High Blood Pressure: Is a Long Term Low Salt Diet the Answer?

by John Laznovsky
The Wolf of Wellness
April 4, 2024

If you have high blood pressure (BP) or know someone with high BP, you’ve probably heard that you should follow a low salt diet to reduce your blood sodium levels because it will help to lower BP. There is ample evidence to indicate that this strategy works quite well in the short term to lower BP, but what about the long term effects of following a low salt diet? How exactly does salt intake impact BP? Are there any ramifications to following a low salt diet? To answer these questions we need to know how the body regulates salt and water balance, and what happens to these systems in response to salt intake.

The Substances Involved in Regulating Water and Salt Balance:

The body regulates water balance through the use of hormones such as anti-diuretic hormone (ADH), aldosterone, renin, and angiotensin 1 and 2, as well as osmolytes (soluble substances that are involved in osmosis), such as ions (i.e. sodium and potassium), plasma proteins (albumins), and other molecules. Our primary focus for this conversation will be on the hormones and ions involved in regulating water and electrolyte balance, since they play a significant role in balancing these processes.

Anti-Diuretic Hormone (ADH):

ADH (also called vasopressin) is produced by the hypothalamus, is then passed to the posterior pituitary gland, where it can be secreted into the blood stream. Neurons in the hypothalamus contain osmoreceptors, which are special receptors that monitor osmotic pressure (water pressure/ volume). In response to conditions, such as hypernatremia (high blood sodium content relative to water), and hypovolemia (low blood volume), osmoreceptors in the hypothalamus will be stimulated. The hypothalamus will then direct the posterior pituitary gland to release ADH. Hypernatremia is something that would take place if you ate a very salty meal, and hypovolemia would occur if you are dehydrated. Both of these conditions can trigger the release of ADH. (1, 2)

The primary role for ADH is to reduce water excretion by increasing water reabsorption in the late distal tubule and collecting duct of the kidneys. The reabsorbed water enters the blood stream and increases blood volume. ADH can also act as a vasoconstrictor, narrowing the blood vessels. Both an increase in blood volume, and vasoconstriction can lead to a concomitant increase in BP. (1, 2)

The Renin-Angiotensin System (RAS):

The RAS involves several hormones, including aldosterone, renin, and angiotensin 1 and 2. This system is described through a direct link or axis between the kidneys and the heart. In this axis, the heart functions to circulate the blood and the kidneys function to maintain the blood volume. (9) As you now know, ADH also plays a role in maintaining blood volume and has a large impact on the RAS. The RAS is typically activated by low blood volume (hypovolemia)/ low BP, or low blood sodium levels (hyponatremia) and is considered to be a long term regulator of BP. Due to its long term regulatory effects on vascular tone and salt and water homeostasis, the RAS is considered to play a major role in the development of pathophysiological conditions, such as hypertension, heart failure, cardiovascular disease (CVD), and renal diseases. (3, 9)

Baroreceptors, which are specialized nerve endings located within the aortic arch and bilateral carotid sinuses, monitor quick changes in BP. Therefore, baroreceptors are considered short term regulators of BP and will monitor and adjust BP throughout the day. It should be noted that dysfunction in the baroreflex feedback pathway (nerve pathway involving baroreceptors) has also been suspected to play a role in high BP that is associated with a high salt diet. (4)

As previously mentioned, conditions involving low blood volume)/ low BP, or low blood sodium levels can activate the RAS system. Renin, which is the rate limiting enzyme of the RAS, is stored in the juxtaglomerular cells of the kidney. (3) It is released when: the afferent arterioles of the kidney sense reduced renal perfusion (low blood volume/ BP), the delivery of sodium is reduced to the distal convoluted tubule (DCT), and when there is increased beta-sympathetic activity in the beta-1 adrenergic receptor, which is part of the sympathetic nervous system (fight or flight response). Renin then cleaves (breaks up) angiotensin, which is synthesized by cells of the liver, at the N-terminal, to form angiotensin 1. Angiotensin 1 is then converted to angiotensin 2 by the enzyme, Angiotensin-Converting Enzyme (ACE). ACE is located on the plasma membranes of vascular endothelial cells. (3, 9)

