Elevated blood pressure (BP) remains an extraordinarily common and important risk factor for cardiovascular (CV) and renal diseases throughout the world. According to the 2011-2012 National Health and Nutrition Examination Survey (NHANES), around 70 million adult Americans (29%) have hypertension (a systolic BP ≥ 140 mm Hg, a diastolic BP ≥ 90 mm Hg, or are being treated with antihypertensive medication), and at least as many Americans have prehypertension (systolic BP of 120 to 139 mm Hg or diastolic BP of 80 to 89 mm Hg, not on medication). Regrettably, the prevalence of hypertension remains essentially unchanged for the past 2 decades, and control rates remain low, at about 53%.
Systolic BP progressively rises with age, such that hypertension becomes almost ubiquitous among the elderly. As a result of the age-related rise in systolic BP, around 90% of adult Americans will develop hypertension over their lifetime. Elevated BP afflicts both men and women. African Americans, on average, have higher BP than non-African Americans, as well as an increased risk of BP-related disease, particularly stroke and kidney disease.
Blood pressure is a strong, consistent, continuous, independent and etiologically relevant risk factor for CV and renal disease. Importantly, there is no evidence of a BP threshold, that is, the risk of CV disease increases progressively throughout the range of BP, including in the prehypertensive range. It has been estimated that almost a third of BP-related deaths from coronary heart disease (CHD) occur in individuals with BP in the nonhypertensive range. Accordingly, prehypertensive individuals not only have a high probability of developing hypertension, but also carry an excess risk of CV disease compared with those with a normal BP (systolic BP < 120 mm Hg and diastolic BP < 80 mm Hg). About 54% of strokes and 47% of ischemic heart disease events worldwide have been attributed to an elevated BP.
Elevated BP results from environmental factors (including dietary factors), genetic factors, and interactions among these factors. Of the environmental factors that affect BP (diet, physical inactivity, toxins, and psychosocial factors), diet likely has the predominant role in BP homeostasis. Well-established dietary modifications that lower BP are a reduced sodium intake, weight loss, moderation of alcohol consumption (among those who drink excessively), and healthy dietary patterns, specifically, dietary approaches to stop hypertension (DASH)-style diets, vegetarian diets, and to a lesser extent, Mediterranean-style diets.
In nonhypertensive individuals, dietary changes that lower BP have the potential to prevent hypertension and reduce the risk of BP-related CV disease. Indeed, even an apparently small BP reduction, if applied broadly to an entire population, could have an enormous, beneficial impact. For example, it has been estimated that a 3 mm Hg average reduction in systolic BP could lead to an 8% reduction in stroke mortality and a 5% reduction in mortality from CHD (see Fig. 21.1 ). In uncomplicated stage I hypertension (systolic BP 140 to 159 mm Hg or diastolic BP 90 to 99 mm Hg), dietary changes can serve as first-line therapy before antihypertensive medication. Among hypertensive individuals who are already on medication, dietary changes can further lower BP and make it possible to reduce the number and doses of medications. In general, the magnitude of BP reduction from dietary changes is greater in hypertensive individuals than in nonhypertensive individuals.
Although dietary changes lower BP, there is considerably less evidence on whether dietary changes blunt the age-related rise in systolic BP. On average, systolic BP rises by around 0.6 mm Hg per year. Efforts to prevent this age-associated rise in systolic BP hold the greatest promise as a means to prevent elevated BP and curb the epidemic of BP-related disease. Unfortunately, even the longest diet-BP intervention trials have lasted less than 5 years. Whether the BP reductions observed in these trials have merely shifted the age-associated rise in BP curve downward, without a change in slope ( Fig. 21.2A ) or actually reduced its slope ( Fig. 21.2B ) cannot be determined. Still, evidence from migration studies, ecologic studies, and most recently observational analyses of trial data, suggest that dietary factors should reduce the rise in systolic BP with age.
