Sodium and Other Dietary Factors
The most recent report of the Sixth Joint National Committee on the Prevention, Detection, Evaluation and Treatment of High Blood Pressure (JNC VI) has recommended a trial of lifestyle intervention as initial therapy in individuals with high-normal (130-139 mmHg systolic/85-89 diastolic) or stage I (140-159/90-99 mmHg) blood pressure levels without end-organ disease, concomitant cardiovascular disease, or diabetes mellitus. This chapter examines the evidence in support of dietary alterations and their effect on blood pressure. The constituents that are considered include calories (body weight), salt (sodium chloride), potassium, calcium, and combinations of these minerals, other dietary components, and alcohol. Rather than attempting an encyclopedic review of the studies of all these dietary elements, this chapter succinctly summarizes what is currently known.
Body weight
Body weight has long been linked to blood pressure levels. More recent findings indicate that the distribution of body fat may be a more important determinant of blood pressure elevation and the risk for cardiovascular disease. An increase in visceral abdominal fat (the central or “apple” form) in contrast to the lower body adiposity pattern (the “pear” shape) is linked not only to blood pressure elevation but also to insulin resistance, dyslipidemia, and an increased risk for cardiovascular events. These associations have been based largely on epidemiologic evidence. However, there are now several intervention trials in which it has been demonstrated that weight loss, often as little as 5 kg rather than a reduction to “ideal” body weight, is associated with a decrease in blood pressure and an improvement in insulin sensitivity. Studies on both humans and experimental animals suggest that the sympathetic nervous system is involved in the pathophysiology of the weight-blood pressure-insulin resistance relationship, but therapeutic interventions based on these findings are not yet available to confirm this connection.
Another mediator of the body weight-blood pressure relationship appears to be the kidney. In experimental animals, obesity has been associated with alterations in renal blood flow and glomerular filtration rate or intraglomerular pressure. In humans, urinary microalbumin excretion was increased among obese subjects, supporting an abnormality in renal function in humans as well. Moreover, microalbuminuria has been linked to an increased risk of cardiovascular events in hypertensive individuals.
Salt (sodium chloride)
The relationship between dietary salt consumption and elevated blood pressure is well-known. The prevalence of hypertension and its consequences is linearly related to dietary salt intake in societies throughout the world. Hypertension and its sequelae are virtually absent in societies in which habitual salt intake is <50-100 mmol/d. However, there are other differences between these groups and those that habitually consume larger amounts of salt. The “low-salt” societies tend to be isolated, genetically homogeneous, physically fit, and consume increased amounts of potassium and calcium in the form of fresh fruits and vegetables. Increased salt intake is associated with societal “acculturation.” This implies a crowded and sedentary lifestyle as well as many other behavioral factors that may affect blood pressure and cardiovascular risk. In addition, the age-related increase in blood pressure is observed only in societies in which salt intake is high. Many of the elderly individuals in low-salt cultures have blood pressure levels that are no higher than those of young adults.
Despite this convincing evidence, controversy still exists concerning the importance of salt in human blood pressure in general, in hypertension, and as a treatment modality. Without considering the various reasons for this controversy, suffice it to say that the magnitude of the effect of salt intake on blood pressure is diluted by the fact that there is substantial heterogeneity in the blood pressure responses of humans to alterations in salt intake. Numerous studies have demonstrated that salt-sensitive and salt-resistant individuals can be identified within both the hypertensive and normotensive populations. Salt-sensitive subjects will demonstrate a decrease in blood pressure with dietary sodium reduction, usually to the level of 100 mmol/d (2.4 g/d). The human need for sodium is about 10 mmol/d (230 mg/d). Thus, the threshold for blood pressure responsiveness to a reduction in salt intake is many times higher than the physiologic requirements. It is often difficult to differentiate between salt-sensitive and salt-resistant subjects without sophisticated research techniques. However, a trial of modest dietary salt restriction or diuretic administration should identify those most likely to benefit from this dietary intervention. Moreover, there have been no adverse reports when a modest reduction in salt intake such as 80-100 mmol/d has been followed.
