In the Dietary Approach to Stop Hypertension (DASH) trial, the DASH diet reduced blood pressure (BP) in a diverse sample of US adults. Subsequent analyses of this trial documented the efficacy of the DASH diet in several subgroups. Although subgroup analyses in individuals with metabolic syndrome (MS) have not been performed, the DASH diet has been recommended in MS patients. This paper is a subgroup analysis of the DASH trial, in which we examined the effect of study diets on BP in participants with and without MS. Participants were stratified according to MS status (99 with MS, 311 without MS (Non-MS)). The trial was a dietary intervention study in which participants were randomized to receive a control diet, a diet rich in fruits and vegetables, or the DASH diet. Outcomes were (i) the difference in BP between the end and the beginning of intervention and (ii) control of hypertension. We found no significant interaction between MS status and diet assignment on BP (each P-interaction >0.05). In the MS subgroup, the DASH diet compared with the control diet reduced systolic BP by 4.9 mm Hg (P=0.006) and diastolic BP by 1.9 mm Hg (P=0.15). In the Non-MS subgroup, corresponding net BP reductions were 5.2 mm Hg (P<0.001) and 2.9 mm Hg (P<0.001), respectively. The DASH diet controlled hypertension in 75% of hypertensive participants with MS (adjusted odds ratio=9.5 vs the control diet, P=0.05). In conclusion, the DASH diet similarly reduces BP in those with and without MS. Our findings provide direct evidence for existing recommendations.
Metabolic syndrome (MS) is a common health problem in the United States that afflicts approximately a quarter of US adults.1 Similar high rates of MS have been reported in many other countries.2 The MS cluster is defined by abdominal obesity, elevated triglycerides, low high-density lipoprotein (HDL)-cholesterol, elevated blood pressure (BP) and glucose intolerance.3 Physical inactivity and obesity are etiologically related to the development of MS, and insulin resistance is important in its pathogenesis.4 Concurrent with the rising obesity epidemic, the prevalence of MS has increased by 17% over the past decade.5
The MS cluster includes elevated BP. Those with MS have a twofold risk of developing hypertension (HTN).6 Moreover, the presence of HTN within the MS cluster carries higher risks than the presence of HTN without the MS cluster.7, 8 MS augments end-organ damage and doubles the risk of incident cardiovascular events in hypertensive patients.7, 8 Thus, lowering BP in MS patients should have substantial health benefits. However, currently available BP reduction therapies, specifically lifestyle modification and pharmacotherapy, have limitations. Although weight loss and increased physical activity target the causes of MS, achieving and maintaining weight loss is challenging. Furthermore, antihypertensive drug therapy may be less effective in patients with MS than in those without MS.9 Thus, additional approaches are needed to lower BP and treat HTN in MS patients. One such approach is improved diet quality.
The Dietary Approach to Stop Hypertension (DASH) trial was a randomized dietary intervention study that documented the benefits of modifying dietary patterns on BP in a diverse sample of US adults.10 The most effective dietary pattern, now termed the DASH diet, reduced BP significantly more than the other dietary patterns and is widely recommended.11 The DASH diet has also been recommended as a means to lower BP in those with MS.12, 13, 14, 15 However, this recommendation was based on overall trial results. The effects of the DASH diet in individuals with MS have not been reported from the DASH trial or any other dietary intervention study. We therefore performed a subgroup analysis of the DASH trial to examine the effects of the dietary patterns on BP in patients with and without MS.
Materials and methods
The methods have been described in detail elsewhere.16 A brief description follows.
Setting and design
At each of the four clinical centers, participants went through three phases: screening, run-in and intervention. During the screening phase, individuals ate their own diets. During the run-in phase (3 weeks), eligible individuals were fed the control diet, described below. During the intervention phase (8 weeks), participants ate one of three randomly assigned diets: the control diet, a fruits and vegetables (F&V) diet or a dietary pattern, now termed the DASH diet. Staff monitored weight and adjusted calorie intake so that weight remained constant.
