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Human Nutrition and Metabolism

Decreasing Dietary Sodium While Following a Self-Selected Potassium-Rich Diet Reduces Blood Pressure¹

Centre for Physical Activity and Nutrition Research, School of Health Sciences, Deakin University, Burwood Highway, Burwood, VIC 2125, Australia; ^* Department of Physiology, University of Melbourne, Parkville, VIC 3152, Australia

²To whom correspondence should be addressed. E-mail: nowson{at}deakin.edu.au.

	ABSTRACT

TOP ABSTRACT SUBJECTS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
Reducing dietary sodium reduces blood pressure (BP), a major risk factor for cardiovascular disease, but few studies have specifically examined the effect on BP of altering dietary sodium in the context of a high potassium diet. This randomized, crossover study compared BP values in volunteer subjects self-selecting food intake and consuming low levels of sodium (Na⁺; 50 mmol/d) with those consuming high levels of sodium (120 mmol/d), in the context of a diet rich in potassium (K⁺). Sodium supplementation (NaSp) produced the difference in Na⁺ intake. Subjects (n = 108; 64 women, 44 men; 16 on antihypertensive therapy) had a mean age of 47.0 ± 10.1 y. Subjects were given dietary advice to achieve a low sodium (LS) diet with high potassium intake (50 mmol Na⁺/d, >80 mmol K⁺/d) and were allocated to NaSp (120 mmol Na⁺/d) or placebo treatment for 4 wk before crossover. The LS diet decreased urinary Na⁺ from baseline, 138.7 ± 5.3 mmol/d to 57.8 ± 3.8 mmol/d (P < 0.001). The NaSp treatment returned urinary Na⁺ to baseline levels 142.4 ± 3.7 mmol/d. Urinary K⁺ increased from baseline, 78.6 ± 2.3 to 86.6 ± 2.1 mmol/d with the LS diet and to 87.1 ± 2.1 mmol/d with NaSp treatment (P < 0.001). The LS diet reduced home systolic blood pressure (SBP) by 2.5 ± 0.8 mm Hg (P = 0.004), compared with the NaSp treatment. Hence, reducing Na⁺ intake from 140 to 60 mmol/d significantly decreased home SBP in subjects dwelling in a community setting who consumed a self-selected K⁺-rich diet, and this dietary modification could assist in lowering blood pressure in the general population.

KEY WORDS: • home blood pressure • sodium • potassium • diet • community

There is a continuous graded relationship between blood pressure and cardiovascular disease, and strokes occur in a large number of people whose blood pressure levels are in the high normal range, outside the current classification criteria for hypertension (1). Therefore, lifestyle modifications that achieve even small reductions in blood pressure are likely to reduce rates of cardiovascular disease significantly. Large population studies have demonstrated a positive association between dietary sodium intake and blood pressure within a wide range of sodium intake, from <10 to >240 mmol/d (2,3). Intervention studies have demonstrated that reducing sodium intake decreases blood pressure (4,5), and this effect has been confirmed by metaanalysis of clinical trials in which sodium intake was altered (6). A few studies have assessed the effect of modestly reducing sodium intake, to a range of 50 to 90 mmol/d (7,8). The Dietary Approaches to Stop Hypertension (DASH)² sodium study (in which all food was provided) recently demonstrated that reducing sodium intake to a range of 67 to 107 mmol/d lowered blood pressure within the context of a diet rich in vegetables, fruits and low fat dairy products (9). A number of studies in different settings have found that vegetarian diets and diets high in potassium lower blood pressure, independent of dietary sodium intake (10–12).

