Urinary sodium and potassium excretion and risk of
hypertension in Chinese: report from a community-based
cohort study in Taiwan
Kuo-Liong Chien
a,b, Hsiu-Ching Hsu
b, Pei-Chun Chen
c, Ta-Chen Su
b,
Wei-Tien Chang
d, Ming-Fong Chen
band Yuan-Teh Lee
bBackground Dietary sodium intake is associated with blood pressure and hypertension risk. However, most of the studies have been conducted in whites and it is not clear whether the effects exist in Asian populations.
Objective The purpose of the present study was to investigate the role of 24-h urinary sodium excretion and hypertension risk among ethnic Chinese.
Design A prospective cohort design on community. Setting and participants One thousand five hundred and twenty middle-aged and elderly participants who were free from hypertension at baseline and had available urine electrolyte data.
Main outcome measures Hypertension incidence. Results During a median 7.93 years of follow-up (interquartile range U 4.07–9.04 years), we documented 669 cases of incident hypertension. The multivariate risk was 1.26 (95% confidence interval U 1.01–1.57;P U 0.043) for individuals in the highest quartile of urinary sodium excretion as compared with those in the second quartile. A significant J-shape relationship between urinary sodium excretion and the risk of hypertension was observed, with the test for linear relation being rejected (P U 0.046). Participants who were in the highest quartile of urinary
sodium excretion and higher baseline blood pressure had a 2.43-fold increased risk of hypertension (95% confidence interval U 1.72–3.22) compared with those in the lowest quartiles of urinary sodium and lower blood pressure. Conclusion Urinary sodium excretion was associated with the risk of hypertension among ethnic Chinese. Urinary sodium excretion, as a marker of dietary sodium intake, can be useful for a comprehensive evaluation of hypertension risk in Asian populations.J Hypertens 26:1750 –1756 Q 2008 Wolters Kluwer Health | Lippincott Williams & Wilkins.
Journal of Hypertension2008, 26:1750–1756 Keywords: cohort, hypertension, urinary sodium
Abbreviations: HDL-C, high density lipoprotein cholesterol; LDL-C, low density lipoprotein cholesterol
a
Institute of Preventive Medicine, College of Public Health, National Taiwan University,b
Department of Internal Medicine, National Taiwan University Hospital,
c
Institute of Environmental Health, College of Public Health, National Taiwan University andd
Department of Emergency Medicine, National Taiwan University Hospital, Taipei, Taiwan
Correspondence to Yuan-Teh Lee, MD, PhD, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan 100
Tel: +886 2 2356 2830; fax: +886 2 2392 0456; e-mail: [email protected]
Received1 January 2008 Revised 23 April 2008 Accepted28 April 2008
Introduction
Hypertension appreciably increases the cardiovascular risk and has a great public burden worldwide. High hypertension incidence rates are found among middle-to-elderly-aged adults, and the risk factors for hyper-tension incidence include age, sex, obesity, metabolic syndrome, and lifestyle factors [1,2]. Among lifestyle factors, dietary sodium and potassium intakes are associ-ated with blood pressure (BP) and hypertension risk in many ecological and cross-sectional studies [3,4]. For example, a cross-sectional European study showed a linear trend between sodium intake and BP levels [5]. However, the ecological and cross-sectional studies were confounded by various modifying factors and were susceptible to bias [6]. Furthermore, geographical and ethnic variations on
sodium intake were found [3,4,7]. Information about the role of urinary sodium and potassium excretion in hyper-tension risk has been relatively rare from the ethnic Chinese community, which actually has the highest sodium intake [3]. Therefore, prospective cohort data from community participants may provide a valid answer for the relationship between urinary sodium excretion and hyper-tension risk.