The control diet was typical of what many Americans eat. Its carbohydrate, fat, protein and fiber intakes were close to the 50th percentile of American consumption, whereas its content of potassium, magnesium and calcium was close to the 25th percentile.17 The F&V diet was similar to the control diet except that it was rich in fruits and vegetables and reduced in carbohydrate-rich snacks and sweets; thus, it was rich in potassium, magnesium and fiber in comparison with the control diet. Similar to the F&V diet, the DASH diet was rich in fruits and vegetables. In contrast to the F&V diet, the DASH diet was rich in low-fat dairy products and reduced in saturated and total fat; thus, the DASH diet was rich in calcium and protein in comparison with the F&V diet. To control for the effects of body weight on BP, weight was held constant during the run-in and intervention periods by providing isocaloric diets. The sodium content of the three diets was similar.
Participants were at least 22 years old, and each had a mean diastolic BP (DBP) of 80–95 mm Hg and a mean systolic BP (SBP) of <160 mm Hg. Among those on antihypertensive drug therapy, medications were withdrawn over 21 days; thereafter, individuals were allowed to enter the screening phase if their BP was within the eligibility range. Participants remained off of antihypertensive medications until the end of the study. Exclusion criteria included poorly controlled diabetes mellitus, renal insufficiency, body mass index (BMI) >35 kg m−2 and serum total cholesterol >260 mg dl−1.
Classification of MS status
Adult Treatment Panel III (ATP III) defined MS as the presence of three or more of the following criteria:3 (1) abdominal obesity (waist circumference: men >102 cm; women > 88 cm); (2) triglycerides ⩾150 mg dl−1 (1.7 mmol l−1); (3) low HDL cholesterol (men <40 mg dl−1 (1.0 mmol l−1), women <50 mg dl−1 (1.3 mmol l−1)); (4) BP ⩾130/85 mm Hg; (5) and fasting blood glucose (FBG) ⩾110 mg dl−1 (6.1 mmol l−1). Because the DASH trial did not measure waist circumference, we instead used BMI, as has been done previously.18, 19 Those DASH participants with BMI >30 kg m−2 were considered to meet the criterion of abdominal obesity. This cutoff was chosen according to the World Health Organization’s definition of MS.20
FBG was not measured in 189 participants. As described below, we were able to assign MS status in the absence of FBG measurements in 141 persons. Ninety-nine participants met the criteria for MS because each of these participants had at least three components of the syndrome; of these 99 participants, 50 did not have FBG measurements. Another 231 participants had less than two components of the MS syndrome and were classified as without MS (Non-MS); 91 of these participants did not have an FBG measurement, which even if elevated would not have changed their status. Those with two components of MS and with subthreshold FBG (n=81) were also classified as without MS. Those with two components of MS but without FBG measurements (n=48) were classified as ‘uncertain’, because their FBG, had it been measured, would have determined whether they had had MS or not. These 48 individuals were not included in our analyses. This approach ensured correct classification of each participant included in our analysis (MS, n=99; Non-MS, n=312). See Supplementary Figure at the Journal of Human Hypertension’s website for a display of our approach.
Outcomes and measurements
The primary outcomes of this study were: (i) the change in BP (separately in those with and without MS) and (ii) HTN control (just among those who were hypertensive at baseline). Change in BP (ΔBP) was defined as the difference in BP between the end of intervention and baseline. The end-of-intervention BP was defined as the mean of five pairs of measurements during the last 2 weeks of the intervention phase. Baseline BP was defined as the mean of seven pairs of measurements (three pairs during screening visits and four pairs during run-in visits). Control of HTN was defined as a BP <140/90 mm Hg among those who previously had an SBP ⩾140 and/or a DBP ⩾90 mm Hg.11
Baseline characteristics were compared across intervention arms with one-way analysis of variance for continuous variables and with χ2 for categorical variables. Wilcoxon’s rank-sum test was used when analysis of variance assumptions were not met, and Fisher’s exact test was used instead of χ2 when expected frequencies were <5.21 Consistent with conventional approaches to subgroup analyses, we tested for an interaction between diet assignment and MS status and then reported effects within each subgroup.22 The difference in ΔBP between each pair of diets was tested by fitting a multiple linear regression model; ΔBP was the dependent variable, whereas diet and MS were independent variables. Analyses were also adjusted for clinical center. In a similar manner, HTN control was compared across diets by fitting a logistic regression model. To test for interaction between randomized diet and MS status, we included two interaction terms in each model, one term for interaction between DASH diet and MS and a second term for interaction between F&V diet and MS. STATA statistical package was used (StataCorp, 2005, Stata Statistical Software: Release 9; StataCorp LP, College Station, TX, USA).
