Good Calories, Bad Calories (29 page)

Despite the intimate association of these diseases, public-health authorities for the past thirty years have insisted that salt is the dietary cause of hypertension and the increase in blood pressure that accompanies aging. Textbooks recommend salt reduction as the best way for diabetics to reduce or prevent hypertension, along with losing weight and exercising. This salt-hypertension hypothesis is nearly a century old. It is based on what medical investigators cal biological plausibility—it makes sense and so seems obvious. When we consume salt—i.e., sodium chloride—our bodies maintain the concentration of sodium in our blood by retaining more water along with it. The kidneys should then respond to the excess by excreting salt into the urine, thus relieving both excess salt and water simultaneously. Stil , in most individuals, a salt binge wil result in a slight increase in blood pressure from the swel ing of this water retention, and so it has always been easy to imagine that this rise could become chronic over time with continued consumption of a salt-rich diet.

That’s the hypothesis. But in fact it has always been remarkably difficult to generate any reasonably unambiguous evidence that it’s correct. In 1967, Jeremiah Stamler described the evidence in support of the salt-hypertension connection as

“inconclusive and contradictory.” He stil cal ed it “inconsistent and contradictory” sixteen years later, when he described his failure in an NIH-funded trial to confirm the hypothesis that salt consumption raises blood pressure in school-age children.

The NIH has funded subsequent studies, but little progress has been made. The message conveyed to the public, nonetheless, is that salt is a nutritional evil—“the deadly white powder,” as Michael Jacobson of the Center for Science in the Public Interest cal ed it in 1978. Systematic reviews of the evidence, whether published by those who believe that salt is responsible for hypertension or by those who don’t, have inevitably concluded that significant reductions in salt consumption—cutting our average salt intake in half, for instance, which is difficult to accomplish in the real world—wil drop blood pressure by perhaps 4 to 5 mm Hg in hypertensives and 2 mm Hg in the rest of us. If we have hypertension, however, even if just stage 1, which is the less severe form of the condition, it means our systolic blood pressure is already elevated at least 20 mm Hg over what’s considered healthy. If we have stage 2 hypertension, our blood pressure is elevated by at least 40 mm Hg over healthy levels. So cutting our salt intake in half and decreasing our systolic blood pressure by 4 to 5 mm Hg makes little difference.

Our belief in the dangers of salt in the diet is once again based on Geoffrey Rose’s philosophy of preventive medicine. Public-health authorities have continued to recommend that we al eat less salt because they believe that any benefit to the individual, no matter how clinical y insignificant, wil have a significant impact on the public health. But this evades the scientific question that stil has to be answered: if excessive salt consumption does not cause hypertension, as these clinical trials suggest it does not, then what does? Moreover, embracing a suspect public-health pronouncement serves to inhibit rigorous scientific research.

Let’s recal that hypertension is a disease of civilization, an observation that dates back to the late 1920s. Just as physicians in Europe and the United States took to measuring blood pressure in their patients with the availability of an instrument that could do so easily and reliably (the sphygmomanometer), missionary and colonial physicians throughout the world took to measuring blood pressure in native populations. Within a decade, noted the British physician Cyril Donnison in 1938 in Civilization and Disease, hypertension was already among the best-documented examples of a disease that seemed specific to Western societies and the more affluent social classes elsewhere. The average blood pressure in isolated populations eating traditional diets was inevitably low, but not dissimilar to the average blood pressure of Europeans and Americans who had not yet reached middle age. Hypertension was never seen in these populations, and blood pressure, if anything, dropped lower with age, which is the opposite of what happens in developed nations. In 1929, Donnison reported that he had measured the blood pressure in a thousand Kenyan nomads and found it similar to that of Europeans for those men under forty, but not so after that: “It tends to come down in the African,” Donnison wrote, “whereas in the white races it continues its tendency to rise until the eighth decade.” The Kenyan nomads in their sixties had an average systolic blood pressure forty points lower than that of European men of the same age. Over the next forty years, these observations would be confirmed in isolated populations throughout the world.