Methods
Study design and population
Details of the present cohort study have been published previously [2,8,9]. Briefly, the Chin-Shan Community Cardiovascular Cohort Study (CCCC) began in 1990 by recruiting 1703 men and 1899 women of Chinese
ethnicity aged 35 years and older from the Chin-Shan township, 30 km north of metropolitan Taipei, Taiwan. Information about anthropometry, lifestyle, and medical conditions was assessed by interview questionnaires in 2-year cycles for the initial 6 years, and the validity and reproducibility of the collected data and measurements have been reported in detail elsewhere [9]. In brief, all study participants were individually interviewed with a structured questionnaire in the baseline survey. Trained medical students canvassed door-to-door with the assist-ance of community leaders to extend invitations for the baseline survey to collect information on sociodemo-graphic characteristics, lifestyle behaviors, regular exer-cise, and a personal and family history of diseases and hospitalizations. With the consent of participants, phys-icians and students conducted physical examinations and laboratory tests for those participants invited to the clinic. BMI was calculated as weight (kg)/height (m2). From 1992, the waist circumference was measured by using a measuring tape positioned at the midway between the lowest rib and the iliac crest. The measurement was made at minimal respiration status, with the tape snug but without compressing the skin. BP was measured twice in the right arm by a mercury sphygmomanometer with the participant seated comfortably and arms supported and positioned at the level of the heart. The average of the BP measurements was used as described previously [2,10].
Participants with a baseline diagnosis of hypertension (BP 140/90 mmHg or with an antihypertensive medi-cation history, n¼ 1096) or incomplete urine collection data at baseline (n¼ 986) were excluded from this inves-tigation. After these exclusions, the final analytic sample included 1520 participants with complete urine data. Because the recruitment strategy was volunteer based and the participants were from just one community, our participants were not representative of the general population. The National Taiwan University Hospital Committee Review Board approved the study protocol. Incident hypertension cases were ascertained through biennial BP measurements and medication history was obtained from questionnaires, and was defined as sitting systolic BP of at least 140 mmHg, diastolic BP of at least 90 mmHg, or antihypertensive treatment.
Measurement of urine sodium and potassium
excretion
The 24-h urine collection was considered the most reliable method to evaluate sodium and potassium intake amounts [11,12]; however, other modifications, such as causal urine specimens [13] and second morning voiding urine collection [12], were more feasible methods and have been validated in epidemiological studies. We used the second morning voiding urine amount as follows. We dispersed a plastic container to all participants and instructed them to collect the overnight urine and record
their sleep time. Participants were asked to collect their overnight urine after voiding all urine before sleep. The sleep time was recorded and the 24-h urine amount was calculated from the sleep time and morning voiding urine. We did not ask the participants to change their dietary patterns during the collection so that the urine sodium and potassium excretion amount could be considered as a marker for usual intake. Electrolytes in the urine were measured by selective electrodes of the Dimension autoanalyzer (Du Pont, Wilmington, Delaware, USA) [14,15].
Biochemical markers
The procedure for blood collection has been reported elsewhere [16,17]. Briefly, all venous blood samples drawn after a 12-h overnight fast were immediately refrigerated and transported within 6 h to the National Taiwan Uni-versity Hospital. Serum samples were then stored at 708C before batch assay for levels of total cholesterol, triglyceride, and high-density lipoprotein cholesterol (HDL-C) were performed. Standard enzymatic tests for serum cholesterol and triglyceride were used (Merck 14354 and 14366, Merck Chemical, Darmstadt, Germany, respectively). HDL-C levels were measured in super-natants after the precipitation of specimens with magnes-ium chloride phosphotungstate reagents (Merck 14993). The low-density lipoprotein cholesterol (LDL-C) concen-tration was calculated as the total cholesterol concenconcen-tration minus the concentration of cholesterol in the supernatant obtained with the precipitation method (Merck 14992) [18]. Plasma uric acid concentrations were assayed with commercial kits (Merck Chemical, Darmstadt, Germany) and placed in an Eppendorf 5060 autoanalyzer (Eppendorf Corp, Hamburg, Germany) [19]. The diagnosis of diabetes was done by fasting glucose levels of at least 126 mg/dl or by the use of oral hypoglycemic medications or insulin.
