Effects of the Dietary Approach to Stop Hypertension (DASH) diet on cardiovascular risk factors: a systematic review and meta-analysis.

Systematic Review with Meta-Analysis
Effects of the Dietary Approach to Stop Hypertension (DASH) diet on
cardiovascular risk factors: a systematic review and meta-analysis
Mario Siervo1*, Jose Lara1, Shakir Chowdhury1, Ammar Ashor1,2, Clio Oggioni1 and John C. Mathers1
1Human Nutrition Research Centre, Institute of Cellular Medicine, Newcastle University, Campus for Ageing and Vitality,
Newcastle upon Tyne NE4 5PL, UK
2College of Medicine, University of Al-Mustansiriyah, Baghdad, Iraq
(Submitted 15 April 2014 – Final revision received 30 August 2014 – Accepted 18 September 2014 – First published online 28 November 2014)
Abstract
The Dietary Approach to Stop Hypertension (DASH) is recommended to lower blood pressure (BP), but its effects on cardiometabolic
biomarkers are unclear. A systematic review and meta-analysis of randomised controlled trials (RCT) was conducted to determine the effects
of the DASH diet on cardiovascular risk factors. Medline, Embase and Scopus databases were searched from inception to December 2013.
Inclusion criteria were as follows: (1) DASH diet; (2) RCT; (3) risk factors including systolic and diastolic BP and glucose, HDL, LDL,
TAG and total cholesterol concentrations; (4) control group. Random-effects models were used to determine the pooled effect sizes.
Meta-regression analyses were carried out to examine the association between effect sizes, baseline values of the risk factors, BMI, age, quality
of trials, salt intake and study duration. A total of twenty articles reporting data for 1917 participants were included in the meta-analysis. The
duration of interventions ranged from 2 to 24 weeks. The DASH diet was found to result in significant decreases in systolic BP (25·2 mmHg,
95% CI 27·0, 23·4; P,0·001) and diastolic BP (22·6 mmHg, 95% CI 23·5, 21·7; P,0·001) and in the concentrations of total cholesterol
(20·20 mmol/l, 95% CI 20·31, 20·10; P,0·001) and LDL (20·10 mmol/l, 95% CI 20·20, 20·01; P¼0·03). Changes in both systolic and
diastolic BP were greater in participants with higher baseline BP or BMI. These changes predicted a reduction of approximately 13% in
the 10-year Framingham risk score for CVD. The DASH diet improved cardiovascular risk factors and appeared to have greater beneficial
effects in subjects with an increased cardiometabolic risk. The DASH diet is an effective nutritional strategy to prevent CVD.
Key words: Dietary Approach to Stop Hypertension diet: Meta-analyses: Hypertension: Dyslipidaemia: Diabetes:
Cardiovascular risk
CVD are the leading cause of mortality worldwide, accounting
for 30% of all global deaths(1). Haemodynamic (elevated
blood pressure (BP)) and metabolic (hyperlipidaemia and
hyperglycaemia) stressors are important cardiovascular risk
factors and linked to the onset and progression of
atherosclerosis(2). Models incorporating risk factors such as
age, smoking status, sex, diabetes, BP, and total cholesterol
and HDL-cholesterol concentrations have been developed for
predicting the risk of cardiovascular events and mortality(3,4).
Dietary and lifestyle interventions are important behavioural
strategies for cardiovascular risk reduction(5,6). The Dietary
Approach to Stop Hypertension (DASH) is a dietary pattern
that promotes the consumption of fruits, vegetables, and
low-fat dairy products; includes whole grains, poultry, fish,
and nuts; and attempts to reduce the intakes of red meat,
sweets, sugar-containing beverages, total fat, saturated fat and
cholesterol(7). Thus, the DASH dietary pattern promotes a
higher intake of protective nutrients such as K, Ca, Mg, fibre
and vegetable proteins and, at the same time, a lower intake of
refined carbohydrates and saturated fat. Furthermore, feeding
trials have demonstrated the additive effects of salt restriction
on the efficacy of the DASH dietary pattern in reducing BP.
The DASH diet is recommended by the American Heart
Association for the non-pharmacological management of
hypertension(8). Compared with a typical American diet, the
DASH diet has been found to significantly reduce systolic
and diastolic BP in hypertensive individuals(9). Importantly,
the beneficial effects of the DASH diet are not limited to BP
and some studies have reported significant improvements in
insulin sensitivity(10), inflammation(11), oxidative stress(12) and
* Corresponding author: Dr M. Siervo, email mario.siervo@ncl.ac.uk
Abbreviations: ADV, dietary advice; BP, blood pressure; CON, controlled feeding; DASH, Dietary Approach to Stop Hypertension; RCT, randomised
controlled trials.
British Journal of Nutrition (2015), 113, 1–15 doi:10.1017/S0007114514003341
q The Authors 2014
British Journal of Nutrition
Downloaded from https://www.cambridge.org/core. IP address: 51.9.206.53, on 08 May 2019 at 20:30:22, subject to the Cambridge Core terms of use, available at https://www.cambridge.org/core/terms. https://doi.org/10.1017/S0007114514003341
recognised cardiovascular risk factors including concentrations
of fasting glucose(13) and total cholesterol(14). However,
other studies have observed non-significant effects of the
DASH diet on BP(15 – 17), fasting glucose concentrations(18,19)
and total cholesterol concentrations(18 – 20).
We systematically reviewed the evidence from randomised
controlled trials (RCT) investigating the effects of the DASH
diet on BP (systolic and diastolic) and on the concentrations
of glucose and lipids (total cholesterol, HDL, LDL and TAG)
in human subjects. We also investigated whether the effects
of the DASH diet on each cardiovascular risk factor were
modified by methodological (trial design, duration and type
of control diet, and dietary Na intake) and phenotypic (systolic
and diastolic BP, plasma concentrations of metabolic biomarkers
and BMI) characteristics. In addition, we examined
the effects of the DASH diet on the 10-year risk for CVD,
CHD, myocardial infarction and stroke estimated using the
Framingham risk equations(3).
Methods
The systematic review was conducted, and it details are
reported, according to Preferred Reporting Items for Systematic
Reviews and Meta-Analyses (PRISMA) guidelines(21). The protocol
was registered in the Prospective Register of Systematic
Reviews database (registration no. CRD4201007296).
Types of studies
RCT carried out in human subjects were included in the metaanalysis
and the specific characteristics and the effects of trial
design (including dietary intervention used for the control
group, delivery of the nutritional interventions, parallel or
cross-over design, run-in period, blinding of the measurement
protocols, duration, compliance, randomisation procedure,
and use of intention-to-treat analysis) were assessed.
Participants
Publications reporting trials carried out in adult male and
female participants (age .18 years) with or without comorbidities
(hypertension, diabetes, the metabolic syndrome
or gestational diabetes) were included. There were no restrictions
with respect to participants’ BMI or ethnic background.
Types of interventions
RCT investigating the effects of the DASH diet on cardiovascular
risk factors and providing information on the energy and
macronutrient contents of both DASH and control interventions
were included in the meta-analysis. The minimum
duration of the RCT for inclusion in the meta-analysis was
2 weeks. An important inclusion criterion was that the DASH
and control diet interventions had to be comparable in
terms of energy intake and other lifestyle interventions, e.g.
physical activity. In other words, RCT were included only if
both control and DASH diet interventions involved a similar
degree of energy restriction and/or physical activity to avoid
the confounding effects of changes in body weight on cardiovascular
risk factors. In addition, RCT were included if
they altered minor components of the DASH interventions
(e.g. modified DASH), but retained the core characteristics
of the archetypical DASH dietary plan(7). Examples of DASH
dietary plan modifications include reduction of salt intake,
increased consumption of lean red meat, and combination
with other interventions such as weight loss or physical
activity. Similarly, RCT having either a typical dietary pattern
or a healthier dietary pattern (healthy diet) as a control were
included, provided that these patterns matched the DASH
intervention in terms of both energy intake and physical
activity level. Finally, RCT were not excluded according to
dietary Na intake, as information regarding this variable was
not consistently reported across trials; this approach was
intended to minimise the risk of publication bias.
Outcome measures
The primary outcomes of the analyses were changes in cardiovascular
risk factors including systolic and diastolic BP and concentrations
of total cholesterol, glucose, TAG, HDL and LDL.
Search strategy and selection of studies
A literature search of the Medline, Embase and Scopus databases
was undertaken from inception to December 2013.
The systematic review was restricted to articles published in
English. The search was conducted based on predefined
search terms (DASH, BP, glucose, diabetes, lipids, cholesterol,
metabolic syndrome, insulin resistance, homeostatic model of
assessment (HOMA), lipoproteins, HDL and LDL) and using
specific building blocks (Boolean terms and truncation) to
create algorithms entered into each database. Articles were
assessed for eligibility independently by two investigators
(M. S. and S. C.). Complete details of the algorithms and selection
process are reported in the online supplementary Box S1.
Data extraction and bias measurement
Data extraction was performed independently by two investigators,
and a list of the extracted variables is provided in
the online supplementary Box S2. Attempts were made to
contact the corresponding authors if data were incomplete. The
quality of the RCT was assessed using a modified Jadad score
against the following criteria: blinding; randomisation procedure;
adherence to the interventions(22). As blinding to the dietary
interventions was not possible, blinding of the research staff to
the measurement protocols contributed to the overall quality
score. Scores ranged from 0 (low quality) to 5 (high quality).
