Last Updated on February 4, 2021 by Sagar Aryal
- Vitamins refer to any of a group of organic compounds which are essential for normal growth and nutrition and are required in small quantities in the diet.
- Vitamins are biologically important. Although a micronutrient, it enhances the metabolism of macronutrients like proteins, carbohydrates and fats. Vitamins are also required for growth in children, formation of hormones, blood cells, tissues and bones.
- Vitamins cannot be synthesized or produced by the human body, thus, our diet must contain vitamins. Vitamins crucial for the body include:
- Vitamin A, or Retinol
- Vitamin B1, or Thiamin
- Vitamin B2, or Riboflavin
- Vitamin B3, or Niacin
- Vitamin B5, or Pantothenic Acid
- Vitamin B6, or Pyridoxine
- Vitamin B7, or Biotin
- Vitamin B9, or Folic Acid (Folate)
- Vitamin B12, or Cobalamin
- Vitamin C
- Vitamin D
- Vitamin E
- Vitamin K
They are divided into two groups-
(1) Fat soluble vitamins, and
(2) Water soluble vitamins.
- Fat soluble vitamins– A, D, E and K.
- Water soluble vitamins – Vitamin B1, B2, B3, B5, B6, B12, C, Folic acid and Biotin.
Solubility, Source, Functions and Deficiencies of Water Soluble Vitamins
Whole grains; breads; cereals
Precursor for TPP; involved in nerve conduction
Thiamine acts as a precursor molecule for TPP, which is a coenzyme for enzymes involved in carbohydrate and amino acid metabolism. These enzymes include pyruvate dehydrogenase (glycolysis), α-ketoglutarate dehydrogenase (citric acid cycle), transketolase (pentose phosphate pathway), and branched-chain keto acid dehydrogenase (amino acid metabolism). TPP has also been implicated in nerve conduction.
Vitamin B1 (Thiamine) Deficiency
Most commonly associated with alcoholism, which leads to thiamine deficiency through poor dietary nutrition and impaired absorption of thiamine. Thiamine deficiency is also associated with malnutrition, malabsorption syndromes, and dialysis treatment.
- Early disease presents with muscle cramps, poor appetite, and peripheral motor and sensory neuropathy (dry beriberi).
- More advanced disease may present with wet beriberi (dilated cardiomyopathy resulting in high-output heart failure and pulmonary edema) or Wernicke-Korsakoff syndrome, which is a combination of Wernicke encephalopathy (characterized by the triad of confusion, ataxia, and ophthalmoplegia) and Korsakoff syndrome (amnesia and confabulation).
Treatment and Prognosis
About half of patients will only have partial or no resolution of their symptoms with treatment.
Bread; cereals; milk
Precursor for FAD and FMN
- Vitamin B2 (Riboflavin) Deficiency
Usually caused by dietary deficiency or other conditions associated with malnutrition, such as alcoholism.
Usually occurs in conjunction with other B vitamin deficiencies. Symptoms of riboflavin deficiency include dermatitis, glossitis, corneal vascularization, angular cheilitis (cracking at corners of lips), weakness, and anemia.
Vitamin B2 supplementation.
Chicken; fish; whole grains; cereals
- Precursor for NAD and NADP
- Niacin serves as a precursor for coenzymes NAD and NADP, both of which act as electron acceptors in a variety of oxidation-reduction reactions, especially in the citric acid cycle and the electron transport chain.
Niacin is supplied to the body through dietary ingestion or by endogenous synthesis from the amino acid tryptophan.
- Vitamin B3 (Niacin) Deficiency
Causes include dietary inadequacy, alcoholism, Hartnup disease (results in deficiency of tryptophan), isoniazid treatment, and carcinoid syndrome.
Symptoms of mild deficiency include poor appetite with weight loss, weakness, and glossitis. More advanced deficiency results in pellagra, which consists of the triad of dermatitis (usually on sun-exposed areas), dementia, and diarrhea.
Toxicity/ Side effects
High doses of niacin supplementation have been found to reduce LDL and VLDL levels and to increase HDL levels and thus can be used to treat hypercholesterolemia and hypertriglyceridemia. Side effects of high-dose niacin include peripheral flushing (caused by vasodilation) and GI upset.
Chicken; beef; cereals; potatoes
Constituent of coenzyme A and fatty acid synthase
Vitamin B5 (pantothenic acid) is a constituent of CoA and fatty acid synthase. Deficiency is rarely seen, but when it does occur (usually in conjunction with other B vitamin deficiencies), it may present with dermatitis, hair loss, and GI upset.
Cereals; soy; liver
Precursor for pyridoxal phosphate; involved in heme synthesis.
- Vitamin B6 is a precursor forpyridoxal phosphate, which is a coenzyme that acts as a carrier of amine groups during the transamination reaction in amino acid breakdown, as a cofactor for cystathionine synthase during methionine metabolism, and as a cofactor during other decarboxylation and trans-sulfuration reactions. Pyridoxal phosphate is also involved in the synthesis of heme.