Statistical analysis
Participants were categorized on the basis of quartiles of 24-h urinary sodium excretion, continuous variables were presented by mean and standard deviation, and analysis of variance was used to test the difference across the quartiles. Correlations between urinary sodium and potassium excretion and other cardiovascular risk factors were estimated by Spearman’s partial correlation coefficients adjusted for age and sex. Incidence rates of hypertension were calculated by dividing the number of cases by the person-years of follow-up for each quartile of urinary sodium and potassium excretion. The relative risk (RR) of hypertension was calculated by dividing the incidence rate of urinary sodium excretion in each quartile by the rate in the second quartile. We chose the second quartile as the reference group because the median sodium excretion value in the second quartile was nearly identical to the recommended upper limit (100 mmol per day) in the general population [20]. We used the Cox proportional-hazards models to adjust for
potential confounding variables, including age groups (35–44, 45–54, 55–64, 65–74, 75 years of age), sex, BMI (<18, 18–20.9, 21–22.9, 23–24.9, or 25 kg/m2), alcohol intake (nondrinker/current), smoking (yes/no), regular exercise (yes/no), marital status (single, married, or divorced), educational level (<9 years,9 years), occu-pation (no work, manual work, or professional), and regular physical activity (yes/no). We further adjusted for con-tinuous systolic BP and diabetes (yes/no) to examine whether the effects were reduced by baseline BP and diabetes status. In addition, we examined the nonlinear relationship between urinary sodium excretion and the risk of hypertension nonparametrically with restricted cubic splines [21]. Tests for nonlinearity included the likelihood ratio test, comparing the model with only the linear term with the model with the linear and the cubic spline terms. Furthermore, we examined whether the association between urinary sodium excretion and hypertension was mediated through several confounding factors, including sex, age, BMI, and systolic BP. The likelihood ratio tests were used to compare the model with the interaction terms and the model without the interaction terms. We also tested the goodness of fit for the model by using the Hosmer and Lemeshow test [22], and the goodness-of-fit test was acceptable (P¼ 0.85). Finally, we conducted
joint analyses to evaluate potential additive effects by baseline BMI and systolic BP using median values as the cutoffs. All statistical tests were two-tailed with a type I error of 0.05, and P < 0.05 was considered statis-tically significant. Analyses were performed using the SAS software version 9.1 (SAS Institute, Cary, North Carolina, USA).
Results
Participants in the highest quartile of urinary sodium excretion had a higher education level and diabetes rate and were more likely to have a higher BMI, systolic and diastolic BP, and total cholesterol and LDL-C levels than the participants in the other quartiles (Table 1). Similar distributions of sex, age, triglyceride, HDL-C, fasting glucose, and uric acid levels were found across various quartiles of urinary sodium excretion, and there was no difference in the lifestyle and socioeconomic status across the urinary sodium excretion quartiles.
The correlations between urinary sodium and other risk factors ranged from 0.011 for triglycerides to 0.099 for BMI, and those between urinary potassium and other risk factors were higher, ranging from 0.035 for systolic BP to 0.133 for BMI (Table 2). The urinary sodium excretion
Table 1 Distribution of various baseline demographic, lifestyle, and socioeconomic factors in the study population in the CCCC cohort, specified by urinary sodium excretion quartiles
Q1 Q2 Q3 Q4 P Sodium (mmol/24 h) <84 84–122 122–178 178 Median (mmol/24 h) 63 103 147 231 Number 380 380 380 380 Sex (%) 0.61 Men 50.0 47.9 48.7 45.3 Women 50.0 52.1 51.3 54.7 Current smoker (%) 36.1 36.1 35.0 33.7 0.89 Alcohol drinking (%) 32.6 30.3 29.7 25.0 0.13 Marital status (%) 0.52 Single 3.2 2.1 1.9 2.9