Certain population groups have been reported to be more likely to be salt sensitive than others. Hypertensive individuals are more salt sensitive than those with normal blood pressure. Among hypertensive subjects, salt sensitivity of blood pressure is more frequent among African-Americans (75%) than Caucasians (50%) and increases with increasing age. The latter finding is also observed in the normotensive population, with the finding that significant salt sensitivity of blood pressure is not seen until the age decade of 60 yr or more. Individuals with reduced renin responses to sodium and volume depletion, the so-called low-renin subjects, are more likely to be salt sensitive than those with brisk renin responses.
In addition to a possible permissive effect of sluggish renin responses to salt sensitivity, a variety of substances have been reported to be involved in the pathophysiology of salt sensitivity of blood pressure. An extensive scientific critique of the many studies that have been conducted in this area is beyond the scope of this chapter; however, note that the sympathetic nervous system, endothelin, insulin sensitivity, atrial natriuretic factor, alterations in renal hemodynamics, and leptin have all been implicated in the patho-physiology of salt sensitivity. It remains to be determined which of these many factors are primary events and which are simply compensatory responses or epiphenomena.
It has been shown that salt sensitivity requires the administration of sodium as the chloride salt and that other forms of sodium do not have the same pressor effect. However, this is a moot point because >95% of the sodium found in foods is in the chloride form. Moreover, most of the salt found in food is added in the preparation, processing, and preservation of food, and only 15% is added as the discretionary form (as table salt). Thus, it is important for the food preparer as well as the patient to become familiar with identifying the salt content of foods at the grocery store and restaurant as well as in cooking.
Another important recent finding related to salt and blood pressure is the observation that long-term follow-up of salt-sensitive normotensive subjects over a period of 10 yr or more demonstrated an eightfold greater rate of blood pressure increase compared with those who were initially salt resistant. This finding supports the epidemiologic observations relating the age-associated rise in blood pressure to increased salt intake.
Potassium
As already mentioned, in societies in which there is alow prevalence of hypertension and its complications as well as little age-related increase in blood pressure, people tend to consume increased amounts of potassium (and calcium, as discussed in the next section) and follow a reduced salt diet. Fewer studies have examined the relationship between potassium and blood pressure than those involving sodium. However, the findings regarding potassium tend to be consistent. In general, the effect of potassium is smaller than that of sodium based on interventional trials. Again, heterogeneity in responsiveness of blood pressure to alterations in potassium intake or balance has been demonstrated. Among potassium-replete normotensive subjects, typically those consuming 60 mmol/d of potassium or more, little effect on blood pressure can be demonstrated with additional potassium administration. However, in hypertensive populations, particularly those comprising substantial numbers of individuals in whom dietary potassium intake is traditionally deficient (the elderly, African Americans) or those in whom diuretic-induced potassium loss occurs, potassium supplementation has been shown to lower blood pressure. It has also been observed that potassium is more likely to lower blood pressure in hypertensive individuals consuming a high salt intake, further suggesting a link between sodium and potassium intake in their effects on blood pressure.
The amount of potassium intake required for optimal reduction in blood pressure in those who are sensitive to this mineral is not clear. Most studies indicate that dietary potassium deficiency begins at levels of intake <50 mmol/d and is clearly observed at intakes of 30 mmol/d or less. Dietary sources of potassium are largely fresh fruits and vegetables. In environments where these are scarce, e.g., because of cold climate or high cost, potassium deficiency is more likely. Among a group of normotensive nurses in whom dietary intakes of potassium, calcium, and magnesium were deficient, only potassium supplementation reduced blood pressure. Recent studies using diets involving multiple mineral manipulations, such as the Dietary Approaches to Stop Hypertension (DASH) trial, are discussed in the Combination Diets section.
