Published online before print September 15, 2003, doi: 10.1161/01.HYP.0000094221.86888.AE
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(Hypertension. 2003;42:878.)
© 2003 American Heart Association, Inc.
Scientific Contributions |
Influence of Weight Reduction on Blood Pressure
A Meta-Analysis of Randomized Controlled Trials
From the Division of Human Nutrition, Wageningen University (J.E.N., B.E.S., F.J.K., J.M.G.), Wageningen, and the Julius Center for Health Sciences and Primary Care, Utrecht University (D.E.G.), Utrecht, Netherlands.
Correspondence to Dr Johanna M. Geleijnse, Wageningen University, Division of Human Nutrition, PO Box 8129, 6700 EV Wageningen, The Netherlands. E-mail marianne.geleijnse{at}wur.nl
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Abstract |
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Increased body weight is a strong risk factor for hypertension. A meta-analysis of randomized controlled trials was performed to estimate the effect of weight reduction on blood pressure overall and in population subgroups. Twenty-five randomized, controlled trials (comprising 34 strata) published between 1966 and 2002 with a total of 4874 participants were included. A random-effects model was used to account for heterogeneity among trials. A net weight reduction of -5.1 kg (95% confidence interval [CI], -6.03 to -4.25) by means of energy restriction, increased physical activity, or both reduced systolic blood pressure by -4.44 mm Hg (95% CI, -5.93 to -2.95) and diastolic blood pressure by -3.57 mm Hg (95% CI, -4.88 to -2.25). Blood pressure reductions were -1.05 mm Hg (95% CI, -1.43 to -0.66) systolic and -0.92 mm Hg (95% CI, -1.28 to -0.55) diastolic when expressed per kilogram of weight loss. As expected, significantly larger blood pressure reductions were observed in populations with an average weight loss >5 kg than in populations with less weight loss, both for systolic (-6.63 mm Hg [95% CI, -8.43 to -4.82] vs -2.70 mm Hg [95% CI, -4.59 to -0.81]) and diastolic (-5.12 mm Hg [95% CI, -6.48 to -3.75] vs -2.01 mm Hg [95% CI, -3.47 to -0.54]) blood pressure. The effect on diastolic blood pressure was significantly larger in populations taking antihypertensive drugs than in untreated populations (-5.31 mm Hg [95% CI, -6.64 to -3.99] vs -2.91 mm Hg [95% CI, -3.66 to -2.16]). This meta-analysis clearly shows that weight loss is important for the prevention and treatment of hypertension.
Key Words: obesity • body weight • blood pressure • hypertension, obesity • meta-analysis • clinical trials
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Introduction |
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Hypertension is an established risk factor for cardiovascular diseases and is common among obese subjects.1 In Western societies, the prevalence of obesity is increasing, which is likely to increase the burden of hypertension and consequently, of cardiovascular mortality.2 From 1960 to 2000, the prevalence of obesity (body mass index [BMI]
30 kg/m2) for American adults aged 20 to 74 years increased from 13.4% to 30.9%. In 2000, the prevalence of overweight (BMI 25 kg/m2) for American adults was 64.5%.3 Weight loss has been proposed as an effective, nonpharmacologic means for the primary prevention of hypertension.4 An early meta-analysis by Staessen et al5 in 1988 showed a reduction in systolic blood pressure (SBP) and diastolic blood pressure (DBP) of -2.4 and -1.5 mm Hg per kilogram weight loss, respectively. Targeted weight loss interventions in population subgroups might be more effective for the prevention of hypertension than a general-population approach because of interindividual differences in BP and body weight. In the present meta-analysis of 25 randomized controlled trials (RCTs), both the overall and subgroup effects of body weight reduction on BP were assessed. This stratified meta-analysis could strengthen the scientific basis for weight control as an important ingredient of hypertension control programs in the community and in individual patients.