The estimated dietary sodium intake of the Australian population, as derived from 24-h urine collection, is 120 mmol/d for women and 160 mmol/d for men (13,14). Fruit and vegetable intake of the Australian population tends to be higher than that of the U.S. population. For Australian adults, the average intake of fruit, a major source of dietary potassium, is 114 g/d (excluding fruit juice), and the average intake of vegetables is 286 g/d (15), whereas in the United States, estimated mean intakes of fruit and vegetables are 88 and 189 g/d, respectively (16). The effect of a modest change in sodium intake on blood pressure has been assessed in Australians with untreated mild hypertension (7,17). However, the effect of a modest reduction in sodium intake in conjunction with a high potassium diet on blood pressure in those with and without hypertension in a community setting is not known. This study aimed to specifically assess the effect of a moderately low sodium, high potassium diet on blood pressure, compared with sodium intake typical for the Australian population (14) and high potassium intake. This was achieved by maintaining a low sodium (50 mmol/d), high potassium dietary pattern for 8 wk and utilizing sodium supplementation for half of that time to produce a total dietary sodium intake of 120 mmol/d (i.e., a difference in dietary sodium intake of 70 mmol/d).

	SUBJECTS AND METHODS

TOP ABSTRACT SUBJECTS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
Subjects.

Subjects were recruited through the National Health and Medical Research Council Twin Registry. Twins were chosen to permit study of genetic and environmental effects; however, the fact that they were twins was not utilized for analysis of this crossover study. Adult twins (30+ years of age) listed with the registry and living in the Melbourne metropolitan area received an invitation letter. Twins and their family members were invited to participate in the study. Subjects currently undergoing treatment for cancer or renal disease and subjects requiring insulin treatment for diabetes were excluded after screening by telephone questionnaire. Subjects currently receiving medication for high blood pressure were defined as hypertensive. This study was approved by both the University of Melbourne and the Deakin University Human Research Ethics Committees.

Design.

The study was a randomized crossover trial in which subjects were instructed to follow a self-selected low sodium (Na⁺; 50 mmol/d), high potassium (K⁺; >80 mmol/d) diet (LS diet) for 8 wk. Subjects were randomized to ingest either placebo or slow-release Na⁺ tablets for 4 wk, then were crossed over to the alternative tablets for 4 wk. The chief investigator used a system of random numbers generated by Microsoft Excel (Microsoft, Redmond, WA) to randomize subjects within twin pairs and their family groups. Hence, all twin pairs and participants within a household underwent the same treatment at the same time, to eliminate possible detection of tablet allocation. Research personnel were unaware of the randomization status of subjects and tablet allocation.

During the 1- to 2-wk baseline period, subjects provided a 24-h urine collection, performed home blood pressure measurements and underwent a 24-h ambulatory blood pressure measurement (ABPM). After this baseline period, subjects were counseled on achieving the LS diet and were randomly allocated Na⁺ supplement (120 mmol/d) or placebo tablets for 4 wk. Blood pressure was measured by home blood pressure monitors for 3 consecutive days during the baseline period and in the first 3 wk of each 4-wk phase and then daily in the final week. The 24-h ABPM was recorded in the last week of the baseline period and at the end of each 4-wk phase. Investigators measured blood pressure with a mercury sphygmomanometer once during the baseline period (mean of 3 measurements) and once per week during the study period. Mean urinary electrolyte levels were assessed with three 24-h urine collections in each 4-wk phase, performed in weeks 2, 3 and 4, allowing assessment of compliance with dietary advice and tablet treatment. Plasma retin activity was measured with blood samples collected in the baseline period (after fasting 8 h) and in weeks 3 and 4 of each 4-wk phase (after fasting 4 h). Mean renin levels were calculated from the mean of the two measurements in each phase (weeks 3 and 4). All procedures were conducted in the subjects’ own homes.

Tablet supplementation.

Subjects were instructed to ingest 12 tablets per day (3 tablets, 4x/d) with food. The first 10 twin pairs and their family members (n = 28) ingested slow-release Na⁺ supplement tablets (10 mmol Na⁺/tablet) (Heinz Haupt, Berlin, Germany) or matched placebo tablets (lactose and cellulose) (Heinz Haupt). However, these tablets caused diarrhea in a significant number of subjects, so the remaining subjects ingested a different slow-release Na⁺ supplement (ex-Ciba brand; Novartis Pharmaceuticals, Surrey, UK) and a placebo matched in color and size (lactose, microcystalline cellulose and magnesium stearate; Institute of Drug Technology, Melbourne, Australia). The sodium supplementation (NaSp) level of 120 mmol/d was chosen to increase Na⁺ intake by 70 mmol/d, based on knowledge of previous compliance levels.

