12): 2222 - 2227. [Abstract] [Full Text]
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X. H. Zhang, S. Sasaki, and H. Kesteloot Changes in the Sex Ratio of Stroke Mortality in the Period of 1955 Through 1990 Stroke, October 1, 1995; 26(10): 1774 - 1780. [Abstract] [Full Text]
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