Journal of Nutrition OpenSOurce Diets- www.ResearchDiets.com

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Nowson, C. A.
Right arrow Articles by Godfrey, S. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nowson, C. A.
Right arrow Articles by Godfrey, S. J.
© 2004 The American Society for Nutritional Sciences J. Nutr. 134:2322-2329, September 2004


Human Nutrition and Metabolism

Blood Pressure Response to Dietary Modifications in Free-Living Individuals1,2

Caryl A. Nowson3, Anthony Worsley, Claire Margerison, Michelle K. Jorna, Amanda G. Frame, Susan J. Torres and Sandra J. Godfrey

Centre for Physical Activity and Nutrition, School of Health Sciences, Deakin University, Burwood, Australia

3To whom correspondence should be addressed. E-mail: nowson{at}deakin.edu.au.


    ABSTRACT
 TOP
 ABSTRACT
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 LITERATURE CITED
 
A diet rich in fruits, vegetables, and low-fat dairy foods has been shown to lower blood pressure (BP) when all foods are provided. We compared the effect on BP (measured at home) of 2 different self-selected diets: a low-sodium, high-potassium diet, rich in fruit and vegetables (LNAHK) and a high-calcium diet rich in low-fat dairy foods (HC) with a moderate-sodium, high-potassium, high-calcium DASH-type diet, high in fruits, vegetables and low-fat dairy foods (OD). Subjects were randomly allocated to 2 test diets for 4 wk, the OD and either LNAHK or HC diet, each preceded by a 2 wk control diet (CD). The changes in BP between the preceding CD period and the test diet period (LNAHK or HC) were compared with the change between the CD and the OD periods. Of the 56 men and 38 women that completed the OD period, 43 completed the LNAHK diet period and 48 the HC diet period. The mean age was 55.6 ± 9.9 (±SD) years. There was a fall in systolic pressure between and the CD and OD [–1.8 ± 0.5 mm Hg (P < 0.001)]. Compared with OD, systolic and diastolic BPs fell during the LNAHK diet period [–3.5 ± 1.0 (P < 0.001) and –1.9 ± 0.7 (P < 0.05) mmHg, respectively] and increased during the HC diet period [+3.1 ± 0.9 (P < 0.01) and +0.8 ± 0.6 (P = 0.15) mm Hg, respectively]. A self-selected low-sodium, high-potassium diet resulted in a greater fall in BP than a multifaceted OD, confirming the beneficial effect of dietary intervention on BP in a community setting.


KEY WORDS: • home blood pressure • dietary sodium • dietary potassium • dietary calcium • community setting

Evidence from multiple studies indicates that dietary sodium intake is positively associated with blood pressure (BP),4 (1,2) and that sodium reduction reduces BP (3,4). As a result, even small reductions in the mean dietary sodium intake of the population are predicted to significantly reduce the financial and social effect of cardiovascular disease (5). Increased dietary calcium was found in some studies (6,7) to reduce BP; however, many studies found no effect (8,9), and a meta-analysis revealed only a small effect (10). A comprehensive dietary approach (DASH: Dietary Approaches to Stop Hypertension) tested the efficacy of a diet high in fruit, vegetables and low-fat dairy products on BP in a large dietary intervention study with all food provided to participants (11). That study demonstrated large falls in systolic and diastolic BPs (11 and 5 mm Hg in hypertensives; 5 and 3 mm Hg in normotensives, respectively), much greater than previously seen in single dietary intervention strategies. Furthermore, in a subsequent study, the blood pressure–lowering effect of this multifaceted dietary approach was enhanced through a dietary sodium reduction (4). The feasibility and effectiveness of these types of dietary interventions in free-living individuals and in other countries is not known.

This study compared the effect on BP of a low-sodium, high-potassium diet (LNAHK) and a high-calcium diet (HC) to a DASH-type diet (OD) in community-dwelling subjects who, after dietary advice, selected and prepared their own foods.


    SUBJECTS AND METHODS
 TOP
 ABSTRACT
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 LITERATURE CITED
 
    Subjects. Subjects were recruited through newspaper articles advertising the study and BP measurement sessions provided in workplaces and shopping centers. Subjects were eligible if they were >25 y old and had a BP measured at the center by research staff (office BP) ≥ 120 mm Hg systolic blood pressure (SBP) or ≥ 80 mm Hg diastolic blood pressure (DBP) at their 2nd visit (mean of last 3 of 4 measurements, taken at 1-min intervals) or a BP measured at home (home BP) ≥ 116 mm Hg SBP or ≥ 78 mm Hg DBP (mean of 7 d). Partners of participants were eligible for entry into the study even if they did not satisfy these BP criteria because this was deemed to be helpful in maintaining dietary compliance. Subjects who were taking antihypertensive medication were included, provided they were willing to maintain their current medication level. Subjects were excluded if they had an office BP > 160 mm Hg SBP or > 90 mm Hg DBP, had a cardiovascular event in the past 6 mo, had insulin-dependent diabetes, were taking medications such as Warfarin or Dilantin, ate their main meal outside the home more than 2 times/wk, drank >30 standard (10 g alcohol) alcoholic drinks/wk, were planning to change smoking habits, or were unwilling to cease taking dietary supplements (including vitamins). All subjects provided written informed consent before starting the study, which was approved by the Deakin University Human Research Ethics Committee.