Measurement of the treatment effect
The meta-analysis was based on the absolute differences
between the DASH and control intervention groups. Baseline
and end-of-study mean, standard deviation and sample size
for each outcome variable were extracted for each treatment
group. Where appropriate, baseline–end-of-study mean
2 M. Siervo et al.
British Journal of Nutrition
Downloaded from https://www.cambridge.org/core. IP address: 51.9.206.53, on 08 May 2019 at 20:30:22, subject to the Cambridge Core terms of use, available at https://www.cambridge.org/core/terms. https://doi.org/10.1017/S0007114514003341
differences, standard deviation values and sample size were
used. For cross-over studies, the effect size was calculated as
the difference between the DASH and control groups at the
end of each intervention. Results presented as medians and
interquartile ranges (25th–75th percentiles) were transformed
into means and standard deviations using the method
proposed by Hozo et al.(23).
Statistical analysis
A meta-analysis was conducted using the Comprehensive
Meta-Analysis 2 software (Biostat). Data are presented as mean
differences (in mmHg for BP and in mmol/l for the
remaining metabolic risk factors) and 95% CI. The differences
were combined across trials using a random-effects model. The
paired nature of the cross-over trials was taken into account in
the meta-analysis to minimise unit-of-analysis errors and underestimation
of the effect size(24). Forest plots were generated for
graphical presentations of the cardiovascular risk factors.
Statistical heterogeneity across the trials was assessed using the
I 2 andQ tests according to specific categories (low,25 %, moderate
25–75%, or high .75 %) and significance level (P,0·10),
respectively(25). Funnel plots and Egger’s regression test were
used to evaluate publication bias. Additional analyses were
conducted to evaluate the impact of potential confounding
factors. Sensitivity analyses were conducted to evaluate whether
changes in cardiovascular risk factors were influenced by study
design (parallel or cross-over), type of control diet (typical diet
or healthy diet) and delivery of nutritional interventions
(controlled feeding (CON) study or provision of dietary advice
(ADV)). Results obtained in individual trials were retrieved
from the majority of the articles. However, for some cardiovascular
risk factors (i.e. glucose, HDL, total cholesterol, LDL
and TAG), results were obtained but not reported in the
articles(16,26,27); in such cases, attempts were made to obtain the
required data. Where such attempts failed, RCT were included
in the primary meta-analysis by entering into the model a null
effect size and the pooled standard error for each of these studies.
A sensitivity analysis was conducted to evaluate the influence of
these assumptions on the overall estimates by excluding studies
with missing information from the models. In addition, results
obtained for glucose and TAG in the Lifestyle Interventions for
Blood Pressure Control (PREMIER) study(26) were reported as
geometric mean and 95% CI. The effect of the DASH diet on
these two risk factors was not significant, and therefore a null
effect and a pooled standard error were entered into the final
model. The results of the PREMIER trial (total cholesterol, LDL
and HDL)(26) and the DASH-Na trial (all risk factors)(28,29) were
stratified by metabolic syndrome diagnosis and dietary Na
intake (low, medium or high), respectively, and average values
were calculated and entered into the final model. Metaregression
analyses were conducted to evaluate whether
changes in the cardiovascular risk factors were influenced by
baseline concentrations of outcome variables, study duration
(in weeks), sample size, age, BMI, Jadad score and difference
in dietary Na intake (mg/d) between the DASH and control
intervention groups. A summary of the differences in dietary
Na intake for each trial is given in Table S1 (available online).
A mixed-effects meta-regression model (unrestricted maximum
likelihood) was used.
Estimated 10-year risk scores for CVD, CHD, myocardial
infarction and stroke were calculated using the Framingham
CVD risk equation(3) incorporating the following: age and
pre- and post-intervention mean values for systolic BP and
total cholesterol and HDL concentrations. Risk scores were
calculated for a non-diabetic population and stratified by sex
and smoking status.
Results
Main search
A total of 5395 articles were identified during the primary
search and, after the removal of duplicates (n 4562), 833
articles were screened based on titles and abstracts. After
screening, sixty-five articles were selected for a full-text
review and twenty articles(9,13 – 20,26 – 36) were selected for
inclusion in the systematic review. Results for independent
groups (men, women; lean, obese) were reported by three
trials(13,19,31), and results obtained for these groups were
analysed separately in the meta-analysis. A flowchart depicting
the different stages leading to the selection of trials included in
the meta-analysis is shown in Fig. 1. Among the trials included
in the meta-analysis, four had a cross-over study
design(16,19,31,34) and thirteen had a parallel-group
design(9,13,15,17,28,30,32,33,35,36). The trials were conducted
between 1997 and 2013 and included a total of 1917 participants
(range: 19–537 participants per study). The duration
of the interventions ranged from 2(36) to 24 weeks(13,18). The
majority of the trials were conducted in the USA (nine
trials)(9,13,18,19,30 – 33,36), four in Australia(16,17,27,35) and three
in Iran(13,15,34). The main characteristics of the trials are
given in Table 1.
Participant characteristics
Otherwise healthy individuals with above-optimal BP and
stage 1 hypertension were recruited in the majority of the
studies. Individuals with the metabolic syndrome were
recruited in three trials(13,19,31) and those with type 2 diabetes
in one trial(34), and one study was conducted in women with
gestational diabetes(15). The baseline average age of participants
recruited in each trial ranged from 31 to 60 years.
Most trials had an approximately equal sex distribution, but
two trials recruited only men(17) or women(15). The mean
BMI of the participants ranged from 23 to 37 kg/m2 in individual
studies(31,36); BMI was not reported in one study(34).
Changes in body weight during the trial were not reported
in one study(15); five trials either reported adjustment of
energy intake to meet energy requirements or mentioned
maintenance of body weight during the trial(16,28,30,31,36).
Nutritional interventions
The DASH diet as originally described in the first DASH trials was
prescribed without modification in ten trials(9,15,16,19,30 – 34,36)
Dietary patterns and cardiovascular risk 3
British Journal of Nutrition
Downloaded from https://www.cambridge.org/core. IP address: 51.9.206.53, on 08 May 2019 at 20:30:22, subject to the Cambridge Core terms of use, available at https://www.cambridge.org/core/terms. https://doi.org/10.1017/S0007114514003341
and five trials modified the DASH dietary plan by incorporating
additional components such as dietary energy restriction or
physical exercise(13,17,18,27,35). These protocol variations
resulted in between-study differences in the magnitude of
weight change. The greatest weight loss was observed in a
24-week trial combining the DASH diet with dietary energy
restriction to investigate effects on BP and metabolic risk factors
(control group was only energy restricted); both groups
exhibited similar levels of body weight loss (approximately
14 kg)(13). Similarly, the inclusion of an exercise intervention
in both groups within a study did not induce differential changes
in body weight(35). However, the majority of the trials aimed
at maintaining stable weight and reported weight changes
,1·5 kg during the intervention period.
Dietary counselling was employed to deliver the nutritional
interventions in several trials(13,15–19,27,31–35). In such cases,
a nutritionist/dietitian regularly met with the study participants
(weekly, fortnightly or monthly) to instruct them on the
specific dietary and lifestyle interventions (DASH or control). In
contrast, four studies controlled dietary intake more carefully by
providing participants with all their meals(9,28,30,36). Salt intake
was standardised and participants were asked to maintain a
record of the non-study foods that they consumed in the latter
studies. Trials differed in their attempts to standardise Na intake
in the DASH and control intervention groups; five trials
reported marginal differences (,210mg/d) in dietary Na
intake(9,18,27,31,36), eight trials reported differences .300mg/d
(range: 319–2481 mg/d)(13,15–17,19,32–34) and one trial(28)
Articles identified through
database searching
(n 5395)
Included Eligibility Screening Identification
Duplicates removed
(n 4562)
Articles screened
(n 833)
Full-text articles
assessed for eligibility
(n 65)
Articles included in
qualitative synthesis
(n 20)
Blood pressure
(n 19)
Glucose
(n 10)
HDL
(n 15)
LDL
(n 13)
Cholesterol
(n 13)
TAG
(n 15)
Articles included in
quantitative synthesis
(meta-analysis)
(n 20)*
Articles excluded
(n 768)
Full-text articles excluded (n 45)
Twenty-two articles: duplication of results
Nine articles: not reporting outcomes
Two articles: not randomised
Three articles: no control group
Seven articles: DASH diet combined
with other interventions
Two articles: follow-up study
Additional articles identified
through other sources
(n 0)
Fig. 1. Flowchart depicting the different stages leading to the selection of trials included in the meta-analysis. * The different number of articles (n) included in the
analyses for specific cardiovascular risk factors is related to the selective reporting of the risk factors in each article. The number of articles and number of
independent subgroups included in the meta-analysis are given in Table 1. DASH, Dietary Approach to Stop Hypertension.