Living with spouse 87.9 89.5 92.3 90.0 Divorced or separated 9.0 8.4 5.8 7.1 Education level (%) 0.030 <9 years 92.9 94.5 96.3 91.3 9 years 7.1 5.5 3.7 8.7 Job status (%) 0.26 No job 47.9 43.2 46.3 42.9 Blue collar 34.5 39.7 36.3 34.5 White collar 17.6 17.1 17.4 22.6
Regular exercise habit (%) 14.0 15.3 14.0 14.2 0.95 Family history of CHD (%) 12.1 14.0 9.7 9.7 0.19 Diabetes (%) 10.6 9.8 10.3 15.1 0.08 Age (year) 51.5 12.0 52.9 11.9 52.4 11.4 51.3 10.6 0.18 BMI (kg/m2) 22.7 3.1 22.8 3.0 23.3 3.0 23.6 3.6 0.0001 Systolic BP (mmHg) 115.1 11.3 114.5 11.3 115.5 10.9 117.0 10.8 0.017 Diastolic BP (mmHg) 72.4 7.8 72.3 8.2 72.7 7.8 74.0 7.6 0.011 Cholesterol (mg/dl) 188.9 42.2 197.7 44.6 196.2 43.3 201.6 46.2 0.001 Triglyceride (mg/dl) 117.1 91.1 119.3 96.2 112.7 84.6 118.4 83.9 0.75 HDL-C (mg/dl) 47.2 12.2 48.9 12.3 48.6 12.1 48.6 12.9 0.26 LDL-C (mg/dl) 129.7 39.3 137.2 44.5 135.2 41.3 140.2 44.9 0.007 Fasting glucose (mg/dl) 107.3 25.3 106.9 26.6 108.9 34.1 111.1 29.3 0.19 Uric acid (mg/dl) 5.63 1.68 5.50 1.79 5.44 1.54 5.47 1.57 0.41 Urine sodium (mmol/24 h) 60 17 103 11 148 16 248 72 <0.0001 Urine sodium (g/24 h) 1.39 0.40 2.36 0.26 3.40 0.37 5.70 1.66 <0.0001 The values are mean SD. BP, blood pressure; CCCC, Chin-Shan Community Cardiovascular Cohort; CHD, coronary heart disease; HDL-C, high-density lipoprotein cholesterol; LDL, low-density lipoprotein cholesterol.
was significantly correlated with BP (0.067–0.075) and cholesterol (0.059–0.070), and the urinary potassium excretion was significantly correlated with glucose (0.108) and uric acid (0.084).
During a median 7.93 years of follow-up (interquartile range¼ 4.07–9.04 years) among 1520 participants with available urinary sodium excretion data, we documented 669 cases of incident hypertension. Except for the first quartile, the incidence rates of hypertension increased with increasing quartiles of urinary sodium excretion (Table 3). In age and sex-adjusted analyses, the RR comparing individuals in the fourth quartile with those in the second quartile of urinary sodium excretion was 1.48 [95% confidence interval (CI)¼ 1.19–1.83; P¼ 0.004], and the RR for individuals in the first quartile was 1.31 (95% CI¼ 1.05–1.64; P ¼ 0.018). The magni-tude of risk of hypertension remained significant even after controlling for BMI, lifestyle, socioeconomic status,
baseline diabetes status, and systolic BP; for individuals in the highest quartile, the multivariate RR was 1.26 (95% CI¼ 1.01–1.57; P ¼ 0.043) as compared with those in the second quartile. However, the risk for the participants in the first quartile became borderline significant (RR¼ 1.24; 95% CI ¼ 0.99–1.56; P ¼ 0.07). A significant J-shape relationship between urinary sodium excretion and the risk of hypertension was observed (Fig. 1), with the test for a linear relation being rejected (P¼ 0.046). In contrast, the incidence rates were similar across the quartiles for urinary potassium and sodium as compared with potassium ratio values, and the RRs were not significant (Table 2).
In joint analyses of BMI as well as systolic BP and urinary sodium excretion, participants with a higher BMI and systolic BP had a consistently higher risk than those with lower values, independent of quartiles of urinary sodium excretion (Fig. 2). The association between urinary
Table 2 Age-adjusted and sex-adjusted Spearman partial correlation coefficients between various measurements and urinary electrolyte excretion among the study participants in the CCCC Study cohort
BMI Systolic BP Diastolic BP Cholesterol Triglyceride HDL-C LDL-C Glucose Uric acid Urinary sodium 0.099MMM 0.067MM 0.075MMM 0.070MM 0.011 0.034 0.059M 0.052M 0.018 Urinary potassium 0.133MMM 0.035 0.052M 0.078MM 0.049 0.020 0.082MM 0.108MMM 0.084MMM
Urinary sodium : potassium ratio 0.018 0.022 0.026 0.012 0.021 0.055M
0.005 0.010 0.108MMM
BP, blood pressure; CCCC, Chin-Shan Community Cardiovascular Cohort; HDL-C, high-density lipoprotein cholesterol; LDL, low-density lipoprotein cholesterol.