    Study design. This study utilized a crossover design, which minimized the interference of the time-dependent reduction in BP, by comparing BP during each test diet period with an immediately preceding control diet (CD) period. Our CD period was similar to the DASH control diet (low calcium, low potassium, and low magnesium) with a macronutrient profile and fiber content that corresponded to average Australian consumption and an electrolyte profile close to the 25th percentile of Australian intakes. Potassium and magnesium intakes in our CD period, however, were higher than the DASH study because Australians consume greater amounts of these nutrients (12). This was a randomized, crossover trial that compared the difference in BP between the CD period and 2 test diet periods to the difference in BP between the CD period and the OD period (Fig. 1). All subjects received two 4-wk dietary interventions (1 was the OD), each preceded by a 2-wk CD period. Subjects were randomly allocated to 1 of 4 groups, which determined the order of test diets followed (Fig. 1). Therefore, all subjects completed 2 CD periods, all followed the OD period, and approximately half followed the LNAHK diet period and half the HC diet period.



View larger version (16K):
[in this window]
[in a new window]
 
FIGURE 1 Study Design. The study was a randomized crossover design. Subjects were randomly allocated to 1 of 4 groups to determine the order of dietary intervention. Group 1: Diet 1, OD; Diet 2, LNAHK; Group 2: Diet 1, LNAHK; Diet 2, OD; Group 3: Diet 1, OD, Diet 2 HC diet; Group 4: Diet 1, HC diet; Diet 2, OD. Blood pressure was measured at home daily for each CD and the last 2 wk of each test diet period. The mean of two 24-h urine collections (during the last 3 wk) was used for each test diet period and 1 for each CD period. The mean of two 24-h dietary records for each 2-wk period was used for each test diet period and 1 for each CD period. Blood samples were taken from fasting subjects at the end of each control diet period and test diet period.

 
Randomization was performed by the chief investigator (C.N.) using a random number generator in blocks of 8 (Excel, Microsoft Corporation, 2000). Subjects who met the inclusion criteria commenced the study and completed a 1-wk run-in phase, measuring baseline home BP daily. If their home SBP or DBP, or that of their partner, was within the acceptable range, they commenced a 2-wk CD period and were then randomized into the study, with all partners allocated to the same dietary interventions.

Subjects attended the center (n = 65) or were visited every 2 wk by a researcher at their worksite (n = 29) for weight, office BP measurements (data not included), and dietary counseling. The main outcome was home BP, which was performed daily for the 2-wk CD period and for the last 2 wk of each test diet period. Subjects performed 24-h urine collections and 24-h dietary records every 2 wk. Blood samples were taken from fasting subjects (10 h overnight fast) at the end of each CD and test diet period.

    Diets. Dietary counseling was overseen by the coordinating dietitian (C.M.) and provided by trained research staff. Initial dietary counseling took between 10 and 30 min and was reinforced at every 2-wk contact. Participants were provided with printed materials explaining the diets in detail. The relative target nutrient differences of the diets are outlined in Table 1. The LNAHK diet was designed to be higher in potassium (and therefore higher in magnesium) with a greater reduction in sodium (compared with the OD), and the HC diet was designed to be higher in calcium. The CD was a low-potassium (and therefore low-magnesium), low-calcium diet, during which subjects were instructed to consume a maximum of the following daily: 1 serving dairy [1 serving = milk (200 mL), yogurt (200 g), or cheese (40 g)]; 1.5 servings fruit/fruit juice [1 serving = 1 medium piece of fruit (100 g) or fruit juice (200 mL)]; 3 servings vegetables [1 serving = 1/2 cup cooked vegetables (50 g)]; and to limit potatoes to 3 servings per week (1 serving = 90 g), tomatoes to 2 servings per week (1 serving = 100 g), and fish to 1 serving per week (1 serving = 120 g). Subjects were asked to maintain their usual intake of dietary fat and salt. The 3 diets tested in this study are described below.


View this table:
[in this window]
[in a new window]
 
TABLE 1 Summary of the nutrient basis of the dietary advice differences between the diets

 
    DASH-type diet (OD). This diet is based on the U.S. DASH study (11); it is rich in vegetables, fruits and low-fat dairy products, with increased fish, nuts and legumes and a moderate sodium restriction. Therefore, the diet would be high in potassium (also magnesium and fiber), lower in saturated fat, and lower in sodium. Subjects were advised to avoid butter, added table/cooking salt, and obviously salty foods and to use mono- or polyunsaturated margarine. Salt-reduced products were recommended (sodium ≤ 120 mg/100 g) and salt-reduced (50%) margarine was provided. The OD recommendations included ≥3 servings low-fat dairy (up to 2% fat) and ≥8 servings of fruit and vegetables daily (serving sizes as listed above), including at least 3–4 servings fruit, at least 4–5 servings vegetables. Subjects were instructed to include ≥3 servings fish, ≥ 1 serving (100 g cooked) legumes, and ≥4 servings (30 g) unsalted nuts and seeds weekly, and to limit red meat to ≤3 servings (100–120 g) weekly.