Body weight and blood pressure measurement.

Body weight was measured with a digital scale placed on a firm surface; subjects wore light clothing. A trained research assistant measured blood pressure with a mercury sphygmomanometer (model ALPK2; Stethoscope and Sphygmomanometer Specialists, Melbourne, Australia) while subjects were seated, after a 5 min rest. Three measurements were taken on the left arm; the mean of the last two measurements was used in analysis. Diastolic pressure was assessed by the disappearance of Korotokoff’s sounds (phase V). Home blood pressure was measured with an AND Model UA-767 automated blood pressure monitor (A&D, Tokyo, Japan) on the left arm, after 10 min rest in a quiet room. Three measurements were taken; the mean of the last two measurements was used for analysis. Subjects were taught to apply the cuff correctly and were instructed to measure blood pressure while alone at approximately the same time on each occasion. Subjects recorded three measurements, waiting 1 min between measurements. The 24-h ABPM was recorded at home with an AND Model TM2421 ambulatory monitor (A&D, Tokyo, Japan). Blood pressure measurements were taken every 30 min from 0600 to 2300, and every 60 min from 2300 to 0600. Blood pressure observations were classified as daytime or nighttime by self-reported sleeping and waking times. Standard sleeping and waking times (2300 and 0700, respectively) were used when subjects failed to report sleeping and waking times. Data were considered valid when at least 80% of blood pressure readings were made in each 24-h period.

Dietary advice.

Subjects received dietary advice designed to reduce Na⁺ intake to 50 mmol/d, increase dietary K⁺ and reverse the Na⁺:K⁺ ratio. Subjects received written and verbal instructions on choosing and preparing food to reduce Na⁺ intake to 50 to 70 mmol/d. Instructions were based on dietary education materials and recipes used in previous studies (7,17). Salt-free bread, salt-free margarine, salt-reduced stock powder and Na⁺-free baking powder were provided to facilitate dietary compliance. Subjects were also advised to replace high Na⁺ foods, including snack foods, with fruits, salad vegetables and unsalted nuts (all high K⁺ foods). However, subjects were not required to consume specific amounts of any foods.

Biochemical analysis.

The 24-h urinary Na⁺ and K⁺ concentrations were measured with ion-selective electrodes and creatinine was assessed by the Jaffe reaction, all using a Hitachi 704 analyzer (Hitachi, Tokyo, Japan) with Boehringer Mannheim electrodes and reagents (Boehringer Mannheim, Mannheim, Germany). Plasma renin activity (PRA) and concentration (PRC) were determined by RIA measurement of angiotensin 1, using an enzyme kinetic approach.

Statistical methods.

Descriptive statistics calculations and general linear modeling were performed using SPSS for Windows version 11.0 (SPSS, Chicago, IL). All blood pressure values were adjusted by regression through the origin, with robust SEM and adjusted P-values, to account for lack of independence within pairs, using STATA statistical software (Stata, College Station, TX, 1997). Values were expressed as means ± SD or means ± SEM. Differences in the effects of NaSp and the LS diet and between the baseline measures and the effects of the LS diet were analyzed using two-tailed paired t-tests; P = 0.05 was considered to be significant. Potential effects of the order of tablet treatment, antihypertensive therapy and gender were investigated by multivariate regression analysis, using STATA statistical software (Stata, College Station, TX, 1997). Investigators measured blood pressure in the last week of each dietary phase. The mean home blood pressure readings collected for three consecutive days during the baseline period and the mean blood pressure measurements for the final 7 d of each dietary phase were used in the analyses. Previous studies indicated that changes in blood pressure are evident after 2 wk with dietary alterations (7,9), and the primary analysis assessed blood pressure in week 4 of each dietary phase, ensuring that there was no carryover effect. Dietary compliance was assessed with the mean electrolyte excretion over each 4-wk dietary period.