The objective of this chapter is to synthesize evidence on the relationship of diet and BP. The summary of evidence and corresponding recommendations largely reflect previous reviews. Table 21.1 provides a summary of this evidence, whereas Table 21.2 provides a summary of recommendations.
| Hypothesized Effect | Evidence | |
|---|---|---|
| Weight | direct | ++ |
| Sodium chloride (Salt) | direct | ++ |
| Potassium | inverse | ++ |
| Magnesium | inverse | +/− |
| Calcium | inverse | +/− |
| Alcohol | direct | ++ |
| Fat | ||
| Saturated fat | direct | +/− |
| Omega-3 polyunsaturated fat | inverse | ++ |
| Omega-6 polyunsaturated fat | inverse | +/− |
| Monounsaturated fat | inverse | + |
| Protein | ||
| Total protein | uncertain | + |
| Vegetable protein | inverse | + |
| Animal protein | uncertain | +/− |
| Carbohydrate | uncertain | +/− |
| Fiber | inverse | + |
| Cholesterol | direct | +/− |
| Vitamin C | uncertain | +/− |
| Dietary Patterns | ||
| Vegetarian diets | inverse | ++ |
| DASH diet | inverse | ++ |
| Mediterranean | inverse | + |
| Lifestyle Modification | Recommendation |
|---|---|
| Weight loss | For overweight or obese persons, lose weight, ideally attaining a body mass index < 25 kg/m 2 For nonoverweight persons, maintain desirable body mass index < 25 kg/m 2 |
| Reduced sodium intake | Lower sodium intake as much as possible, with a goal of no more than 2300 mg/day in the general population and no more than 1500 mg/day in blacks, middle- and older-aged persons, and individuals with hypertension, diabetes, or chronic kidney disease |
| Dietary pattern | Consume a dietary approach to stop hypertension (DASH)-style dietary pattern rich in fruits and vegetables (8 to 10 servings/day), rich in low-fat dairy products (2 to 3 servings/day), and reduced in saturated fat and cholesterol. Vegetarian diets and to a lesser extent, Mediterranean style diets, are effective options |
| Increased potassium intake | Increase potassium intake to 4.7 gm/day, which is also the level provided in the DASH diet |
| Moderation of alcohol intake | For those who drink alcohol, consume ≤ 2 alcoholic drinks/day (men) and ≤ 1 alcohol drinks/day (women) a |
a One alcoholic drink is defined as 12 oz of regular beer, 5 oz of wine (12% alcohol), or 1.5 oz of 80 proof distilled spirits.
Dietary Factors That Reduce Blood Pressure
Weight Loss
Weight is directly associated with BP. The importance of this relationship is reinforced by the high and increasing prevalence of obesity throughout the world. In the United States, around 69% of adults have a body mass index (BMI) 25 kg/m 2 or higher and therefore are classified as either overweight or obese; around 35% of adults are obese (BMI ≥ 30 kg/m 2 ). Likewise, among infants, toddlers, children and adolescents, the prevalence of high weight persists, with scant evidence of any improvement.
Weight loss lowers BP. Reductions in BP occur before, and even without, attainment of a desirable body weight. In a meta-analysis of 25 trials, an average weight loss of 5.1 kg reduced systolic BP by a mean of 4.4 mm Hg and diastolic BP by a mean of 3.6 mm Hg. In subgroup analyses, BP reductions were greater in those who lost more weight. Within trial, dose-response analyses and observational studies, also provide evidence that greater weight loss leads to greater BP reduction. However, given the potential for huge reductions in weight, a linear dose response relationship is unlikely.
Other research has documented that modest weight loss, with or without sodium reduction, can prevent hypertension by around 20% among overweight, nonhypertensive individuals, and can facilitate the reduction of the number and doses of medications. Behavioral intervention trials have uniformly achieved short-term weight loss, primarily through a reduction in energy intake. In several instances, substantial weight loss has also been maintained over 3 or more years. Regular physical activity is well-recognized as a critical factor in sustaining weight loss. Whether or not weight loss can blunt the age-related rise in systolic BP is uncertain. In one of the longest weight loss trials, those individuals who sustained a greater than 10-pound weight loss achieved a lower BP that nonetheless rose over time (see Fig. 21.3 ).
In aggregate, available evidence strongly supports weight reduction as an effective approach to prevent and treat hypertension.