    Low-sodium, high-potassium diet (LNAHK). This diet differed from the OD recommendations in that it was lower in calcium and sodium. There were no specific dietary recommendations for dairy products, fish, red meat, or the use of polyunsaturated and monounsaturated fats. Salt-free bread and margarine were provided and subjects were advised to avoid added table/cooking salt and obviously salty foods. One additional serving of fruit/vegetables was recommend (compared with OD). Using the same serving sizes, the LNAHK diet recommendations included ≥4 servings fruit and ≥5 servings vegetables daily. Subjects were instructed to include ≥2 servings legumes and ≥4 servings unsalted nuts and seeds weekly.

    High-calcium diet (HC). This diet had only 1 specific dietary recommendation, i.e., to include ≥4 servings reduced-fat dairy products daily, with a maximum of 40 g/d of reduced fat cheese (up to 25% fat). No other dietary advice was provided.

During the CD period and all test diet periods, a maximum of 4 caffeine-containing drinks (e.g., cola drinks, coffee, and tea) and 2 standard (10 g alcohol) alcoholic drinks were permitted daily.

    Anthropometry and blood pressure measurement. Height was measured using a wall-mounted stadiometer. Body weight was measured at each visit on a digital scale with subjects wearing light clothing and no shoes. BP was measured at home on the left arm using an automated BP monitor (AND Model UA-767 or UA-767-PC, A&D). Subjects were trained to correctly apply the cuff and instructed to take their BP measurements alone at the same time of day, after 5 min rest in a quiet room, taking 3 measurements with a 1-min interval (mean of last 2 each day used for analysis). Those using Model UA-767 recorded their BP; for those using Model UA-767-PC, BP measurement data were downloaded directly to a computer at the center visit.

    Clinical biochemistry. Twenty-four hour urinary electrolytes and creatinine were assayed using a Hitachi 704 analyzer (electrodes and reagents supplied by Boehringer Mannheim GmbH). Serum total cholesterol, HDL cholesterol, and triglycerides were measured on the Hitachi 704 analyzer using enzymatic reagents (Boehringer, Mannheim). LDL cholesterol was calculated by the Friedewald equation (13).

    Dietary assessment. Subjects completed a 24-h dietary record on the day before their visit with study staff. Trained research personnel verified this record. Dietary information was entered into a dietary analysis program (Foodworks, Professional Edition, Version 3.02, Xyris Software) to calculate daily nutrient intakes. The mean of two 24-h dietary records (at the end of wk 2 and 4) was used in the analysis to assess nutrient intake during the test diet period; 1 record was used in each CD period.

    Statistical analysis. Data were analyzed using SPSS for WINDOWS (version 11.0) to calculate the descriptive statistics and perform regression analysis. Values are expressed as means ± SD or means ± SEM. SDs were used when describing the distribution of variables in tables. SEMs were used in tables and text when comparisons between groups were made, i.e., the main comparative analysis. The box plot represents median, 25th, and 75th percentiles (excluding outliers) for the difference between the control diet period and the OD period.

BP readings taken for the 2-wk CD period, and the final 2 wk of each dietary phase; the mean of two 24-h urine collections taken in the last 3 wk of the dietary intervention phase were used in the analysis. Previous studies indicated that changes in BP are evident after 2 wk of dietary alterations (3,11,14), and the analysis assessed BP in the final 2 wk of each dietary phase, ensuring that there was no carry-over effect.

The change in BP was assessed by subtracting the mean value during the test diet period from the mean value during the preceding CD period. The difference between the changes in BP between the OD period and the LNAHK diet period, and the OD period and the HC diet period were analyzed using 2-tailed paired t tests; differences with P = 0.05 were considered significant. Multivariate regression analysis was used to determine predictors of blood pressure change.


    RESULTS
 TOP
 ABSTRACT
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 LITERATURE CITED
 
People who responded to advertisements or participated in BP screening sessions (n = 348) were sent a screening questionnaire and invited to attend further screening. Of these, 118 met the screening criteria and were present for BP measurement at the center. There were 93 subjects who met the entry criteria for BP using either measurement and wished to participate. Four partners were also included who did not meet the BP criteria. Ninety-seven subjects commenced the study; 3 men dropped out before the completion of at least 1 test diet period (1 during the HC diet period, 2 during the LNAHK diet period) and their data were not included. A further 2 women and 1 man failed to complete the 2nd dietary intervention (1 during the HC diet period, 2 during the LNAHK diet period) and their data were included for the OD period only. Four cited inability to follow the diet and 2 cited illness as reasons for dropping out. Therefore, 94 subjects (81 subjects and 13 partners, 56 men, 38 women) completed the OD period, 43 completed the LNAHK diet period and 48 completed the HC diet period. Fifty subjects completed the OD period in the 1st 4-wk period and 44 in the 2nd 4 wk. Twenty subjects completed the LNAHK diet period in the 1st 4-wk period and 23 in the 2nd. Twenty-four subjects completed the HC diet period in the 1st 4 wk and 24 in the 2nd. Twenty-nine subjects manually recorded their home BP (self-reported); for 65 subjects, the home BP measurements were downloaded directly via computer.