4 M. Siervo et al.
British Journal of Nutrition
Downloaded from https://www.cambridge.org/core. IP address: 51.9.206.53, on 08 May 2019 at 20:30:22, subject to the Cambridge Core terms of use, available at https://www.cambridge.org/core/terms. https://doi.org/10.1017/S0007114514003341
Table 1. Summary of findings from studies included in the meta-analysis
Author (year,
country) Inclusion criteria Design
Duration
(weeks) Run-in ITT Groups
Subjects
(n)
Age
(years)
Females
(n)
Caucasians
(n)
BMI
(kg/m2) Diet Feeding
Weight
loss (kg)
Completion
(%)
Risk
factors
Jadad*
score
Appel† (1997,
USA)(9)
Age .22 years C 154 44 72 48 28 TD Controlled 20·1 95 BPR‡
SBP ,160mmHg PMC‡ 8 Yes Yes G
DBP: 80–95mmHg I 151 44 77 53 29 DASH Controlled 20·4 99 HDL 5
Stop HT drugs TC
TAG
LDL
Sacks† (2001,
USA)(28)
Age .22 years C 204 49 110 81 30 TD Controlled NRWS‡ 95 BPR‡ 5
SBP: 120–159mmHg PMC,SS‡ 12 Yes Yes G
DBP: 90–95mmHg I 208 47 122 83 29 DASH Controlled NRWS‡ 94 HDL
BMI: 18·5–45 kg/m2 TC
TAG
LDL
Appel† (2003,
USA)(18)
Age $25 years C 269 50 154 163 33 HD Counselling 24·9 71 BPR‡ 5
SBP: 120–159mmHg PMC‡ 24 Yes Yes G
DBP: 80–95mmHg I 268 50 174 181 33 M-DASH Counselling 25·8 78 HDL
TC
TAG
LDL
Conlin (2003,
USA)(30)
SBP: 140–179mmHg C 28 52 15 10 30 TD Controlled NREI‡ 100 BPAMBP‡ 3
DBP: 90–109mmHg PMC,SL‡ 8 Yes Yes G
Stop HT drugs I 27 52 15 10 32 DASH Controlled NREI‡ 100 HDL
TC
TAG
LDL
Lopes (2003,
USA)(19)
NW: BMI ,25 kg/m2 C 12 39 6 6 23 LAO Counselling 0 100 BPR‡ 3
No MetS§ CO 4 Yes No G
I 12 39 6 6 23 DASH Counselling 0 100 HDL
TC
TAG
LDL
Lopes (2003,
USA)(19)
OW: BMI .27 kg/m2 C 12 35 6 6 34 LAO Counselling 0 100 BPR‡ 3
MetS§ CO 4 Yes No G
I 12 35 6 6 34 DASH Counselling 21 100 HDL
TC
TAG
LDL
Harsha† (2004,
USA)(29)
Age .22 years C 193 49 104 110 30 TD Controlled NRRP‡ 95RP‡ BPR
‡ 5
SBP: 120–160mmHg PMC,SS‡ 8 Yes Yes G
DBP: 90–95mmHg I 197 48 116 112 29 DASH Controlled NRRP‡ 94RP‡ HDL
TC
TAG
LDL
Nowson (2004,
Australia)(16)
Age .25 years C 94 56 38 NR 29 TD Counselling NRWS‡ 97 BPR‡ 3
SBP: 120–160mmHg CO 4 Yes No G
DBP: 80–90mmHg I 94 56 38 NR 29 DASH Counselling NRWS‡ 97 HDL k
TC k
TAG k
LDL k
Nowson (2005,
Australia)(17)
Age .25 years C 27 49 0 NR 31 LF{ Counselling 24·6 87 BPR‡ 3
SBP $120mmHg P 12 No No G
DBP $80mmHg I 27 47 0 NR 30 M-DASH{ Counselling 24·9 85 HDL
BMI: 25–35 kg/m2 TC
TAG
LDL
Azadbakht
(2005,
Iran)(13)
MetS** C 11 41†† 0 NR 30†† WL{ Counselling 214 100 BPR‡ 3
BMI $25 kg/m2 P 24 Yes NA G
I 11 41†† 0 NR 30†† M-DASH{ Counselling 215 100 HDL
TC
TAG
LDL
Dietary patterns and cardiovascular risk 5
British Journal of Nutrition
Downloaded from https://www.cambridge.org/core. IP address: 51.9.206.53, on 08 May 2019 at 20:30:22, subject to the Cambridge Core terms of use, available at https://www.cambridge.org/core/terms. https://doi.org/10.1017/S0007114514003341
Table 1. Continued
Author (year,
country) Inclusion criteria Design
Duration
(weeks) Run-in ITT Groups
Subjects
(n)
Age
(years)
Females
(n)
Caucasians
(n)
BMI
(kg/m2) Diet Feeding
Weight
loss (kg)
Completion
(%)
Risk
factors
Jadad*
score
Azadbakht
(2005,
Iran)(13)
MetS** C 27 41†† 27 NR 30†† WL{ Counselling 212 100 BPR‡ 3
BMI $25 kg/m2 P 24 Yes NA G
I 27 41†† 27 NR 30†† M-DASH{ Counselling 214 100 HDL
TC
TAG
LDL
Lien† (2007,
USA)(26)
Age $25 years C 269 50 154 163 33 HD Counselling 24·9 71 BPR‡ 5
SBP: 120–159mmHg PMC‡ 24 Yes Yes G
DBP: 80–95mmHg I 268 50 174 181 33 M-DASH Counselling 25·8 78 HDL
TC
TAG
LDL
Nowson (2009,
Australia)(27)
Age: 45–75 years C 49 58 49 NR 30 HD Semi-controlled 0·8 85 BPR‡ 3
BMI: 18–35 kg/m2 P 14 Yes No G
SBP: 120–159mmHg I 46 60 46 NR 29 M-DASH Semi-controlled 1·1 87 HDL k
DBP: 80–94mmHg TC k
HT diagnosis TAG k
LDL k
Al Solamain
(2010,
USA)(31)
Age: 21–49 years C 15 37 12 10 23 TD Counselling NRWS‡ 83 BPR‡ 3
NW: BMI ,25 kg/m2 CO 3 Yes NA G
No MetS‡‡ I 15 37 12 10 23 DASH Counselling NRWS‡ 83 HDL
TC
TAG
LDL
Al Solamain
(2010,
USA)(31)
Age: 21–49 years C 15 40 12 7 34 TD Counselling NRWS‡ 78 BPR‡ 3
OW: BMI .27 kg/m2 CO 3 Yes NA G
MetS‡‡ I 15 40 12 7 34 DASH Counselling NRWS‡ 78 HDL
TC
TAG
LDL
Blumenthal†
(2010,
USA)(32)
Age .35 years C 48 52 34 29 33 TD Counselling 0·9 98 BPR‡ 4
BMI: 25–40 kg/m2 P 16 Yes Yes G
SBP: 130–159mmHg I 46 52 29 23 33 DASH Counselling 20·3 100 HDL
DBP: 85–99mmHg TC
TAG
LDL
Blumenthal†
(2010,
USA)(20)
Age .35 years C 48 52 34 29 33 TD Counselling 0·9 98 BPR‡ 4
BMI: 25–40 kg/m2 P 16 Yes Yes G
SBP: 130–159mmHg I 46 52 29 23 33 DASH Counselling 20·3 100 HDL
DBP: 85–99mmHg TC
TAG
LDL
Chen† (2010,
USA)(14)
Age .22 years C 144 44 66 47 28 TD Controlled 20·1 95 BPR‡ 5
SBP ,160mmHg PMC‡ 8 Yes Yes G
DBP: 80–95mmHg I 146 44 75 53 29 DASH Controlled 20·4 99 HDL
Stop HT drugs TC
TAG
LDL
Malloy-McFall
(2010,
USA)(33)
Age: 22–60 years C 10 38 3 NR 26 TD Counselling 20·6 NR BPR‡ 1
SBP: 120–160mmHg P 4 No No G
DBP: 80–95mmHg I 10 38 5 NR 34 DASH Counselling 21·3 NR HDL
TC
TAG
LDL
Azadbakht
(2011,
Iran)(34)
T2D C 31 NR 18 NR NR§§ HD Counselling 22 70 BPR‡ 3
G $126 mg/dl
(6·993 mmol/l)
CO 8 Yes No G
I 31 NR 18 NR NR§§ DASH Counselling 25 70 HDL
TC
TAG
LDL
6 M. Siervo et al.
British Journal of Nutrition
Downloaded from https://www.cambridge.org/core. IP address: 51.9.206.53, on 08 May 2019 at 20:30:22, subject to the Cambridge Core terms of use, available at https://www.cambridge.org/core/terms. https://doi.org/10.1017/S0007114514003341
Table 1. Continued
Author (year,
country) Inclusion criteria Design
Duration
(weeks) Run-in ITT Groups
Subjects
(n)
Age
(years)
Females
(n)
Caucasians
(n)
BMI
(kg/m2) Diet Feeding
Weight
loss (kg)
Completion
(%)
Risk
factors
Jadad*
score
Edwards
(2011,
Australia)(35)
Age: 25–60 years C 25 46 13 NR 30 EX Counselling 20·2kk NR BPR‡ 3
SBP: 120–170mmHg P 12 No No G
DBP: 80–95mmHg I 12 48 6 NR 31 EX-DASH Counselling 20·8kk NR HDL
Stop HT drugs TC
TAG
LDL
Lin (2012,
USA)(36)
Age .22 years C 9 42 6 2 37 TD Controlled NREI‡ 90 BPR‡ 4
BMI: 18·5–40 kg/m2 P 2 Yes Yes G
SBP: 140–159mmHg I 10 46 7 3 31 DASH Controlled NREI‡ 100 HDL
DBP: 90–99mmHg TC
TAG
LDL
Asemi (2013,
Iran)(15)
Pregnant women C 17 29 17 NR 31 TD Counselling NR 85 BPR‡ 3
GD (24–26 weeks) P 4 No No G
Age: 18–40 years I 17 31 17 NR 29 DASH Counselling NR 85 HDL
TC
TAG
LDL
ITT, intention to treat; SBP, systolic blood pressure; DBP, diastolic blood pressure; HT, hypertension; P, parallel study design; C, control group; I, intervention group; TD, typical diet; DASH, Dietary Approach to Stop Hypertension;
BP, blood pressure; G, glucose; TC, total cholesterol; HD, healthy diet; M-DASH, modified DASH diet; NW, normal weight; MetS, metabolic syndrome; CO, cross-over study design; LAO, low antioxidant; OW, overweight; NR,
not reported in the article; LF, low-fat; NA, not applicable; WL, weight loss; T2D, type 2 diabetes; EX, exercise intervention; EX-DASH, DASH diet combined with EX; GD, gestational diabetes. , results reported in the article and
included in the meta-analysis; , results not reported in the article.