Angiotensin 2 is the primary hormone responsible for the effects of the RAS. These effects include: vasoconstriction in the arterioles, secretion of aldosterone from the adrenal cortex, increased sodium reabsorption in the proximal convoluted tubule of the kidneys, increased sympathetic activity in the central nervous system, and the release of ADH. (3) Aldosterone, which is synthesized in the zona glomerulosa of the adrenal cortex, aids angiotensin 2 by increasing sodium reabsorption, as well as potassium release, from the DCT in the kidneys. (5) Through these responses, angiotensin 2 and aldosterone produce an array of effects in the circulatory system, including increased BP (from increased peripheral resistance), an increase in heart rate (HR), and an increase in oxidative stress/strain on vascular tissues (with prolonged release). Thus, angiotensin 2 and aldosterone from the RAS have been linked with many pathophysiological conditions including: hypertension, atherosclerotic disease, heart failure, and kidney disease. (3, 5, 6, 7, 8)

The Effects of A Long Term Low Salt Diet:

In cases of high BP, a long term low salt diet is usually recommended in addition to medications such as ACE inhibitors. Remember, ACE was the enzyme that converted angiotensin 1 to angiotensin 2. ACE inhibitors block the conversion of angiotensin 1 to angiotensin 2, thereby reducing BP. In the short term, a low salt diet appears to be very effective at reducing BP. One cross over study showed significant reductions in BP in just one week (14) However, it is still highly controversial as to whether or not a low salt diet actually decreases cardiovascular morbidity or mortality (in the long term). (15, 16, 17, 18, 26, 27) 

Interestingly, several studies have indicated that a long term low salt diet may actually increase cardiovascular morbidity and mortality! Therefore, a long term low salt diet has been correlated with an increased risk of high BP and CVD. (10, 11, 12, 13, 16, 17, 27) Researchers suspect that this is most likely due to over activation of the RAS, which is associated with elevated levels of angiotensin 2 and aldosterone. As you now know, elevated levels of these hormones can lead to increases in HR (sympathetic activity), BP, and oxidative stress in vascular tissues.

This makes sense because the RAS is the long term regulator of BP (through salt and water balance), and responds to low blood volume / low BP and low blood sodium levels. Initially, a low salt diet will most likely produce conditions of low BP/ blood volume/ blood sodium levels. Eventually, the RAS will probably respond to these conditions by releasing angiotensin 2 and aldosterone, causing an increase sodium reabsorption, blood volume and pressure. A continued low salt intake may continuously activate the RAS, allowing a vicious cycle to take place.

The Antagonistic Interplay Between Sodium and Potassium:

Sodium (Na+ ion) and potassium (K+ ion) are essential minerals involved in maintaining many vital processes, such as fluid and blood volume regulation, muscular contraction and nerve transduction. Sodium is generally found in larger quantities in the extracellular fluid (fluid outside of cells such as interstitial fluid and plasma), which is why sodium is able to have such a large impact on BP. Potassium, on the other hand, is found in larger quantities in the intracellular fluid (fluid inside cells). Therefore, h; sodium is involved with maintaining extracellular fluid volume, while potassium is involved in maintaining intracellular fluid volume. (22)

More mild symptoms of sodium deficiency (hyponatremia) include nausea, vomiting, weakness, headache, and mild neurocognitive deficits. More severe symptoms associated with hyponatremia include delirium, confusion, impaired consciousness, ataxia, seizures, and, brain herniation, and death (23), as well as high BP and increased risk of CVD/ mortality. (10, 11, 12, 13, 16, 17, 27) Hyponatremia can be caused by certain medications, excessive alcohol consumption, very low-salt diets, and excessive free water intake during exercise without electrolytes. (23)

Symptoms of potassium deficiency include muscle weakness and paralysis, which can lead to respiratory failure if not corrected, tachycardia, gallop rhythm, and dilatation of the heart. The primary causes of potassium deficiency include reduced intake due to intravenous feedings that did not contain potassium, increased loss of potassium in the urine due to accelerated tissue breakdown, or renal lesions, loss from the gastrointestinal tract due to diarrhea, or fistulae, change between serum and cells, associated with metabolic causes, medications or shifts in pH. (24)

Thus, both sodium (from high quality salt) and potassium (whole food sources such as avocados) should be consumed regularly in the diet and in adequate amounts! Even “salt sensitive” individuals still need a certain amount of sodium in order to function properly and avoid pathological disorders, and very low salt diets may cause deleterious effects in these populations. Indeed, a large review of the body of evidence to support the efficacy of a very low sodium diet (from reduced salt intake) concluded that there is insufficient and potentially biased evidence (due to self reported sodium intakes by the subjects) to support the recommendation of low sodium diets. This study also concluded that intakes of at least 2.3 grams and up to almost 5 grams (4.6 g) a day of salt were associated with a reduced risk of CVD. (26) Therefore, based on this evidence, we can define a very low salt diet as an average consumption of less than 2.3 grams of salt per day. What’s even more interesting is that medical associations such as The American Heart Association (AHA) and The American Medical Association (AMA) typically recommend a salt intake below 2.3 grams of salt a day for the general population. Moreover, an Italian cohort study on elderly populations ages 62-102 years found an increased risk of mortality associated with a diet of less than 6 grams of salt per day! (27)