Of the 94 subjects who completed at least 1 dietary phase, 42 were undergoing antihypertensive therapy. These included 22 subjects receiving single therapy: ß-blocker, n = 2; angiotensin-converting enzyme inhibitor (ACE), n = 3; angiotensin II receptor antagonist (AT1), n = 12; diuretic n = 1; and calcium channel blocker, n = 4. A further 4 were receiving combination therapy in combined tablet form (ACE + diuretic n = 3, AT1 + diuretic n = 1); 13 were receiving other dual drug combinations and 3 took a combination of 3 drugs.

The baseline characteristics of the subjects indicated that those taking antihypertensive therapy were older (+8.0 ± 1.8 y, P < 0.001) and had a higher BMI, (+1.8 ± 0.8 kg/m2, P = 0.024); however, there were no differences in baseline home BP or urinary electrolytes (Table 2). The baseline characteristics and distribution of antihypertensive medication did not differ among the diet groups (data not shown).


View this table:
[in this window]
[in a new window]
 
TABLE 2 Baseline characteristics of subjects indicating those taking antihypertensive medication1

 
    Differences between 1st and 2nd control diet periods. Comparing the 2 control diet periods, the only difference was that during the 2nd CD period, urinary potassium was 5.3 ± 2.4 mmol/d higher (P < 0.05) and home SBP was 1.3 ± 0.6 mm Hg lower (P < 0.05).

    Dietary intake. The energy intake was similar in all test diet periods (Table 3). However, compared with the CD period, there was a higher intake of energy (1.4 ± 0.2 MJ), percentage of energy from protein (1.4 ± 0.4), fiber (13.2 ± 1.0 g), potassium (61.9 ± 3.4 mmol), calcium (603.0 ± 42.4 mg), magnesium (189.9 ± 14.0 mg), and phosphorus (622.4 ± 54.6 mg) and a lower intake of percentage of energy from fat (2.9 ± 0.8), saturated fat (1.9 ± 6.3), and sodium (26.5 ± 4.9 mmol) during the OD period (all P < 0.001).


View this table:
[in this window]
[in a new window]
 
TABLE 3 Daily nutrient intakes during the 3 dietary intervention periods and the CD period1

 
Assessing the difference in the dietary changes between the test diets and the CD periods (test diet – CD), there was a greater increase during the LNAHK diet period in dietary fiber (+7 ± 3 g/d) and potassium (+21 ± 8 mmol/d) and a greater decrease during the LNAHK diet period in dietary sodium (–38 ± 11 mmol/d) and calcium (–287 ± 85 mg/d) compared with the OD period (all P < 0.05). There was a greater increase during the HC diet period in saturated fat (+7 ± 3 g/d), sodium (+49 ± 12 mmol/d) and calcium (+442 ± 77 mg/d) and a lesser increase during the HC diet period in fiber (–9 ± 3 g/d), potassium (–28 ± 5 mmol/d) and magnesium (–118 ± 24 mg/d) compared with the OD period difference (all P < 0.05) (Table 4).


View this table:
[in this window]
[in a new window]
 
TABLE 4 The difference in the changes in blood pressure measured at home, body weight, serum lipids, urinary electrolytes, and nutrient intakes between the LNAHK or HC diet periods compared with the OD period1

 
    Dietary compliance. Dietary compliance, assessed by urinary excretion, indicated that there was a 20% reduction in urinary sodium during the OD period (Table 5) and a 54% reduction during the LNAHK diet period compared with the CD period. There was a 26% increase in urinary potassium during the HC diet period compared with the CD period, which was approximately half that of the increase during the LNAHK diet period or the OD period. Urinary urea, however, increased by 23 ± 9 mmol/d (P < 0.01) during the OD period compared with the CD period, indicating an increase in dietary protein (Table 5).


View this table:
[in this window]
[in a new window]
 
TABLE 5 Blood pressure measured at home, body weight, serum lipids, and urinary electrolytes during the 3 dietary intervention periods and the CD period1

 
There was a decrease in urinary sodium during the LNAHK diet period compared with the OD period. There was a greater increase in urinary sodium, calcium, phosphorus, and urea and less of an increase in potassium during the HC diet period compared with the OD period (Table 4).

    Blood pressure. Between the test diets and the preceding CD period, there was a small but significant fall in SBP of 1.8 ± 0.5 mm Hg during the OD period (Fig. 2), and BP fell by 4.4 ± 0.8 /2.0 ± 0.6 mm Hg during the LNAHK diet period. There was no significant change, however, in BP during the HC diet period compared with the CD period. Compared with the OD period, there was a greater fall in SBP and DBP during the LNAHK diet period, and a rise in SBP during the HC diet period (Fig. 3) (Table 4).



