|DATE||Friday, March 03|
|AUTHOR||Dr. Carlos Orozco (BSc, MSc, ND, MD, PhD, FPAMS)|
Pantothenic acid, also known as vitamin B5, as well as the “anti-stress vitamin” is part of the B group vitamins and classified as a water-soluble vitamin. This nutrient can be manufactured in the body by the intestinal flora.
Biological Function of Vitamin B5
Pantothenic acid is involved in the synthesis of acetylcholine, antibody production, cholesterol, cortisone, coenzyme A, fibroblast multiplication, steroid hormone production, lipid metabolism, protein metabolism; it reduces arthritic pain and maintains normal uric acid levels. Vitamin B5 is also helpful to fight wrinkles as well as the graying of the hair.
Pantothenic acid, also known as vitamin B5, is essential to all forms of life (1). Pantothenic acid is found throughout living cells in the form of coenzyme A (CoA), a vital coenzyme in numerous chemical reactions (2).
Pantothenic acid is a component of coenzyme A (CoA), an essential coenzyme in a variety of reactions that sustain life. CoA is required for chemical reactions that generate energy from food (fat, carbohydrates, and proteins). The synthesis of essential fats, cholesterol, and steroid hormones requires CoA, as does the synthesis of the neurotransmitter, acetylcholine, and the hormone, melatonin. Heme, a component of hemoglobin, requires a CoA-containing compound for its synthesis. Metabolism of a number of drugs and toxins by the liver requires CoA (3).
Coenzyme A was named for its role in acetylation reactions. Most acetylated proteins in the body have been modified by the addition of an acetate group that was donated by CoA. Protein acetylation affects the 3-dimensional structure of proteins, potentially altering their function, the activity of peptide hormones, and appears to play a role in cell division and DNA replication. Protein acetylation also affects gene expression byfacilitating the transcription of mRNA. A number of proteins are also modified by the attachment of long-chain fatty acids donated by CoA. These modifications are known as protein acylation, and appear to play a central role in cell signaling (1).
The acyl-carrier protein requires pantothenic acid in the form of 4′-phosphopantetheine for its activity as an enzyme (1, 4). Both CoA and the acyl-carrier protein are required for the synthesis of fatty acids. Fatty acids are a component of some lipids, which are fat molecules essential for normal physiological function. Among these essential fats are sphingolipids, which are a component of the myelin sheath that enhances nerve transmission, and phospholipids in cell membranes.
Signs and Symptoms of Deficiency in vitamin B5
With Vitamin B5 in short supply symptoms like fatigue, headaches, nausea, tingling in the hands, depression, personality changes and cardiac instability have been reported.
Naturally occurring pantothenic acid deficiency in humans is very rare and has been observed only in cases of severe malnutrition. World War II prisoners in the Phillipines, Burma, and Japan experienced numbness and painful burning and tingling in their feet, which was relieved specifically by pantothenic acid (1). Pantothenic acid deficiency in humans has been induced experimentally by administering a pantothenic acid antagonist together with a pantothenic acid deficient diet. Participants in this experiment complained of headache, fatigue, insomnia, intestinal disturbances, and numbness and tingling of their hands and feet (5). In a more recent study, participants fed only a pantothenic acid free diet did not develop clinical signs of deficiency, though some appeared listless and complained of fatigue (6). Homopantothenate is a pantothenic acid antagonist with cholinergic effects (similar to those of the neurotransmitter, acetylcholine). It was used in Japan to enhance mental function, especially in Alzheimer’s disease. A rare side effect was the development of hepatic encephalopathy, a condition of abnormal brain function resulting from the failure of the liver to eliminate toxins. The encephalopathy was reversed by pantothenic acid supplementation suggesting, but not proving, it was due to pantothenic acid deficiency caused by the antagonist (4).