	RESULTS

TOP ABSTRACT SUBJECTS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
Subjects.

Subjects (n = 128) commenced the study by completing a baseline measurement of blood pressure (home or 24-h ABPM) and a 24-h urine collection. Of these, 108 subjects completed the intervention study by providing blood pressure measurements (home or ABPM) in each of the two 4-wk phases. These consisted of 43 pairs of twins (none of which lived together), 17 of their live-in partners or family members and 1 individual twin (87 households total). Ten subjects dropped out because of gastrointestinal side effects attributed to the first batch of Na⁺ tablets, 2 subjects declined after being allocated tablets, and 8 dropped out because they were unable to comply with the demands of the study. The mean age of the 20 subjects (5 male, 15 female) who dropped out was 50.2 ± 13.7 y (mean ± SD), and 3 were undergoing antihypertensive therapy. No measured demographic characteristic of subjects differed between those who dropped out and those who completed the study.

Study characteristics.

Ninety-two normotensive subjects and 16 hypertensive subjects completed the study (Table 1). Hypertensive subjects did not change antihypertensive medication during the study. Compliance with treatment as assessed by tablet count was 70 ± 16.0% for placebo and 73 ± 15.2% for NaSp. Good adherence to sodium restriction was confirmed by a significant decrease in mean 24-h Na⁺ excretion in the LS diet phase, compared with the baseline phase (Fig. 1). Subjects whose Na⁺ excretion decreased <20 mmol/d (n = 5; 4 normotensive, 1 hypertensive) were included in the analysis. The NaSp treatment returned Na⁺ excretion to 141.6 ± 3.8 mmol/d, which was not different from the baseline value of 138.7 ± 5.3 mmol/d (Fig. 1). The NaSp treatment in conjunction with the LS diet produced an increment in urinary Na⁺ excretion of 89.4 ± 4.2 mmol/d, which was close to that predicted from the tablet compliance (i.e., 73% of 120 mmol NaSp = 88 mmol Na⁺/d). Urinary K⁺ excretion increased significantly, to 86.6 ± 2.1 and 87.1 ± 2.1 mmol/d for the LS diet and NaSp, respectively (P < 0.001), compared with the baseline level of 78.6 ± 2.3 mmol/d. Urinary creatinine excretion was constant in the three study phases, indicating similar urinary collections overall in each period (13.1 ± 0.3, 12.8 ± 0.3 and 12.8 ± 0.8 mmol/d, respectively). Home blood pressure (BP) measurements were lower than 24-h ABPM at every time point [e.g., baseline home BP was lower by 4.1 ± 1.2 (P = 0.001)/1.8 ± 0.8 (P = 0.031) mmHg]. At baseline, the correlations among the different methods of measurement for systolic blood pressure (SBP) were as follows (P < 0.01): home measurement versus ABPM, r = 0.73; home measurement versus investigator measurement, r = 0.76; ABPM versus investigator measurement, r = 0.67. The coefficient of variation for baseline SBP was 13% for investigator measurement, 12% for ABPM and 7% for home measurement.

View larger version (52K): [in this window] [in a new window]   FIGURE 1 Home-measured blood pressure readings and levels of urinary sodium and potassium excretion for all subjects during the baseline phase, low sodium diet phase, and sodium supplementation treatment phase. Values are means ± SEM; P-values: *P < 0.05, P < 0.01, P < 0.001 (paired t test). Study phases: baseline = baseline measurement phase; LS diet = low sodium, high potassium diet phase; NaSp = sodium supplementation phase. Phase comparisons: (a) baseline compared with LS diet (n = 88), (b) LS diet compared with NaSp (n = 106). Measurement data: (i) systolic blood pressure, (ii) diastolic blood pressure, (iii) urinary sodium, (iv) urinary potassium.

Effect of Na⁺ supplementation.