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Methods |
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Selection of Studies
Systematic literature searches in electronic databases (Cab Abstract, Current Contents, FSTA, and MEDLINE Advanced) were conducted for RCTs of weight reduction and BP by using the search phrase (overweight OR weight reduction OR obes* OR weight OR diet*) AND (hypertension OR blood pressure) AND (trial OR intervention OR random* OR study) as title words or MeSH terms. Article reference lists were examined for additional articles.
Trials that fulfilled the following criteria were eligible for meta-analysis: (1) an RCT design, (2) published after 1966, (3) conducted in humans, (4) written in English, and (5) nonpharmacologic reduction of body weight. A total of 97 articles was identified, of which 72 were excluded on the basis of the predefined criteria (literature list of excluded trials is available from the authors); ie, they did not fulfill the inclusion criteria (n=21), the intervention period was <8 weeks (n=2), there were co-interventions from which the effect of weight loss could not be separated (n=28), inappropriate or missing BP data (n=5), study objective was not weight reduction (n=4), or overlapping data with other publication(s) (n=12). Figure 1 shows the number of studies that were identified and excluded at different stages of the selection process. A total of 25 trials6–30 proved eligible for this meta-analysis.
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Data Abstraction
Original articles were retrieved for data abstraction. Two investigators (J.E.N., B.E.S.) independently collected data on population characteristics, study design, and treatment effect on a standard form. For trials in which BP and body weight measurements were recorded at several points in time,6–14 data were abstracted for the intervention period during which the maximal BP effect was achieved. If intermediate measurements were not reported, then the total intervention period was used.15–30 Different types of weight intervention could have been examined within the same trial, ie, energy restriction, increased physical activity, or the combined intervention. When this was the case, these interventions were analyzed as separate strata. For 2 trials, the authors were contacted to obtain missing data.15,25 For 1 trial, in which the age of the trial population was not reported, the mean age of other trial populations combined (ie, 46 years) was imputed in the data analysis.28
Quantitative Data Synthesis
Changes in BP from baseline in the control group were subtracted from changes in the intervention group to obtain the net BP effect of weight reduction. SEs of the treatment effect were also abstracted. If not reported, SEs were derived from SDs or SEs for BP effects within groups, confidence intervals (CIs), test statistics, or probability values. For estimations of SE, a correlation of 0.5 between the variances at baseline and at follow-up within each group was assumed, according to Follmann et al,31 as follows:
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In one article,26 variance measures were not presented, so SE was predicted from all other trials by means of linear regression by using the trial sample size as the independent variable.
A random-effects model was chosen for meta-analysis to account for heterogeneity in BP effect among trials. An advanced statistical technique for meta-analysis of continuous outcomes was applied that takes into account both within- and between-study variation (SAS PROC MIXED).32 The weight factor by which BP effects were weighted was 1/(SE2+
2), where is the between-study variation.
To examine the effect modification of BP response to weight loss, meta-analyses were performed in predefined strata of mean age (
45 vs >45 years), gender (<50% vs 50% females), type of intervention (energy restriction vs increased physical activity vs combined intervention), race (white vs black vs Asian), initial BMI (<30 vs 30 kg/m2), antihypertensive treatment (no vs yes; coded as "yes" if 1 or more subjects were being treated with antihypertensive drugs), weight loss (5 vs >5 kg), and baseline hypertensive status (yes vs no; based on initial BP level only, ie, <140/90 vs 140/90 mm Hg). Stratified meta-analyses were repeated with a multivariate model to adjust for potential confounders, ie, mean age, gender (percent females), initial BP, change in body weight of trial populations, and duration of intervention.
A funnel plot of SBP effect against the weight factor was visually examined for potential publication bias (Figure 2). The funnel plot was roughly symmetrical about the mean-effect size line, except for the outlying study by Reisin et al.27 For this reason, meta-analyses were also performed after exclusion of this study.
