2006：饮食疗法预防和治疗高血压（AHA）

ISSN: 1524-4563 Copyright © 2006 American Heart Association. All rights reserved. Print ISSN: 0194-911X. Online 72514 Hypertension is published by the American Heart Association. 7272 Greenville Avenue, Dallas, TX DOI: 10.1161/01.HYP.0000202568.01167.B6 2006;47;296-308 Hypertension Elmer and Frank M. Sacks Lawrence J. Appel, Michael W. Brands, Stephen R. Daniels, Njeri Karanja, Patricia J. From the American Heart Association Dietary Approaches to Prevent and Treat Hypertension: A Scientific Statement http://hyper.ahajournals.org/cgi/content/full/47/2/296 located on the World Wide Web at: The online version of this article, along with updated information and services, is http://www.lww.com/reprints Reprints: Information about reprints can be found online at journalpermissions@lww.com 410-528-8550. E-mail: Fax:Kluwer Health, 351 West Camden Street, Baltimore, MD 21202-2436. Phone: 410-528-4050. Permissions: Permissions & Rights Desk, Lippincott Williams & Wilkins, a division of Wolters http://hyper.ahajournals.org/subscriptions/ Subscriptions: Information about subscribing to Hypertension is online at by on April 12, 2009 hyper.ahajournals.orgDownloaded from Dietary Approaches to Prevent and Treat Hypertension A Scientific Statement From the American Heart Association Lawrence J. Appel, MD, MPH; Michael W. Brands, PhD; Stephen R. Daniels, MD, PhD; Njeri Karanja, PhD; Patricia J. Elmer, PhD; Frank M. Sacks, MD Abstract—A substantial body of evidence strongly supports the concept that multiple dietary factors affect blood pressure (BP). Well-established dietary modifications that lower BP are reduced salt intake, weight loss, and moderation of alcohol consumption (among those who drink). Over the past decade, increased potassium intake and consumption of dietary patterns based on the “DASH diet” have emerged as effective strategies that also lower BP. Of substantial public health relevance are findings related to blacks and older individuals. Specifically, blacks are especially sensitive to the BP-lowering effects of reduced salt intake, increased potassium intake, and the DASH diet. Furthermore, it is well documented that older individuals, a group at high risk for BP-related cardiovascular and renal diseases, can make and sustain dietary changes. The risk of cardiovascular disease increases progressively throughout the range of BP, beginning at 115/75 mm Hg. In view of the continuing epidemic of BP-related diseases and the increasing prevalence of hypertension, efforts to reduce BP in both nonhypertensive and hypertensive individuals are warranted. In nonhypertensive individuals, dietary changes can lower BP and prevent hypertension. In uncomplicated stage I hypertension (systolic BP of 140 to 159 mm Hg or diastolic BP of 90 to 99 mm Hg), dietary changes serve as initial treatment before drug therapy. In those hypertensive patients already on drug therapy, lifestyle modifications, particularly a reduced salt intake, can further lower BP. The current challenge to healthcare providers, researchers, government officials, and the general public is developing and implementing effective clinical and public health strategies that lead to sustained dietary changes among individuals and more broadly among whole populations. (Hypertension. 2006;47:296-308.) Key Words: AHA Scientific Statements � blood pressure � diet � hypertension Elevated blood pressure (BP) remains an extraordinarilycommon and important risk factor for cardiovascular and renal diseases, including stroke, coronary heart disease, heart failure, and kidney failure. According to the most recent NHANES survey (1999 to 2000), 27% of adult Americans have hypertension (systolic BP �140 mm Hg, diastolic BP �90 mm Hg, or use of antihypertensive medication), and another 31% have prehypertension (systolic BP of 120 to 139 mm Hg or diastolic BP of 80 to 89 mm Hg, not on medication).1 Prehypertensive individuals have a high prob- ability of developing hypertension and carry an excess risk of cardiovascular disease as compared with those with a normal BP (systolic BP �120 mm Hg and diastolic BP �80 mm Hg).2 It has been estimated that among adults �50 years of age, the lifetime risk of developing hypertension approaches 90%.3 Recent data indicate that the prevalence of hypertension is increasing4 and that control rates among those with hypertension remain low.5 On average, blacks have higher BP than nonblacks,4 as well as an increased risk of BP-related complications, particularly stroke6,7 and kidney failure.8 BP is a strong, consistent, continuous, independent, and etiologically relevant risk factor for cardiovascular and renal disease.9 Notably, no evidence of a BP threshold exists; ie, the risk of cardiovascular disease increases progressively throughout the range of BP, including the prehypertensive range.10 It has been estimated that almost a third of BP-related deaths from coronary heart disease occur