- Vitamin B6 (Pyridoxine) Deficiency
Caused by dietary malnutrition, alcoholism, pregnancy, certain metabolic diseases (eg, homocystinuria), or certain pharmacologic agents (isoniazid, penicillamine, oral contraceptives) that interfere with pyridoxine metabolism or act as competitive inhibitors at pyridoxinebinding sites.
Mild deficiency results in personality disturbances (irritability, depression), dermatitis, and glossitis. More severe deficiency manifests as a peripheral neuropathy, seizures, and a sideroblastic anemia.
Vitamin B6 supplementation.
Vitamin B6 toxicity can occur in patients receiving large doses of vitamin B6 over a long time. It generally manifests as a sensory neuropathy, which can be irreversible.
Vitamin B7 (Biotin)
Found in small amounts in many foods such as eggs, milk, or bananas.
Biotin can be ingested in the diet and is also synthesized in the bowel by intestinal flora.
- Biotin Deficiency
Associated with long-term antibiotic use, increased ingestion of raw egg whites (which contain avidin, a protein that interferes with biotin digestion), and long-term parenteral nutrition.
Biotin acts as a cofactor for three different carboxylase enzymes:
- Pyruvate carboxylase (converts pyruvate to oxaloacetate during gluconeogenesis),
- Propionyl CoA carboxylase (involved in breakdown of propionyl CoA, a product of β-oxidation in fatty acid metabolism, to methylmalonyl CoA), and
- Acetyl CoA carboxylase (converts acetyl CoA to malonyl CoA in fatty acid synthesis).
Deficiency is rarely seen, but symptoms include alopecia, dermatitis, GI upset, muscle pain with paresthesias, and elevated cholesterol levels.
Biotin supplementation for patients requiring parenteral nutrition or long-term antibiotic use.
Vitamin B9 (Folic Acid)
- Solubility: Water
- Sources: Dark green leafy vegetables, liver, and lentils.
The reduced form of folic acid (tetrahydrofolate) acts as a cofactor for many one-carbon transfer reactions in nucleotide synthesis (especially the conversion of dUMP to dTMP in the synthesis of thymidylate), in methionine synthesis (especially the conversion of homocysteine to methionine), and in the conversion of serine to glycine and vice versa.
- Folic Acid Deficiency
Caused by inadequate dietary intake (especially seen in alcoholics), medications that decrease folate absorption in the intestine (eg, sulfasalazine, phenytoin, TMP-SMX), sprue, methotrexate use (inhibits conversion of folic acid to active form), or conditions in which folic acid requirements are increased (eg, pregnancy or chronic hemolytic anemia).
Glossitis and diarrhea; neural tube defects can result from maternal folate deficiency.
Folic acid supplementation.
Liver; fruits; meats
- Cofactor in methionine metabolism and in propionyl coenzyme A metabolism.
- In methionine metabolism, vitamin B12 serves as a cofactor in the conversion of homocysteine to methionine.
- In the metabolism of propionyl CoA, a final product of fatty acid β-oxidation, vitamin B12 serves as a cofactor in the conversion of methylmalonyl CoA to succinyl CoA.
When ingested, vitamin B12 becomes bound to intrinsic factor, a protein secreted by the parietal cells of the gastric mucosa. The vitamin B12-intrinsic factor complex is then absorbed in the distalileum, and the vitamin B12 is stored in the liver.
- Vitamin B12 (Cobalamin) Deficiency
Causes include dietary deficiency (usually seen only in vegans), pancreatic insufficiency, decreased production of intrinsic factor (eg, pernicious anemia or gastrectomy), decreased ileal absorption of vitamin B12 (eg, Crohn disease, Diphyllobothrium latum infection, sprue, or surgicalresection of small intestine), or blind loop syndrome (leading to bacterial overgrowth and resulting competition for vitamin B12).
Neurologic abnormalities (ataxia, impaired proprioception, and vibratory sensation); glossitis; diarrhea; symptoms of autoimmune gastritis (if vitamin B12 deficiency is caused by pernicious anemia).
Vitamin B12 supplementation.
Citrus fruits; peppers; broccoli
- Facilitates collagen synthesis; increases iron absorption in GI tract
- Vitamin C acts as a cofactor for several different oxidation-reduction reactions, including the hydroxylation of proline and lysine in the synthesis of collagen leading to decreased osteoid matrix synthesis, metabolism of tyrosine, conversion of dopamine to norepinephrine, and synthesis of carnitine.
- Vitamin C also has antioxidant properties and facilitates iron absorption in the intestine by keeping iron in a reduced state (Fe2+), which is more amenable to absorption.
- Vitamin C (Ascorbic Acid) Deficiency
Usually caused by dietary inadequacy.
More often seen in the elderly, alcoholics, the homeless, or patients with chronic illnesses such as cancer or chronic renal failure.
Manifests as scurvy: subperiosteal hemorrhage; bleeding into joint spaces; purpura and petechiae; bleeding from gums; osteoporosis; gingival swelling; fatigue; weakness; anemia; impaired wound healing.
Vitamin C supplementation.
- Suzanne J. Baron and Christoph I. Lee (2013).Biochemistry & Genetics. Second Edition. Mc Graw Hill: New York.
- David Hames and Nigel Hooper (2005). Biochemistry. Third ed. Taylor & Francis Group: New York.