The kidneys manage potassium concentrations through responses to dietary intake of sodium and potassium. A low intake of salt (sodium) or a high intake of potassium will typically lead to the release of potassium through urinary excretion. Remember, low salt intake eventually leads to elevated levels of aldosterone, which promotes excretion of potassium from the DCT in the kidneys. (5) Several studies have revealed that increasing potassium intake may play a crucial role in sustaining healthy BP, reducing risk of CVD and kidney stone formation. (19, 20, 21, 22, 25) Potassium has been shown to be vasoactive, in that it can cause vasodilation (opening) in the blood vessels, which can help to reduce BP. (25) Based on this research, adequate levels of potassium appear to negate the negative effects of sodium on BP. The only issue is that these studies recommend a very low intake of sodium and a high intake of potassium to produce a more favorable ratio for BP control. As we now know, a very low sodium intake can not only increase excretion of potassium, but may also increase risk of high BP, CVD, impaired cognitive function, brain herniation etc. Therefore, an adequate intake of both sodium and potassium appear to be vital for managing BP and reducing risk of CVD.

Processed Table Salt Vs. The Salt of The Earth:

If you search the differences between higher quality salts, such as sea salt, and refined table salt, most medical/ health articles will tell you there is no difference between the two in regard to health or mineral content. These sources will also tell you that there is no evidence to indicate sea salt is better for BP control or reduced risk of CVD. The first thing you should be aware of is that there are clear differences between these two salts.

Salt is formed through an ionic bond between sodium (Na) and chloride (Cl), with Na+ being the cation (positive ion) and Cl- being the anion (negative ion). Remember, opposites attract. When sodium and chloride come together, an ionic bond is formed, and electrons are transferred from the metal cation (Na+) to the non-metal anion (Cl-). Thus, salt is made up mostly of sodium and chloride (NaCl). One study compared the differences between sea salt and refined salt and found that the sea salt used contained 85.7% NaCl, whereas the refined salt contained 99.9% NaCl. The reason for this is because the sea salt had a higher overall mineral content. Indeed, sea salt contains additional minerals, such as calcium (1.5 mg/g), potassium (2.9 mg/g), magnesium (3.9 mg/g), and trace amounts of iron, manganese and zinc. While refined table salt contains almost no amount of these vitally important minerals. Therefore, refined salt is said to be mineral deficient. (29)

Research has also shown that sea salt may confer additional protection against high BP and CVD compared to refined salt. (28, 29, 30) These studies noted lower BP and risk of CVD in rats that consumed mineral rich salt (sea salt), in contrast to rats that consumed mineral deficient salt (refined salt). Researchers suspect this is most likely due to the higher mineral content in quality salt sources such as sea salt. In addition, one study showed that mineral rich salt produced less oxidative stress in vascular tissues (blood vessels) compared to mineral deficient salt (refined salt)! (30) While this research is intriguing, more research should be conducted to further investigate the differences between mineral rich salt sources and mineral poor salt sources and their impacts on BP and CVD.


Based on the evidence, a low salt diet appears to be very effective at reducing BP levels in the short term. (14) Conversely, a long term low salt diet appears to increase risk of sodium deficiency, high BP and CVD. (10, 11, 12, 13, 16, 17, 23, 27) It is recommended that even salt sensitive individuals should consume at least 2.3 grams, and up to 4.6 grams of salt per day, to reduce risk of sodium deficiency, high BP and CVD. (26) While non-salt sensitive individuals, and those with no signs of CVD, may be able to safely consume amounts greater than 6 grams of salt per day. (27) Potassium has been identified as a vasoactive mineral that may be able to counteract the negative effects of sodium on BP; thus, adequate amounts of potassium should also be consumed to reduce risk of CVD. (19, 20, 21, 22, 25) The quality of salt consumed (i.e. overall mineral content) appears to play a role in reducing risk of high BP and CVD. (28, 29, 30) Therefore, the efficacy of a long term very low salt diet should be re-evaluated, and higher mineral salt sources should be recommended to reduce overall risk of CVD.


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