* The Jadad score ranges from 0 to 5(22). One point was assigned by default to the blinding scale as dietary interventions could not be blind. The other point was assigned based on whether personnel performing the measurements
were blind to the interventions.
† The results of the following pairs of publications were obtained from the same trial design: Appel(9) and Chen(14); Sacks(28) and Harsha(29); Appel(18) and Lien(26); Blumenthal(32) and Blumenthal(20).
‡ MC, multicentre study; R, resting BP; SS, stratified by salt intake (three groups, cross-over design); NRWS, weight not reported in the article, but weight stability of participants mentioned in the ‘Results’ section of the article; SL,
stratified by losartan treatment (cross-over, double blind); NREI, weight not reported in the article, but adjustment of energy intake to maintain body weight mentioned in the ‘Methods’ section of the article; AMBP, ambulatory 24 h
BP; RP, article refers to related publications for details.
§ Inclusion criteria for the study were as follows: (1) OW group (BMI $27 kg/m2), dyslipidaemic (TAG concentration .150 mg/dl (.1·7 mmol/l) and/or HDL-cholesterol concentration ,45 mg/dl (,1·17 mmol/l) for women or
,40 mg/dl (,1·04 mmol/l) for men) subjects with high-normal to stage 1 HT (BP 130–159/85–99 mmHg) and twelve lean (BMI ,25 kg/m2) normotensives (BP ,130/85mmHg) with normal lipid concentrations.
k Results obtained for lipids after the intervention period were not provided in the article. A summary of the main findings was provided in the ‘Results’ section of the article. These results have been included in the meta-analysis.
{WL studies including a DASH diet intervention. Studies demonstrated a similar level of energy deficit in the DASH and C groups as shown by the similar WL. The C of these studies have been classified as HD in the
meta-analysis.
** Inclusion criteria for the study were as follows: NW (waist:hip ratio ,0·80 for women and ,0·85 for men, BP ,130/85 mmHg, glucose concentration ,110 mg/dl (,6·105 mmol/l), TAG concentration ,125 mg/dl (,1·4 mmol/l),
and HDL concentration .40mg/dl (.1·04 mmol/l) for men and .45 mg/dl (.1·17 mmol/l) for women) and obese (waist circumference (WC) . 101cm for men and 88cm for women, BP within 130/85 and 159/99 mmHg, glucose
concentration ,126 mg/dl (,6·993 mmol/l), TAG concentration .170 mg/dl (.1·9 mmol/l), and HDL concentration ,40 mg/dl (,1·04 mmol/l) for men and ,50 mg/dl (,1·30 mmol/l) for women).
†† Baseline subjects’ characteristics were not reported by sex in the article.
‡‡ Inclusion criteria for the study were as follows: NW (BMI ,25 kg/m2, WC ,102 cm for men and ,88cm for women, blood pressure consistently ,130/85mmHg during all three visits before the first study, fasting glucose
concentration ,100 mg/dl (,5·550 mmol/l), fasting TAG concentration ,125 mg/dl (,1·4 mmol/l), HDL-cholesterol concentration .40 mg/dl (.1·04 mmol/l) for men and .50 mg/dl (.1·30 mmol/l) for women and/or TC/HDL
concentration ,3·5) and OW (blood pressure in the 130–159/85–99mmHg range during the three screening visits, BMI .27 kg/m2 and WC $40 inches ($102 cm) for men and $35 inches ($88 cm) for women). They also had
at least one other risk factor including impaired fasting glucose concentration (100–125 mg/dl; 5·550–6·938 mmol/l), fasting TAG concentration .150 mg/dl (.1·7 mmol/l) or HDL-cholesterol concentration ,50 mg/dl
(,1·30 mmol/l) for women and ,40 mg/dl (,1·04 mmol/l) for men.
§§ Only body weight was reported in the article.
kk Changes in BMI.
Dietary patterns and cardiovascular risk 7
British Journal of Nutrition
Downloaded from https://www.cambridge.org/core. IP address: 51.9.206.53, on 08 May 2019 at 20:30:22, subject to the Cambridge Core terms of use, available at https://www.cambridge.org/core/terms. https://doi.org/10.1017/S0007114514003341
specifically evaluated the additive effects of a stepwise
reduction in dietary Na intake on the BP-lowering effects of
the DASH diet (see online supplementary Table S1).
Study quality
The following factors were considered while determining the
quality of studies included in the meta-analysis: type of dietary
intervention; study design; compliance monitoring; measurement
protocols. On occasion, some important information
was missing or incomplete, e.g. intakes of energy, macronutrients
and micronutrients, and there was large variability in the
assessment of compliance with the dietary interventions with
respect to monitoring changes in body weight and physical
activity levels. An important aspect of the nutritional interventions
was the inclusion of a run-in period (both parallel and
cross-over studies) and/or a washout period (cross-over
studies). Specifically, a run-in period (duration: 1–4 weeks)
was included in twelve trials(9,13,16,18,19,27,28,30 – 32,34,36) and a
washout period (duration: 2 and 4 weeks) was included in
two cross-over trials(16,34). There was considerable variability
in the effectiveness of monitoring compliance with the dietary
interventions, which was influenced by the intervention protocol
(e.g. CON study v. provision of ADV). Urinary or plasma
mineral and electrolyte concentrations (i.e. Mg, Na, K, phosphate
and Ca) were measured in eleven trials to evaluate
the adherence to the dietary interventions(9,16 – 19,27,28,30 – 32,36).
Only seven trials reported whether the personnel involved
in the collection of outcome data were unaware of participants’
diet assignment(9,15,18,28,32,34,36).
Meta-analysis results and estimated CVD risk
The DASH diet resulted in significant decreases in systolic BP
(25·2 mmHg, 95% CI 27·0, 23·4, P,0·001; Fig. 2(a)) and
diastolic BP (22·6 mmHg, 95% CI 23·5, 21·7, P,0·001;
Fig. 2(b)) and in the concentrations of total cholesterol
(20·20 mmol/l, 95% CI 20·31, 20·10, P,0·001; Fig. 2(d))
and LDL (20·10 mmol/l, 95% CI 20·20, 20·01, P¼0·03;
Fig. 2(f)). The pooled effect of the interventions was not
significant for the concentrations of glucose (20·19 mmol/l,
95% CI 20·39, 20·17, P¼0·07; Fig. 2(c)), HDL (0·003 mmol/l,
95% CI 20·05, 0·05, P¼0·95; Fig. 2(e)) and TAG
(20·005 mmol/l, 95% CI 20·06, 0·05, P¼0·87; Fig. 2(g)).
There was no change in the estimates for glucose, HDL,
LDL, total cholesterol and TAG concentrations after the
exclusion of trials(16,26,27) with missing information (see
online supplementary Table S2). The DASH diet resulted in
highly significantly lowered BP when the analyses were
stratified by the type of intervention (CON(9,28,30,36) and
ADV(13,15 – 19,27,31 – 35)) and by the type of the control diet
(typical diet(9,15,16,28,30 – 33,36) and healthy diet(13,17 – 19,27,34,35)),
albeit the decline in systolic BP was greater when a typical
diet was used as the control intervention (see online supplementary
Table S3). Using the Framingham risk equations(3),
it was estimated that the concomitant changes in BP and
cholesterol concentrations elicited by the DASH diet would
lead to a reduction of approximately 13% in the estimated
10-year risk for CVD (see online supplementary Fig. S1).
Meta-regression analysis
Reductions in systolic and diastolic BP following randomisation
to the DASH diet were greater in participants with higher BP or
BMI at baseline. For each mmHg increase in baseline systolic
and diastolic BP, the effect size for both BP variables increased
by about 0·1mmHg. Similarly, baseline BMI was directly associated
with changes in both systolic BP (b 20·1 (SE 0·06)mmHg,
P¼0·02) and diastolic BP (b 20·1 (SE 0·04)mmHg, P,0·001)
(Table 2). Differences in dietary Na intake between the DASH
and control intervention groups were not associated with
changes in systolic and diastolic BP as well as with glucose and
lipid concentrations (Table 2).
Publication bias and heterogeneity
Funnel plots generated for all the cardiovascular risk factors
revealed an overall symmetric distribution for BP (systolic
and diastolic) and for total cholesterol, glucose, HDL and
LDL concentrations, indicating the absence of publication
bias (see online supplementary Fig. S2). In addition, Egger’s
regression test for these risk factors was not significant (see
online supplementary Table S4). In contrast, funnel plots
generated for TAG concentrations revealed some asymmetry,
which was confirmed by a significant Egger regression test
(P¼0·01). The heterogeneity of the models was high for systolic
BP (I 2 ¼ 76·0 %) and HDL concentrations (I 2 ¼ 75·6 %),
whereas the lowest value was observed for TAG concentrations
(I 2 ¼ 0%; online supplementary Table S4).
