Salt Is Not the Nutritional Evil It Is Made Out to Be

This post could just as well have been titled "Sugar, Not Salt, Should Be the Primary Suspect for Causing High Blood Pressure." The basic argument is that the effects of salt on blood pressure are quite small, while blood pressure has a strong association with insulin and insulin resistance, which in turn are strongly associated with eating refined carbohydrates such as sugar that spike insulin. To make this case, I will turn primarily to excerpting some of what Gary Taubes says in his excellent history of thought about nutrition Good Calories, Bad Calories, which chronicles a great deal of dogmatic arrogance by influential nutrition scientists who outshouted the ideas of other nutrition scientists who had just as much evidence on their side. This claim about dogmatic arrogance can be easily (if laboriously) documented from the historical record, as Gary Taubes does.

The quotations below are from Chapter 8: "The Science of the Carbohydrate Hypothesis."

First, Gary Taubes makes the case that high blood pressure is associated with the pre-diabetes condition of insulin resistance, which is also called metabolic syndrome:

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.

Next, Gary discusses the weakness of the evidence for any serious harm from salt. In particular, even cutting salt in half would reduce blood pressure by only 4 or 5 points ("millimeters of mercury"), while even mildly high blood pressure is 20 points higher than normal, and serious high blood pressure is 40 points higher than normal. 

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.

Salt may cause some water retention, but perhaps surprisingly, so do sugar and other carbohydrates: 

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 well 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 “remarkable sodium and water retaining effect of concentrated carbohydrate food,” as the University of Wisconsin endocrinologist Edward Gordon called it, was then explained physiologically 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 theoretically 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.

The reduction of bloating when someone goes on a low-carb diet is so substantial that weight loss in the first week or two can be quite dramatic, because this water loss is added to whatever fat loss there is. 

In the progression above, I skipped over Gary's discussion of how high blood pressure is one of the "Diseases of Civilization," later renamed more politically correctly as "Western Diseases." That is, people from non-European cultures who eat traditional diets have very little high blood pressure, just as they have very little obesity, very little heart disease and very little cancer. This is true for a wide range of different traditional diets, including the fatty-red-meat-laden traditional Inuit diet, the traditional Masai diet of milk, meat and blood, and diet of coconuts and fish (later coconuts, fish and breadfruit) on the Pacific island of Tokelau. Thus, high blood pressure seems most likely to be due to non-traditional foods, such as sugar, white flour and other highly refined carbohydrates. More generally, it seems likely to be something to which advanced European food-processing technology contributed that was the culprit. When any group began eating distinctively Western foods—of which processed foods are the most distinctive—something in that menu seems to have led to a wide range of chronic diseases. 

Gary does not say this, but salt in particular does not seem to be a good candidate as a cause for one of the "Western Diseases" since it would be quite surprising if there were not some traditional diets that were heavy on salt—perhaps because of a location near the sea—that would have revealed clearly any strong association of salt with high blood pressure. 

Finally, given the importance of sugar and other refined carbohydrates in causing insulin spikes, the following passages about insulin are damning for sugar and refined carbohydrates more generally:

Finally, by the mid-1990s, diabetes textbooks, such as Joslin’s Diabetes Mellitus, contemplated the likelihood that chronically 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. ...

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.


Update: Mark Fontana points me to Gina Kolata's May 8, 2017 New York Times article "Why Everything We Know About Salt May Be Wrong," which complicates the story further. What is clear is that the traditional story about salt is wrong and there is no adequate reason to worry about salt intake in the normal range because there simply isn't enough science to justify worry (unless you like worrying). Gina Kolata's article is also interesting one of her interviewees illustrates the way in which many in the nutritional establishment continue to assert the same thing they didn't have enough evidence for in the first place in the face of further contradictory evidence:

“The work suggests that we really do not understand the effect of sodium chloride on the body,” said Dr. Hoenig.

“These effects may be far more complex and far-reaching than the relatively simple laws that dictate movement of fluid, based on pressures and particles.”

She and others have not abandoned their conviction that high-salt diets can raise blood pressure in some people.

But now, Dr. Hoenig said, “I suspect that when it comes to the adverse effects of high sodium intake, we are right for all the wrong reasons.”

 On what basis does Dr. Hoenig say “I suspect that when it comes to the adverse effects of high sodium intake, we are right for all the wrong reasons,” other than out of sheer stubbornness?

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