View larger version (32K):
[in this window]
[in a new window]
 
FIGURE 2 Box plots of the differences in blood pressure measured at home, body weight, and urinary electrolytes between the OD period and the preceding CD period. Change in blood pressure, body weight, and urinary electrolytes and urea during the OD period (OD minus preceding CD). The box plot represents the 25th and 75th percentiles (ends of box). The box includes 50% of all values and the median (white line within box), and the ends of the errors bars include the entire distribution (excluding outliers). {ddagger}P < 0.001, {dagger}P < 0.01 compared with the preceding CD period. (a) SBP = systolic blood pressure; (b) DBP = diastolic blood pressure; (c) Wt = weight; (d) U Na+ = daily urinary sodium excretion; (e) U K+ = daily urinary potassium excretion; (f) U Ca++ = daily urinary calcium excretion; (g) U Mg++ = daily urinary magnesium excretion; (h) U P+++ = daily urinary phosphorus excretion; (i) U Ur = daily urinary urea excretion.

 


View larger version (32K):
[in this window]
[in a new window]
 
FIGURE 3 The difference in the changes in blood pressure measured at home, body weight, and urinary electrolytes between the LNAHK diet period or the HC diet period compared with the OD period. Changes in BP, body weight, and urinary electrolytes and urea during the LNAHK and the HC diet periods are compared with the changes during the OD period (mean and 95% CI). Zero lines denote OD, • indicates the mean value, {circ} indicates the 95% CI. If {circ} crosses the zero line, the value does not differ from the OD period; (a) SBP = systolic blood pressure; (b) DBP = diastolic blood pressure; (c) Wt = weight; (d) U Na+ = daily urinary sodium excretion; (e) U K+ = daily urinary potassium excretion; (f) U Ca++ = daily urinary calcium excretion; (g) U Mg++ = daily urinary magnesium excretion; (h) U P+++ = daily urinary phosphorus excretion; (i) U Ur = daily urinary urea excretion.

 
Multiple regression analysis indicated that a model that included preintervention home SBP [ß = 0.11(0.03) (SE)], preintervention home DBP [ß = –0.97(0.04)], and the difference in urinary sodium to potassium ratio [ß = 1.98(0.50)] together explained 40% of the variance (R2 = 0.40, P < 0.001) of the difference in home SBP between the OD period and the CD period. Urinary sodium and potassium excretion did not predict changes in BP with the other test diets.

    Body weight. There was no change in body weight during the OD period compared with the CD period (Fig. 2); however, during the LNAHK diet period, body weight decreased by 0.4 ± 0.2 kg (P < 0.05). There was no difference, however, between the change in body weight during the OD period and the change in body weight during the LNAHK diet period (Table 4). Body weight during the HC diet period increased by 0.9 ± 0.1 kg (P < 0.001) compared with the preceding CD period, and there was a greater increase in body weight during the HC diet period than in the OD period (Table 4).

    Serum lipids. Serum lipid concentrations did not change during the study except for HDL cholesterol, which increased more during the HC diet period than during the OD period (Table 4).


    DISCUSSION
 TOP
 ABSTRACT
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 LITERATURE CITED
 
This study investigated the effects of 3 dietary interventions in a "real world setting," using dietary recommendations based on numbers of servings of foods. Our OD was based on the DASH study (11) but with a moderate sodium reduction. The LNAHK diet was designed to be high in dietary potassium and low in sodium, and the HC diet had a simple "stand alone" dietary message to increase calcium-containing dairy foods. We found that SBP fell during both the OD and the LNAHK diet periods (compared with the CD period), but the change during the LNAHK diet period was greater and also produced a reduction in DBP. Although we demonstrated a fall of 2 mm Hg SBP during the OD period, this was considerably less than that reported for the DASH study. There are a number of reasons why our results might differ. First, our contrast in dietary intake was not as great as in the DASH study. Although there was a significant increase in the percentage of energy from protein, potassium, magnesium, fiber, and calcium, and a decrease in the percentage of energy from fat, percentage of energy from saturated fat, and sodium during the OD period (electrolyte and protein intakes confirmed by changes in urinary sodium, potassium, magnesium and urea), the magnitude of these changes was less than that in the DASH study, except for the change in sodium, which was greater in our study and calcium, which was similar. This is due in part to the higher potassium and magnesium content of our CD, which was representative of the 25th percentile of intakes of the Australian population, who eat more fruits and vegetables than the U.S. population. Perhaps the most notable dietary difference was in potassium intake. Urinary potassium excretion was 39 mmol/d (1531 mg/d) during the DASH study control diet and 67 mmol/d (2620 mg/d) during our CD period. It is possible that the size of a BP fall is related to the magnitude of the difference in dietary intake between the control and test diets, and we did not demonstrate such a large difference in dietary potassium (52% change vs. 91% in DASH). Magnesium also followed a similar pattern. Because the DASH sodium study demonstrated the effectiveness of sodium reduction within the context of a DASH-type diet (4), we also included a recommendation to choose salt-reduced products. Therefore, during the OD period, there was a 20% reduction in urinary sodium, which confirmed the results of the DASH sodium study that sodium reduction within in the context of this type of dietary pattern is effective in reducing blood pressure.

