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Dietary Salt Impairs the Endothelial Glycocalyx: The Most Important Cardiovascular Disease Risk Factor You May Never Have Heard About

Frequently, important physiological discoveries made by scientists who study obscure topics escape the attention of the general public, health professionals, and even other scientists. Such has been the case for the endothelial glycocalyx: a delicate and fragile structure lining the inside surface of all blood vessels.

The endothelial glycocalyx had been inferred from blood flow measurements as far back as the 1940’s, but due to its fragile configuration the structure had never been viewed until 1966 when it was first detected with an electron microscope using special staining procedures (1). Over the next 30 years, scientists speculated about the function of the endothelial glycocalyx, but it was not until 1996 that two researchers, Vink and Duling (2), provided an answer. They concluded that the endothelial glycocalyx “may represent the true active interface between blood and the capillary wall”.

Okay, no big deal. A tiny and fragile blood vessel structure was first visualized 50 years ago and then it took scientists another 30 years to assign what many would consider a minor function to it. But is the function of the endothelial glycocalyx really that minor?

In fact, the glycocalyx is so important that its dysfunction plays a critical role in almost every step of atherosclerosis – the process that leads to heart disease and stroke. And as you’ll see, dietary sodium can directly contribute to this dysfunction and start the disease process.

Visualizing the Glycocalyx

I tend to be a visual learner, as do many people. So, let’s take a look at the cross section of an artery, the way many cardiologists visualized it prior to 1996. Figure 1 below shows that the inner-most surface of arteries is lined by cells called the endothelium. However, nowhere in sight is the endothelial glycocalyx. This perception of blood vessel structure was commonly held until about 1994 when a select group of scientists developed a new staining procedure (alcian blue) to better visualize the endothelial glycocalyx (1).

Figure 1. Classical visualization of an artery cross section

The widespread impression of blood vessels devoid of an endothelial glycocalyx gave scientists studying cardiovascular disease an imperfect view of the atherosclerotic process which underlies heart attacks and strokes. Figure 2 shows the commonly held perspective of the day for atherosclerosis in a blood vessel without an endothelial glycocalyx.

Figure 2. Classical visualization of atherosclerosis without the endothelial glycocalyx.

In contrast, Figure 3 shows the cross section of a capillary taken in 2003 using electron microscopy with alcian blue staining procedures. It provides indisputable evidence of the endothelial glycocalyx (3).

Figure 3. Electron microscope overview of an alcian blue stained rat left ventricular myocardial capillary showing the endothelial glycocalyx (3).

When an atherosclerotic plaque forms in the intima of arteries, a number of key steps occur which can ultimately lead to cardiovascular disease: 1) Inflammation (8, 14, 19, 77) causes the endothelial glycocalyx to be shed (14-29), promoting further inflammation. 2) The glycocalyx becomes thinner in areas of turbulent blood flow (1, 7, 21, 23) where atherosclerotic plaques form. 3) The shedding of the glycocalyx promotes movement of LDL cholesterol from the bloodstream into the intima (20, 22, 28). 4) The LDL cholesterol becomes oxidized and continues to promote glycocalyx shedding. 5) Leukocytes, monocytes, T cells, other leukocytes and platelets, attach to adhesion molecules on the surface of endothelial cells (4-6, 12, 15, 17, 18, 26, 33) and then enter the intima. 6) After entry into the arterial intima, a specific type of leukocyte, called monocytes, are transformed into macrophages. 7) Macrophages consume oxidized LDL cholesterol and other elements to become foam cells. 8) Over time and continued inflammation, these foam cells become the atherosclerotic plaques that clog arteries. 9) Eventually a fibrous cap forms over the plaque which, if ruptured via the continued inflammatory processes, can precipitate heart attacks and strokes.

The atherosclerotic process is more complex than these simple nine steps, but these steps will provide you with sufficient information to understand how a high salt diet promotes atherosclerosis at nearly every step along the way.

However, before I show you how a high salt diet damages the endothelial glycocalyx and promotes CVD, heart attacks and strokes, one more important detail must be known. An additional revealing clue to the atherosclerotic process is the anatomical location of atherosclerotic plaques within arteries. As far back as 1971, C.G. Caro and colleagues (52, 53) showed that early atherosclerotic lesions developed almost exclusively in areas of turbulent blood flow near bifurcations (forks) of arteries, and rarely in areas of non-turbulent (laminar) blood flow. This fact has been verified in all modern studies of atherosclerosis (1, 7, 21, 21, 23, 53). Figure 5 below shows this phenomenon of plaque formation in areas of turbulent flow where the thickness and density of the endothelial glycocalyx is reduced. Current evidence indicates that atherosclerosis arises in these areas of turbulent flow because they are less able (than areas of non-turbulent flow) to respond to inflammatory conditions in the bloodstream, which promote glycocalyx shedding (8, 14, 19, 77).

Figure 5. Effect of turbulent blood flow and laminar (non-turbulent) blood flow upon the distribution of atherosclerotic plaques in arteries.

How a High Salt Diet Promotes Atherosclerosis and Cardiovascular Disease (CVD)

Normally, plasma concentrations of sodium are maintained within a narrow range that varies in the general population from 134 to 148 mmol/L (54-56). Increasing dietary salt in subjects without hypertension elevates plasma sodium concentrations within or beyond the normal range (57, 58).

