Weight Loss. Weight is directly associated with BP. The importance of this relationship is evident by the high and increasing prevalence of overweight and obesity worldwide. Approximately 65% of US adults are classified as overweight or obese and more than 30% of US adults are obese.18 Over the past decade, the prevalence of overweight in US children and adolescents has increased, as have levels of BP.19
With rare exception, trials have documented that weight loss lowers BP. Importantly, reductions in BP occur without attainment of a desirable body weight. In one meta-analysis of 25 trials, mean systolic/diastolic BP reductions were 4.4/3.6 mm Hg from an average weight loss of 5.1 kg.20 Within-trial, dose-response analyses21,22 and prospective observational studies23 have documented that greater weight loss leads to greater BP reduction. Other trials have documented that modest weight loss, with or without sodium reduction, can prevent hypertension by approximately 20% among prehypertensive individuals 24 and can facilitate medication stepdown and drug withdrawal.25,26 Nonetheless, the long-term effects of sustained weight loss on BP are uncertain, with some studies suggesting attenuated BP reduction over time.22,27
In aggregate, available data strongly support weight reduction as an effective approach to prevent and treat elevated BP. In view of the well-recognized challenges of maintaining weight loss, public health efforts to prevent overweight and obesity are critically important.
Reduced Salt Intake. On average, as salt (sodium chloride) intake increases, so does BP. To date, more than 50 predominantly short-term trials have been conducted. In a recent meta-analysis,28 a median reduction in urinary sodium of approximately 1.8 g/d (78 mmol/d) lowered systolic/diastolic BP (DBP) by 2.0/1.0 mm Hg in nonhypertensive and by 5.0/2.7 mm Hg in hypertensive adults. In a meta-analysis of trials conducted in children, sodium reduction lowered mean SBP/DBP by 1.2/1.3 mm Hg.29
In addition to lowering BP, clinical trials have documented that reduced sodium intake prevents hypertension (relative risk reduction of approximately 20% with or without concurrent weight loss),24 lowers BP in the setting of antihypertensive medications,30,31 and improves hypertension control.25,26 In observational studies, reduced sodium intake is associated with a blunted age-related rise in systolic BP.32 To date, policy recommendations have relied on evidence that sodium reduction lowers BP. Recently, two trials of behavioral interventions to lower sodium and one trial of reduced sodium/high potassium salt have reported clinical outcomes. In each instance, there was a 21% to 41% reduction in clinical CVD events (significant reduction in 2 trials33,34 and nonsignificant trend in the third31) in those who received a reduced-sodium intervention. Such evidence highlights the potential for sodium reduction to prevent CVD and should dispel any residual concern that sodium reduction might be harmful.35
The BP response to changes in dietary sodium intake is heterogeneous.36 In general, the effects of sodium on BP tend to be greater in blacks and middle- and older-aged individuals. Genetic and dietary factors also influence the BP response to sodium. In the setting of either the Dietary Approaches to Stop Hypertension (DASH) diet37 or high potassium intake,38,39 the rise in BP for a given increase in sodium intake is blunted. While it is possible to identify subgroups that benefit more from sodium reduction, there is considerable overlap within subgroups. Importantly, there are no effective means to distinguish persons who are more or less salt-sensitive. Hence, the concept of salt sensitivity, while an important biological construct, has no clear clinical or public health application.
Available evidence supports population-wide sodium reduction, as recommended by the 2005 Dietary Guidelines for Americans. Specific recommendations are an upper limit of 2300 mg/d in the general population and an upper limit of 1500 mg/d in blacks, middle- and older-aged persons, and individuals with hypertension, diabetes, or chronic kidney disease. Together these groups comprise 69% of US adults.40 Survey data indicate that most children and adults exceed these limits. For example, median sodium intake (mg/d) in 1988–1994 was 3700 and 3100 in boys and girls, aged 9 to 13 years, respectively, and 4300 and 2900 in men and women, aged 31 to 50 years, respectively.41
To reduce sodium intake, consumers should choose foods low in sodium and limit the amount of added salt. However, because more than 75% of sodium comes from processed foods,42 any effective strategy to reduce sodium intake must involve the cooperation of food manufacturers and restaurants, which should progressively reduce the sodium added to foods by 50% over the next 10 years, as recommended by the American Medical Assocation.2,43 Public health efforts designed to reduce sodium intake are underway in several countries (eg, Great Britain, Finland).44 Additional efforts are likely, in large part because of the World Action on Salt and Health (WASH), an international advocacy group.
