“Blood pressure” refers to the force exerted against the walls of the arteries as blood is pumped throughout the body by the heart. This pressure can be measured, and abnormally high levels indicate a condition of “high blood pressure,” or hypertension, which is classified into two types. Secondary hypertension is that resulting from a known cause, such as a disease of the kidneys, whereas essential or primary hypertension arises with no evident cause. More than 90 percent of hypertension cases fall into the latter category (Wilson and Grim 1993).
Salt consumption was linked with blood pressure long ago - as early as the second century B. C. in ancient China. In the Huang-ti nei-ching (“The Inner Classic of the Yellow Emperor”), it was written that “if too much salt is used for food, the pulse hardens” (Swales 1975:1).
In 1836, Richard Bright reported on the kidneys and hearts of 100 patients who had died of kidney problems. He noted that, in most instances, when the kidney was small and shrunken, the heart was often markedly enlarged - an indication of high blood pressure (Bright 1836). In the late nineteenth century, R. Tigerstedt and T. G. Bergman (1898) coined the term “renin” in their report that saline extracts from kidney tissue raised blood pressure. A few years later, French researchers L. Ambard and E. Beaujard noted that blood pressure was lowered by the dietary restriction of sodium chloride and raised by its addition or increase; they believed, however, that chloride was the culprit because they were unable to measure sodium content (Ambard and Beaujard 1904).
Many attempts to induce high blood pressure in experimental animals followed but proved inconclusive. In 1934, however, Harry Goldblatt noted that when he placed an adjustable clamp so that it partially blocked the renal artery of a dog, the animal developed a rapid increase in blood pressure that was sustained so long as the clamp remained in place. Research to determine the mechanism causing this high blood pressure began, and by 1940, two teams of investigators (Eduardo Braun-Menendez and colleagues in Buenos Aires and Irving Page and O. M. Helmer in Indianapolis) succeeded in isolating a material that caused vasoconstriction. Both groups reported that there was a substance - coming from the kidneys - that, when mixed with blood, generated a potent vasoconstricting and blood-pressure-raising substance. The South American group called this “hypertensin” and the U. S. group “angiotonin,” but eventually the two were determined to be the same chemical, which was named “angiotensin.”
Within a few years, W. Kempner (1944) reported that a low-sodium diet decreased blood pressure and heart size even in cases of malignant hypertension. The following year, he described the effects of a low-sodium diet on 65 patients who were hypertensive but showed no evidence of renal disease. After an average of only 48 days on a rice-fruit diet, the average blood-pressure readings decreased from a systolic blood pressure (SBP) of 197 mm Hg and a diastolic blood pressure (DBP) of 115 mm Hg to an SBP of 151 mm Hg and a DBP of 97 mm Hg. In those patients who experienced a decrease in blood pressure, the response was obvious within the first 7 to 10 days on the low-sodium diet, and Kempner observed that the maximum decrease in blood pressure was first attained after only 10 days.
Most early blood-pressure studies were on whites, yet the prevalence of high blood pressure in blacks is much greater and, as mentioned, is thought to result, at least in part, from salt intake. The first report of an association between salt intake and blood pressure in African-Americans was by A. Grollman and colleagues (1945), who studied patients given less than 1 gram (<1,000 mg) of sodium chloride in their daily diets. In the case of two black women, blood pressure declined to normal, promptly rose when salt intake was increased, and then fell again when the low-sodium diet was resumed.
Five years later, V. P. Dole and colleagues (1950) reported the results of a series of studies to evaluate the sodium content of Kempner’s rice-fruit diet and its effect on blood pressure and heart size. They confirmed all of Kempner’s observations and, further, documented that the effect of the diet was related to its low sodium content and not low chloride (Dole et al. 1950).
The introduction of diuretics, which act to excrete sodium and water via the kidneys, came in the late 1950s, and these were quickly shown to lower blood pressure significantly (Freis et al. 1958). In the 1970s, however, a series of observations made by a research group in Indianapolis (which included Clarence E. Grim, co-author of this chapter) once again focused attention on the relationship between dietary sodium and blood pressure. This culminated in several reports indicating that even a normoten-sive individual would experience an increase in blood pressure if enough salt was consumed (Murray et al. 1978; Luft et al. 1979). In addition, ethnic differences in sodium metabolism and blood-pressure responses were documented in normotensive subjects; such evidence demonstrated, for the first time, that blacks were more sensitive to salt than whites. These studies also demonstrated the enormous capacity of human kidneys to excrete sodium, which was proof of Guyton’s hypothesis that excess salt will always increase blood pressure (Guyton et al. 1995).
Current Thinking on Sodium and Hypertension
Cardiovascular disease is now a major cause of death in all countries of the world, and high blood pressure is the most common (although treatable) precursor of heart disease. Unfortunately, as pointed out in a recent review by J. P Midgley, A. G. Matthew, C. M. T. Greenwood, and A. G. Logan (1996), most sodium-reduction trials in hypertensive subjects have not yet produced definitive evidence that reducing sodium intake improves long-term health (but see also Staessen et al. 1997). Indeed, some have argued (based on a single observational study) that reducing salt intake may do more harm than good (Alderman et al. 1995).
Nonetheless, high dietary salt intake has been reported to be associated with other adverse medical outcomes, including death from stroke, enlargement of the heart (a precursor to congestive heart failure), and even asthma mortality (Antonios and McGregor 1995). Moreover, recent population-based studies seem to confirm that the major cause of high blood pressure is an excessive dietary intake of sodium. Using a standardized protocol in a 52-center worldwide study, INTERSALT showed a positive, significant, linear relationship between salt intake and blood pressure. The statistical relationship suggested that each 100 mmol of sodium intake was responsible for a 2 mm Hg increase in systolic blood pressure. In addition, the INTERSALT findings suggest a powerful effect of dietary sodium intake on the rise in blood pressure with age. It has also been argued that a reduction in the average intake of sodium in Britain - from 150 mmol to 100 mmol per day - could reduce strokes and heart attacks in that nation by 22 percent and 16 percent, respectively, and would have a greater impact than that of all of the drugs used to treat high blood pressure (McGregor and Sever 1996).
For the majority of hypertensive persons, it seems well established that lifestyle improvements, such as lowering dietary sodium intake while increasing dietary potassium intake, reducing body weight, and increasing exercise, can lower blood pressure. Although such efforts would likely lower a person’s blood pressure by “only” 5 mm Hg, it is important to consider the societal health benefits of such a downward shift across the entire population. From a population-wide perspective, this could dramatically reduce the prevalence of hypertension and cardiovascular disease.
It has been estimated that it costs $1,000 per year to treat each hypertensive person (Elliott 1996). If lifestyle changes could lower the average blood pressure by only 5 mm Hg, then 21.4 million persons would no longer require treatment. This would save the United States about $21 billion a year in the cost of health care for hypertension alone, not to mention the costs saved by the reduction of strokes by about 40 percent and cardiovascular disease by about 25 percent. The potential economic advantage of implementing low-cost lifestyle changes to lower blood pressure across society should be obvious. Indeed, it is clear that most countries of the world will not be able to afford expensive medical therapies to control high blood pressure and should be implementing public-health strategies to lower blood pressure and the devastating consequences of hypertension for a country’s workforce.
Thomas W Wilson Clarence E. Grim
World History