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Results |
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Overview of Trials
The population and study characteristics of trials of weight reduction and BP are presented in Table 1. The analysis was based on 25 parallel trials published between 1978 and 2002, comprising 34 strata with a total of 4874 subjects. The duration of intervention until the maximal BP effect (or, if not reported the overall BP effect) was achieved varied between 8 and 260 weeks. Most studies (82%) included both men and women. The mean age of trial populations ranged from 37 to 66 years. Half of the populations were hypertensive (on the basis of initial BP cutoff level of 140/90 mm Hg), and 24% of the populations were taking antihypertensive medication. Mean total duration was 66.6 weeks, and mean duration until the maximal BP effect was achieved was 35.3 weeks. The overall percentage of subjects in RCTs who dropped out after randomization was small (4.8%).
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Changes in Body Weight
Mean initial body weight and BMI were 88.3 kg and 30.7 kg/m2, respectively. Mean net change in body weight of the population was -5.8% of initial body weight, ie, -5.1 kg (95% CI, -6.03 to -4.25), ranging from -0.6 to -11.9 kg. Average weight reductions in the energy restriction, increased physical activity, and combined intervention subgroups were -6.7 kg (95% CI, -8.27 to -5.11), -3.1 kg (95% CI, -4.54 to -1.75), and -6.2 kg (95% CI, -7.87 to -4.55), respectively.
Changes in BP
Forest plots for net changes in SBP and DBP due to weight reduction, with 95% CIs, are presented in Figure 3. An average net weight reduction of -5.1 kg by means of energy restriction, increased physical activity, or the combined intervention was associated with a significant reduction in SBP of -4.44 mm Hg (95% CI, -5.93 to -2.95) and a significant reduction in DBP of -3.57 mm Hg (95% CI, -4.88 to -2.25). When expressed per kilogram of weight loss, reductions in SBP and DBP were -1.05 mm Hg (95% CI, -1.43 to -0.66) and -0.92 mm Hg (95% CI, -1.28 to -0.55), respectively. Exclusion of the outlying study by Reisin et al27 caused a small attenuation of the overall estimates, ie, -4.17 mm Hg (95% CI, -5.55 to -2.80) for SBP and -3.12 mm Hg (95% CI, -4.17 to -2.07) for DBP.
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BP Response in Subgroups
Findings from stratified meta-analyses are presented in Table 2. In the stratified meta-analysis, larger BP reductions were observed in populations with an average weight loss >5 kg than in populations with less weight loss, both for SBP (-6.24 mm Hg [95% CI, -8.06 to -4.41] vs -2.44 mm Hg [95% CI, -4.38 to -0.49]) and DBP (-4.97 mm Hg [95% CI, -6.62 to -3.31] vs -1.97 mm Hg [95% CI, -3.71 to -0.21]). BP reductions were also larger in populations who were taking antihypertensive medication than in untreated populations, both for SBP (-7.00 mm Hg [95% CI, -10.02 to -3.98] vs -3.77 mm Hg [95% CI, -5.33 to -2.22]) and DBP (-5.49 mm Hg [95% CI, -8.06 to -2.93] vs -2.97 mm Hg [95% CI, -4.39 to -1.55]). When subgroups were compared on the basis of initial BP level (<140/90 mm Hg vs 140/90 mm Hg), there was no difference in SBP response, but reductions in DBP were approximately twice as large in hypertensives, although this difference was not statistically significant (-4.92 [95% CI, -6.73 to -3.12] vs -2.35 [95% CI, -4.05 to -0.65]). Weight loss caused larger BP reductions in Asian than in white or black populations, both for SBP and DBP, but findings must be interpreted with caution because of limited statistical power. Age, initial BMI, gender (percent females), and type of intervention did not significantly influence SBP and DBP response to weight loss in unadjusted analyses (Table 2).