Reduced Salt (Sodium Chloride) Intake
On average, as dietary sodium intake rises, so does BP. Available types of evidence include animal studies, epidemiologic studies, dose-response trials, and meta-analyses of trials. To date, over 100 randomized trials have been performed. In one of the most recent meta-analyses, a reduction in sodium intake of 2.3 grams per day lowered systolic BP by 3.8 in adults; larger BP reductions occurred in older rather than younger persons, African Americans compared with whites, and hypertensive individuals compared with normotensive individuals. In a small but well-done trial of patients with medication-treated, resistant hypertension, reducing sodium intake by around 4.5 grams per day lowered systolic/diastolic BP by 22.7/9.1 mm Hg.
The most persuasive evidence on the effects of sodium intake on BP comes from rigorously controlled, dose-response studies. Each of these trials tested at least three sodium levels, and each documented statistically significant, direct, progressive, dose-response relationships. The largest of these trials, the DASH Sodium trial, tested the effects of three different sodium intakes separately in two diets: the DASH diet (see subsequent section) and a control diet more typical of what Americans usually eat. As estimated from 24-hour urine collections, the three sodium levels (termed lower, intermediate, and higher) provided 65, 107, and 142 mmol of sodium per day, respectively (corresponding to 1.5, 2.5, and 3.3 g per day).
The main results of this trial are displayed in Fig. 21.4 . The BP response to sodium reduction, although direct and progressive, was nonlinear. Decreasing sodium intake by approximately 0.9 grams per day (40 mmol/day) caused a greater BP reduction when the starting sodium intake was below 100 mmol per day than when it was above this level. In subgroup analyses of this trial, a reduced sodium intake significantly lowered BP in each of the major subgroups studied (i.e., African American, non-African American, men, women). Importantly, sodium reduction significantly lowered BP in nonhypertensive individuals on both diets.
In addition to lowering BP, trials have documented that a reduced sodium intake can prevent hypertension (relative risk reduction of ∼20% with or without concomitant weight loss), can lower BP even in the setting of BP-lowering medications, and can improve hypertension control. In observational studies, a reduced sodium intake is associated with a blunted age-related rise in systolic BP. Several observational studies have explored the relationship of sodium intake with CV disease. These reports have been notable for their inconsistent and occasionally paradoxical results, which likely result from methodological limitations, particularly, the potential for reverse causality and the challenge of accurately estimating usual sodium intake.
To date, few trials have reported the effects of a reduced sodium intake on clinical CV events. Two trials tested reduced sodium lifestyle interventions, and one trial assessed the effects of a reduced sodium/high potassium salt substitute. In each, there was a 21% to 41% reduction in clinical CV disease events in those who received the reduced sodium intervention (significant reduction in 2 studies ). A fourth trial with few CVD outcomes had a null result. In a meta-analysis of these trials, there was a 20% reduction in CVD outcomes. Hence, direct evidence from trials, albeit limited, is consistent with indirect evidence on the health benefits of sodium reduction.
Similar to other interventions, the BP response to changes in dietary sodium intake is heterogeneous. Despite attempts to classify individuals in research studies as salt sensitive and salt resistant, the change in BP in response to a change in sodium intake is not binary. Rather, the change in BP from a reduced sodium intake has a continuous distribution, that is, individuals have greater or lesser degrees of BP reduction. In general, the extent of BP reduction as a result of reduced sodium intake is greater in African Americans, middle-aged and older-aged persons, and individuals with hypertension and likely those with diabetes or kidney disease. These groups tend to have a less responsive renin-angiotensin-aldosterone system. It has been hypothesized that sodium sensitivity is a phenotype that reflects subclinical kidney dysfunction. As discussed later, genetic and dietary factors also influence the response to sodium. The rise in BP for a given increase in sodium is blunted in the setting of either the DASH diet or a high dietary potassium intake.
A reduced sodium intake should have other beneficial effects that are independent of its effects on BP. Potential benefits include a reduced risk of subclinical CVD (i.e., left ventricular hypertrophy, ventricular fibrosis, and diastolic dysfunction), kidney damage, gastric cancer, and disordered mineral metabolism (i.e., increased urinary calcium excretion, potentially leading to osteoporosis). Specifically, in cross-sectional studies, left ventricular (LV) mass is directly related to sodium intake, and one small trial in the early 1990s documented that sodium reduction can reduce LV mass.