Discussion
Summary of the main results
DASH diet interventions resulted in significant improvements in
systolic and diastolic BP along with significant reductions in
total cholesterol and LDL concentrations. However, these interventions
did not affect TAG, glucose and HDL concentrations.
The responses of both systolic and diastolic BP to the DASH
diet were greater in participants with higher BP or BMI at baseline.
The responses appeared to be independent of differences
in dietary Na intake. Importantly, measures of the effectiveness
of the DASH diet were not modified by the type of study design
or feeding protocol and the characteristics of control diet.
Study quality and applicability of evidence
In general, the quality of the trials was good (median Jadad
score $3). Most trials provided a summary of the randomisation
process and evidence of adherence to the study
protocols and to the dietary interventions. Compliance appeared
to be superior in controlled interventions(9,28,30,36). Lesscontrolled
trials (those based on ADV) and longer-duration
trials tended to report greater dropout rates(13,15 – 19,27,31 – 35).
The stratification of the meta-analysis by the type of dietary
8 M. Siervo et al.
British Journal of Nutrition
Downloaded from https://www.cambridge.org/core. IP address: 51.9.206.53, on 08 May 2019 at 20:30:22, subject to the Cambridge Core terms of use, available at https://www.cambridge.org/core/terms. https://doi.org/10.1017/S0007114514003341
intervention (CON v. ADV) did not modify the effects on BP.
Although there is evidence for greater changes in total cholesterol,
HDL and LDL concentrations in controlled trials, this
finding should be treated with caution as only two studies
included in the sensitivity analysis used the CON trial approach.
The lack of a significant association between changes in BP and
dietary Na intake is unanticipated. However, the results may
require a cautious interpretation in consideration of differences
(a) First author and year
(b)
Difference in means and 95% Cl
Lower
limit
–2·6
7·2
2·5
Conlin (2003)(30)
Lopes (2003)(19) (L)
Lopes (2003)(19) (OB)
Nowson (2004)(16)
Nowson (2005)(17)
3·1
Azadbakht (2005)(13) (W)
0·3
Al Solamain (2010)(31) (L)
Al Solamain (2010)(31) (OB)
Blumenthal (2010)(20,32)
–9·0
Azadbakht (2011)(34)
Edwards (2011)(35)
Lin (2012)(36)
Asemi (2013)(15)
–3·4
0·00
Decrease
Statistics for each study
Difference
in means
Upper
limit
Relative
weight
Appel (1997)(9) –5·2 –7·8 7·3
Sacks (2001)(28) –4·4 –7·0 –1·8
Appel (2003)(18) –0·6 –3·7 6·8
–6·4 –14·4 1·6 3·1
–1·6 –6·7 3·5 5·0
–8·0 –13·5 –2·5 4·7
–1·9 –3·9 0·1 7·7
–5·5 –11·8 0·8 4·1
Azadbakht (2005)(13) (M) –1·0 –9·1 7·1
–8·0 –13·0 –3·0 5·1
Nowson (2009)(27) –2·9 –6·1 6·7
–2·0 –3·7 –0·3 7·9
–9·8 –11·5 –8·1 7·9
–7·8 –12·1 –3·5 5·7
Malloy (2010)(33) –17·1 –0·9 3·1
–13·2 –19·4 –7·0 4·2
–5·4 –12·7 1·9 3·5
–8·7 –21·0 3·6 1·7
–4·3 –9·3 0·7 5·1
–5·2 –7·0
–15·00 –7·50 7·50 15·00
Increase
First author and year Difference in means and 95% Cl
Lower
limit
–1·9
9·5
1·3
2·6
1·0
–0·9
–1·7
0·00
Decrease
Statistics for each study
Difference
in means
Upper
limit
Relative
weight
–3·0 –4·1 11·2
–2·1 –3·7 –0·5
–0·9 –3·1 7·3
–4·2 –8·3 –0·1 3·4
–1·8 –4·2 0·6 6·6
–5·4 –9·8 –1·0 3·1
–0·7 –2·4 1·0 9·1
–4·4 –8·7 –0·1 3·2
–5·7 –10·6 –0·8
–5·0 –11·7 1·7 1·5
–1·2 –3·4 7·3
–1·0 –2·3 0·3 10·7
–5·0 –7·2 –2·8 7·4
–3·7 –6·1 –1·3 6·7
–6·8 5·0 1·9
–8·7 –14·2 –3·2 2·2
–2·8 –9·8 4·2 1·4
–10·2 –19·3 –1·1 0·9
0·1 –3·6 3·8 4·0
–2·6 –3·5
–15·00 –7·50 7·50 15·00
Increase
Conlin (2003)(30)
Lopes (2003)(19) (L)
Lopes (2003)(19) (OB)
Nowson (2004)(16)
Nowson (2005)(17)
Azadbakht (2005)(13) (W)
Al Solamain (2010)(31) (L)
Al Solamain (2010)(31) (OB)
Blumenthal (2010)(20,32)
Azadbakht (2011)(34)
Edwards (2011)(35)
Lin (2012)(36)
Asemi (2013)(15)
Appel (1997)
Sacks (2001)(28)
Appel (2003)(18)
Azadbakht (2005)(13) (M)
Nowson (2009)(27)
Malloy (2010)(33)
Dietary patterns and cardiovascular risk 9
British Journal of Nutrition
Downloaded from https://www.cambridge.org/core. IP address: 51.9.206.53, on 08 May 2019 at 20:30:22, subject to the Cambridge Core terms of use, available at https://www.cambridge.org/core/terms. https://doi.org/10.1017/S0007114514003341
(c) Study name
(d)
(e)
Difference in means and 95% Cl
Lower
limit
Lopes (2003)(19) (L) 5·7
Lopes (2003)(19) (OB
4·3
Azadbakht (2005)(13) (W)
Al Solamain (2010)(31) (L)
Al Solamain (2010)(31) (OB)
Blumenthal (2010)(20,32)
Azadbakht (2011)(34)
Asemi (2013)(15)
0·00
Decrease
Statistics for each study
Difference
in means
Upper
limit
Relative
weight
0·0 3·2
4·0
Appel (2003)(18)
1·0 4·7
–8·0 15·7
–5·0 2·5
–2·6 18·3
0·0 18·1
1·1 18·3
Azadbakht (2005)(13) (M)
–27·5
–8·1 8·8
–3·4
–19·5
–9·6
–14·3
–13·2
–27·3
–6·4
–3·9
–2·7
–42·6
–17·9
–7·1
19·5
17·6
16·3
–2·8
17·3
1·2
3·9
4·9
–12·4
1·7
0·3
–25·00 –12·50 12·50 25·00
Increase
First author and year Difference in means and 95% Cl
Lower
limit
0·00
Decrease
Statistics for each study
Difference
in means
Upper
limit
Relative
weight
1·2
–8·0
1·0
–16·6
–3·9
–3·9
0·0
–7·0
–10·0
1·0
–13·0
–12·3
–26·7
–7·9
–10·2
–19·9
–13·1
–22·9
–11·4
–24·5
–21·7
–27·2
–27·7
–12·8
–20·1
–23·7
–58·1
–12·0
12·6
3·9
15·1
–10·3
3·6
16·7
27·7
13·2
7·7
14·8
–5·9
–0·9
4·7
–3·8
8·7
8·3
6·4
16·1
14·0
3·5
3·2
3·6
4·5
6·7
14·7
8·7
1·6
–40·00 –20·00 20·00 40·00
Increase
Lopes (2003)(19) (L)
Lopes (2003)(19) (OB)
Nowson (2004)(16)
Harsha (2004)(29)
Nowson (2005)(17)
Nowson (2009)(27)
Al Solamain (2010)(31) (L)
Al Solamain (2010)(31) (OB)
Blumenthal (2010)(20,32)
Azadbakht (2011)(34)
Chen (2010)(14)
Asemi (2013)(15)
Appel (2003)(18)
First author and year Difference in means and 95% Cl
Lower
limit
Lopes (2003)(19) (L)
Lopes (2003)(19) (OB)
Nowson (2004)(16)
Harsha (2004)(29)
Nowson (2005)(17)
Azadbakht (2005)(13) (M)
Azadbakht (2005)(13) (W)
Al Solamain (2010)(31) (L)
Al Solamain (2010)(31) (OB)
Blumenthal (2010)(20,32)
Azadbakht (2011)(34)
Chen (2010)(14)
Asemi (2013)(15)
0·00
Decrease
Statistics for each study
Difference
in means
Upper
limit
Relative
weight
–1·3
–6·0
Appel (2003)(18)
–2·0
–3·5
0·0
5·0
8·0
–2·3
0·0
–1·0
Nowson (2009)(27)
–1·7
–1·0
–2·8
3·1
4·7
0·1
–4·3
–14·3
–9·0
–5·2
–2·3
1·2
4·3
–7·1
–10·9
–8·0
–7·0
–5·9
–5·8
1·1
–5·8
–2·0
1·7
2·3
5·0
–1·7
2·3
8·8
11·7
2·5
10·9
6·0
3·6
3·9
0·2
5·1
15·2
2·1
8·7
3·8
4·7
9·9
9·4
7·7
7·9
6·7
2·6
4·7
6·2
6·5
8·7
9·7
2·8
–15·00 –7·50 7·50 15·00
Increase
10 M. Siervo et al.
British Journal of Nutrition
Downloaded from https://www.cambridge.org/core. IP address: 51.9.206.53, on 08 May 2019 at 20:30:22, subject to the Cambridge Core terms of use, available at https://www.cambridge.org/core/terms. https://doi.org/10.1017/S0007114514003341
between the trials with regard to dietary Na intake in both
DASH and control intervention groups, assessment of dietary
Na intake (dietary intake or 24 h urinary excretion assessment)
and type of dietary intervention (CON or ADV).