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Excluding the study of Reisin et al27 yielded a smaller contrast in BP response between treated and untreated populations, ie, -5.87 mm Hg (95% CI, -8.79 to -2.94) versus -3.79 mm Hg [95% CI, -5.25 to -2.32] for SBP and -3.90 mm Hg (95% CI, -6.10 to -1.70) versus -2.90 mm Hg (95% CI, -4.06 to -1.74) for DBP.
Findings from multivariate stratified analyses were consistent with univariate results (Table 2), except for strongly increased BP estimates for intervention with physical activity (-4.74 mm Hg [95% CI, -7.60 to -1.88] for SBP and -4.65 mm Hg [95% CI, -6.84 to -2.45] for DBP), which resulted from correction for the amount of weight reduction.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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This meta-analysis of 25 RCTs comprising 4874 participants from different ethnic populations showed a BP reduction of -4.4/-3.6 mm Hg for an
5-kg weight loss by means of energy restriction, physical activity, or both. Larger BP reductions were achieved in populations that included subjects taking antihypertensive drugs. Our meta-analysis was based on trials with an RCT design, which have high internal validity. For trials in which BP measurements were repeatedly recorded during follow-up, data were abstracted at the time point when the maximal effect of weight reduction on BP was achieved (32% of the strata). In most of these RCTs, the maximal effect was reached before the end of the trial. A likely explanation is lack of compliance during long-term intervention.
A previous meta-analysis of 12 trials by Staessen et al,5 published in 1988, showed a BP reduction of -2.4/-1.5 mm Hg per kilogram weight loss, which is substantially larger than our estimate (-1.1/-0.9 mm Hg per kg). However, half of the studies in the meta-analysis by Staessen et al5 were not randomized, and only 2 trials overlapped with our study, which might explain this discrepancy. The results of our subgroup analysis by hypertensive status are not consistent with the meta-analysis of 8 RCTs by Ebrahim and Smith,33 in which the BP response was larger in hypertensive populations (-5.2/-5.2 mm Hg) than in normotensive populations (-2.8/-2.3 mm Hg). However, hypertension in our analysis was defined on the basis of BP level only and not on use of antihypertensive medication, which accounts for part of this difference. The Cochrane review by Mulrow et al34 showed that modest weight loss in the range of 3% to 9% of initial body weight was roughly associated with a 3-mm Hg reduction in BP in overweight, hypertensive persons, which is smaller than in our study. Mulrow et al34 did not perform pooling of trials because of marked heterogeneity in study designs, entry criteria, and outcome measurement. Most of the 18 trials in their meta-analysis included combined interventions (eg, weight reduction plus sodium restriction), from which the effect of body weight reduction could not be separated.
A meta-analysis of aerobic exercise and BP by Whelton et al35 showed that BP was significantly reduced even in trials in which overall weight loss was minimal. This suggests that exercise reduces BP independently of changes in body weight. In our multivariate analysis, which was standardized for the amount of weight loss, the effect on DBP was larger when body weight was reduced by physical activity compared with energy restriction. This confirms the idea that physical activity also reduces BP by mechanisms unrelated to weight loss.
Although the exact mechanism of the relation between hypertension and obesity and the effect of weight loss on BP is unknown, there are several plausible biologic pathways.1 The renin-angiotensin-aldosterone system is overactivated in obese subjects, and renin activity and aldosterone concentrations are higher than in lean subjects.36–38 Furthermore, activity of the sympathetic nervous system is increased in hypertensive, obese subjects, which could induce obesity-related renal effects.38–40 Alternatively, there might be inhibition of the natriuretic peptides system, of which the functional effects are vasodilatation and natriuresis.38,41,42 Decreased insulin sensitivity and hyperinsulinemia as part of the metabolic syndrome might also form an essential link between obesity and hypertension, although this interrelation is still not fully understood.43
Additional studies are needed to investigate the long-term effects of weight reduction on BP. It is also important to examine whether weight loss has a persistent beneficial effect on cardiovascular risk, even after regaining weight. Data on weight reduction and BP in children and adolescents are scanty. Trials in this field are clearly warranted because of the increasing prevalence of obesity and hypertension at younger ages, which is becoming a major medical problem and a threat to public health.44
In conclusion, the results from this meta-analysis provide unequivocal evidence that weight loss makes an important contribution to the treatment of hypertension, especially in subjects taking antihypertensive medication. Prevention of weight gain is likely to have a large impact on the burden of hypertension and consequently, cardiovascular diseases in the general population.