in individuals with BP in the nonhypertensive range.11 Elevated BP results from environmental factors, genetic factors, and interactions among these factors. Of the environ- mental factors that affect BP (diet, physical inactivity, toxins, The American Heart Association makes every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside relationship or a personal, professional, or business interest of a member of the writing panel. Specifically, all members of the writing group are required to complete and submit a Disclosure Questionnaire showing all such relationships that might be perceived as real or potential conflicts of interest. This statement was approved by the American Heart Association Science Advisory and Coordinating Committee on November 4, 2005. A single reprint is available by calling 800-242-8721 (US only) or writing the American Heart Association, Public Information, 7272 Greenville Ave, Dallas, TX 75231-4596. Ask for reprint No. 71-0353. To purchase additional reprints: up to 999 copies, call 800-611-6083 (US only) or fax 413-665-2671; 1000 or more copies, call 410-528-4121, fax 410-528-4264, or e-mail kramsay@lww.com. To make photocopies for personal or educational use, call the Copyright Clearance Center, 978-750-8400. Expert peer review of AHA Scientific Statements is conducted at the AHA National Center. For more on AHA statements and guidelines development, visit http://www.americanheart.org/presenter.jhtml?identifier�3023366. © 2006 American Heart Association, Inc. Hypertension is available at http://www.hypertensionaha.org DOI: 10.1161/01.HYP.0000202568.01167.B6 296 AHA Scientific Statement by on April 12, 2009 hyper.ahajournals.orgDownloaded from and psychosocial factors), dietary factors have a prominent, and likely predominant, role in BP homeostasis. In nonhy- pertensive individuals, including those with prehypertension, dietary changes that lower BP have the potential to prevent hypertension and more broadly to reduce BP and thereby lower the risk of BP-related clinical complications. Indeed, even an apparently small reduction in BP, if applied to an entire population, could have an enormous beneficial impact. For instance, it has been estimated that a 3–mm Hg reduction in systolic BP could lead to an 8% reduction in stroke mortality and a 5% reduction in mortality from coronary heart disease (see Figure 1).12 In uncomplicated stage I hyperten- sion (systolic BP of 140 to 159 mm Hg or diastolic BP of 90 to 99 mm Hg), dietary changes can serve as initial treatment before the start of drug therapy. Among hypertensive indi- viduals who are already on drug therapy, dietary changes, particularly a reduced salt intake, can further lower BP and facilitate medication step-down. In general, the extent of BP reduction from dietary therapies is greater in hypertensive than in nonhypertensive individuals. The purpose of this scientific statement, which updates prior AHA recommendations,13 is to summarize evidence on the efficacy of diet-related factors that lower BP and to present recommendations for healthcare providers, policy makers, and the general public. This document relies primar- ily on evidence as compiled in systematic reviews. Individual studies that document seminal findings are also discussed. Recommendations in this document are broadly consistent with those expressed in federal policy documents.9,14 Dietary Factors That Lower BP See Table 1 for a summary of diet-related lifestyle modifica- tions that effectively lower BP. Weight Loss A substantial and largely consistent body of evidence from observational studies and clinical trials documents that weight is directly associated with BP. The importance of this relationship is reinforced by the high and increasing preva- lence of overweight and obesity in the United States and throughout the world. Approximately 65% of US adults have a body mass index (BMI) �25 kg/m2 and therefore are classified as either overweight or obese; �30% of US adults are clinically obese (BMI �30 kg/m2).15 In US children and adolescents, the prevalence of overweight has increased over the past decade, as have levels of BP.16 With rare exception, clinical trials have documented that weight loss lowers BP. Importantly, reductions in BP occur before, and without, attainment of a desirable body weight. In one meta-analysis that aggregated results across 25 trials, mean systolic and diastolic BP reductions from an average weight loss of 5.1 kg were 4.4 and 3.6 mm Hg, respectively.17 In subgroup analyses, BP reductions were similar for nonhy- pertensive and hypertensive subjects but were greater in those who lost more weight. Within-trial dose–response analy- ses18,19 and prospective observational studies20 also document that greater weight loss leads to greater BP reduction. Additional trials have documented that modest weight loss, with or without sodium reduction, can prevent hypertension by �20% among overweight, prehypertensive