The primary outcome of the trials was change in systolic
or diastolic BP, and subgroup analyses were conducted
to determine the effects on other cardiovascular risk
factors(14,26,29,32). Most of the clinical trials using the DASH
diet targeted the primary prevention of hypertension and
chronic metabolic diseases, although, more recently, the
DASH diet has been used in studies aiming to prevent
progression and complications in other conditions including
heart failure(37) and uncontrolled asthma(38). Prospective
cohort studies have found that adherence to a DASH-style
diet is associated with a lower risk of CHD and stroke(39).
The effectiveness of the DASH diet as a nutritional strategy
for the prevention and management of hypertension was
confirmed and its significant beneficial effects on other
Fig. 2. Forest plots of randomised clinical trials investigating the effects of DASH diet interventions on (a) systolic and (b) diastolic blood pressure (mmHg),
(c) glucose (mg/dl) and lipid profile (in mg/dl) ((d) total cholesterol, (e) HDL, (f) LDL and (g) TAG). A random-effects model was used to obtain the pooled mean
differences for each metabolic component. L, lean; OB, overweight and obese; M, men; W, women. SI conversion factors: to convert glucose to millimol per litre,
multiply by 0·0555; HDL-, LDL- and total cholesterol to millimol per litre, multiply by 0·0259; TAG to millimol per litre, multiply by 0·0113.
First author and year Difference in means and 95% Cl
Lower
limit
Lopes (2003)(19) (L)
Lopes (2003)(19) (OB)
Nowson (2004)(16)
Harsha (2004)(29)
Nowson (2005)(17)
Al Solamain (2010)(31) (L)
Al Solamain (2010)(31) (OB)
Blumenthal (2010)(20,32)
Azadbakht (2011)(34)
Chen (2010)(14)
Asemi (2013)(15)
0·00
Decrease
Statistics for each study
Difference
in means
Upper
limit
Relative
weight
1·5
1·0
Appel (2003)(18)
2·0
–12·8
0·0
–8·0
0·0
4·0
–7·0
1·0
Nowson (2009)(27)
–10·0
–10·5
–27·0
–4·0
–8·4
–7·9
–11·8
–22·7
–7·7
–24·9
–11·9
–6·7
–21·1
–11·2
–16·5
–17·8
–58·2
–7·7
11·4
9·9
15·8
–2·9
7·7
8·9
11·9
14·7
7·1
13·2
–3·5
–3·2
4·2
–0·3
8·5
9·7
5·4
8·6
11·3
3·9
6·7
7·7
5·3
6·5
13·1
11·9
1·3
–40·00 –20·00 20·00 40·00
Increase
(g) First author and year
(f)
Difference in means and 95% Cl
Lower
limit
0·00
Favours A
Statistics for each study
Difference
in means
Upper
limit
Relative
weight
0·0
–15·0
–3·0
1·8
9·0
–3·0
–1·0
–26·6
2·0
–6·1
–1·0
3·5
–8·0
–43·0
–0·4
–62·6
–39·6
–77·7
–10·8
–9·0
–17·2
–27·0
–63·9
–11·7
–31·9
–22·0
–7·4
–39·7
–94·9
–5·6
62·6
9·6
71·7
14·4
27·0
11·2
25·0
10·7
15·7
19·7
20·0
14·4
23·7
8·9
4·7
0·7
4·4
0·5
16·8
8·2
13·1
3·9
1·9
14·3
4·0
6·0
22·5
2·7
1·0
–50·00 –25·00 25·00 50·00
Favours B
Lopes (2003)(19) (L)
Lopes (2003)(19) (OB)
Nowson (2004)(16)
Harsha (2004)(29)
Nowson (2005)(17)
Al Solamain (2010)(31) (L)
Al Solamain (2010)(31) (OB)
Blumenthal (2010)(20,32)
Azadbakht (2005)(13) (M)
Chen (2010)(14)
Asemi (2013)(15)
Appel (2003)(18)
Azadbakht (2005)(13) (W)
Azadbakht (2011)(34)
Dietary patterns and cardiovascular risk 11
British Journal of Nutrition
Downloaded from https://www.cambridge.org/core. IP address: 51.9.206.53, on 08 May 2019 at 20:30:22, subject to the Cambridge Core terms of use, available at https://www.cambridge.org/core/terms. https://doi.org/10.1017/S0007114514003341
cardiovascular risk factors including total cholesterol and LDL
concentrations were revealed in this meta-analysis. Taken
together, these changes are expected to translate into a
reduction of approximately 13% in the 10-year Framingham
risk scores for CHD, myocardial infarction and stroke.
The analysis highlights the beneficial effects of higher
consumption of unrefined carbohydrates, fruits and vegetables
and lower consumption of saturated fat on the risk of primary
heart disease. However, the efficacy of the DASH diet in
reducing the risk of complications, reoccurrence of major
cardiovascular events, and mortality in patients with more
severe heart conditions is currently not known.
Table 2. Summary of the results of the meta-regression analyses investigating the association of the individual
cardiovascular risk factors with covariates that may modify the results of the meta-analysis*
(Regression coefficients (b) with their standard errors)
Covariates b SE Q (df ¼ 1) P
Systolic BP (mmHg; n 19)
Baseline systolic BP (mmHg) 2 0·1 0·06 5·1 0·02
Duration (weeks) 0·08 0·1 0·6 0·43
Age (years) 0·1 0·1 1·0 0·30
BMI (kg/m2) 2 0·5 0·2 5·9 0·01
Total sample size (n) 0·007 0·004 2·4 0·12
Jadad score 1·0 0·7 1·7 0·18
Dietary Na intake (mg/d) 0·006 0·001 0·1 0·67
Diastolic BP (mmHg; n 19)
Baseline diastolic BP (mmHg) 2 0·1 0·04 12·7 , 0·001
Duration (weeks) 2 0·006 0·06 0·01 0. 91
Age (years) 0·03 0·05 0·3 0·56
BMI (kg/m2) 2 0·2 0·1 6·0 0·01
Total sample size (n) 0·002 0·002 1·1 0·28
Jadad score 0·2 0·4 0·4 0·52
Dietary Na intake (mg/d) 2 0·0001 0·0007 0·05 0·81
Glucose (mmol/l; n 10)
Baseline glucose concentration (mmol/l) 2 0·0167 0·0056 12·5 , 0·001
Duration (weeks) 2 0·0167 0·0056 6·4 0·01
Age (years) 2 0·0033 0·0167 0·1 0·72
BMI (kg/m2) 0·0056 0·0222 0·09 0·76
Total sample size (n) 0·0002 0·0006 0·03 0·86
Jadad score 0·0500 0·1110 0·22 0·63
Dietary Na intake (mg/d) 0·0002 0·0001 4·6 0·03
HDL (mmol/l; n 15)
Baseline HDL concentration (mmol/l) 2 0·0104 0·0021 19·4 , 0·001
Duration (weeks) 0·0052 0·0026 3·9 0·04
Age (years) 2 0·0026 0·0026 0·7 0·39
BMI (kg/m2) 0·0026 0·0104 0·2 0·67
Total sample size (n) 2 0·0003 0·0001 3·7 0·05
Jadad score 2 0·0544 0·0078 40·5 , 0·001
Dietary Na intake (mg/d) 2 0·0001 0·0001 3·3 0·06
LDL (mmol/l; n 13)
Baseline LDL concentration (mmol/l) 2 0·0008 0·0026 0·05 0·81
Duration (weeks) 0·0026 0·0078 0·3 0·58
Age (years) 0·0026 0·0078 0·2 0·66
BMI (kg/m2) 2 0·0078 0·0130 0·4 0·54
Total sample size (n) 2 0·0002 0·0003 0·5 0·47
Jadad score 2 0·0233 0·0440 0·3 0·56
Dietary Na intake (mg/d) 0·0001 0·0001 0·2 0·62
Total cholesterol (mmol/l; n 13)
Baseline total cholesterol concentration (mmol/l) 0·0010 0·0026 0·09 0·76
Duration (weeks) 0·0104 0·0078 1·6 0·19
Age (years) 0·0078 0·0078 0·9 0·32
BMI (kg/m2) 0·0207 0·0181 1·5 0·21
Total sample size (n) 2 0·0002 0·0003 0·5 0·47
Jadad score 2 0·0466 0·0440 1·0 0·31
Dietary Na intake (mg/d) 2 0·0002 0·0001 0·02 0·86
TAG (mmol/l; n 15)
Baseline TAG concentration (mmol/l) 2 0·0007 0·0006 1·5 0·21
Duration (weeks) 2 0·0007 0·0034 0·02 0·86
Age (years) 0·0011 0·0045 0·1 0·77
BMI (kg/m2) 2 0·0045 0·0090 0·4 0·52
Total sample size (n) 0·0001 0·0001 1·0 0·29
Jadad score 0·0237 0·0237 1·0 0·33
Dietary Na intake (mg/d) 0·0001 0·0001 2·4 0·12
BP, blood pressure.