M
P < 0.05.MM
P < 0.01.MMM
P < 0.001.
Table 3 Relative risks (and 95% confidence intervals) of hypertension incidence during a median 7.9 years of follow-up according to quartiles of urinary sodium and potassium excretion in the CCCC Study
Q1 Q3 Q4 Urinary sodiuma RR 95% CI P Q2 RR 95% CI P RR 95% CI P Model 1 1.31 1.05–1.64 0.018 1 1.16 0.92–1.44 0.21 1.48 1.19–1.83 0.0004 Model 2 1.32 1.05–1.65 0.016 1 1.10 0.88–1.37 0.42 1.41 1.14–1.76 0.002 Model 3 1.28 1.02–1.61 0.033 1 1.11 0.88–1.39 0.39 1.41 1.13–1.76 0.002 Model 4 1.24 0.99–1.56 0.07 1 1.11 0.89–1.39 0.37 1.26 1.01–1.57 0.043 Q2 Q3 Q4 Urinary potassiumb Q1 RR 95% CI P RR 95% CI P RR 95% CI P Model 1 1 1.16 0.93–1.44 0.19 1.10 0.88–1.37 0.40 1.17 0.94–1.46 0.16 Model 2 1 1.09 0.88–1.36 0.44 1.04 0.83–1.30 0.72 1.07 0.86–1.34 0.55 Model 3 1 1.10 0.88–1.37 0.40 1.06 0.85–1.33 0.60 1.09 0.87–1.37 0.44 Model 4 1 0.97 0.77–1.21 0.75 1.01 0.80–1.26 0.95 0.98 0.78–1.23 0.88 Q2 Q3 Q4 Sodium vs. potassiumc Q1 RR 95% CI P RR 95% CI P RR 95% CI P Model 1 1 0.96 0.77–1.19 0.71 1.01 0.81–1.26 0.92 1.07 0.87–1.33 0.52 Model 2 1 1.00 0.80–1.25 0.99 1.03 0.83–1.28 0.79 1.10 0.89–1.37 0.38 Model 3 1 0.99 0.79–1.23 0.90 1.04 0.83–1.30 0.72 1.10 0.89–1.37 0.38 Model 4 1 0.96 0.76–1.19 0.69 0.99 0.79–1.24 0.94 1.09 0.88–1.36 0.44 Incidence rates presented as per 1000 person-years. Model 1: adjusted for age groups (35–44, 45–54, 55–64, 65–74,75 years of age) and sex. Model 2: Model 1 and BMI (<18, 18–20.9, 21–22.9, 23–24.9, or25 kg/m2
). Model 3: Model 2 and smoking (yes/no or abstinence), current alcohol drinking (regular/no), marital status (single, married and living with spouse, or divorced and separated), education level (less than 9 years, at least 9 years), occupation (no work, labor, official or business), and regular exercise habit (yes/no). Model 4: Model 3 and baseline systolic blood pressure (continuous variable) and diabetes status (yes/no). CCCC, Chin-Shan Community Cardiovascular Cohort; CI, confidence interval; RR, relative risk.aQ1: cases: 165; person-years: 2432; rates (/1000): 67.8. Q2: cases: 144; person-years: 2558; rates
(/1000): 56.3. Q1: cases: 167; person-years: 2581; rates (/1000): 64.7. Q1: cases: 193; person-years: 2453; rates (/1000): 78.7.bQ1: cases: 151; person-years: 2455; rates (/1000): 61.5. Q2: cases: 177; person-years: 2498; rates (/1000): 70.9. Q3: cases: 169; person-years: 2585; rates (/1000): 65.4. Q4: cases: 172; person-years: 2487; rates (/1000): 69.2.cQ1: cases: 160; years: 2482; rates (/1000): 64.5. Q2: cases: 163; years: 2565; rates (/1000): 63.5. Q3: cases: 168;
sodium excretion and hypertension risk appears to be stronger among those with a higher systolic BP than those with a lower BP, and the interaction between urinary sodium excretion and BMI and BP was significant (both P-values for interaction <0.001). Participants who were in the highest quartile of urinary sodium excretion and higher baseline BP had a 2.43-fold increased risk of hypertension (95% CI¼ 1.72–3.22) compared with those in the lowest quartiles of urinary sodium excretion and lower BP.