With exposure to Western lifestyles and diets, however, blood pressure among these native populations began to rise with age, as it does in Europe and America, and the average blood pressure and the incidence of hypertension increased as wel . In Kenya and Uganda, British physicians considered hypertension to be nonexistent among their African patients in the late 1930s. By the 1950s, more than 10 percent of native Africans checking into hospitals for any reason were diagnosed with clinical hypertension. That number had risen to over 30 percent by the mid-1960s. By the 1970s, hypertension was considered as frequent in the native African populations as it was in Europe or America. In some urban populations, hypertension rates as high as 60 percent were reported.

Until the salt hypothesis began receiving serious attention in the 1960s, the investigators paid little attention to nutritional explanations for the rise in blood pressure that accompanied Western diets and lifestyles. Instead, they debated whether it was the stress and tension of what they considered civilized life that led blood pressure to rise, as Donnison believed. Once the salt hypothesis raised the possibility that diet was responsible, investigators began to perceive the presence or absence of hypertension in isolated populations purely as a test of the salt hypothesis. Since hypertension only appeared in these populations when they gained access to Western diets, which frequently included salt-rich processed foods, the investigators saw their studies as confirming the salt hypothesis. By the 1990s, the absence of hypertension in isolated populations eating their traditional diets was stil the most compel ing evidence in support of the hypothesis.

Of course, the same societies that ate little or no salt ate little or no sugar and white flour, so the evidence supported both hypotheses, although the investigators were interested in only one. The notion that the refined-carbohydrate hypothesis could explain many of the other chronic changes in health among these populations was rarely discussed. In two cases—Gerald Shaper’s studies of nomadic tribes in Kenya and Uganda, and Ian Prior’s studies of South Pacific Islanders—the investigators first implicated refined carbohydrates as a possible cause of the emergence of hypertension in their populations, because sugar and flour constituted the conspicuous additions to the diet with Western influence. Then they embraced salt as the culprit, after they became aware that investigators in the U.S. believed salt to be the problem. In the early 1970s, when the Harvard hypertension specialist Lot Page and his col eagues set out to study “the antecedents of cardiovascular disease” in the Solomon Islands, they, too, considered their research to be solely a test of the salt hypothesis, so salt was the only aspect of the Solomon Islanders’ diet that they assessed. In what came to be considered a seminal study in the field, they concluded natural y enough that suspicion of the cause of high blood pressure among the islanders “fal s most heavily on salt intake.”

The laboratory evidence that carbohydrate-rich diets can cause the body to retain water and so raise blood pressure, just as salt consumption is supposed to do, dates back wel over a century. It has been attributed first to the German chemist Carl von Voit in 1860. In 1919, Francis Benedict, director of the Nutrition Laboratory of the Carnegie Institute of Washington, described it this way: “With diets predominantly carbohydrate there is a strong tendency for the body to retain water, while with diets predominantly fat there is a distinct tendency for the body to lose water.” The context of Benedict’s discussion was the weight loss that occurs in the first few weeks of any calorie-or carbohydrate-restricted diet, and particularly the latter.

As Benedict pointed out, this weight loss is to a large extent water, not fat, which has to be factored into any discussion of the apparent benefits of a reducing scheme. In the late 1950s, a new generation of investigators rediscovered the phenomenon, and it was then used to rationalize the popularity of carbohydrate-restricted diets as due not to the ease of losing fat, but entirely to the water lost in the first few weeks of the diet.

The “remarkable sodium and water retaining effect of concentrated carbohydrate food,” as the University of Wisconsin endocrinologist Edward Gordon cal ed it, was then explained physiological y in the mid-1960s by Walter Bloom, who was studying fasting as an obesity treatment at Atlanta’s Piedmont Hospital, where he was director of research. As Bloom reported in the Archives of Internal Medicine and The American Journal of Clinical Nutrition, the water lost on carbohydrate-restricted diets is caused by a reversal of the sodium retention that takes place routinely when we eat carbohydrates. Eating carbohydrates prompts the kidneys to hold on to salt, rather than excrete it. The body then retains extra water to keep the sodium concentration of the blood constant. So, rather than having water retention caused by taking in more sodium, which is what theoretical y happens when we eat more salt, carbohydrates cause us to retain water by inhibiting the excretion of the sodium that is already there. Removing carbohydrates from the diet works, in effect, just like the antihypertensive drugs known as diuretics, which cause the kidneys to excrete sodium, and water along with it.