The effect of NaSp treatment was assessed by comparing the difference between LS diet and NaSp values. In the entire sample group, home-measured SBP was 2.5 ± 0.8 mmHg (P = 0.004) lower on the LS diet compared to the NaSp treatment and home-measured diastolic blood pressure was 1.1 ± 0.6 (P = 0.074) lower. In normotensive subjects, home-measured SBP was 2.3 ± 0.9 (P = 0.015) lower during the LS diet compared to NaSp treatment (Table 2).

Effect of changes in dietary Na⁺.

Comparison of the BP on the LS diet to baseline BP provided an indication of the effects of a low sodium, high potassium diet on blood pressure. The LS diet lowered all SBP and most DBP values, compared with baseline values. In the 87 subjects who completed home BP measurements during both the baseline and intervention periods, the LS diet lowered home-measured SBP by 3.3 ± 1.0 mmHg (P = 0.001), compared with baseline measurements. In the normotensive subjects, the LS diet lowered home-measured BP by 2.9 ± 1.0 (P = 0.006)/1.4 ± 0.7 (P = 0.041) mmHg, compared with baseline measurements. In the entire subject group, the LS diet lowered 24-h ABPM by 3.3 ± 0.9 (P = 0.0001)/1.9 ± 0.4 (P = 0.0001) mmHg, compared with baseline measurements. In the normotensive subjects, the LS diet again lowered 24-h ABPM significantly, by 3.0 ± 0.8 (P = 0.001)/1.6 ± 0.4 (P = 0.001) mmHg, compared with baseline measurements. The effect on investigator-measured BP was similar; the LS diet lowered values by 5.7 ± 1.5 (P = 0.001)/2.1 ± 0.9 (P = 0.02) mmHg, compared with baseline measurements. In the entire subject group, the LS diet decreased body weight by 1.2 ± 0.2 kg (P < 0.001), compared with baseline measurements.

In the entire subject group, NaSp treatment lowered 24-h ABPM by 2.9 ± 1.0 (P = 0.01)/1.4 ± 0.7 (P = 0.04) mmHg, compared with baseline measurements. Similarly, NaSp treatment lowered investigator-measured SBP by 5.5 ± 1.3 (P < 0.001) mmHg, compared with baseline measurements, although Na⁺ intake was similar in the treatment and baseline periods. Conversely, NaSp treatment did not affect home-measured BP, compared with baseline measurements [entire subject group, 1.2 ± 1.0 (P > 0.2)/0.6 ± 0.7 (P > 0.2) mmHg; normotensive subjects, 0.8 ± 1.1 (P > 0.4)/0.6 ± 0.7 (P > 0.4) mmHg)].

Effect of gender.

Multivariate regression analysis, adjusting for the correlation between twins, hypertensive therapy and gender, indicated a marginally significant interaction of gender and diet for home-measured DBP: the fall in DBP between the LS diet and NaSp treatment was greater in women (ß = 2.4 ± 1.3 mmHg; P = 0.063). A similar nonsignificant effect was also seen for home-measured SBP in women (ß = 2.1 ± 1.2 mmHg; P = 0.077). Baseline BP was significantly lower in women compared with men, with a difference in home-measured SBP/DBP of 11.2 ± 3.1 (P = 0.001)/3.9 ± 2.0 (P = 0.049) mmHg in the entire subject group and 9.1 ± 3.1(P = 0.005)/3.3 ± 2.1 (P = 0.121) mmHg in normotensive subjects.

	DISCUSSION

TOP ABSTRACT SUBJECTS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
This study confirmed the effect of dietary Na⁺ reduction in lowering blood pressure and specifically produced an important finding. In the context of a K⁺-rich diet, the low Na⁺ intake (LS) diet significantly lowered home-measured BP relative to the high Na⁺ phase (NaSp). Therefore, we confirmed that reducing dietary Na⁺ within the context of a diet high in K⁺ effectively reduced home-measured SBP by 2.5 mmHg in a group of subjects dwelling in a community setting and by 2.3 mmHg in a subgroup of normotensive subjects (not taking antihypertensive medication) within 4 wk.