Increased Potassium Intake. High potassium intake is associated with lower BP. While data from individual trials have been inconsistent, 3 meta-analyses have each documented that increased potassium intake lowers BP in nonhypertensives and hypertensives.45–47 In one meta-analysis,46 average SBP/DBP reductions associated with a net increase in urinary potassium excretion of 2 gm/d (50 mmol/d) were 4.4/2.5 mm Hg in hypertensives and 1.8/1.0 in nonhypertensive individuals. Potassium appears to reduce BP to a greater extent in blacks than whites.46 Because high intake of potassium can be achieved through diet and because potassium derived from foods is also accompanied by other nutrients, particularly bicarbonate precursors, the preferred strategy to increase potassium intake is consumption of potassium-rich foods rather than pills.
The extent of BP reduction from potassium depends on concurrent levels of salt intake and vice versa. Specifically, potassium lowers BP to a greater extent in the setting of a high salt intake compared with a low salt intake. Conversely, a reduced salt intake lowers BP to a greater extent when potassium intake is low rather than high. These data are consistent with subadditive effects from reduced salt intake and increased potassium intake. This pattern, namely, a subadditve effect when ≥2 lifestyle interventions are implemented together, appears to occur with other combinations of effective BP-lowering therapies.24,48
The lack of dose response trials hinders recommendations on desirable levels of potassium intake as a means to lower BP. However, an intake of at least 4.7 gm/d (120 mmol/d) is reasonable given several considerations. This level of intake corresponds to the average total potassium intake in clinical trials of potassium supplements,46 the highest dose in the one available dose response trial,39 the potassium content of the DASH diet intake,49 and the adequate intake level set by an Institute of Medicine committee.50 Few Americans achieve this level of potassium intake. In the National Health and Nutrition Examination Survey (NHANES) III, the average intake of potassium was 2.9 to 3.2 mg/d (74–82 mmol/d) in adult men and 2.1 to 2.3 g/d (54–59 mmol/d) in adult women; only 10% of men and <1% of women consumed 4.7 gm/d (120 mmol/d) or more of potassium.50
In healthy individuals with normal kidney function, a potassium intake >4.7 gm/d (120 mmol/d) from foods poses no risk because excess potassium is excreted in the urine. However, in persons with impaired ability to excrete potassium, an intake <4.7 g/d (120 mmol/d) is appropriate because of the potential for adverse cardiac effects (arrhythmias) from hyperkalemia. Common drugs that can substantially impair potassium excretion are angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, nonsteroidal anti-inflammatory agents, and potassium-sparing diuretics. Medical conditions that are associated with impaired potassium excretion include advanced diabetes, chronic renal insufficiency, end-stage renal disease, severe heart failure, and adrenal insufficiency.
Moderation of Alcohol Intake. Observational studies have documented a direct dose-dependent relationship between alcohol intake and BP, particularly above approximately 2 drinks per day.51,52 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. Although some studies suggest that the alcohol-BP relationship also extends into the light drinking range (≤2 drinks per day), this is the range in which alcohol may reduce the risk of coronary heart disease. In a recent meta-analysis of 15 trials,52 decreased consumption of alcohol (median reduction in self-reported alcohol consumption of 76%, range of 16%–100%) lowered SBP/DBP by 3.3/2.0 mm Hg. BP reductions were similar in nonhypertensives and hypertensives.
In aggregate, available data support moderation of alcohol intake, among those who drink, as an effective approach to reduce BP. Alcohol consumption should be limited to no more than 1 alcoholic drink per day in women and lighter-weight persons and to no more than 2 alcoholic drinks per day in most men.