Perspectives
This meta-analysis of 25 RCTs showed reductions in SBP and DBP of 1 mm Hg for each kilogram of weight loss. In particular, subjects on antihypertensive drug treatment might benefit from weight reduction. This study provides unequivocal evidence that lifestyle modifications to reduce body weight should be a major component in the treatment of hypertension. The prevalence of overweight in Western societies has strongly increased in the past decades. Weight control in the population is of the utmost importance to prevent an increase in the prevalence of hypertension and consequently, of cardiovascular morbidity and mortality.
Received June 17, 2003; first decision July 10, 2003; accepted August 25, 2003.
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J. A. Cutler, P. D. Sorlie, M. Wolz, T. Thom, L. E. Fields, and E. J. Roccella Trends in Hypertension Prevalence, Awareness, Treatment, and Control Rates in United States Adults Between 1988-1994 and 1999-2004 Hypertension, November 1, 2008; 52(5): 818 - 827. [Abstract] [Full Text] [PDF]
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P. Pacher, P. Mukhopadhyay, R. Mohanraj, G. Godlewski, S. Batkai, and G. Kunos Modulation of the Endocannabinoid System in Cardiovascular Disease: Therapeutic Potential and Limitations Hypertension, October 1, 2008; 52(4): 601 - 607. [Full Text] [PDF]
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 A. L. Hague and R. Touger-Decker Weighing in on Weight Screening in the Dental Office: Practical Approaches J Am Dent Assoc, July 1, 2008; 139(7): 934 - 938. [Abstract] [Full Text] [PDF]
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 D. A. Calhoun, D. Jones, S. Textor, D. C. Goff, T. P. Murphy, R. D. Toto, A. White, W. C. Cushman, W. White, D. Sica, et al. Resistant Hypertension: Diagnosis, Evaluation, and Treatment: A Scientific Statement From the American Heart Association Professional Education Committee of the Council for High Blood Pressure Research Circulation, June 24, 2008; 117(25): e510 - e526. [Abstract] [Full Text] [PDF]
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S. S. Bassuk and J. E. Manson Lifestyle and Risk of Cardiovascular Disease and Type 2 Diabetes in Women: A Review of the Epidemiologic Evidence American Journal of Lifestyle Medicine, June 1, 2008; 2(3): 191 - 213. [Abstract] [PDF]
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D. A. Calhoun, D. Jones, S. Textor, D. C. Goff, T. P. Murphy, R. D. Toto, A. White, W. C. Cushman, W. White, D. Sica, et al. Resistant Hypertension: Diagnosis, Evaluation, and Treatment: A Scientific Statement From the American Heart Association Professional Education Committee of the Council for High Blood Pressure Research Hypertension, June 1, 2008; 51(6): 1403 - 1419. [Abstract] [Full Text] [PDF]
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D. W. Harsha and G. A. Bray Weight Loss and Blood Pressure Control (Pro) Hypertension, June 1, 2008; 51(6): 1420 - 1425. [Full Text] [PDF]
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P. M. Janiszewski, T. J. Saunders, and R. Ross Themed Review: Lifestyle Treatment of the Metabolic Syndrome American Journal of Lifestyle Medicine, April 1, 2008; 2(2): 99 - 108. [Abstract] [PDF]
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 L. P. Svetkey, V. J. Stevens, P. J. Brantley, L. J. Appel, J. F. Hollis, C. M. Loria, W. M. Vollmer, C. M. Gullion, K. Funk, P. Smith, et al. Comparison of Strategies for Sustaining Weight Loss: The Weight Loss Maintenance Randomized Controlled Trial JAMA, March 12, 2008; 299(10): 1139 - 1148. [Abstract] [Full Text] [PDF]