A graduated reduction in blood pressure has been demonstrated with dietary Na⁺ reduction in large population studies [e.g., Intersalt (2)] and by a large metaanalysis of Na⁺ intervention studies (6,8). Our results are consistent with the reported range of BP–urinary Na⁺ relationships. A recent metaanalysis of modest Na⁺ restriction studies predicted a fall in BP of 3.6/1.7 mmHg in normotensive subjects and 7.1/3.9 mmHg in hypertensive subjects per 100-mmol/d reduction in Na⁺ intake (20). We found a significant difference on BP between the NaSp (sodium-supplemented, high potassium) and LS diet (low sodium, high potassium) phases: a reduction of 90 mmol Na⁺/d decreased home-measured SBP by 2.5 mmHg. This fall in blood pressure was demonstrated in a community group comprised of 85% normotensive subjects and 15% hypertensive subjects undergoing antihypertensive therapy.

It is likely that the increased dietary K⁺ intake with the LS diet assisted in lowering BP. Two recent metaanalyses of K⁺ supplementation studies (11,20) found that the pooled estimates for all trials showed that K⁺ significantly lowered blood pressure. Previous studies (12,21) have found that the effect of a low Na⁺ diet on BP is less with a high K⁺ intake. The DASH sodium study (9) clearly demonstrated that reducing Na⁺ intake from 141 to 64 mmol/d produced the greatest decreases in BP in subjects who were consuming a low K⁺ control diet (40 mmol K⁺/d), a change in dietary Na⁺:K⁺ ratio from 3.8 to 1.4. The cumulative reduction of 7 mmHg in clinical SBP contrasted with the 3-mmHg reduction measured in subjects consuming a high K⁺ diet (81 mmol K⁺/d), a change in Na⁺:K⁺ ratio from 1.5 to 0.7. The Na⁺:K⁺ ratio of the diet may therefore be an important predictor of blood pressure response, as indicated by previous studies (4,22). The urinary excretion of K⁺ at baseline in our study was 79 mmol/d, similar to the urinary excretion of 81 mmol K⁺/d in the DASH low Na⁺ diet. Importantly, our study achieved a significant difference in Na⁺ intake of 84 mmol/d between the low Na⁺ phase (58 mmol Na⁺/d) and the Na⁺ supplemented phase (142 mmol Na⁺/d), while subjects were consuming the same relatively high K ⁺ diet (86 mmol K⁺/d), resulting in significant decreases in blood pressure in this community-based population.

We detected no association between change in body weight and change in BP, although mean body weight did fall by 1.0 kg throughout the study. Consuming a low Na⁺ diet has been found to cause a reduction in body weight (17), perhaps because of a reduction in plasma volume and/or reduced energy intake (22), both of which lower BP.

We found that NaSp treatment had no effect on home-measured BP compared with baseline measures; conversely, both investigator-measured BP and 24-h ABPM decreased markedly over time, an effect that is not generally seen with ABPM. The decrease in SBP of 3 mmHg SBP from baseline measures apparently caused by the LS diet could be attributed to familiarization and/or regression to the mean, but the dietary intervention is very likely responsible for a component of this effect. This is confirmed by the fact that significantly lower BP measurements were recorded for subjects in the LS diet phase, compared with the NaSp treatment, in which regression to the mean and familiarization effects did not apply, because subjects ingested the Na⁺ supplement and placebo treatments in random order.

We measured BP by three different methods; home-measured BP correlated significantly with both investigator-measured BP and ABPM (r > 0.7). As expected, investigator-measured BP was higher than home-measured BP. Unexpectedly, however, investigator-measured BP was no higher than ABPM. This may be due to taking investigator-measured BP readings in the home (not in a clinical setting) and to recording both home- and investigator-measured BP readings mainly in the late afternoon or early evening, when BP levels tend to be low. The home-measured BP values represented multiple readings generally taken at the same time of day and under standard conditions. Subjects wrote down their home-measured BP readings themselves, but these records were checked fortnightly and there is no reason to suspect that this task was performed incorrectly.