This water loss leads to a considerable drop in blood pressure, so much so that it led critics of these diets, such as Philip White, author of a nutrition column in the The Journal of the American Medical Association, to worry publicly about the

“low blood pressure resulting from…losses of…fluid, sodium, and other minerals.” Discussions of the treatment of obesity with very low-carbohydrate diets would address the need to retain some carbohydrates in the diet to maintain “fluid balance”

and “avoid large shifts in weight due to changes in water balance.” By the early 1970s, researchers had demonstrated that the water-retaining effect of carbohydrates was due to the insulin secreted, which in turn induced the kidneys to reabsorb sodium rather than excrete it, and that insulin levels were indeed higher, on average, in hypertensives than in normal individuals. Final y, by the mid-1990s, diabetes textbooks, such as Joslin’s Diabetes Mellitus, contemplated the likelihood that chronical y elevated levels of insulin were “the major pathogenetic defect initiating the hypertensive process” in patients with Type 2 diabetes. But such speculations rarely extended to the potential implications for the nondiabetic public.

There are several possible explanations for why this phenomenon rarely entered into the discussions of hypertension and heart disease. Those investigators concerned with the dangers of hypertension might simply have considered the obesity literature or even the diabetes literature of little significance to their research, other than the obvious observation that obese and diabetic patients tend to be hypertensive and vice versa. Another possibility is that by the 1960s hypertension and high cholesterol were two of the three major risk factors associated with premature coronary heart disease (the third was smoking), so it was difficult to imagine that eating carbohydrates might be beneficial for one risk factor, cholesterol, while being detrimental for another, blood pressure.

Though this carbohydrate-induced water retention and the hypertensive effect of insulin were occasional y discussed in nutrition and dietetics textbooks—Modern Nutrition in Health and Disease, for example, which was published in 1951 and was in its fifth edition by the 1970s—they would appear solely in the technical context of water and electrolyte balance (sodium is an electrolyte), whereas the discussion of hypertension prevention would focus exclusively on the salt hypothesis.

When they were discussed in obesity conferences after the 1960s, the implications were restricted to a very narrow range, usual y as evidence against any metabolic advantage of carbohydrate-restricted diets. (“One claim which is often made for the low-carbohydrate diet is that 3,000 [calories]/day or more can be eaten and the patient wil stil lose weight if the carbohydrate intake is restricted,” explained George Bray at the Second International Conference on Obesity in 1977. “There are no convincing studies to support this claim. On the contrary…it is now wel -established that a low-carbohydrate diet is fol owed by the excretion of water and that carbohydrate ingestion leads to retention of both salt and water.”) Since lower weight is associated with lower insulin levels, overweight hypertensives were advised to lose weight to reduce their blood pressure, but then low-calorie diets—usual y low-fat and thus high in carbohydrates—would be recommended as the means to do it.

On very rare occasions, “carbohydrate overeating” would be acknowledged as a nutritional factor involved in the genesis of hypertension, at least in obese patients, and then both carbohydrate restriction and salt restriction would be recommended as treatment. Those investigators, too, had come to assume that the salt hypothesis must be true.

Since the late 1970s, investigators have demonstrated the existence of other hormonal mechanisms by which insulin raises blood pressure—in particular, by stimulating the nervous system and the same flight-or-fight response incited by adrenaline. This was first reported by Lewis Landsberg, an endocrinologist who was then at Harvard Medical School and would later become dean of the Northwestern University School of Medicine. Landsberg showed that, by stimulating the activity of the nervous system, insulin increases heart rate and constricts blood vessels, thereby raising blood pressure. The higher the insulin level, the greater the stimulation of the nervous system, Landsberg noted. If insulin levels remained high, so Landsberg’s research suggested, then the sympathetic nervous system would be constantly working to raise blood pressure. The heart-disease research community has paid attention to Landsberg’s work, but has considered it relevant only for the obese. Because obesity is associated with higher insulin levels, and because it’s now believed that obesity causes higher insulin levels (whereas obesity itself is al egedly caused by the consumption of excess calories of al types), any possible link to carbohydrate consumption or “carbohydrate overfeeding” is overlooked. Even Landsberg has concentrated almost exclusively on the obesity-insulin-hypertension connection and ignored the idea that the increase in insulin levels due to excessive carbohydrate consumption, or due to the consumption of refined and easily digestible carbohydrates, might have a similar effect.