Tables 1 and 2 display baseline characteristics, stratified by MS status. The MS subgroup differed from the Non-MS subgroup only in those characteristics that defined the syndrome (Tables 1 and 2). Baseline characteristics did not significantly differ across the three randomized arms within either the MS or Non-MS subgroups (Table 1). Participants with an uncertain MS classification status (n=48) did not differ in baseline characteristics from those with certain MS classification (data not shown).
Within-group BP change
Figure 1 displays mean BP at baseline and during each week of dietary intervention. The greater variability in mean BP by week in the MS compared with the Non-MS subgroup likely reflects the lower sample size in the MS subgroup compared with the Non-MS subgroup. As reported previously, BP changes tended to occur early, approximately 2 weeks after randomization. At the end of the trial, in the MS subgroup, the DASH diet reduced BP as compared with baseline (ΔSBP=−5.5 mm Hg; 95% confidence interval (CI), −8.3 to −2.8 mm Hg; ΔDBP=−2.0 mm Hg; 95% CI, −3.8 to −0.3 mm Hg), as did the F&V diet (ΔSBP =−4.4 mm Hg; 95% CI, −7.3 to −1.5 mm Hg; ΔDBP=−2.7 mm Hg; 95% CI, −5.0 to −0.4 mm Hg). Both diets reduced BP in the Non-MS subgroup as well (DASH, ΔSBP=−6.8 mm Hg (95% CI, −8.2 to −5.4 mm Hg) and ΔDBP=−4.0 mm Hg (95% CI, −5.0 to −2.9 mm Hg); F&V, ΔSBP=−4.1 mm Hg (95% CI, −5.6 to −2.6 mm Hg) and ΔDBP=−1.6 mm Hg (95% CI, −2.7 to −0.6 mm Hg)).
Between-group differences in BP change
Table 3 displays pairwise, between-diet comparisons, separately in the MS and Non-MS subgroups. Tests for interaction between the DASH diet and MS status were nonsignificant (SBP, P=0.91; DBP, P=0.48). In the MS subgroup, the DASH diet significantly reduced SBP by 4.9 mm Hg, net of BP change in the control diet (P=0.006). The corresponding difference for DBP was 1.9 mm Hg (P=0.15). In the Non-MS subgroup, corresponding net reductions in SBP and DBP were statistically significant (P<0.001 each). In the MS subgroup, the F&V diet reduced SBP by 3.8 mm Hg, net of BP change in the control diet (P=0.04), whereas the net reduction in DBP was 2.3 mm Hg (P=0.075).
The pattern of BP responses to the F&V diet in the Non-MS subgroup was similar to that of the MS subgroup and the whole sample. Tests for interaction between the F&V diet and MS status were nonsignificant (SBP, P=0.52; DBP, P=0.25). Still, in MS, the extent of mean BP reduction from the F&V and DASH diets appeared similar, and there was no significant difference between BP change in the DASH and F&V groups, for SBP and DBP.
Figure 2 displays HTN control rates by diet and by MS status among those individuals who were hypertensive at baseline. In general, there was a gradient across diets in both the MS and Non-MS subgroups. In the MS subgroup, the DASH diet was more effective than the control diet at controlling HTN (67% vs 17%, odds ratio (OR)=9.5, P=0.05). There were no significant differences between the F&V and control diet (41% vs 17%, OR=3.3, P=0.22). The pattern of diet effects in the Non-MS subgroup was similar to that of the MS subgroup (DASH vs control, 57% vs 15%, OR=7.7, P=0.001; F&V vs control, 29% vs 15%, OR=2.3, P=0.12). There were no significant interactions between diet and MS status on HTN control (each P-interaction >0.05).