individuals21 and can facilitate medication step-down and drug withdraw- al.22,23 Lifestyle intervention trials have uniformly achieved short-term weight loss, primarily through a reduction in total caloric intake. In several instances, substantial weight loss has been sustained over �3 years.23,24 Maintaining a high level of physical activity is well recognized as a critical factor in sustaining weight loss. Whether weight loss can blunt the age-related rise in BP is unclear. In one trial with long-term follow-up, those individuals who sustained a �10-lb weight loss achieved a lower BP that nonetheless rose over time.19 In aggregate, available evidence strongly supports weight reduction, ideally attainment of a BMI �25 kg/m2, as an effective approach to prevent and treat hypertension. More importantly, in view of the well-recognized difficulties of sustaining weight loss, efforts to prevent weight gain among those who have normal body weight are critically important. Figure 1. Estimated effects of population-wide shifts in systolic BP distributions on mortality. Adapted with permission from Stamler.12 TABLE 1. Diet-Related Lifestyle Modifications That Effectively Lower BP Lifestyle Modification Recommendation Weight loss For overweight or obese persons, lose weight, ideally attaining a BMI �25 kg/m2; for nonoverweight persons, maintain desirable BMI �25 kg/m2 Reduced salt intake Lower salt (sodium chloride) intake as much as possible, ideally to �65 mmol/d sodium (corresponding to 1.5 g/d of sodium or 3.8 g/d sodium chloride) DASH-type dietary patterns Consume a diet rich in fruits and vegetables (8–10 servings/d), rich in low-fat dairy products (2–3 servings/d), and reduced in saturated fat and cholesterol Increased potassium intake Increase potassium intake to 120 mmol/d (4.7 g/d), which is also the level provided in DASH-type diets Moderation of alcohol intake For those who drink alcohol, consume �2 alcoholic drinks/d (men) and �1 alcoholic drink/d (women) Appel et al Dietary Prevention and Treatment of Hypertension 297 by on April 12, 2009 hyper.ahajournals.orgDownloaded from Reduced Salt Intake On average, as dietary salt (sodium chloride) intake rises, so does BP. Evidence includes results from animal studies, epidemiological studies, clinical trials, and meta-analyses of trials. To date, �50 randomized trials have been conducted. In one of the most recent meta-analyses,25 a median reduction in urinary sodium of �1.8 g/d (78 mmol/d) lowered systolic BP and diastolic BP by 2.0 and 1.0 mm Hg in nonhyperten- sive and by 5.0 and 2.7 mm Hg in hypertensive individuals. The most persuasive evidence about the effects of salt on BP comes from rigorously controlled, dose–response tri- als.26–28 Each of these 3 trials tested at least 3 sodium levels, and each documented statistically significant, direct, progres- sive dose–response relationships. The largest of the dose– response trials, the DASH-Sodium trial, tested the effects of 3 different sodium intakes separately in 2 distinct diets: the DASH (Dietary Approaches to Stop Hypertension) diet (see subsequent section for a complete description) and a control diet more typical of what Americans eat. As estimated from 24-hour urine collections, the 3 sodium levels (lower, inter- mediate, and higher) provided 65, 107, and 142 mmol/d, respectively, corresponding to approximate intakes of 1.5, 2.5, and 3.3 g, respectively. The main results of the DASH-Sodium trial are shown in Figure 2. The BP response to sodium reduction, while direct and progressive, was nonlinear. Specifically, decreasing so- dium intake by �0.9 g/d (40 mmol/d) caused a greater lowering of BP when the starting sodium intake was 100 mmol/d than when it was above this level. In subgroup analyses of the DASH-Sodium trial,29,30 reduced sodium intake significantly lowered BP in each of the major sub- groups studied (ie, men, women, blacks, and nonblacks). Importantly, sodium reduction significantly lowered BP in nonhypertensive individuals on both diets. In addition to reduced BP, clinical trials have documented that a reduced sodium intake can prevent hypertension (relative risk reduction of�20% with or without concomitant weight loss),21 can lower BP in the setting of antihypertensive medication,31,32 and can facilitate hypertension control.22,23 In observational studies, reduced sodium intake is associated with a blunted age-related rise in systolic BP.33 In other observational studies, reduced salt intake is associated with a reduced risk of atherosclerotic cardiovascular events34,35 and congestive heart failure.36 The BP response to changes in dietary sodium intake is heterogeneous37 (as is the BP response to other dietary changes). Despite use of the terms “salt sensitive” and “salt resistant” to classify individuals in research studies, the change in BP in response to a change in salt intake is not binary.38 Rather, the reduction in BP from a reduced