Don’t Blame the Salt for What the Sugar did

This review, led by cardiovascular research scientist, James DiNicolantonio, challenges the “Salt Hypothesis” which claims dietary salt will increase blood pressure (i.e., hypertension), and therefore increase the risk of cardiovascular disease. High blood pressure is indeed a risk factor for cardiovascular disease; however, the science to support salt-induced hypertension remains inconsistent and inadequate. Instead, this review suggests that sugar, not salt, is more likely the food additive contributing to hypertension and cardiovascular disease.

Despite the lack of data to prove salt’s promotional role in high blood pressure, numerous health organizations, dietary guidelines, and government agencies across the globe continue to recommend reducing salt intake. Paradoxically, salt restriction may lead to worse health outcomes.

Salt is a combination of sodium and chloride­, together forming the beloved white crystals we sprinkle on our food to make it taste better. And through all its disparage, sodium remains an essential mineral, meaning we have an absolute requirement for it in order to survive. Sodium acts in controlling blood volume, maintaining the body’s overall fluid balance, facilitating proper nerve and muscle function, among other roles.

Across the globe, the average sodium intake falls around 3.5–4 g (just over 8.5g of salt) per day, despite the current Dietary Guidelines for Americans recommending a sodium intake of less than 2300 mg/day (~5.7g of salt). It is suggested that we are not “over-consuming” sodium out of ignorance to these recommendations, we are merely responding to bodily needs (salt cravings), and these average levels currently being consumed are actually optimal.

The low-salt recommendations are primarily based on opinion and data from a subset of individuals who are “salt-sensitive” (i.e. those who see a modest increase in blood pressure with higher salt intake). These individuals tend to be older, insulin resistant, and/or have reduced kidney function. While some people may respond to a reduction in blood pressure by reducing salt intake, it may be accompanied by an increased risk for many concerning metabolic side-effects.

Younger people with normal blood pressure and kidney function are typically “salt-resistant” (i.e. those who do not see a rise in blood pressure with higher salt intake), and in these individuals, higher salt intake may actually be protective against health problems. It’s even possible that healthy individuals that lower their salt intake can experience an increase in blood pressure (the opposite of what they are trying to achieve).

Internal sodium levels are tightly regulated — too much, and we excrete more in our urine, too little, and our kidneys conserve and reabsorb it. Part of our body’s response to low sodium levels is the activation of the renin-angiotensin-aldosterone system, which leads to the release of catecholamines (stress response), and activation of our sympathetic nervous system (fight or flight mode). Although, inconsistencies remain around sympathetic nervous system activity depending on the state of health of the individual. Low salt intake in healthy individuals may lower blood pressure by ~1–3%, but at the cost of increasing the hormones involved in this system (renin, aldosterone, adrenaline, and noradrenaline), an increase in heart rate, and increased cholesterol and triglycerides (undesirable effects).

Dr. DiNicolantonio argues that when we limit salt intake, our desire for salty foods increases, and in our modern food environment, these cravings tend to be satisfied with processed foods. Processed foods are in fact, where the majority of sodium in the diet comes from. Low-salt recommendations could, therefore, inadvertently lead to the over-consumption of processed foods, which not only increases salt intake but sugar and refined carbohydrate intake too. The potential unintended consequences of these actions that Dr. DiNicolantonio points out are obesity and insulin resistance, among other metabolic disturbances that contribute to hypertension. Salt, in this case, may simply be the innocent bystander.

There is evidence to suggest high-sugar diets are more likely to increase blood pressure and drive salt-sensitive hypertension than high-salt diets. A meta-analysis of randomized controlled trials found high-sugar diets increase blood pressure at levels that nearly double that of high-salt diets. Insulin resistance itself, driven by high-sugar diets, has been identified as the more likely cause of hypertension, shown to increase levels of atherogenic lipid particles, dyslipidemia, hypertension, and cardiovascular disease. It has also been demonstrated that uncontrolled glucose levels and chronically elevated insulin levels may worsen salt sensitivity, likely in part due to the damaging effects glucose can have on the kidneys. High blood glucose levels can cause draw water to blood vessels, increase blood volume, and lead to hyponatremia (low blood sodium levels). A high-sugar diet can trigger an increase in blood pressure that is nearly twice that observed with high-salt diets. In essence, the consequences of excess sugar are more likely driving hypertension, and salt is simply taking the brunt. Removing sugar, not salt, could help correct these problems, in addition to normalizing salt sensitivity.

Altogether, we may have been misled into believing the reduced-sodium versions of our favorite canned soups, crackers, and potato chips are the healthier option when in reality we’re cutting out the wrong ingredient. Keep the salt, ditch the sugar.