Calcium
Epidemiologic surveys have suggested a relationship between reduced dietary calcium intake and hypertension. Several studies have demonstrated a small and inconsistent effect of calcium supplementation to lower blood pressure. Again, this appears to be largely owing to the heterogeneity in human responses to calcium supplementation. Subgroup analyses of some of the larger studies suggest that those in whom dietary calcium intake is often reduced (African-Americans, the elderly) are more likely to demonstrate a reduction in blood pressure with calcium supplementation than other groups in whom intake is higher. Because both subgroups are traditionally salt sensitive, we conducted a study of calcium supplementation in a group of normal and hypertensive subjects who had been previously categorized with respect to salt sensitivity of blood pressure. We found no significant effect of calcium supplementation on blood pressure for the entire group. However, when the subjects were separated on the basis of salt-sensitivity status, we found a significant decrease in blood pressure when the salt-sensitive subjects received calcium supplements and a significant increase in blood pressure when calcium was given to the salt-resistant subjects. These findings suggested a reciprocal relationship between the effects of calcium and sodium on blood pressure that was confirmed by the results of the DASH trial.
Other dietary constituents
There is, at present, no convincing evidence to link alterations in magnesium intake with blood pressure, and thus the JNC VI report did not advocate an increase in this mineral for the purpose of lowering blood pressure. Caffeine may raise blood pressure acutely in caffeine-naive individuals but does not appear to be a factor in the chronic elevation of blood pressure. Moreover, there is no evidence that withdrawal of caffeine in habitual consumers produces a decrease in blood pressure. Although some studies have suggested a beneficial effect of large amounts of omega-3 fatty acids in reducing blood pressure, intolerance of these doses makes this an impractical approach for most individuals.
Combination diets
A variety of studies have examined the effect of combined dietary approaches on blood pressure as nonpharmacologic treatment of hypertension or for the prevention of hypertension in those at increased risk (high-normal blood pressure). These combined studies have been fraught with problems resulting from recidivism, inadequate achievement of dietary goals, or relatively short duration. In general, it can be stated that weight loss appears to be the most effective single intervention as long as the weight loss can be maintained. There does not appear to be an additive benefit when potassium supplementation is combined with modest dietary salt restriction beyond that seen with salt restriction alone. However, in the DASH trial, when a specific diet incorporating modest salt restriction with an increase in fresh fruits and vegetables and low-fat dairy products (presumably increasing potassium, calcium, and magnesium intake) was followed, a significant reduction in blood pressure was observed over the 8-wk study period. This benefit appeared to be greatest among African-Americans and those with higher initial blood pressure levels. Another study examining multiple dietary changes was a subgroup of the Nurses Health Study II, which compared the effects of supplemental potassium, calcium, magnesium, or all three minerals to placebo in normotensive nurses in whom dietary deficiencies of these minerals were documented. As previously mentioned, potassium supplementation alone, but not combination supplementation, lowered blood pressure.
Alcohol
Alcohol consumption has been shown to have a biphasic effect on blood pressure. Small amounts of alcohol appear to lower blood pressure, presumably secondary to a vasodilator effect, but as alcohol consumption increases, blood pressure rises. The dose-response characteristics vary from individual to individual and may be based on factors such as body surface area, gender, and race. The racial differences may be explicable, in part, by virtue of genetic differences in alcohol metabolism. The mechanism for the alcohol-induced increase in blood pressure appears to be related to activation of, or increased responsiveness to, the sympathetic nervous system. This is manifested by an increase in cardiac output when more than one ounce of alcohol is consumed. Thus, a prudent recommendation to hypertensive subjects is to limit their daily alcohol consumption to no more than 2 oz (60 iriL) of 100-proof spirits (or 2.5 oz of 80-proof whiskey), 24 oz (720 inL) of beer, or 10 oz (300 iriL) of wine. For those hypertensive individuals in whom habitual alcohol consumption exceeds these levels, a reduction in intake may lower blood pressure or make it easier to control.
Conclusion
A variety of dietary and lifestyle factors can influence blood pressure. The ideal recommendation for individuals who are hypertensive or are at increased risk for its development are to maintain a body weight as close to ideal as possible; to consume a diet modest in salt content and enriched with fresh fruits, vegetables, and low-fat dairy products, and to consume no more than the recommended optimal amounts of alcohol.
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