In this subgroup analysis of the DASH trial, we documented that the DASH diet lowered BP in adults with MS and improved BP control in those MS patients with HTN. Furthermore, the effects of the DASH diet were similar in those with and without MS; each interaction test of diet and MS status was nonsignificant. These data provide empiric support for BP recommendations in patients with MS. Several authoritative bodies, including the American Heart Association, have already recommended the DASH diet for reducing BP in persons with MS.12, 13, 14, 15 However, these recommendations were based on overall results from the DASH trial, rather than an explicit subgroup analysis of patients with and without MS. Our analyses address this research gap.
Previous studies have suggested that the presence of MS might blunt the benefits of antihypertensive pharmacotherapy9 and lifestyle therapy.23 In a study of patients with MS and without MS, persons with MS required more medications to achieve BP control than persons without MS.9 In a trial of non-pharmacologic therapy, a multicomponent lifestyle intervention did not reduce BP in those with MS, whereas the intervention lowered BP in those without MS.23 It is reassuring that in our study we documented similar levels of BP reduction and HTN control in the MS and Non-MS subgroups.
The effects of the F&V diet on BP were intermediate between those of the control and the DASH diets. These findings reflect the design of the study, that is, the composition of F&V diet is intermediate between the control and the DASH diets; it had similar fat, protein and calcium content to that of the control diet and similar potassium, magnesium and fiber content to that of the DASH diet. The observed reduction in BP with the F&V diet is consistent with other trials.16, 24 However, one trial did not document BP reduction from increased F&V intake among those with MS, perhaps related to the high intake of F&V at baseline.25
Major strengths of our study were the type of study, namely, a controlled dietary intervention study with high adherence, as self-reported by participants and confirmed by biomarkers.10 Food was provided to all participants. An additional strength was the diverse sample, including both prehypertensive and hypertensive individuals and the large numbers of ethnic minorities. Limitations included the relatively small number of patients with MS, just 99 persons across the three randomized groups. Hence, the lack of statistical significance in certain subgroup analyses, for example, the nonsignificant difference in ΔDBP between the DASH and control groups (1.9 mm Hg, P=0.15) likely resulted from inadequate power. This explanation is supported by the fact that the DASH diet significantly reduced DBP in the Non-MS subgroup in the absence of interaction. Another limitation is the absence of fasting blood sugar in 189 participants. However, on the basis of the number and pattern of other components of MS, we are able to accurately classify MS status in 141 of these persons; only 48 persons had indeterminate MS status and were not included in our analyses. Finally, the DASH trial did not measure waist circumference. In place of waist circumference, we used BMI, as done in other studies.18, 19
Our study has clinical implications. The presence of MS challenges the management of HTN because treatment options are limited and therapy might be less efficacious. For example, the European Society of Hypertension suggests avoidance of diuretics and β-blockers in MS patients.26 The presence of MS appears to reduce the efficacy of antihypertensive drug therapy, creating the need for an additional drug, on average, to achieve BP control.9 In this context, the DASH diet provides an additional and effective option to achieve BP control in MS patients who are hypertensive. Specifically, we have shown that the DASH diet reduces BP in those with MS by 4.9/1.9 mm Hg, which is similar to what is achieved by adding one drug to a multidrug regimen in hypertensive patients with MS.9
The public health context is also important. It has been estimated that seven million patients with MS in the United States have uncontrolled HTN despite antihypertensive therapy.27 In such patients, the magnitude of BP reduction from the DASH diet is substantial and should reduce the risk of BP-related cardiovascular disease.28 Furthermore, the DASH diet can potentially control HTN in 75% of MS patients with Stage 1 HTN. This extent of BP control could potentially prevent 28% of coronary heart disease events in men with MS, and 12.5% of such events in women.29
In conclusion, although the American Heart Association and other authorities have recommended the DASH diet for reducing BP in individuals with MS, such recommendations were based on overall effects of the DASH diet, rather than an explicit subgroup analysis. Our study provides direct evidence that the DASH diet reduces BP and controls HTN in patients with MS, as well as patients without MS.