Discussion
In the present prospective cohort study, 24-h urinary sodium excretion amounts were significantly associated with the risk of developing hypertension over a median of 7.9 years of follow-up. The J-shape relationship was independent of BMI, diabetes, physical activity, and other conventional risk factors and not explained by baseline BP levels. We did not find the urinary potassium excretion as a protective factor for hypertension risk. Intrapopulation and interpopulation studies on sodium intake and the risk of hypertension have proven that there
is a significant individual variation in daily sodium intake [23]. For example, the ecological Intersalt study showed that populations with a daily sodium intake of less than 1.3 g had low BP [3]. In contrast, a high-sodium diet was prevalent in both developed and developing countries. Among these Intersalt populations, northern Chinese have the highest sodium intake, up to 242 mmol/24 h, which is higher than median levels of the highest quartiles in our study population.
Increasing sodium intake is linked to arterial resistance, fluid intake and associated with platelet activation [23]. Excessive sodium also induces harmful effects, such as renal function impairment and aggravates the hyper-tension burdens [24]. Furthermore, increased sodium sen-sitivity is associated with less renin–angiotensin system activation and increased insulin resistance and therefore induces increased vasoconstriction and high BP [25]. A hypothesis of a threshold relationship between sodium intake and hypertension has been proposed [26]; individ-uals who ingest less than the amount for an increasing BP
Fig. 1 6.6 6.0 5.4 4.8 4.2 3.6 Adj u s te d re la ti ve r is k 3.0 2.4 1.8 1.2 0.6 0 80 160 240 320
Urinary sodium excretion (mmoI/24 h) 400 480 560 640 720 800
Relationship between urinary sodium excretion and risk of hypertension. The multivariate adjusted relative risk is plotted as a function of the baseline urinary sodium excretion value with the 95% confidence bands shown as the shaded areas.
Fig. 2 Q4 Q3 Q2 Q1 SBP < 116 mmHg SBP ≥ 116 mmHg 2.4 2.1 1.9 2.3 1.1 0.7 0.6 1.0 0 1 2 3 Relative risk Relative risk Q4 Q3 Q2 Q1 BMI < 22.7 BMI ≥ 22.7 1.6 1.4 1.4 1.7 1.2 1.0 0.7 1.0 0 1 2 3
Multivariate adjusted relative risk of hypertension incidence during a median 7.9 years of follow-up according to quartiles of urinary sodium excretion and BMI as well as blood pressure status. Cutoff points for the quartiles of urinary sodium excretion were less than 84 mmol, 84–122 mmol, 122–178 mmol and at least 178 mmol and cutoff points as the median values of BMI (22.7 kg/m2) and systolic blood pressure (116 mmHg). SBP, systolic blood pressure.
effect of sodium do not develop hypertension; the lower limit is probably near 50 mmol/day sodium, and taking more than 100 mmol/day is enough to induce hyperten-sion. However, our study supports that high urinary sodium excretion is related to hypertension risk. Further-more, we found a J-shape relationship between BP and hypertension incidence; sodium intake in the lowest quartile (63 mmol/day) had a higher risk of hypertension, and those in the highest quartile (231 mmol/day) had a much higher risk. The median sodium excretion value in the second quartile was similar to the recommended upper limit (100 mmol/day) [20], and the median value of the third quartile was almost identical to the average intake in the United States (150 mmol/day) [27].
Although there is overwhelming evidence supporting dietary sodium as a major cause of raised BP [23,28], the findings with respect to an extremely low sodium risk have been inconclusive. Extremely low salt intake has been associated with increased cardiovascular risk, especially in vulnerable populations such as the elderly [29], although moderate sodium reduction is recom-mended [23,30]. Severe sodium restriction has been associated with elevated plasma catecholamine levels, which increases neurohormonal stress, and is related to a higher cardiovascular risk [31]. Participants in the lowest quartile of sodium intake from the National Health and Nutrition Examination Survey (NHANES) were likely to have a higher myocardial infarction and cardiovascular mortality [32,33]. According to the NHANES data, participants in the lowest quartile of sodium intake were more likely to have a lower body weight and to smoke more [34]. Putative dangers in strict sodium reduction have been proposed: (i) extremely low salt intake induces less cardiovascular reserve and the inability to reconsti-tute losses in stressful conditions and (ii) the activation of renin–angiotensin and sympathetic activity would make susceptible individuals at a higher risk for vascular damage [29,30]. Our study also showed similar patterns and our findings supported the hypothesis that a very low sodium intake was associated with increased hyper-tension risk. Further studies are warranted to clarify the underlying mechanism.
