13.2: Sodium

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Salt (\(\ce{NaCl}\)) contributes almost all the sodium that we consume. 75-85% of the salt we consume is from processed foods, 10% is naturally in foods, and added salt contributes 10-15% of total salt intake1.

95-100% of consumed sodium is absorbed2. Sodium is taken up into the enterocyte through multiple mechanisms before being pumped out of the enterocyte by sodium-potassium (\(\ce{Na+}\)/\(\ce{K+}\)) ATPase. Sodium-potassium ATPase is an active carrier transporter that pumps 3 sodium ions out of the cell and 2 potassium ions into the cell, as shown below. It is the reason that sodium is the major extracellular cation and potassium is the major intracellular cation.

Figure \(\PageIndex{1}\): Sodium-potassium ATPase (aka sodium-potassium pump), an active carrier transporter3

Sodium is the major cation in extracellular fluid.

ADAPT \(\PageIndex{1}\)

Sodium has 3 main functions1:

Fluid balance
Aids in monosaccharide and amino acid absorption
Muscle contraction and nerve transmission (not discussed further below)

Fluid balance

The body regulates sodium and fluid levels through a series of processes as shown below. A decrease in plasma volume and blood pressure signals the kidney to release the enzyme renin. Renin activates angiotensin that is converted to angiotensin II. Angiotensin II signals the adrenal glands to secrete the hormone aldosterone. Aldosterone increases sodium reabsorption in the kidney, thus decreasing sodium excretion. These actions cause plasma sodium concentrations to increase (these could also be increased by sodium intake), which is detected by the hypothalamus. The hypothalamus stimulates the pituitary gland to release antidiuretic hormone (ADH) that causes the kidneys to reabsorb water, decreasing water excretion. The net result is an increase in blood volume and blood pressure1.

Figure \(\PageIndex{2}\): Response to decreased plasma volume and blood pressure

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Aids in monosaccharide and amino acid absorption

Glucose and galactose are taken up into the enterocyte by sodium-glucose cotransporter 1 (SGLT1), which requires sodium to be transported along with glucose or galactose.

Figure \(\PageIndex{3}\): Monosaccharide Uptake and Absorption

Amino acids are taken up and transported into circulation through a variety of amino acid transporters. Some of these transporters are sodium-dependent (require sodium to transport amino acids).

Figure \(\PageIndex{4}\): Protein absorption

Sodium deficiency is rare, and is normally due to excessive sweating. Sweat loss must reach 2-3% of body weight before sodium losses are a concern1,2. Losses of this magnitude are uncommon, but can occur in marathon runners and ultra-marathon runners who sweat for many hours straight (without proper liquid intake). But in general some practices like consuming salt pills to replace loss from sweating are not needed. Low blood sodium levels (hyponatremia) can result in1:

Headache
Nausea
Vomiting
Fatigue
Muscle Cramps

Sodium is not toxic because we can readily excrete it, but higher sodium intake increases the risk of developing high blood pressure. High sodium intake also increases calcium excretion, and a recent meta-analysis has found a positive association between dietary sodium intake and the risk of osteoporosis4, such that high intakes are associated with a higher risk of developing osteoporosis. However, hyponatremia (low sodium in the body) has also been associated with an increased risk of developing osteoporosis due to the release of sodium from the bone matrix. The prevalence of hyponatremia is estimated to be between 3-26%5. The extraction of sodium from bone has been hypothesized to affect bone quality, such that the bone is less efficient at healing microfractures which can eventually lead to lower bone density5. High sodium intake may also increase the risk of developing kidney stones (by increasing calcium excretion), because calcium oxalate is the most common form of kidney stone1.

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References

Byrd-Bredbenner C, Moe G, Beshgetoor D, Berning J. (2009) Wardlaw's perspectives in nutrition. New York, NY: McGraw-Hill.
Gropper SS, Smith JL, Groff JL. (2008) Advanced nutrition and human metabolism. Belmont, CA: Wadsworth Publishing.
http://frontalcortex.com/?page=oll&topic=2314&qid=2468
Fatahi S, Namazi N, Larijani B, Azadbakht L. (2018). The Association of Dietary and Urinary Sodium With Bone Mineral Density and Risk of Osteoporosis: A Systematic Review and Meta-Analysis, Journal of the American College of Nutrition, 37:6, 522-532.
Holm JP, Amar AOS, Hyldstrup L, Jensen JEB. (2016). Hyponatremia, a risk factor for osteoporosis and fractures in women. Osteoporos Int, 27, 989-1001.