*A mixed-effects meta-regression model (unrestricted maximum likelihood) was used.
12 M. Siervo et al.
British Journal of Nutrition
Downloaded from https://www.cambridge.org/core. IP address: 51.9.206.53, on 08 May 2019 at 20:30:22, subject to the Cambridge Core terms of use, available at https://www.cambridge.org/core/terms. https://doi.org/10.1017/S0007114514003341
The majority of the trials were conducted in the USA
and there was a lack of RCT investigating the effects of the
DASH diet in European populations. One clinical trial was
conducted in the UK, but it was excluded from the main
meta-analysis because the allocation to the dietary interventions
was not randomised(40). These findings suggest that the
evidence on the applicability and acceptability of the DASH
diet in populations outside the USA is limited, and this
warrants further investigation(41).
Potential biases in the review process
This meta-analysis has some limitations. First, all such
meta-analyses are based on retrospective analytical inference
using data reported in peer-reviewed journals from original
studies that may not have been designed primarily to
investigate the risk factors considered in this meta-analysis.
However, our clear delineation of the research questions
and inclusion and exclusion criteria, the comprehensive
search strategy used and the objective assessment of
the quality of the trials may have minimised bias and
increased the validity of the findings. The suitability of the
extracted studies for meta-analysis is confirmed by the
absence of significant publication bias for most risk factors.
Significant publication bias was observed for only TAG
concentrations.
In some articles, relevant information was either not
reported or described only in the text(16,26,27). All studies
with missing numerical information reported a non-significant
effect of the DASH diet on risk factors for which data were
missing. These trials were included in the main analyses
where the missing data were imputed by assigning a null
effect to each non-significant result. This conservative
approach was implemented to avoid potential inflation of
the effect size. A subsequent analysis, after exclusion of
these trials, revealed a marginal modification of the effects
of the interventions. In some trials, the DASH diet was used
in combination with restriction of energy or Na intakes or
with attempts to increase physical activity. Such trials were
included in the main meta-analysis provided that the absence
of the DASH diet was the only intervention difference
when compared with the control group so that any effect
on the cardiovascular risk factors of interest could be ascribed
to the DASH diet.
Biological mechanisms
The DASH dietary pattern involves increased consumption of
whole-grain cereals, dietary fibre, unsaturated fatty acids and
vegetable proteins compared with typical Western diets(8). In
addition, it involves lower salt intake and promotes the
consumption of foods rich in vitamins (vitamin C and
folate), minerals (K, Ca, Mg and P), amino acids (arginine)
and other substances with biological activity in human cells
(flavonoids and inorganic nitrate)(8,36,42). All these factors
may contribute to the significant beneficial effects of the
DASH diet on cardiovascular risk factors; the putative
mechanistic links between altered intakes of these substances
and changes in cardiovascular and metabolic functions have
been reviewed extensively(43). Briefly, the multi-organ
protective effects of the DASH diet may be due to the
combined effects of these molecules on multiple physiological
mechanisms including the modification of antioxidant
capacity(44), inflammatory response(11), hepatic function(11),
coagulation(11), natriuresis(45), sympathetic activation(35),
endothelial function(32) and gluco-insular control(10).
The effects of the DASH diet may be related to the high
intake of inorganic nitrate and its role in the non-enzymatic
generation of NO(46). Hord et al.(42) have estimated that the
nitrate-rich foods in a DASH dietary plan (including leafy
vegetables, raw or cooked vegetables, vegetable juice and
fruits) would result in the consumption of approximately
1200 mg nitrate/d. Our group has recently demonstrated a
significant effect of inorganic nitrate supplementation on
systolic BP (24·4 mmHg, P,0·001) and diastolic BP
(21·1 mmHg, P¼0·06)(46).
Agreements and disagreements with previous results
The DASH dietary pattern shares some dietary features with
the Mediterranean dietary pattern including higher consumption
of vegetables and fruits, whole grains, fish and nuts(47).
The Prevencio´n con Dieta Mediterra´nea trial has recently
reported significant beneficial effects of a Mediterranean diet
supplemented with extra-virgin olive oil or nuts on multiple
cardiovascular and metabolic risk factors and primary
prevention of CVD(48). A recent meta-analysis of clinical
studies has shown that adherence to a Mediterranean dietary
pattern improves HDL concentrations (þ0·03 mmol/l), TAG
concentrations (20·07 mmol/l), systolic BP (22·3mmHg)
and diastolic BP (21·5 mmHg) and glucose concentrations
(20·21 mmol/l)(49). The DASH diet appears to have a greater
effect on BP than the Mediterranean diet, but the results of
these meta-analyses confirm that adherence to either dietary
pattern improves multiple cardiovascular risk factors
substantially(47).
Conclusions
The DASH dietary plan has been recommended by several
US health organisations as an effective nutritional strategy
for the prevention and management of elevated BP(8,50).
This systematic review and meta-analysis of RCT investigating
the effects of DASH diet interventions revealed that the mean
change in cardiometabolic markers would yield a reduction of
approximately 13% in the 10-year Framingham risk score for
cardiovascular events. This finding reinforces the evidence
that DASH diet interventions could make a significant contribution
to the prevention of CVD beyond the well-known
BP-lowering effects.
Future studies should include identification of the biological
pathways activated in individuals eating the DASH diet that
are most influential in lowering CVD risk and investigation
of the nutrient–nutrient and gene–diet interactions responsible
for inter-individual difference in responsiveness to
the DASH diet. Findings from such studies may help to
Dietary patterns and cardiovascular risk 13
British Journal of Nutrition
Downloaded from https://www.cambridge.org/core. IP address: 51.9.206.53, on 08 May 2019 at 20:30:22, subject to the Cambridge Core terms of use, available at https://www.cambridge.org/core/terms. https://doi.org/10.1017/S0007114514003341
inform the design of more effective personalised nutritional
interventions for CVD prevention.
Supplementary material
To view supplementary material for this article, please visit
http://dx.doi.org/10.1017/S0007114514003341
Acknowledgements
A. A. received funds from the Ministry of Higher Education
and Scientific Research of Iraq. J. L. and J. C. M. acknowledge
support received from the LiveWell Programme, a research
project funded through a collaborative grant from the Lifelong
Health and Wellbeing initiative, managed by the Medical
Research Council on behalf of the following funders: Biotechnology
and Biological Sciences Research Council; Engineering
and Physical Sciences Research Council; Economic and Social
Research Council; Medical Research Council; Chief Scientist
Office of the Scottish Government Health Directorates;
National Institute for Health Research/The Department of
Health; The Health and Social Care Research & Development
of the Public Health Agency (Northern Ireland); Wales Office
of Research and Development for Health and Social Care
and the Welsh Assembly Government (grant no. G0900686).
The authors’ contributions are as follows: M. S. and J. C. M.
conceived the systematic review; S. C. and M. S. searched and
collected the data; J. L. acted as a third reviewer during
the different phases of the systematic review; M. S. analysed
the data and wrote the manuscript. All authors contributed
to subsequent analyses, interpretation of the results and the
final revision of the manuscript.
The corresponding author (M. S.) is the guarantor for the
manuscript and had full access to all the data and takes
responsibility for the integrity of the data and the accuracy
of the data analysis.
None of the authors has any conflicts of interest to declare.
References
1. World Health Organization (2011) Global Atlas on Cardiovascular
Disease Prevention and Control. Policies, Strategies
and Interventions. Geneva: World Health Organization.
2. Hansson GK (2005) Inflammation, atherosclerosis, and
coronary artery disease. N Engl J Med 352, 1685–1695.
3. D’Agostino RB, Vasan RS, Pencina MJ, et al. (2008) General
cardiovascular risk profile for use in primary care: the
Framingham Heart Study. Circulation 117, 743–753.
4. Hippisley-Cox J, Coupland C, Vinogradova Y, et al. (2008) Predicting
cardiovascular risk in England and Wales: prospective
derivation and validation of QRISK2. BMJ 336, 1475–1482.
5. Eilat-Adar S, Sinai T, Yosefy C, et al. (2013) Nutritional
recommendations for cardiovascular disease prevention.
Nutrients 5, 3646–3683.
6. Stuart-Shor EM, Berra KA, Kamau MW, et al. (2012)
Behavioral strategies for cardiovascular risk reduction in
diverse and underserved racial/ethnic groups. Circulation
125, 171–184.
7. National Heart, Lung, and Blood Institute (2006) Your
Guide to Lowering Your Blood Pressure with DASH.
NIH Publication no. 06-4082. Bethesda, MD: NIH, National
Heart, Lung, and Blood Institute.
8. Appel LJ, Brands MW, Daniels SR, et al. (2006) Dietary
approaches to prevent and treat hypertension: a scientific
statement from the American Heart Association. Hypertension
47, 296–308.
9. Appel L, Moore T, Obarzanek E, et al. (1997) A clinical trial
of the effects of dietary patterns on blood pressure. N Engl J
Med 336, 1117–1124.
10. Shirani F, Salehi-Abargouei A & Azadbakht L (2013) Effects of
Dietary Approaches to Stop Hypertension (DASH) diet on
some risk for developing type 2 diabetes: a systematic
review and meta-analysis on controlled clinical trials.
Nutrition 29, 939–947.
