VITAMINS
DR.BHARGAVI
CONTENTS DEFINITION CLASSIFICATION NUTRITIONAL REQUIREMENT DEFICIENCY EXCESS
DEFINITION VITAMINS ARE A GROUP OF ORGANIC NUTRIENTS, REQUIRED IN SMALL QUANTITIES FOR A VARIETY OF BIOCHEMICAL FUNCTIONS. THEY GENERALLY CANNOT BE SYNTHESIZED BY THE BODY AND MUST THEREFORE BE SUPPLIED IN THE DIET.
CLASSIFICATION They are grouped as
Water soluble vitamins Fat soluble vitamins
WATER SOLUBLE VITAMINS
Thiamine Riboflavin Niacin Vitamin B6 (pyridoxine) Vitamin B12 (cobalamine) Folate Pantothenic acid Biotin Vitamin C (ascorbic acid)
FAT SOLUBLE VITAMINS • • • •
Vitamin A Vitamin D Vitamin E Vitamin K
THIAMINE DEFICIENT STATES In chronic alcoholics Impaired absorption, metabolism, storage Dialysis Chronic PEM Narcotic abuse
CLINICAL DEFICIENCY MANIFESTATIONS Wet beri-beri Dry beri-beri Wernicke-Korsakoff syndrome Acute fulminating beriberi(shoshin beri-beri)
DIAGNOSIS Erythrocyte transketolase activity greater than 15-20% suggests thiamine deficiency.
TREATMENT Large parenteral doses of thiamine
VITAMIN B12 (RIBOFLAVIN) CO-ENZYMES: Flavin mononucleotide (FMN) and Flavin adenine dinucleotide (FAD) Flavin coenzymes are electron carriers in oxidoreduction reactions. Dietary sources: milk and dairy products.
CLINICAL DEFICIENCY Deficiency is widespread but not fatal. Manifestations: Cheilosis, sebhorric dermatitis. DIAGNOSIS: Measurement of activation of erythrocyte glutathione reductase by FAD added in vitro
NIACIN It is strictly not a vitamin as it can be synthesized in the body from essential amino acid Tryptophan. Mg Niacin equivalents= mg preformed niacin+1/60 *mg tryptophan
CLINICAL DEFICIENCY PELLAGRA characterized by a photosensitive dermatitis, dementia and possibly diarrhoea.Fatal if untreated. Despite an adequate intake of tryptophan and niacin pellagra can occur in HARTNUP’S DISEASE and in CARCINOID SYNDROME.
TOXICITY Intakes of both nicotinic acid and nicotinamide in excess of 500mg/day can cause liver damage.
VITAMIN B6 6 compounds have Vitamin B6 activity:Pyridoxine, pyridoxal, pyridoxamine and their 5’-phosphates. Important in amino acid metabolism, steroid hormone action.
CLINICAL DEFICIENCY Vitamin B6 deficiency is rare. Moderate deficiency results in abnormalities of tryptophan and methionine metabolism. VITAMIN B6 STATUS ASSESSMENT Is by activation of erythrocyte transaminases by pyridoxal phosphate added in vitro.
EXCESS Reports suggest that intakes in excess of 200mg/dl are associated with sensory neuropathy.
VITAMIN B12 It is a generic descriptor for the cobalamins which are cobalt containing compounds possessing the corrin ring. Found exclusively in foods of animal origin. Absorbed bound to intrinsic factor which is secreted byparietal cells of gastric mucosa. Methyl-malonyl CoA mutase, leucine aminomutase and methionine synthase are vitamin B12 dependent enzymes.
CLINICAL DEFICIENCY Seen in pancreatic insufficiency cancer chemotherapy, anti-bacterial and antimalarial drug therapy. Vitamin B12 deficiency causes pernicious anaemia and functional folate deficiencyTHE FOLATE TRAP. Folate deficiency causes megaloblastic anaemia.
FOLIC ACID Folic acid supplements reduce the risk of neural tube defects & hyperhomocysteinaemia & may reduce the incidence of cardiovascular disease & some cancers. Folate supplementation will rectify the megaloblastic anaemia of vitamin B12 deficiency but may hasten development of irreversible nerve damage found in vitamin B12 deficiency.
BIOTIN Biotin is synthesized by intestinal flora in excess of requirements and therefore dietary deficiency is unknown except among people maintained at TPN for many months and those who eat uncooked egg white that contains avidin which binds biotin and prevents it’s absorption It is a coenzyme of carboxylate enzymes.
PANTOTHENIC ACID Has a central role in acyl group metabolism. Widely distributed in all food stuffs and deficiency has not been unequivocally reported in humans.
ASCORBIC ACID Vitamin C is an intermediate in the uronic acid pathway of glucose metabolism Vitamin C has specific roles in the copper containing hydroxylases and the alpha-ketoglutarate-linked iron containing hydroxylases. Deficiency causes SCURVY signs of which include skin changes, gum decay, tooth loss, fragility of blood vessels & bone fractures.
BENEFITS OF VIT C Enhances absorption of iron. High doses of Vitamin C may reduce the duration and severity of common cold. At intakes above 100mg/dl the body’s capacity to metabolize Vitamin C is saturated.
VITAMIN A Two groups of compounds have Vitamin A activity:-Retinoids (Retinol,Retinaldehyde, & Retinoic acid) -Carotenoids. 6 microgram of beta-carotene is is equivalent to 1 microgram of preformed retinol. Vitamin A has a function in vision.in the retina, retinaldehyde functions as the prosthetic group of the light sensitive opsin proteins, forming RHODOPSIN (in rods) and IODOPSIN (in cones).
DEFICIENCY Vitamin A deficiency is one of the most important preventable cause of blindness. Prolonged deficiency leads to XEROPHTHALMIA.
EXCESS Symptoms include headache, nausea, ataxia, excessive dryness of skin, & alopecia. Signs include hepatomegaly & desquamation.
VITAMIN D Vitamin D is really a hormone as it can be synthesized in the skin.7dehydrocholesterol undergoes a nonenzymatic reaction on exposure to UV light, yielding pre-vitamin D. Vitamin D is both regulated by and regulates calcium homeostasis.
DEFICIENCY
EXCESS
RICKETS in children & OSTEOMALACIA in adults.
Contraction of blood vessels, high blood pressure, and calcinosis.
VITAMIN E Vitamin E is the generic descriptor for two families of compounds, the TOCOPHROLS and the TOCOTRIENOLS. It is the major lipid-soluble anti-oxidant in cell membranes and plasma proteins.
DEFICIENCY May be seen in patients with severe fat malabsorption, cystic fibrosis, chronic liver disease and in premature infants.
TOXICITY Not documented.
VITAMIN K Three compounds have the biological activity of Vitamin K: -Phylloquinone -Menaquinone -Menadione. Vitamin K is required for the synthesis of blood clotting proteins. It is also important in the synthesis of bone calcium binding proteins.