In the Paleo diet community, a common perception is that adding salt, or particularly sea salt, to a Paleo diet has little or no adverse effect upon health and wellbeing (59-68). Nevertheless, the data reveals that salt, even added to the diet of normotensives (normal blood pressure), elevates plasma sodium concentrations and has important and far-reaching health considerations; particularly if the salt habit is continued throughout life.

Experiments conducted in 2007 on living human endothelial cells incubated outside the body (ex vivo) demonstrated that stiffness of the cells was unaffected by sodium concentrations of < 135 mmol/L, but stiffness rose steeply at concentrations between 135 and 145 mmol/L (70). Further, higher plasma sodium concentrations (~143-150 mmol/L), which are still mostly within normal ranges and can easily be achieved in living humans by adding salt to their diet (54-58), caused the endothelial cells to stiffen and reduce their production of nitric oxide (70, 72): a compound found throughout the body. In blood vessels, nitric oxide suppresses cell inflammation and adhesion of leukocytes and platelets to the endothelium (71). In this way, normal nitric oxide production by arterial endothelial cells inhibits blood clotting and promotes normal blood flow. Nitric oxide metabolism and production is diminished with age and CVD (71).

One of the problems with the ex vivo experiment conducted in 2007 (70) was that the endothelial cells were not only incubated with sodium, but also with a hormone called aldosterone. Accordingly, the interpretation of the experiment was muddled. Was it the sodium, the aldosterone, or both that caused a stiffening of the endothelial cells and decreased production of nitric oxide? In the ensuing years, others researchers replicated these results (46, 72), but the question still remained: what caused the adverse effects upon endothelial function and nitric oxide production?

This question was finally answered in 2016 in a living (in vitro) mouse model that had a genetic mutation preventing it from synthesizing aldosterone [aldosterone synthase knockout mouse] (69). A high salt diet, without aldosterone, increased plasma sodium to 150 mmol/L, increased endothelial cell stiffness by 44 percent, and suppressed nitric oxide production. These results are consistent with two recent randomized controlled human trials showing that a high salt meal (65 mmol Na) increased plasma sodium concentrations and impaired endothelial function while increasing arterial stiffness (74, 75).

In a living (in vivo) animal model, high salt diets fed to mice increased the responsiveness of arterial endothelial cells to a pro-inflammatory cytokine (TNFα), at areas of turbulent blood flow within the arteries. High salt diets also increased adhesion of leukocytes to these same areas of turbulent flow (76). Both of these physiological changes are characteristic of, and precede the development of CVD in humans. As I previously mentioned, high salt diets promote inflammation by impairing the release of nitric oxide (69, 70, 72), while TNFα directly causes endothelial cells to shed the glycocalyx (8, 14, 19, 77). Accordingly, glycocalyx shedding initiated by the inflammation produced from a high salt diet facilitates the formation of atherosclerotic plaques and the development of CVD. Figure 6 below summarizes the effects of high salt diets upon the development of CVD.

Figure 6. How high salt diets promote the development of cardiovascular disease (CVD)

Clinical data from the Atherosclerosis Risk in Communities Study involving 12,779 subjects demonstrated that plasma sodium concentrations represent a significant predictor of 10-years risk of coronary heart disease (77). These findings show that elevation of plasma sodium even within the normal physiological range (134 to 148 mmol/L) is accompanied by cardiovascular changes that facilitate the development of CVD (77).

Practical Implications and Final Thoughts

Perhaps the most obvious implication of this recent, enormous and persuasive scientific literature, is simply not to add salt or sea salt to your already healthful, natural and fresh Paleo foods and recipes. Unadulterated, natural, fresh Paleo foods have very little normally occurring sodium. In a previous blog table, I have demonstrated how it is virtually impossible to ingest more than 2300 mg of sodium from natural, un-salted Paleo foods. From this table, also notice how the potassium content of natural, un-salted Paleo diets typically contains about five times more potassium than sodium.

High dietary levels of potassium are known to overcome many of the adverse cardiovascular effects of sodium by softening vascular endothelial cells (78), increasing nitric oxide production (78) and preventing sodium induced impairment of endothelial function (75). So, practically speaking, it may not always be possible to avoid foods with added salt. If this is the case, try to counter high salt foods with plenty of potassium rich fruits and vegetables. Some of my favorite high potassium foods are peaches, cherries, bananas, dates, raisins, dried figs, pecans, filberts, tomatoes, steamed broccoli and summer squash.

Another practical way to counter the effects of temporary overindulgence in salty foods is to drink more water. For an average person with an elevated plasma sodium concentration of 143 mmol/L, drinking one liter of water over a six to eight-hour period can reduce this value to the lower range of 137 mmol/L, providing no additional high salt foods are consumed (77).

So, the take home message to prevent salt induced CVD is this: 1) don’t put added salt or sea salt into fresh, healthy Paleo foods; 2) avoid salted, processed foods whenever possible. If you happen to overindulge in salted foods: 3) eat plenty of potassium rich fruits and vegetables and 4) drink more water.


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Loren Cordain, Ph.D.

As a professor at Colorado State University, Dr. Loren Cordain developed The Paleo Diet® through decades of research and collaboration with fellow scientists around the world.

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