11. Azadbakht L, Surkan PJ, Esmaillzadeh A, et al. (2011) The
Dietary Approaches to Stop Hypertension eating plan affects
C-reactive protein, coagulation abnormalities, and hepatic
function tests among type 2 diabetic patients. J Nutr 141,
1083–1088.
12. Asemi Z, Samimi M, Tabassi Z, et al. (2013) A randomized
controlled clinical trial investigating the effect of DASH diet
on insulin resistance, inflammation, and oxidative stress in
gestational diabetes. Nutrition 29, 619–624.
13. Azadbakht L, Mirmiran P, Esmaillzadeh A, et al. (2005) Beneficial
effects of a Dietary Approaches to Stop Hypertension
eating plan on features of the metabolic syndrome. Diabetes
Care 28, 2823–2831.
14. Chen ST, Maruthur NM & Appel LJ (2010) The effect of dietary
patterns on estimated coronary heart disease risk: results
from the Dietary Approaches to Stop Hypertension (DASH)
trial. Circ Cardiovasc Qual Outcomes 3, 484–489.
15. Asemi Z, Tabassi Z, Samimi M, et al. (2013) Favourable effects
of the Dietary Approaches to Stop Hypertension diet on
glucose tolerance and lipid profiles in gestational diabetes: a
randomised clinical trial. Br J Nutr 109, 2024–2030.
16. Nowson CA, Worsley A, Margerison C, et al. (2004) Blood
pressure response to dietary modifications in free-living
individuals. J Nutr 134, 2322–2329.
17. Nowson CA, Worsley A, Margerison C, et al. (2005) Blood
pressure change with weight loss is affected by diet type
in men. Am J Clin Nutr 81, 983–989.
18. Appel LJ, Champagne CM, Harsha DW, et al. (2003) Effects
of comprehensive lifestyle modification on blood pressure
control: main results of the PREMIER clinical trial. JAMA
289, 2083–2093.
19. Lopes HF, Martin KL, Nashar K, et al. (2003) DASH diet
lowers blood pressure and lipid-induced oxidative stress in
obesity. Hypertension 41, 422–430.
20. Blumenthal JA, Babyak MA, Sherwood A, et al. (2010) Effects
of the dietary approaches to stop hypertension diet alone
and in combination with exercise and caloric restriction on
insulin sensitivity and lipids. Hypertension 55, 1199–1205.
21. Liberati A, Altman DG, Tetzlaff J, et al. (2009) The PRISMA
statement for reporting systematic reviews and metaanalyses
of studies that evaluate healthcare interventions:
explanation and elaboration. BMJ 339, b2700.
22. Jadad AR, Moore RA, Carroll D, et al. (1996) Assessing the
quality of reports of randomized clinical trials: is blinding
necessary? Control Clin Trials 17, 1–12.
23. Hozo S, Djulbegovic B & Hozo I (2005) Estimating the mean
and variance from the median, range, and the size of a
sample. BMC Med Res Methodol 5, 13.
24. Higgins JPT & Green S (2011) Cochrane Handbook for
Systematic Reviews of Interventions Version 5.1.0 (Updated
March 2011). The Cochrane Collaboration. http://www.
cochrane-handbook.org
14 M. Siervo et al.
British Journal of Nutrition
Downloaded from https://www.cambridge.org/core. IP address: 51.9.206.53, on 08 May 2019 at 20:30:22, subject to the Cambridge Core terms of use, available at https://www.cambridge.org/core/terms. https://doi.org/10.1017/S0007114514003341
25. Higgins JPT & Thompson SG (2002) Quantifying heterogeneity
in a meta-analysis. Stat Med 21, 1539–1558.
26. Lien LF, Brown AJ, Ard JD, et al. (2007) Effects of PREMIER
lifestyle modifications on participants with and without the
metabolic syndrome. Hypertension 50, 609–616.
27. Nowson CA, Wattanapenpaiboon N & Pachett A (2009) Lowsodium
Dietary Approaches to Stop Hypertension-type diet
including lean red meat lowers blood pressure in postmenopausal
women. Nutr Res 29, 8–18.
28. Sacks F, Svetkey L, Vollmer W, et al. (2001) Effects on blood
pressure of reduced dietary sodium and the dietary
approaches to stop hypertension (DASH) diet. N Engl J
Med 344, 3–10.
29. Harsha DW, Sacks FM, Obarzanek E, et al. (2004) Effect of
dietary sodium intake on blood lipids: results from the
DASH-sodium trial. Hypertension 43, 393–398.
30. Conlin PR, Erlinger TP, Bohannon A, et al. (2003) The DASH
diet enhances the blood pressure response to losartan in
hypertensive patients. Am J Hypertens 16, 337–342.
31. Al-Solaiman Y, Jesri A, Mountford WK, et al. (2010) DASH
lowers blood pressure in obese hypertensives beyond
potassium, magnesium and fibre. J Hum Hypertens 24,
237–246.
32. Blumenthal JA, Babyak MA, Hinderliter A, et al. (2010)
Effects of the DASH diet alone and in combination with exercise
and weight loss on blood pressure and cardiovascular
biomarkers in men and women with high blood pressure:
the ENCORE study. Arch Intern Med 170, 126–135.
33. Malloy-McFall J, Barkley JE, Gordon KL, et al. (2010) Effect
of the DASH diet on pre- and stage 1 hypertensive individuals
in a free-living environment. Nutr Metab Insights 3,
15–23.
34. Azadbakht L, Fard NR, Karimi M, et al. (2011) Effects of the
Dietary Approaches to Stop Hypertension (DASH) eating
plan on cardiovascular risks among type 2 diabetic patients:
a randomized crossover clinical trial. Diabetes Care 34,
55–57.
35. Edwards KM, Wilson KL, Sadja J, et al. (2011) Effects on
blood pressure and autonomic nervous system function of
a 12-week exercise or exercise plus DASH-diet intervention
in individuals with elevated blood pressure. Acta Physiol
(Oxf) 203, 343–350.
36. Lin PH, Allen JD, Li YJ, et al. (2012) Blood pressure-lowering
mechanisms of the DASH dietary pattern. J Nutr Metab 2012,
472396.
37. Hummel SL, Seymour EM, Brook RD, et al. (2013) Lowsodium
DASH diet improves diastolic function and
ventricular–arterial coupling in hypertensive heart failure
with preserved ejection fraction. Circ Heart Fail 6, 1165–1171.
38. Ma J, Strub P, Lavori PW, et al. (2013) DASH for asthma: a
pilot study of the DASH diet in not-well-controlled adult
asthma. Contemp Clin Trials 35, 55–67.
39. Salehi-Abargouei A, Maghsoudi Z, Shirani F, et al. (2013)
Effects of Dietary Approaches to Stop Hypertension
(DASH)-style diet on fatal or nonfatal cardiovascular
diseases-incidence: a systematic review and meta-analysis
on observational prospective studies. Nutrition 29, 611–618.
40. Hodson L, Harnden KE, Roberts R, et al. (2010) Does the
DASH diet lower blood pressure by altering peripheral
vascular function? J Hum Hypertens 24, 312–319.
41. Harnden KE, Frayn KN & Hodson L (2010) Dietary
Approaches to Stop Hypertension (DASH) diet: applicability
and acceptability to a UK population. J Hum Nutr Diet 23,
3–10.
42. Hord NG, Tang Y & Bryan NS (2009) Food sources of nitrates
and nitrites: the physiologic context for potential health
benefits. Am J Clin Nutr 90, 1–10.
43. Sacks FM & Campos H (2010) Dietary therapy in hypertension.
N Engl J Med 362, 2102–2112.
44. Al-Solaiman Y, Jesri A, Zhao Y, et al. (2009) Low-sodium
DASH reduces oxidative stress and improves vascular
function in salt-sensitive humans. J Hum Hypertens 23,
826–835.
45. Akita S, Sacks FM, Svetkey LP, et al. (2003) Effects of the Dietary
Approaches to Stop Hypertension (DASH) diet on the pressure–
natriuresis relationship. Hypertension 42, 8–13.
46. Siervo M, Lara J, Ogbonmwan I, et al. (2013) Inorganic
nitrate and beetroot juice supplementation reduces blood
pressure in adults: a systematic review and meta-analysis.
J Nutr 143, 818–826.
47. Mozaffarian D, Appel LJ & Van Horn L (2011) Components
of a cardioprotective diet: new insights. Circulation 123,
2870–2891.
48. Estruch R, Ros E, Salas-Salvado J, et al. (2013) Primary prevention
of cardiovascular disease with a Mediterranean
diet. N Engl J Med 368, 1279–1290.
49. Kastorini C-M, Milionis HJ, Esposito K, et al. (2011) The
effect of Mediterranean diet on metabolic syndrome and
its components: a meta-analysis of 50 studies and 534,906
individuals. J Am Coll Cardiol 57, 1299–1313.
50. Chobanian AV, Bakris GL, Black HR, et al. (2003) Seventh
report of the Joint National Committee on prevention,
detection, evaluation, and treatment of high blood pressure.
Hypertension 42, 1206–1252.
Dietary patterns and cardiovascular risk 15
British Journal of Nutrition
Downloaded from https://www.cambridge.org/core. IP address: 51.9.206.53, on 08 May 2019 at 20:30:22, subject to the Cambridge Core terms of use, available at https://www.cambridge.org/core/terms. https://doi.org/10.1017/S0007114514003341