Taurine: Modulator of Cellular Electrolytes


Jon B. Pangborn, Ph.D.
Bionostics, Inc., St. Charles, IL

Discovered about 175 years ago, taurine (2-aminoethanesulfonic acid) was thought to be an inert artifact of human metabolism until about 1970 when its functions began to be understood. Abundant in human mother’s milk but nearly absent in cow’s milk, taurine was recognized as “semi-essential” and even essential for children in the mid 1980s when it was added to commercial infant formula.  In the 1990s, its antioxidant role as a scavenger of hypochlorite was investigated, and taurine was found to be a critical metabolite for phagocytosis. In the CNS, taurine helps to regulate the activity of two neurotransmitters, GABA and glutamic acid. In liver tissue, it combines with activated cholesterol (“cholyl-Coenzyme-A” to produce taurocholic acid, a primary bile acid that assists uptake of dietary lipids.

Not as well recognized is taurine’s influence on cellular electrolyte levels and on body retention of magnesium.  One of the earliest-discovered functions of taurine was that of regulating the flux of potassium, calcium and magnesium into cells while limiting cellular levels of sodium. In studies with rats, Welty et al.  Discovered that heart muscle cells, when challenged with glucose, had normal electrolyte levels and normal function when taurine was adequate.  When deficient in taurine, however, these same glucose-stressed cells lost potassium and developed an abnormal Ca/Na ratio.  Replenishment of taurine to the surrounding plasma corrected the potassium loss and rectified electrolyte ratios Ca/Na, Mg/Na, and K/Na.

The anti-arrhythmic action of taurine appears to be connected with its abundance in heart tissue in humans (and other mammals).  In addition to beneficial actions for cardiac tissue, taurine is magnesium-sparing for the body globally.  Normalized or healthy blood magnesium levels may decrease blood platelet aggregation and associated vascular disorders.

Assessment of taurine levels can be accomplished by amino acid analysis of fasting blood plasma or 24-hour urine.  Fasting plasma represents the metabolic level (rather than a transient dietary influx), although it also is a point-in-time transport level.  When low, inadequacy is certain.  When normal in plasma, one should also check its primary metabolic precursor, cyst(e)ine.  Low cysteine or cystine suggests limited taurine during periods of increased need. When high in plasma, one must check for blood cell homeolysis, leukocytolysis, infection, or toxicity that causes rupture of cell membranes.  Urinary taurine must be interpreted with great care. Deficient urine taurine (with normal renal clearance), means deficiency. Elevated urine taurine can also mean deficiency due to wasting.  Urinary taurine wasting typically occurs with elevated beta-alanine and possibly occurs with elevated beta-aminosobutyric acid. In renal tubules, beta-alanine blocks reabsorption of taurine.  Elevated beta-alanine occurs with: (1) maldigestion and increased uptake of dietary peptides (anserine, carnosine), (2) infection or intestinal dysbiosis in which bacterial production is abnormally increase, and (3) catabolism of DNA and RNA as occurs with tissue necrosis or molignancy.  Catabolism of tissue produces both beta-alanine and beta-aminoisobutyric acid.

Hair element analysis can suggest cystine and taurine insufficiency – the telltale result being deficient sulfur. Structurally, hair is about 14 to 15% cysteine and about 5% by weight sulfur. Low hair sulfur results often are found to correlate with methionine deficiency, cystinuria, or urinary taurine wasting, all of which are diagnosed by 24 hour urine amino acid analysis.  Both methionine deficiency and urinary cysteine wasting imply limited reserves or capacity for taurine formation.

The following clinical presentations are consistent with taurine insufficiency.
1. Signs of magnesium deficiency (muscle cramps, lower backache, constipation, fatigue, depression)
2. Hypersensitivity to chlorine, bleach or chlorinated water
3. Cardiac arrhythmia
4. Steatorrhea
5. Elevated cholesterol
6. Abnormally enhanced inflammation during infections
7. Frequent infections, leukocytolysis or leukopenia
8. Maldigestion
9. Seizures