Importantly, there is no convincing or consistent evidence of harm from a reduced sodium intake. Although some sodium intake is essential, there is no evidence that inadequate sodium intake is a public health problem. Extreme sodium reduction to less than 20 mmol per day might adversely affect blood lipids and insulin resistance; however, moderate sodium reduction has no such effects. A potential adverse effect of a reduced sodium intake is an increase in plasma renin activity (PRA) and uric acid. However, in contrast to the well-accepted benefits of BP reduction, the clinical relevance of modest rises in PRA and uric acid as a result of sodium reduction and other antihypertensive therapies is uncertain. In fact, thiazide diuretics, a class of antihypertensive drug therapies that raises PRA and uric acid substantially reduces CV disease risk.
Available evidence supports population-wide sodium reduction, as recommended by the U.S. Dietary Guidelines for Americans and numerous other organizations. Current dietary guidelines recommend an upper limit of 2300 mg per day in the general population and an upper limit of 1500 mg per day for African American, middle-aged and older-aged persons, and individuals with hypertension, diabetes, or chronic kidney disease (CKD); together these groups represent well over 50% of U.S. adults. In this setting, the American Heart Association set 1.5 gm (65 mmol) of sodium per day as the recommended upper limit of intake for all Americans. Survey data indicate that most children and adults exceed this limit.
In summary, available data strongly support current, population-wide recommendations to lower sodium intake. Consumers should choose foods low in sodium and limit the amount of sodium added to food. However, because over 75% of consumed sodium comes from processed foods, any meaningful strategy to reduce sodium intake must involve food manufacturers and restaurants. Recent guidelines have recommended that the food industry should progressively reduce the sodium added to foods by 50% over the next 10 years. In the absence of meaningful reductions in sodium intake through voluntary recommendations, a recent Institute of Medicine (IOM) report has recommended a national approach, implemented through the United States Food and Drug Administration (FDA), to accomplish population-wide reductions in sodium intake.
Increased Potassium Intake
High potassium intake is associated with lower BP. Available evidence includes animal studies, observational studies, clinical trials, and meta-analyses of these trials. Although data from individual trials have typically been inconsistent, several meta-analyses have each documented a significant inverse relationship between potassium intake and BP in hypertensive patients and equivocal effects in nonhypertensive individuals. In one meta-analysis, a net increase in urinary potassium excretion of 2 gm per day (50 mmol/day) was associated with average systolic and diastolic BP reductions of 4.4 and 2.5 mm Hg in hypertensive individuals, and 1.8 and 1.0 in nonhypertensive persons. Increased potassium has beneficial effects on BP in the setting of a low potassium intake (e.g., 1.3 to 1.4 gm/day, or 35 to 40 mmol/day), or a much higher intake (e.g., 3.3 gm/day, or 84 mmol/day). Importantly, increased potassium intake reduces BP to a greater extent in African Americans compared with whites, and therefore may be a valuable tool to reduce health disparities related to the prevalence of elevated BP and its complications.
Because a high intake of potassium can be achieved through diet and because potassium contained in 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. In the DASH trial, the two groups that increased fruit and vegetable consumption both lowered BP. The DASH diet provides around 4.7 grams per day (120 mmol/day) of potassium. Another trial documented that increased fruit and vegetable intake lowers BP, but it did not specify the amount of potassium that was provided.
Potassium and sodium interact such that the effects of potassium on BP depend on the concurrent intake of sodium and vice versa. Specifically, an increased intake of potassium has greater BP-lowering effects in the setting of a higher sodium intake and lesser BP effects when sodium intake is already low. Conversely, the BP reduction from a lower sodium intake is greatest when potassium intake is also low. In one trial, a high potassium intake (120 mmol/day) blunted the pressor response to increased sodium intake in nonhypertensive African-American men and to a lesser extent in non-African Americans (see Fig. 21.5 ). A 2 × 2 factorial trial, conducted in Australia, tested the effects of reduced sodium intake and increased potassium intake, alone or together, on BP in 212 hypertensives; in this trial, a reduced sodium intake lowered BP to the same extent as an increased potassium intake; however, the combination did not further lower BP. Overall, available data are consistent with subadditive effects of reduced sodium intake and increased potassium intake on BP.