The dietary intakes assessed during the OD period, apart from a higher intake of cholesterol (265 mg/d) and potassium (130 mmol/d) and a lower sodium intake (92 mmol/d), were comparable to those in the DASH study. Many subjects experienced difficulty in consuming the amount of food recommended and were advised to focus on maintaining the fruit, vegetables, and other dietary requirements; this may explain why the percentage of energy from carbohydrate was slightly lower (51% compared with 55% in the DASH). During the OD and LNAHK diet periods, subjects received margarine as an incentive, and because no salt-free bread is available in supermarkets, during the LNAHK diet period, subjects also received bread. However, subjects were required to select and prepare their own foods following dietary advice; therefore, the level of dietary compliance in our study is representative of dietary changes that are achievable in a group of motivated individuals living in the community, provided that suitable foods are available for purchase.

The blood pressure of our study group was lower than that in the DASH study (4) because we did not include any untreated hypertensive subjects. The fact that 45% were receiving antihypertensive therapy could explain the reduced effectiveness of OD. We did include both men and women, whose mean BMI was similar to that seen in the DASH study (~29 kg/m2); the mean age of our subjects was 55 y compared with 44 y in the DASH study. We did not, however, include large numbers of subjects from ethnic groups. Our dietary intervention lasted 4 wk rather than 8 wk (as in the DASH study), and it is conceivable that a longer period of time may be required to detect BP effects of this type of diet. This does seem unlikely, however, because the full BP effect of the DASH diet was seen after only 2 wk, and we measured blood pressure after subjects had been following the diet for 2 wk, thus allowing for acclimation.

Although changes in the dietary intake of a number of electrolytes have been associated with effects on BP, the majority of the evidence relates to a reduction in sodium intake and an increase in potassium intake. A 30–40% reduction in dietary sodium intake has been found to reduce BP by 3–4 mm Hg SBP and 2 mm Hg DBP in hypertensive subjects, and 2 mm Hg SBP and 0.5 mm Hg DBP in normotensives (1517). Our dietary approach included not only a reduction in dietary sodium, but also a marked increase in dietary potassium. This combined approach appears to exert a greater BP-lowering effect than sodium restriction alone and has also been shown to be effective in normotensives (17,18). Our results confirm the increased effectiveness of a low-sodium, high-potassium diet over a DASH-type diet, and although there was a mean weight loss of 0.4 kg during the LNAHK diet period, this weight change did not differ from that during the OD period. Furthermore, weight loss was not related to blood pressure response. There was no change in serum lipids in this study. However, it may be that a longer period of dietary intervention is required to detect an effect on serum lipids.

BP did not change during the HC diet period (compared with the CD period), but was 3 mm Hg higher compared with the OD period. There was an increase in weight during the HC diet period (compared with both the CD and OD periods), indicating that dietary advice to increase 1 particular food group in isolation results in weight gain. This increase in weight (and the increase in saturated fat during the HC diet period) may have negated any blood pressure–lowering effect of calcium, although intervention studies demonstrate only minimal declines in BP with calcium (10). Although our dietary advice emphasized the use of reduced fat dairy products, many of these (particularly cheese) were not acceptable to the subjects. Dietary advice to increase low-fat dairy products should be provided in the context of other positive dietary changes, such as increasing fruit and vegetables, to prevent undesirable weight gain.

The declines in BP during the LNAHK diet period are somewhat greater than other studies, but some of the difference could be attributed to the different method of BP assessment. BP measured at home, at the same time of day, under the same conditions has less variability. Home BP measurement is now emerging as a preferred method of measuring BP (19) because it has been shown to share some of the advantages of ambulatory BP, that is, to have no white-coat effect (20), be more reproducible (21,22), and be more predictive of the presence and progression of organ damage than office/clinic values (23). Most of our subjects utilized BP monitors that had no possibility of subject error in recording because BP measurements were downloaded directly via study staff.

This study clearly showed that dietary education facilitated a healthier self-selection of foods and in turn improved BP levels and reduced cardiovascular disease risk. Choosing foods low in sodium together with foods high in potassium is likely to provide the most effective strategy in reducing BP. This study did not provide any evidence that other components of the DASH type diet (e.g., increased dietary calcium, reduced saturated fatty acids, and increased fish) provide additional benefits with respect to BP reduction. Other studies however, have indicated that a dietary pattern that incorporates reduced saturated fat, increased polyunsaturated and monounsaturated fats, increased fiber, and adequate calcium would be useful in reducing cardiovascular disease (24), cancer (25), and osteoporosis (26). From a public health perspective, most people are at risk of developing all of these diseases; thus, general dietary recommendations should address all of these. Accordingly, a lower-sodium diet, high in fruits, vegetables, and dietary fiber, which is low in saturated fatty acids and includes low-fat dairy products and more fish is a valid recommendation for good health.

The major dietary changes required to achieve the reduction in sodium intake in this study were the use of salt-free bread and the avoidance of high-sodium foods, together with replacement of sodium-containing snacks with fresh and dried fruit. Therefore, a population-wide reduction in dietary sodium, effected by reducing the sodium content of staple food items (particularly bread), together with an increase in potassium intake (through increased fruit, vegetable, and whole-grain cereal intake), would be achievable and would contribute to the maintenance of optimal blood pressures in the community.


    ACKNOWLEDGMENTS
 
We thank Prof. Damien Jolley for his advice regarding the design and statistical analysis of this study.