The dietary guidelines for sodium restriction to 100 mmol/day are well supported [23,30] because the threshold of a daily 100 mmol sodium intake is supported from short-term intervention trial data [30]. In fact, a moderate sodium reduction to a level of 100 mmol/day is reasonably easy to achieve and feasible [23]. Clinical trial data in Dietary Approaches to Stop Hypertension (DASH)-salt trial demonstrated that sodium reduction could lower BP significantly [27]. The levels of sodium intake were approximately 150 mmol, 100 mmol, and 50 mmol per day in three strata, which induced step-wise BP significantly [27]. Overall, reducing sodium intake by 50 mmol per day decreased BP by an average of
4–6 mmHg [35,36], with great variation between individ-uals. The large-scale well controlled Trials of Hyperten-sion Prevention (TOHP-I) involving 2182 adults with diastolic BP from 80 to 89 mmHg for 18 months treatment on lifestyle interventions such as sodium restriction and weight reduction clearly demonstrated that a significantly substantial BP reduction was associated with decreased urinary sodium excretion [37]. Extended 10–15 years of observations on the 77% of the cohort participants found a 30% reduction in cardiovascular events among the inter-vention group [38]. Our study supports that the optimal daily sodium intake was around 100 mmol, consistent with the DASH-salt findings [27].
Our prospective study did not show the protective roles of urinary potassium excretion in the risk of hypertension incidence, although cross-sectional studies in various countries have shown an inverse relationship between dietary potassium and BP [39]. Our negative results resulted from urinary excretion as a poor surrogate for dietary potassium intake. In addition, our normotensive participants in the baseline may not be affected by a mildly increased potassium intake.
To our knowledge, this is the first extensive investigation of urinary sodium and potassium excretion and the risk of developing hypertension among ethnic Chinese. Because of the prospective cohort design, the baseline measure-ments of our cohort members were unlikely to be affected by disease status. Furthermore, the use of a community-based population could reduce the possibility of a selection bias. We also included important covariates including socioeconomic status, lifestyle factors, and clinical risk factors. Adjustment for these variables did not diminish the role of urinary sodium excretion in predicting hyper-tension incidence.
The study has several potential limitations. First, we only collected a single overnight urine sample, which may not be an adequate measurement of usual sodium intake. A single measurement of 24-h sodium excretion is a valid estimate of dietary sodium intake [13], and data from the overnight urine samples in the study were consistent with other population-based observational data. Furthermore, the participants did not change their dietary habits during the collection period so that the urine sample might be representative of a usual intake. Second, we did not validate the sodium intake through other methods such as a food frequency questionnaire and 24-h dietary recall methods. Furthermore, we did not estimate the processed foods with sodium intake and evaluate the different contents of foods. Methods for sodium intake from a 24-h dietary recall or a food frequency questionnaire are inaccurate measures of usual intake for the general popu-lation [40]. Accordingly, we used the secondary morning voiding urine amount as the surrogate for calculating 24-h urine sodium and potassium excretion [12]. We still did not
exclude measurement errors in quantifying the sodium intake. We believe the misclassification was undifferential and the true biological relationship between dietary sodium intake and BP may be more significant.
In summary, urinary sodium excretion is associated with the risk of hypertension among ethnic Chinese. Because of only a mild correlation between urinary sodium excretion and traditional vascular risk factors, urinary sodium excretion, as a marker of dietary sodium intake, can be useful for a comprehensive evaluation of hyper-tension risk in the Asian populations.
Acknowledgements
We thank the participants in the Chin-Shan community and the cardiologists at the National Taiwan University Hospital for their assistance in this study. This study was supported partly by grants from the National Science Council in Taiwan (NSC 96-2314-B-002-155) and Department of Health (DOH 96D047).
There are no conflicts of interest.
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