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J. B Keogh, G. D Brinkworth, M. Noakes, D. P Belobrajdic, J. D Buckley, and P. M Clifton Effects of weight loss from a very-low-carbohydrate diet on endothelial function and markers of cardiovascular disease risk in subjects with abdominal obesity Am. J. Clinical Nutrition, March 1, 2008; 87(3): 567 - 576. [Abstract] [Full Text] [PDF]
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 P. F. Bodary Links Between Adipose Tissue and Thrombosis in the Mouse Arterioscler Thromb Vasc Biol, November 1, 2007; 27(11): 2284 - 2291. [Abstract] [Full Text] [PDF]
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 Authors/Task Force Members:, G. Mancia, G. De Backer, A. Dominiczak, R. Cifkova, R. Fagard, G. Germano, G. Grassi, A. M. Heagerty, S. E. Kjeldsen, et al. 2007 Guidelines for the Management of Arterial Hypertension: The Task Force for the Management of Arterial Hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC) Eur. Heart J., June 11, 2007; (2007) ehm236v1. [Full Text] [PDF]
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G. Schillaci and M. Pirro Hypoadiponectinemia: A Novel Link Between Obesity and Hypertension? Hypertension, June 1, 2007; 49(6): 1217 - 1219. [Full Text] [PDF]
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M. Shah, B. Adams-Huet, and A. Garg Effect of high-carbohydrate or high-cis-monounsaturated fat diets on blood pressure: a meta-analysis of intervention trials Am. J. Clinical Nutrition, May 1, 2007; 85(5): 1251 - 1256. [Abstract] [Full Text] [PDF]
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G. Fantuzzi and T. Mazzone Adipose Tissue and Atherosclerosis: Exploring the Connection Arterioscler Thromb Vasc Biol, May 1, 2007; 27(5): 996 - 1003. [Abstract] [Full Text] [PDF]
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 A. R. Wilson and D. D. McAlpine The Effectiveness of Screening for Obesity in Primary Care: Weighing the Evidence Med Care Res Rev, October 1, 2006; 63(5): 570 - 598. [Abstract] [PDF]
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 S.D.H. Malnick and H. Knobler The medical complications of obesity QJM, September 1, 2006; 99(9): 565 - 579. [Full Text] [PDF]
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L. B. Goldstein, R. Adams, M. J. Alberts, L. J. Appel, L. M. Brass, C. D. Bushnell, A. Culebras, T. J. DeGraba, P. B. Gorelick, J. R. Guyton, et al. Primary Prevention of Ischemic Stroke: A Guideline From the American Heart Association/American Stroke Association Stroke Council: Cosponsored by the Atherosclerotic Peripheral Vascular Disease Interdisciplinary Working Group; Cardiovascular Nursing Council; Clinical Cardiology Council; Nutrition, Physical Activity, and Metabolism Council; and the Quality of Care and Outcomes Research Interdisciplinary Working Group: The American Academy of Neurology affirms the value of this guideline. Circulation, June 20, 2006; 113(24): e873 - e923. [Abstract] [Full Text] [PDF]
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 L. B. Goldstein, R. Adams, M. J. Alberts, L. J. Appel, L. M. Brass, C. D. Bushnell, A. Culebras, T. J. DeGraba, P. B. Gorelick, J. R. Guyton, et al. Primary Prevention of Ischemic Stroke: A Guideline From the American Heart Association/American Stroke Association Stroke Council: Cosponsored by the Atherosclerotic Peripheral Vascular Disease Interdisciplinary Working Group; Cardiovascular Nursing Council; Clinical Cardiology Council; Nutrition, Physical Activity, and Metabolism Council; and the Quality of Care and Outcomes Research Interdisciplinary Working Group: The American Academy of Neurology affirms the value of this guideline. Stroke, June 1, 2006; 37(6): 1583 - 1633. [Abstract] [Full Text] [PDF]
