The “Salt–Blood Pressure Hypothesis” states that an increase in the intake of salt leads to an increased in blood pressure and subsequently increases the risk for cardiovascular events, which has been a point of contention for decades. This article covers the history and some of the key players pertaining to “The Salt Wars” during the first half of the 1900s, both in Europe and in the United States. Early studies finding benefits with salt restriction in those with hypertension were based on uncontrolled case reports. The overall evidence in the first half of the 1900s suggests that a low-salt diet was not a reasonable strategy for treating hypertension.
In the late 1800s salt was not demonized as a cause of water retention, edema, and kidney disease. In fact, salt restriction was actually thought to cause some of these conditions.1 According to an article published by Branche in 1885, salt depletion resulted in extreme weakness, anemia, albuminuria, and edema; and as early as 1909, heat and muscle cramps from sodium depletion were well recognized symptoms.2, 3 Other side effects of salt restriction included vertigo, headache, apathy, anorexia, nausea, feeble twitching of the muscles, abdominal cramps, and oliguria. More severe side effects included vascular collapse, cold extremities, and large drops in blood pressure (hypotension).1
Carrion and Hallion in 1899 were the first to suggest that excess salt in the body pulled water from bodily tissues, increasing plasma volume.1 This theory was soon championed by Achard in 1901, who suggested that edema of Bright’s disease (chronic inflammation of the kidneys) was caused by the retention of chloride, causing an over-retention of water to dilute excess chloride. Afterward, Achard went on to confirm that chloride was also retained in febrile disease, heart failure, and nephritis (inflammation of the kidneys).1 It was thus argued that salt retention was the cause of numerous diseases rather than its retention being caused by the disease condition. This was essentially the beginning of the end for salt, being considered not a healthy natural substance providing 2 essential minerals (sodium and chloride) but rather a dietary blood pressure–raising demon.
Widal in 1903 and Strauss in 1904 were the first to test a low-salt diet as a treatment of edema, noting “peripheral, pulmonary, and even cerebral edema” with the addition of salt to the diet, whereas limiting salt intake “…occasioned a relatively rapid disappearance of the edema.”1 According to Widal, “Salt…in certain cases of Bright’s disease is a dangerous article of diet”1; and Widal and Archard both claimed credit for the idea that chloride retention causes heart and kidney edema.1
In 1904, 2 French scientists named Ambard and Beaujard (sometimes spelled Beauchard) further promoted the idea that salt retention was a driver of edema and hypertension. These authors were credited for inventing the Salt–Blood Pressure Hypothesis and were some of the first scientists to spark The Salt Wars.4 However, there was tremendous controversy at the time because “…the general German experience was opposed to a strict relationship between retention of chlorids and elevation of blood pressure.”5 In 1907, Lowenstein was unable to demonstrate a correlation between chloride retention and blood pressure in patients with renal hypertension, with only 1 of 10 cases having “a definite relationship between the fall in blood pressure and elimination of chloride from the body.”1
During this time Ambard and Beaujard were testing salt restriction in patients with hypertension and found retention of chloride in hypertensive patients. They studied 6 hypertensive patients (some with valvular heart disease and/or Bright’s disease) with a low-salt diet consisting of 3 g of salt (1.2 g of sodium) and compared it against a high-salt diet (14 g of salt or 5.8 g of sodium). Despite the salt intake being approximately twice that compared with a normal sodium diet (ie, 5.8 vs 3.4 g of sodium), “The changes in blood pressure were not striking but tended to be downward when the low salt diet was given and upward when the higher salt intake was allowed.”1
Ambard and Beaujard believed that both edema and hypertension were caused by a saturation of the body with salt, but even these authors realized that salt restriction did not completely normalize blood pressure in those with hypertension. However, the idea that salt restriction would prevent those with kidney disease from developing permanent severe hypertension made logical sense.1 Soon after, Laufer came up with a diet that was even lower in salt compared with that recommended by Ambard and Beaujard. The diet contained just 100-720 mg of sodium/d (instead of 1200 mg) but provided a sufficient amount of calories and protein. Laufer’s diet consisted of 200 g of rice, 300 g of wheat flour, 500 g of potato, 100 g of white cheese, 100 g of sugar, and 1 L of water. This diet was very similar to that which would be recommended by Walter Kempner 40 years later.1 However, the “low-salt rice diet” was actually first invented in 1904 by Laufer (40 years before Walter Kempner’s rice diet). Interestingly, both diets allowed fairly high amounts of sugar, because back then sugar was considered innocuous. However, the evidence is finally starting to shed light on the harms of sugar, suggesting that we may have blamed the wrong white crystal all along.6, 7, 8, 9
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-James J. DiNicolantonio, PharmD, James H. O’Keefe, MD
This article originally appeared in the September 2017 issue of The American Journal of Medicine.
