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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.
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ABSTRACT |
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 TOP ABSTRACT SUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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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.
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SUBJECTS AND METHODS |
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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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.
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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 = 
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.
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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.
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RESULTS |
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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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).
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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).
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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).
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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).
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DISCUSSION |
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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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 (15–17). 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.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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2 Supported by the Dairy Research and Development Corporation.
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.
Manuscript received 7 April 2004. Initial review completed 28 April 2004. Revision accepted 25 June 2004.
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LITERATURE CITED |
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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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.
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.[Medline]
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.
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.
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.
8. Nowson, C. & Morgan, T. (1989) Effect of calcium carbonate on blood pressure in normotensive and hypertensive people. Hypertension 13:630-639.
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.
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.
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.
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.
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.
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.
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.
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]
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P < 0.001, 
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.
indicates the 95% CI. If