Ford ES, Giles WH, Dietz WH . Prevalence of the metabolic syndrome among US adults: findings from the third National Health and Nutrition Examination Survey. JAMA 2002; 287 (3): 356–359.
Cameron A, Shaw J, Zimmet P . The metabolic syndrome: prevalence in worldwide populations. Endocrinol Metab Clin N Am 2004; 33 (2): 351–375.
National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) final report. Circulation 2002; 106 (25): 3143–3421.
Reaven GM . Banting Lecture 1988. Role of insulin resistance in human disease. 1988. Nutrition 1997; 13 (1): 65 discussion 64, 66.
Mozumdar A, Liguori G . Persistent increase of prevalence of metabolic syndrome among U.S. adults: NHANES III to NHANES 1999-2006. Diabetes Care 2011; 34 (1): 216–219.
Cheung BM, Wat NM, Man YB, Tam S, Cheng CH, Leung GM et al. Relationship between the metabolic syndrome and the development of hypertension in the Hong Kong Cardiovascular Risk Factor Prevalence Study-2 (CRISPS2). Am J Hypertens 2008; 21 (1): 17–22.
Leoncini G, Ratto E, Viazzi F, Vaccaro V, Parodi D, Parodi A et al. Metabolic syndrome is associated with early signs of organ damage in nondiabetic, hypertensive patients. J Intern Med 2005; 257 (5): 454–460.
Schillaci G, Pirro M, Vaudo G, Gemelli F, Marchesi S, Porcellati C et al. Prognostic value of the metabolic syndrome in essential hypertension. J Am Coll Cardiol 2004; 43 (10): 1817–1822.
Rossi R, Nuzzo A, Origliani G, Modena MG . Metabolic syndrome affects cardiovascular risk profile and response to treatment in hypertensive postmenopausal women. Hypertension 2008; 52 (5): 865–872.
Appel LJ, Moore TJ, Obarzanek E, Vollmer WM, Svetkey LP, Sacks FM et al. A clinical trial of the effects of dietary patterns on blood pressure. DASH Collaborative Research Group. N Engl J Med 1997; 336 (16): 1117–1124.
Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL Jr et al. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension 2003; 42 (6): 1206–1252.
Grundy SM, Cleeman JI, Daniels SR, Donato KA, Eckel RH, Franklin BA et al. Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement. Circulation 2005; 112 (17): 2735–2752.
Whaley-Connell A, Palmer J, Sowers JR . Risk stratification and treatment options for patients with hypertension with metabolic syndrome and prediabetes. Adv Stud Med 2005; 5 (10C): S1011–S1018.
Ganne S, Arora SK, Dotsenko O, McFarlane SI, Whaley-Connell A . Hypertension in people with diabetes and the metabolic syndrome: pathophysiologic insights and therapeutic update. Curr Diab Rep 2007; 7 (3): 208–217.
Makaryus AN, Akhrass P, McFarlane SI . Treatment of hypertension in metabolic syndrome: implications of recent clinical trials. Curr Diab Rep 2009; 9 (3): 229–237.
Sacks FM, Obarzanek E, Windhauser MM, Svetkey LP, Vollmer WM, McCullough M et al. Rationale and design of the Dietary Approaches to Stop Hypertension trial (DASH): a multicenter controlled-feeding study of dietary patterns to lower blood pressure. Ann Epidemiol 1995; 5 (2): 108–118.
Carroll MD, Abraham S, Dresser CM . Dietary Intake Source Data: United States, 1976–80. Vital and Health Statistics, Series 11, Data from the National Health Survey 1983, 1–483.
Ridker PM, Buring JE, Cook NR, Rifai N . C-reactive protein, the metabolic syndrome, and risk of incident cardiovascular events: an 8-year follow-up of 14 719 initially healthy American women. Circulation 2003; 107 (3): 391–397.
