It’s widely acknowledged among well-read, perspicacious nutritionists and nutritional scientists that all of the salt that’s entered into our diets over the most recent millennia, and in particular the past century, has had a devastating impact on our health. Salt has been implicated in the pathogenesis of a number of ailments, including various forms of inflammation-driven conditions. Not to mention the fact that it’s well established that sodium is principally involved in the etiology of hypertension (1, 2, 3, 4, 5, 6, 7), which is a risk factor for cardiovascular disease, the leading cause of death in many parts of the world.
What’s not firmly established though, is exactly how salt causes hypertension. Nutritional scientists have a fairly good understanding of the mechanisms, but there’s certainly room for speculation, debate, and generation of novel hypotheses. Very recently, some of the leading scientists operating within the realm of evolutionary nutrition published a paper in which they present a mechanistic hypothesis pertaining to the link between salt and hypertension. In this post, I thought I’d highlight certain critical parts of that article, in an attempt to illuminate and draw attention to the physiological effects of salt consumption.
The links between the dietary sodium/potassium ratio, oxidative stress, and hypertension
At the very beginning of the article, the authors present their theory…
We hypothesize that Americans, and most people in Westernized countries, habitually consume a self-selected daily diet of foods that contain exceedingly suboptimal amounts of dietary potassium and enormously supraphysiological amounts of sodium chloride, a dietary imprudence that causes oxidative stress, which in turn causes dysfunction of the vascular endothelium, vascular smooth muscle, and perivascular tissues. Such dysfunction ultimately results in hypertension, its associated cardiovascular diseases, and salt sensitivity of blood pressure. (8)
This theory is fairly uncontroversial in light of the available data on salt and hypertension. It does have a certain uniqueness to it though, in that it heavily emphasizes the importance of the sodium/potassium ratio in relation to oxidative stress and the development of hypertension.
Later on, the researchers go on to talk about the role potassium and sodium play in our diet, as well as the effects they have on the human body. Here are some of the most relevant parts:
The lineage of our species, Homo sapiens, subsisted as hunters-gatherers for at least 5 million years, during which time they adapted to dietary intakes of potassium in the range of 200 – 400 mmol per day on average. Because Homo sapiens evolved only in the last 1 – 2% of that 5 million year lineage, we can conclude that too little time has elapsed for the requirement for adapted potassium consumption to have changed, given that conserved core metabolic processes depend on potassium.
… A high sodium diet results in oxidative stress-induced vascular endothelial dysfunction and consequent reduced nitric oxide bioavailability and impaired vasodilatation. High sodium diets increase oxidative stress and reduce nitric oxide bioavailability by decreasing the activity of nitric oxide synthase. High sodium intakes increase the production of reactive oxygen species which play an important role in inducing vascular endothelial dysfunction and reducing endothelial mediated vasodilation (see references in). Salt loading increases NADPH oxidase activity and superoxide production and expression. Dietary sodium restriction improves vascular endothelial function by increasing nitric oxide bioavailability. Dietary sodium restriction improves nitric oxide production by enhancing the production of the nitric oxide synthase cofactor, tetrahydrobiopterin (BH4). (8)
Finally, before wrapping up, the authors discuss the implications of their hypothesis. Here’s the key point:
Because the average American consumes foods containing suboptimal amounts of potassium and physiologically excessive amounts of sodium under their usual conditions of daily living, such individuals will already have some degree of oxidative stress. That would imply also that such individuals have some degree of vascular endothelial dysfunction and blood pressures that are already higher than optimal. (8)
The statements presented in the paper concord with my own personal experience, in the sense that I’ve noticed that the impact salt has on my body relates to my intake of potassium-rich fruits and vegetables. I generally stay away from salt; however, every now and then, such as when I’m attending social events, I do eat some salty foods. What I’ve noticed is that if I take in a lot of salt, but little to no fruits and vegetables, I feel worse than if I couple a moderate-high salt intake with a high intake of unprocessed plant foods. Not only that, but at times when I take in more salt than usual, I typically get a craving for fresh fruits and veggies. This probably isn’t solely because such foods are rich in potassium, but it’s likely one of the reasons.
The evidence against salt, in particular sodium, is very strong. There are arguably few nutritional cases that are as clear-cut as the one in which sodium is on trial. This is reflected by the fact that the vast majority of trained nutritionists and nutritional scientists hold the belief that sodium is guilty of several crimes, and that a number of public health agencies have issued warnings stating that people should strive to reduce their salt intake.
There are many possible mechanisms by which salt can inflict damage. Recently, it has become increasingly clear that a high sodium intake is particularly detrimental when coupled with a low potassium intake and that an evolutionarily abnormal intake of these nutritional elements could lead to oxidative stress, which has been postulated to play a critical role in the development of hypertension.