The reduced variability of the home BP measurement method enabled detection of a 2.5-mmHg decrease in BP. Home BP measurement is now emerging as a preferred method of measuring BP (23), because it has been shown to share some of the advantages of ABPM; that is, it causes no white-coat effect (24), and home-measured BP values are more reproducible (25,26) and more predictive of the presence and progression of organ damage than are office- or clinic-measured values (27). The present study confirms that home BP measurement requires only a short period of familiarization and that measurements do not fall over time, supporting the usefulness of home BP monitoring in intervention studies.

Most studies of Na⁺–BP relationships have used subject groups comprised primarily of men. The majority of the subjects in this study were women. Although this study was not designed to assess differences in Na⁺ response by gender, there was some indication that despite the fact that women had lower baseline BP values than men, the LS diet caused greater decreases in home-measured DBP in women (which was of marginal significance), compared with NaSp treatment. There may be significant differences between the sexes with respect to the effect of Na⁺ intake on BP, with reports of greater responsiveness in women to changes in Na⁺ intake (28,29), and the evidently greater effect of the low Na⁺, high K⁺ DASH diet in lowering BP in women compared with men. One small study found that the effects of increased Na⁺ intake on BP were reflected in ABPM values in men but not women, but that there was an increase in clinic-measured BP values in women (30). The imbalance in gender ratio in the present study may account, to some extent, for the observed lack of effect on 24-h ABPM.

This study found that a decrease in dietary Na⁺ of 90 mmol/d, within the context of a high K⁺ diet, caused a significant 2.5-mmHg decrease in home-measured SBP in a group of adults dwelling in a community setting. The magnitude of the effect was comparable to that reported for the DASH low Na⁺ diet, which was similarly high in dietary K⁺. This decrease in SBP is clinically important in terms of shifting the population’s BP downward and potentially reducing stroke and coronary deaths by 6 and 4% in normotensive and hypertensive subjects, respectively (19). Accordingly, dietary Na⁺ reduction should be recommended to assist in reducing the BP of the general population.

The major dietary changes required to achieve the reduction in Na⁺ intake in this study were the use of salt-free bread and avoidance of high Na⁺ foods such as commercial canned and packaged foods, together with replacement of Na⁺-containing snacks with fresh and dried fruit. A previous study in free-living Australian subjects demonstrated a reduction in Na⁺ intake of 70 mmol/d and an increase of dietary K⁺ to 85 mmol/d using a similar dietary approach in a community setting for 12 wk (22). Therefore, a population-wide reduction in dietary Na⁺ intake, effected by reducing the Na⁺ content of staple food items (particularly bread), together with an increase in K⁺ intake (through increased fruit, vegetable and wholegrain cereal intake), is achievable and would contribute to the maintenance of optimal BP levels in the community. Reducing Na⁺ intake and increasing consumption of high K⁺ foods could assist in maintaining lower BP levels and reducing the burden of cardiovascular disease.

	ACKNOWLEDGMENTS

 
We would like to acknowledge the valuable contributions of Gayathri Parasivam and Kathryn Crossland, who were responsible for conducting subject measurements; Sandra Godfrey, who performed the biochemical analysis of samples; Stella O’Connell for her thorough editing of the manuscript; Associate Professor Damien Jolley for his statistical advice and Robert MacInnes for performing some of the statistical analysis. The Australian NHMRC Twin Registry assisted this research. We would also like to thank all the twins and their family members for their valuable contribution to this study.

	FOOTNOTES

 
¹ This work was supported by research grants from the National Health and Medical Research Committee and the Rebecca Cooper Foundation.

³ Abbreviations used: ABPM, ambulatory blood pressure measurement; BP, blood pressure; DASH, Dietary Approaches to Stop Hypertension; DBP, diastolic blood pressure; LS, low sodium, high potassium; NaSp, sodium supplementation; PRA, plasma renin activity; PRC, plasma renin concentration; SBP, systolic blood pressure.

Manuscript received 5 June 2003. Initial review completed 3 July 2003. Revision accepted 9 September 2003.

	LITERATURE CITED

TOP ABSTRACT SUBJECTS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 

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