Good Calories, Bad Calories

fructose, which is found naturally only in small concentrations in fruits and some root vegetables, the human body has also been confronted with having to adjust to radically large amounts of fructose. In this sense, all of the abnormalities of metabolic syndrome and the accompanying chronic diseases of civilization can be viewed as the dysregulation of homeostasis caused by the repercussions throughout the body of the blood- sugar, insulin, and fructose-induced changes in regulatory systems. (As the geneticist James Neel wrote in 1998 about adult-onset diabetes, “The changing dietary patterns of Western civilization had compromised a complex homeostatic mechanism.”)

It’s possible that obesity, diabetes, heart disease, hypertension, and the other associated diseases of civilization all have independent causes, as the conventional wisdom suggests, but that they serve as risk factors for each other, because once we get one of these diseases we become more susceptible to the others. It’s also possible that refined carbohydrates and sugar, in particular, create such profound disturbances in blood sugar and insulin that they lead to disturbances in mechanisms of homeostatic regulation and growth throughout the entire body.

Any assumptions about regulatory mechanisms and disease, as Claude Bernard explained, have to be understood in the context of the entire harmonic ensemble. “We really must learn, then, that if we break up a living organism by isolating its different parts, it is only for the sake of ease in experimental analysis, and by no means in order to conceive them separately,” Bernard wrote. “Indeed when we wish to ascribe to a physiological quality its value and true significance, we must always refer it to this whole, and draw our final conclusion only in relation to its effects in the whole.” When Hans Krebs paraphrased this lesson a century later, he said that if we neglect “the wholeness of the organism—we may be led, even if we experimented skillfully, to very false ideas and very erroneous deductions.”

Perhaps the simplest example of this kind of erroneous deduction is the common assumption that the cause of high blood pressure and hypertension is excess salt consumption.

Hypertension is defined technically as a systolic blood pressure higher than 140 and a diastolic blood pressure higher than 90. It has been known since the 1920s, when physicians first started measuring blood pressure regularly in their patients, that hypertension is a major risk factor for both heart disease and stroke. It’s also a risk factor for obesity and diabetes, and the other way around—if we’re diabetic and/or obese, we’re more likely to have hypertension. If we’re hypertensive, we’re more likely to become diabetic and/or obese. For those who become diabetic, hypertension is said to account for up to 85 percent of the considerably increased risk of heart disease. Studies have also demonstrated that insulin levels are abnormally elevated in hypertensives, and so hypertension, with or without obesity and/or diabetes, is now commonly referred to as an “insulin-resistant state.” (This is the implication of including hypertension among the cluster of abnormalities that constitute metabolic syndrome.) Hypertension is so common in the obese, and obesity so common among hypertensives, that textbooks will often speculate that it’s overweight that causes hypertension to begin with. So, the higher the blood pressure, the higher the cholesterol and triglyceride levels, the greater the body weight, and the greater the risk of diabetes and heart disease.

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 call 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. Still, in most individuals, a salt binge will result in a slight increase in blood pressure from the swelling 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 still called 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 called 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—will 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 all eat less salt because they believe that any benefit to the individual, no matter how clinically insignificant, will have a significant impact on the public health. But this evades the scientific question that still 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 recall 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 well. 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.