    FOOTNOTES
 
1 Presented at the annual meeting of the Nutrition Society of Australia, Dec. 2003 [Nowson, C., Worsley, T., Margerison, C., Jorna, M. K., Frame, A. G., Torres, S. & Godfrey, S. (2003) Dietary approaches to reduce blood pressure in a community setting: a randomized crossover study. Asia Pac. J. Clin. Nutr. 12 (suppl.): S19]. Back

2 Supported by the Dairy Research and Development Corporation. Back

4 Abbreviations used: ACE, angiotensin-converting enzyme inhibitor; AT1, angiotensin II receptor antagonist; BP, blood pressure; CD, control diet; DASH, Dietary Approaches to Stop Hypertension; DBP, diastolic blood pressure; HC, high-calcium diet; home BP, blood pressure measured at home by subject; LNAHK, low-sodium, high-potassium diet; OD, Dash-type diet; office BP, blood pressure taken at the center by research staff; SBP, systolic blood pressure; Wt, weight. Back

Manuscript received 7 April 2004. Initial review completed 28 April 2004. Revision accepted 25 June 2004.


    LITERATURE CITED
 TOP
 ABSTRACT
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 LITERATURE CITED
 

1. Elliott, P., Stamler, J., Nichols, R., Dyer, A. R., Stamler, R., Kesteloot, H. & Marmot, M. (1996) Intersalt revisited: further analyses of 24 hour sodium excretion and blood pressure within and across populations. Intersalt Cooperative Research Group. Br. Med. J. 312:1249-1253.[Abstract/Free Full Text]

2. Law, M. R., Frost, C. D. & Wald, N. J. (1991) By how much does dietary sodium salt reduction lower blood pressure? I. Analysis of observational data among populations. Br. Med. J. 302:811-815.[Abstract/Free Full Text]

3. Chalmers, J., Morgan, T., Doyle, A., Dickson, B., Hopper, J., Mathews, J., Matthews, G., Moulds, R., Myers, J. & Nowson, C. (1986) Australian National Health and Medical Research Council dietary salt study in mild hypertension. J. Hypertens. (suppl.) 4:S629-S637.

4. Sacks, F. M., Svetkey, L. P., Vollmer, W. M., Appel, L. J., Bray, G. A., Harsha, D., Obarzanek, E., Conlin, P. R., Miller, E. R., Simons-Morton, D. G., Karanja, N. & Lin, P. H. (2001) Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group. N. Engl. J. Med. 344:3-10.[Abstract/Free Full Text]

5. Selmer, R., Kristiansen, I., Haglerod, A., Graff-Iversen, S., Larsen, H., Meyer, H., Bonaa, K. & Thelle, D. (2000) Cost and health consequences of reducing the population intake of salt. J. Epidemiol. Community Health 54:697-702.[Abstract/Free Full Text]

6. McCarron, D. A. & Morris, C. D. (1985) Blood pressure response to oral calcium in persons with mild to moderate hypertension. A randomized, double-blind, placebo-controlled, crossover trial. Ann. Intern. Med. 103:825-831.[Medline]

7. Pfeifer, M., Begerow, B., Minne, H. W., Nachtigall, D. & Hansen, C. (2001) Effects of a short-term vitamin D(3) and calcium supplementation on blood pressure and parathyroid hormone levels in elderly women. J. Clin. Endocrinol. Metab. 86:1633-1637.[Abstract/Free Full Text]

8. Nowson, C. & Morgan, T. (1989) Effect of calcium carbonate on blood pressure in normotensive and hypertensive people. Hypertension 13:630-639.[Abstract/Free Full Text]

9. van Beresteyn, E. C., Schaafsma, G. & de Waard, H. (1986) Oral calcium and blood pressure: a controlled intervention trial. Am. J. Clin. Nutr. 44:883-888.[Abstract/Free Full Text]

10. Cappuccio, F. P., Elliott, P., Allender, P. S., Pryer, J., Follman, D. A. & Cutler, J. A. (1995) Epidemiologic association between dietary calcium intake and blood pressure: a meta-analysis of published data. Am. J. Epidemiol. 142:935-945.[Abstract/Free Full Text]

11. Appel, L. J., Moore, T. J., Obarzanek, E., Vollmer, W. M., Svetkey, L. P., Sacks, F. M., Bray, G. A., Vogt, T. M., Cutler, J. A., Windhauser, M. M., Lin, P. H. & Karanja, N. (1997) A clinical trial of the effects of dietary patterns on blood pressure. DASH Collaborative Research Group. N. Engl. J. Med. 336:1117-1124.[Abstract/Free Full Text]

12. Maclean, R. & Podger, A. (1999) National Nutrition Survey 1995—Foods Eaten. ABS Cat. No. 4804.0 1999 Australian Bureau of Statistics Canberra, Australia.

13. Friedewald, W. T., Levy, R. I. & Fredrickson, D. S. (1972) Estimation of the concentration of low density lipoprotein cholesterol in plasma without use of preparative ultracentrifuge. Clin. Chem. 18:499-502.[Abstract]

14. Australian National Health and Medical Research Council (1989) Dietary Salt Study. Fall in blood pressure with modest reduction in dietary salt intake in mild hypertension. Lancet i:399-402.

