Threonine is an essential amino acid, which means that it must be obtained through the diet. It is needed to create glycine and serine, two amino acids that are necessary for the production of collagen, elastin, and muscle tissue (including the heart muscle, where it is found in significant amounts). Threonine is useful in the stabilization of blood sugar because it can be converted into glucose in the liver. It also combines with aspartic acid and methionine to help the liver digest fats and fatty acids. Threonine supports the immune system by aiding in the production of antibodies. Supplementation with threonine may also be useful for treatment of ALS (Amyotropic Lateral Sclerosis) and MS (Multiple Sclerosis) and other spastic diosorders. Threonine is known to require vitamin B6 (pyridoxine), B3 (niacin) [please refer to vitamin B-complex] and magnesium for its optimal utilization and metabolism. Good sources are dairy foods, meat, grains, mushrooms, and leafy vegetables.

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OBJECTIVES: Chronic pancreatitis (CP) and pancreatic cancer (CA) have been associated with intestinal malabsorption and inflammation. However, little is known about the changes in amino acid metabolism in such patients…… In CP patients, significant reductions in the concentrations of citrulline, gamma-aminobutyric acid, taurine, and aspartic acid were found (P < 0.05), whereas in CA patients, the levels of phosphoethanolamine, gamma-aminobutyric acid, aspartic acid, taurine, arginine, threonine, alanine, citrulline, and tryptophan were reduced. There was a significant inverse relationship between the total amino acid levels and the white blood cell counts………. CONCLUSIONS: Both patients with CP and with CA exhibit alterations in amino acid levels. The mechanisms underlying these defects may involve intestinal malabsorption as well as systemic inflammation. Providing selective amino acid supplementation to such patients may minimize the excess morbidity and mortality associated with protein malnutrition.

 o      Schrader, H et al (2009). Amino acid malnutrition in patients with chronic pancreatitis and pancreatic carcinoma. Pancreas, 38(4), 416-21.

To determine whether the naturally occurring amino acid threonine, a potential precursor for glycine biosynthesis in the spinal cord, has an effect on spasticity in multiple sclerosis, 26 ambulatory patients were entered into a randomized crossover trial. Threonine administered at a total daily dose of 7.5 g reduced signs of spasticity on clinical examination, although no symptomatic improvement could be detected by the examining physician or the patient. In contrast to the side effects of sedation and increased motor weakness associated with antispasticity drugs commonly used for the treatment of multiple sclerosis, no side effects or toxic effects of threonine were identified. Levels of threonine were elevated in serum and cerebrospinal fluid during treatment, but glycine levels did not change. Enhancement by threonine of glycinergic postsynaptic inhibition of the motor reflex arc in the spinal cord may represent a non-sedating, nontoxic approach to the management of spasticity in multiple sclerosis.

o      Hauser, SL et al (1992). An antispasticity effect of threonine in multiple sclerosis. Arch Neurol. 49(9), 923-6.

In order to investigate glycinergic mechanisms in spasticity, and other signs of the upper motor syndrome, we gave 4.5 and 6.0 g/day of L-threonine to 18 patients with familial spastic paraparesis (FSP) according to a double-blind, crossover protocol……..Based upon the severity rating scales, there was a statistically significant (p less than 0.02) decrease in motor impairment and spasticity during L-threonine administration compared to placebo treatment…….. Plasma and CSF levels of threonine increased significantly during L-threonine treatment but glycine levels did not change. These data indicate that L-threonine significantly suppressed the signs of spasticity even though the benefits were not clinically valuable.

o      Growdon, JH, Nader, TM, Schoenfeld, J & Wurtman, RJ (1991). L-threonine in the treatment of spasticity. Clin Neuropharmacol. 14(5), 403-12.

We conducted a double-blind, placebo-controlled, crossover study of oral L-threonine at 6 g/day in patients with spinal spasticity. Muscle tone from selected leg muscles, measured by the Ashworth Scale, was the principal measure of spasticity and was evaluated before and at the end of each treatment period. A 10% reduction in Ashworth score was regarded as a positive response to a treatment. The results were analyzed sequentially, patients being classified as threonine-responders, placebo-responders or non-responders (those who responded to both treatments by either less or greater than 10%) and a level of significance of p = 0.05 was chosen. The trial concluded in favour of L-threonine after 33 patients. Side-effects were minimal. L-threonine has a modest but definite antispastic effect.

 o      Lee, A & Patterson, V (1993). A double-blind study of L-threonine in patients with spinal spasticity. Acta Neurol Scand. 88(5), 334-8.

Threonine supplementation (500 mg/day) was given to 6 patients with genetic spasticity syndromes for a period of 12 months, followed by a 4-month observation period without medication. All 6 patients showed partial improvement of spasticity, intensity of knee jerks and muscle spasms without changes in true pyramidal tract signs. The improvement in motor performance, objectively measured, averaged 29% (19% in upper limbs and 42% in lower limbs). The range of overall improvement was 19--35% (7--30% for upper limbs; 25--67% for lower limbs). No toxic clinical or biochemical side effects were encountered. Thus threonine, a precursor of glycine, produced the same effect on spasticity than that previously observed with glycine. It is concluded that threonine supplementation is feasible and safe and that it deserves a controlled trial in well defined (preferably genetic) cases of spasticity.

 o      Barbeau, A, Roy, M & Chouza, C (1982). Pilot study of threonine supplementation in human spasticity. Can J Neurol Sci. 9(2), 141-5.

OBJECTIVE: As is the case with glutamine, requirements for amino acids such as cysteine, taurine, and serine may be increased in stress situations. This study evaluated the potential usefulness of supplementation of total parenteral nutrition with a cysteine, taurine, threonine, and serine mixture (SEAS), with or without glutamine, in an experimental model of turpentine-induced acute inflammation……….. CONCLUSIONS: Improved nitrogen balance and reduction in urinary 3-methylhistidine suggest that SEAS supplementation improves nitrogen homeostasis in an experimental model of acute inflammation. Glutamine addition further improves protein status.

 o      Osowska, S, De Bandt, JP, Chaïb, S, Neveux, N, Bérard, MP & Cynober, L (2003). Efficiency of a cysteine-taurine-threonine-serine supplemented parenteral nutrition in an experimental model of acute inflammation. Intensive Care Med. 29(10), 1798-801.