Good Calories, Bad Calories

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.