15. Cutler, J. A., Follmann, D. & Allender, P. S. (1997) Randomized trials of sodium reduction: an overview. Am. J. Clin. Nutr. 65(2 Suppl):643S-651S.[Abstract/Free Full Text]

16. He, F. J. & MacGregor, G. A. (2002) Effect of modest salt reduction on blood pressure: a meta-analysis of randomized trials. Implications for public health. J. Hum. Hypertens. 11:761-767.

17. Nowson, C., Morgan, T. & Gibbons, C. (2003) Decreasing dietary sodium while following a self-selected potassium-rich diet reduces blood pressure. J. Nutr. 133:4118-4123.[Abstract/Free Full Text]

18. Cappuccio, F. P. & MacGregor, G. A. (1991) Does potassium supplementation lower blood pressure? A meta-analysis of published trials. J. Hypertens. 5:465-473.

19. Guidelines Committee (2003) European Society of Hypertension-European Society of Cardiology guidelines for the management of arterial hypertension. J. Hypertens. 21:1011-1053.[Medline]

20. Mancia, G., Zanchetti, A., Agabiti-Rosei, E., Benemio, G., De Cesaris, R., Fogari, R., Pessina, A., Porchellati, C., Rappelli, A., Salvetti, A., Trimarco, B. & Pessino, A. (1997) Ambulatory blood pressure is superior to clinic blood pressure in predicting treatment-induced regression of left ventricular hypertrophy. SAMPLE Study Group. Study on Ambulatory Monitoring of Blood Pressure and Lisinopril Evaluation. Circulation 95:1464-1470.[Abstract/Free Full Text]

21. Sakuma, M., Imai, Y., Nagai, K., Watanabe, N., Sakuma, H., Minami, N. & Satoh, H. (1997) Reproducibility of home blood pressure measurements over a one-year period. Am. J. Hypertens. 10:798-803.[Medline]

22. Stergiou, G. S., Baibas, N. M., Gantzarou, A. P., Skeva, I. I., Kalkana, C. B., Roussias, L. G. & Mountokalakis, T. D. (2002) Reproducibility of home, ambulatory, and clinic blood pressure: implications for the design of trials for the assessment of antihypertensive drug efficacy. Am. J. Hypertens. 15:101-104.[Medline]

23. Mule, G., Caimi, G., Cottone, S., Nardi, E., Andronico, G., Piazza, G., Volpe, V., Federico, M. R. & Cerasola, G. (2002) Value of home blood pressures as predictor of target organ damage in mild arterial hypertension. J. Cardiovasc. Risk 9:123-129.[Medline]

24. Trichopoulou, A., Costacou, T., Bamia, C. & Trichopoulos, D. (2003) Adherence to a Mediterranean diet and survival in a Greek population. N. Engl. J. Med. 348:2599-2608.[Abstract/Free Full Text]

25. Key, T., Schatzkin, A., Willett, W. C., Allen, N. E., Spencer, E. A. & Travis, R. C. (2004) Diet, nutrition and the prevention of cancer. Public Health Nutr. 7:187-200.[Medline]

26. Prentice, A. (2004) Diet, nutrition and the prevention of osteoporosis. Public Health Nutr. 7:227-243.[Medline]




This article has been cited by other articles:


Home page
J. Am. Coll. Nutr.Home page
P. M. Kris-Etherton, J. A. Grieger, K. F. Hilpert, and S. G. West
Milk Products, Dietary Patterns and Blood Pressure Management
J. Am. Coll. Nutr., February 1, 2009; 28(Supplement_1): 103S - 119S.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Clin. Nutr.Home page
L. Dauchet, E. Kesse-Guyot, S. Czernichow, S. Bertrais, C. Estaquio, S. Peneau, A.-C. Vergnaud, S. Chat-Yung, K. Castetbon, V. Deschamps, et al.
Dietary patterns and blood pressure change over 5-y follow-up in the SU.VI.MAX cohort
Am. J. Clinical Nutrition, June 1, 2007; 85(6): 1650 - 1656.
[Abstract] [Full Text] [PDF]


Home page
J. Nutr.Home page
M. Raff, T. Tholstrup, K. Sejrsen, E. M. Straarup, and N. Wiinberg
Diets Rich in Conjugated Linoleic Acid and Vaccenic Acid Have No Effect on Blood Pressure and Isobaric Arterial Elasticity in Healthy Young Men
J. Nutr., April 1, 2006; 136(4): 992 - 997.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Clin. Nutr.Home page
C. A Nowson, A. Worsley, C. Margerison, M. K Jorna, S. J Godfrey, and A. Booth
Blood pressure change with weight loss is affected by diet type in men
Am. J. Clinical Nutrition, May 1, 2005; 81(5): 983 - 989.
[Abstract] [Full Text] [PDF]


This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Nowson, C. A.
Right arrow Articles by Godfrey, S. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nowson, C. A.
Right arrow Articles by Godfrey, S. J.


Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
Copyright © 2004 by American Society for Nutrition