Hypertension Due to Toxic White Crystals in the Diet: Should We Blame Salt or Sugar?

ByCrossFitFebruary 28, 2020

Question
Does increased salt intake lead to hypertension, and does reducing salt intake reduce blood pressure? Does sugar intake affect blood pressure?
Takeaway
Sodium is an essential nutrient. The behavior of free-living populations suggests humans are adapted toward levels of salt intake significantly higher than those recommended by prominent dietary guidelines. Evidence clearly indicates increased salt intake does not increase blood pressure and lower salt intake leads to only small reductions in blood pressure in the majority of individuals. Other changes that occur alongside salt restriction may in fact increase overall cardiovascular risk. Increased sugar intake is more consistently linked to increased blood pressure via sugar-induced insulin resistance. Taken together, the evidence indicates recommendations to reduce hypertension and incidence of stroke and heart attack should focus on restricting sugar, not salt.

Numerous government bodies and public health institutions recommend population-wide reductions in sodium intake (1). The American Heart Association (AHA) is the most extreme, having at times recommended all Americans reduce sodium intake to 1,500 mg/d or less (2). The theoretical basis for these extreme recommendations is the belief that reducing sodium intake will reduce blood pressure and thus risk of cardiovascular disease and stroke (3).

Note: When the Institute of Medicine evaluated the AHA guidelines, they found no support for this level of sodium restriction. As a result, the 2015 Dietary Guidelines, issued by the USDA, recommended a reduction instead to 2,300 mg/d or less (4).

In the U.S., U.K., Canada, and a variety of other populations, sodium intake has remained stable, between 3.5 and 4 grams per day, despite wide variance in dietary recommendations and patterns (5). Our bodies are adapted to detect sodium deficiency, stimulate an appetite for salt, and detect salt in the environment (through taste), which historically allowed humans to find this essential nutrient in varied environments (6). Rats and sheep consume similar amounts of salt per pound of body weight as humans, suggesting a broad mammalian sodium set point.

High doses of salt have been conclusively shown to have little effect on blood pressure in studies dating back to the early 1900s. In both normotensive and hypertensive subjects, adding as much as 30 grams of salt per day to the diet had little or no effect on blood pressure (BP), with some subjects showing lower BP on high-salt diets and higher BP on low-salt diets (7). One lab (Kawasaki) concluded adding salt “virtually never increases BP significantly in normal subjects.”

Some share of the population (which may be as low as 6% or as high as 50%) will see an increase in BP with increased salt intake, and vice versa (8). Even in these subjects, however, the magnitude of effect is arguably trivial. A meta-analysis of 170 randomized controlled trials found sodium restriction lowers BP by an average of 1-3% in normotensive subjects and 3.5-7% in hypertensive subjects while increasing renin, noradrenaline, aldosterone, triglyceride, and cholesterol levels (9). The longest trial in this survey found 18-36 months of adherence to a low-salt diet decreased blood pressure by an average of 2/1 mmHg (10).

Low-salt diets may lead to other changes that increase cardiovascular risk. Some have argued hypertension is an adaptive response to atherosclerosis that ensures the heart and brain continue to receive adequate blood flow; this argument is supported by an increased risk of heart disease at low blood pressures (11). Low sodium intake reduces blood volume, frustrating this adaptation while leading to an increased heart rate and the metabolic changes noted above, all of which may suggest increased overall heart disease risk. Salt restriction also increases peripheral vascular resistance, which is linked to hypertension (12).

Increased sugar intake, conversely, leads to insulin resistance, which reliably induces hypertension via its effects on kidney function and the sympathetic nervous system (13). Research in rats, monkeys, and humans has consistently shown that high-sugar diets more consistently lead to increased blood pressure — and larger increases in blood pressure — than high-salt diets (14). The “salt sensitive” share of the population noted above may in fact develop sensitivity as the result of insulin resistance-induced kidney damage and other consequences of insulin resistance (15). This is consistent with evidence from some of the animal studies mentioned above, which indicate the effect of salt on blood pressure is exacerbated in the context of a high-sugar diet. Low-salt diets have been linked to increased insulin and C-peptide levels and impaired insulin clearance, all of which exacerbate the deleterious effects of sugar (16).

Taken together, the evidence suggesting excess salt intake leads to hypertension, or that reducing salt intake will treat hypertension, is weak. The evidence is comparatively strong, however, that increased sugar intake directly leads to hypertension and increased risk of metabolic disease, and that sugar restriction can reverse hypertension. Accordingly, recommendations for the treatment of hypertension should focus on the restriction of sugar, not salt.

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Notes