The dearth of dose-response studies precludes a firm recommendation for a specific level of potassium intake to lower BP. However, an IOM committee set the recommended potassium intake level at 4.7 grams per day (120 mmol/day). This level is similar to the average total potassium intake in clinical trials, the highest dose in the one available dose-response trial, and the potassium content of the DASH diet.
In the generally healthy population with normal kidney function, a potassium intake from foods above 4.7 grams per day (120 mmol/day) poses no risk because excess potassium is readily excreted. However, in individuals whose urinary potassium excretion is impaired, an intake less than 4.7 grams per day (120 mmol/day) is appropriate, because of adverse cardiac effects (dysrhythmias) from hyperkalemia. Common drugs that impair potassium excretion are angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, nonsteroidal antiinflammatory drugs (NSAIDs), and potassium-sparing diuretics. Medical conditions associated with impaired renal excretion of potassium include diabetes, CKD, end-stage renal disease, severe heart failure, and adrenal insufficiency. Elderly individuals are at increased risk of hyperkalemia. Available evidence is insufficient to identify the level of kidney function at which individuals with CKD are at risk for hyperkalemia from a high dietary intake of potassium. In this setting, namely, patients with advanced CKD, that is, stage 3 or 4, an expert panel set a wide range of recommended potassium intake of between 2000 and 4000 mg per day.
Moderation of Alcohol Consumption
Observational and experimental studies have documented a direct, dose-response relationship between alcohol intake and BP, particularly as the intake of alcohol increases above two drinks per day. This relationship is independent of potential confounders such as age, obesity, and sodium intake. Although some studies have shown that the alcohol-BP relationship also extends into the “light drinking” range, that is, at or below two drinks per day, this is the range in which alcohol may reduce the risk of coronary heart disease.
A meta-analysis of 15 randomized trials reported that decreased alcohol consumption (median reduction in self-reported alcohol intake of 76%, range 16% to 100%) lowered BP by 3.3/2.0 mm Hg. Reductions were similar in nonhypertensives and hypertensives, and the relationship appeared dose-dependent.
In aggregate, available evidence supports moderation of alcohol intake (among those who drink) as an effective strategy to lower BP. The prevailing consensus is that alcohol consumption should be limited to no more than two alcoholic drinks per day in men and to no more than 1 alcoholic drink per day in women and lighter weight persons [one drink is defined as 12 oz. of regular beer, 5 oz. of wine (12% alcohol), and 1.5 oz. of 80 proof distilled spirits].
Dietary Patterns
Vegetarian Diets
Certain dietary patterns, particularly vegetarian diets, have been associated with low BP. In industrialized countries, where elevated BP is extremely commonplace, individuals who consume a vegetarian diet have markedly lower BP than nonvegetarians. Some of the lowest BPs observed in industrialized countries have been documented in strict vegetarians living in Massachusetts. Vegetarians may also experience a slower, age-related rise in BP.
Several aspects of a vegetarian lifestyle might affect BP. These lifestyle factors include nondietary factors (e.g., physical activity), established dietary risk factors (e.g., sodium, potassium, weight, alcohol), and other aspects of a vegetarian diet (e.g., high fiber, no meat). To a limited extent, observational studies have controlled for the well-established dietary determinants of BP. For instance, in a study of Seventh Day Adventists, analyses were adjusted for weight but not dietary sodium or potassium intake. In a recent meta-analysis of 7 trials and 32 cohort studies, vegetarian diets were associated with lower systolic BP (mean net difference of −6.9 mm Hg) and diastolic BP (mean net difference of −4.7 mm Hg) compared with omnivorous diets.
The Dietary Approaches to Stop Hypertension Diet
The DASH trial was a randomized feeding study that tested the effects of three diets on BP. The most effective diet, now termed the DASH diet, emphasized fruits, vegetables, and low-fat dairy products; included whole grains, poultry, fish and nuts; and was reduced in fats, red meat, sweets, and sugar-containing beverages. It was rich in potassium, magnesium, calcium and fiber, and reduced in total fat, saturated fat and cholesterol; it was also slightly increased in protein. Among all participants, the DASH diet significantly lowered BP by a mean of 5.5/3.0 mm Hg, each net of control. The BP-lowering effects of the diets were rapid, occurring within only 2 weeks (see Fig. 21.6 ).