Sattar N, Gaw A, Scherbakova O, Ford I, O’Reilly DS, Haffner SM et al. Metabolic syndrome with and without C-reactive protein as a predictor of coronary heart disease and diabetes in the West of Scotland Coronary Prevention Study. Circulation 2003; 108 (4): 414–419.
Alberti KG, Zimmet PZ . Definition, diagnosis and classification of diabetes mellitus and its complications. Part 1: diagnosis and classification of diabetes mellitus provisional report of a WHO consultation. Diabet Med 1998; 15 (7): 539–553.
Dawson B, Trapp RG . Basic & Clinical Biostatistics 4th edn. Lange Medical Books-McGraw-Hill, Medical Pub. Division: New York, NY, USA, 2004.
Geller NL . Advances in Clinical Trial Biostatistics. Marcel Dekker: New York, NY, USA, 2004.
Lien LF, Brown AJ, Ard JD, Loria C, Erlinger TP, Feldstein AC et al. Effects of PREMIER lifestyle modifications on participants with and without the metabolic syndrome. Hypertension 2007; 50 (4): 609–616.
Karlsen A, Svendsen M, Seljeflot I, Laake P, Duttaroy AK, Drevon CA et al. Kiwifruit decreases blood pressure and whole-blood platelet aggregation in male smokers. J Hum Hypertens 2013; 27 (2): 126–130.
Uusitupa M, Hermansen K, Savolainen MJ, Schwab U, Kolehmainen M, Brader L et al. Effects of an isocaloric healthy Nordic diet on insulin sensitivity, lipid profile and inflammation markers in metabolic syndrome? a randomized study (SYSDIET). J Intern Med 2013.
Redon J, Cifkova R, Laurent S, Nilsson P, Narkiewicz K, Erdine S et al. The metabolic syndrome in hypertension: European society of hypertension position statement. J Hypertens 2008; 26 (10): 1891–1900.
Wong ND, Lopez VA, L’Italien G, Chen R, Kline SE, Franklin SS . Inadequate control of hypertension in US adults with cardiovascular disease comorbidities in 2003–2004. Arch Intern Med 2007; 167 (22): 2431–2436.
Turnbull F, Neal B, Algert C, Chalmers J, Chapman N, Cutler J et al. Effects of different blood pressure-lowering regimens on major cardiovascular events in individuals with and without diabetes mellitus—results of prospectively designed overviews of randomized trials. Arch Intern Med 2005; 165 (12): 1410–1419.
Wong ND, Pio JR, Franklin SS, L’Italien GJ, Kamath TV, Williams GR . Preventing coronary events by optimal control of blood pressure and lipids in patients with the metabolic syndrome. Am J Cardiol 2003; 91 (12): 1421–1426.
This work was supported by a Fulbright Grant (15043737) from the Institute of International Education to Dr Fadi Hikmat. This work was also supported by the late Mr Hikmat A Bihnam. The DASH clinical trial was supported by Grants (HL50981, HL50968, HL50972, HL50977, HL50982, HL02642, RR02635 and RR00722) from the National Heart, Lung and Blood Institute, the Office of Research on Minority Health and the National Center for Research Resources of the National Institutes of Health. We are indebted to the trial participants for their sustained commitment to DASH, and to the following companies, which donated food: Best Foods, Campbell’s Soup Company, Coca-Cola Foods Company, Comstock Michigan Fruit, The Dannon Company, Dole Food Company, HJ Heinz Company, Harris Teeter Company, Hershey Foods Corporation, Lifelines Technology Inc., McCormick & Company Inc., Nabisco Foods Group, Ocean Spray Cranberries Inc., Procter & Gamble, Quaker Oats Company, Ralston Foods, Sunkist Growers, Vandenbergh Foods and Wawona Frozen Foods.
The authors declare no conflict of interest.
Supplementary Information accompanies this paper on the Journal of Human Hypertension website
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Hikmat, F., Appel, L. Effects of the DASH diet on blood pressure in patients with and without metabolic syndrome: results from the DASH trial. J Hum Hypertens 28, 170–175 (2014). https://doi.org/10.1038/jhh.2013.52
- metabolic syndrome
- blood pressure
- dietary intervention study
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