sodium intake has a continuous distribution, with individuals having greater or lesser degrees of BP reduction. In general, the effects of sodium reduction on BP tend to be greater in blacks; middle-aged and older persons; and individuals with hypertension, diabetes, or chronic kidney disease. These groups tend to have a less responsive renin-angiotensin- aldosterone system.39 It has been hypothesized that salt sensitivity is a phenotype that reflects subclinical renal disease.40 As discussed later in this statement, genetic and dietary factors also influence the response to sodium reduc- tion. For example, the rise in BP for a given increase in sodium intake is blunted in the setting of either the DASH diet28 or high potassium intake.41,42 Some salt intake is required. Recently, an Institute of Medicine committee set 1.5 g/d (65 mmol/d) sodium as an adequate intake level, primarily to ensure nutrient adequa- cy.43 Although a sodium intake below this level is associated with lower BP,44 little information is available about the nutrient content of diets that provide �1.5 g/d of sodium. From the DASH-Sodium trial, it is apparent that Western- type diets can provide this level of sodium intake and that such a diet can also provide adequate levels of other nutri- ents.45 Because the relationship between sodium intake and BP is direct and progressive without an apparent threshold, it is difficult to set an upper level of sodium intake, which also could be 1.5 g/d (65 mmol/d). However, in view of the available food supply and the currently high levels of sodium consumption, a reduction in sodium intake to 1.5 g/d (65 mmol/d) is not easily achievable at present. In the interim, a reasonable recommendation is an upper limit of 2.3 g/d (100 mmol/d), which is similar to earlier recommendations for the prevention and treatment of hypertension.9,14 In aggregate, available data strongly support current, population-wide recommendations to lower salt intake. To reduce salt intake, consumers should choose foods low in salt and limit the amount of salt added to food. However, because �75% of consumed salt comes from processed foods,46 any meaningful strategy to reduce salt intake must involve the efforts of food manufacturers and restaurants, which should progressively reduce the salt added to foods by 50% over the next 10 years.9,47 Increased Potassium Intake High potassium intake is associated with reduced BP. Evi- dence includes animal studies, observational epidemiological studies, �30 clinical trials, and meta-analyses of these trials. Although data from individual trials have been inconsistent, 3 meta-analyses of these trials have documented a significant inverse relationship between potassium intake and BP in nonhypertensive and hypertensive individuals.48–50 In the meta-analysis by Whelton et al,49 average systolic and dia- Figure 2. Mean systolic BP changes in the DASH-Sodium trial. Solid lines indicate the effects of sodium reduction in the 2 diets; hatched lines, the effects of the DASH diet at each sodium level. Adapted with permission from Sacks et al.28 298 Hypertension February 2006 by on April 12, 2009 hyper.ahajournals.orgDownloaded from stolic BP reductions associated with a net increase in urinary potassium excretion of 2 g/d (50 mmol/d) were 4.4 and 2.5 mm Hg in hypertensive and 1.8 and 1.0 mm Hg in nonhypertensive individuals. Because no trial has tested the effects of �3 levels of dietary potassium intake on BP, inferences on the dose– response relationship between potassium and BP must be drawn from individual trials. Available data suggest that increased potassium has beneficial effects on BP in the setting of a low intake (eg, 1.3 to 1.4 g/d, or 35 to 40 mmol/d)51 or a much higher intake (eg, 3.3 g/d, or 84 mmol/d).52 Potassium reduces BP to a greater extent in blacks than in whites.49 In several trials, the effects of increased potassium intake in blacks have been particularly striking.53 Because a high potassium intake can be achieved through diet rather than pills and because potassium derived from foods is also accompanied by a variety of other nutrients, the preferred strategy to increase potassium intake is to consume foods such as fruits and vegetables that are rich in potassium, rather than supplements. In the DASH trial, the 2 groups that increased fruit and vegetable consumption both lowered BP.28,54 The 2100-kcal version of the DASH diet provides �4.7 g/d (120 mmol/d) potassium.55 Another trial docu- mented that increased fruit and vegetable consumption lowers BP, but it did not specify the amount of potassium provided in the fruits and vegetables.56 The effects of potassium on BP depend on the concurrent intake of salt and vice versa. Specifically, an increased intake of potassium has a greater BP-lowering effect in the context of a higher salt intake and lesser BP reduction in the setting of a lower salt intake. Conversely, the BP reduction from a reduced