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P. J. Elmer, E. Obarzanek, W. M. Vollmer, D. Simons-Morton, V. J. Stevens, D. R. Young, P.-H. Lin, C. Champagne, D. W. Harsha, L. P. Svetkey, et al. Effects of Comprehensive Lifestyle Modification on Diet, Weight, Physical Fitness, and Blood Pressure Control: 18-Month Results of a Randomized Trial Ann Intern Med, April 4, 2006; 144(7): 485 - 495. [Abstract] [Full Text] [PDF]
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 J. D. Fernstrom, A. P. Courcoulas, P. R. Houck, and M. H. Fernstrom Long-term Changes in Blood Pressure in Extremely Obese Patients Who Have Undergone Bariatric Surgery. Arch Surg, March 1, 2006; 141(3): 276 - 283. [Abstract] [Full Text] [PDF]
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D. G. Simons-Morton, E. Obarzanek, and J. A. Cutler Obesity Research--Limitations of Methods, Measurements, and Medications JAMA, February 15, 2006; 295(7): 826 - 828. [Full Text] [PDF]
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L. J. Appel, M. W. Brands, S. R. Daniels, N. Karanja, P. J. Elmer, and F. M. Sacks Dietary Approaches to Prevent and Treat Hypertension: A Scientific Statement From the American Heart Association Hypertension, February 1, 2006; 47(2): 296 - 308. [Abstract] [Full Text] [PDF]
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 J. G Ray Screening and active management reduced perinatal complications more than routine care in gestational diabetes Evid. Based Med., December 1, 2005; 10(6): 171 - 171. [Full Text] [PDF]
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 Prepared by: British Cardiac Society, British Hype JBS 2: Joint British Societies' guidelines on prevention of cardiovascular disease in clinical practice Heart, December 1, 2005; 91(suppl_5): v1 - v52. [Full Text] [PDF]
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J.A. Iestra, D. Kromhout, Y.T. van der Schouw, D.E. Grobbee, H.C. Boshuizen, and W.A. van Staveren Effect Size Estimates of Lifestyle and Dietary Changes on All-Cause Mortality in Coronary Artery Disease Patients: A Systematic Review Circulation, August 9, 2005; 112(6): 924 - 934. [Abstract] [Full Text] [PDF]
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 M. J. Chapman, M. J. Craven, and D. D. Chadwick Fighting fit?: An evaluation of health practitioner input to improve healthy living and reduce obesity for adults with learning disabilities J Intellect Disabil., June 1, 2005; 9(2): 131 - 144. [Abstract] [PDF]
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L. P. Svetkey Management of Prehypertension Hypertension, June 1, 2005; 45(6): 1056 - 1061. [Full Text] [PDF]
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L. Aucott, A. Poobalan, W. C. S. Smith, A. Avenell, R. Jung, and J. Broom Effects of Weight Loss in Overweight/Obese Individuals and Long-Term Hypertension Outcomes: A Systematic Review Hypertension, June 1, 2005; 45(6): 1035 - 1041. [Abstract] [Full Text] [PDF]
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C. A Nowson, A. Worsley, C. Margerison, M. K Jorna, S. J Godfrey, and A. Booth Blood pressure change with weight loss is affected by diet type in men Am. J. Clinical Nutrition, May 1, 2005; 81(5): 983 - 989. [Abstract] [Full Text] [PDF]
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 K. P. Davy and J. E. Hall Obesity and hypertension: two epidemics or one? Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2004; 286(5): R803 - R813. [Abstract] [Full Text] [PDF]
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 BP Effect of Weight Reduction Journal Watch Cardiology, January 9, 2004; 2004(109): 3 - 3. [Full Text]
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