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 DIAGNOSIS

Wet beri-beri Erythrocyte

Dry beri-beri transketolase activity
Wernicke-Korsakoff greater than 15-20%
syndrome suggests thiamine
deficiency.
Acute fulminating beri-
beri(shoshin beri-beri)
 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 deficiency-
THE 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 EXCESS

 Vitamin A deficiency is  Symptoms include

one of the most headache, nausea,
important preventable ataxia, excessive dryness
cause of blindness. of skin, & alopecia.
 Prolonged deficiency  Signs include
leads to hepatomegaly &
XEROPHTHALMIA. desquamation.
 VITAMIN D
Vitamin D is really a hormone as it can be
synthesized in the skin.7-
dehydrocholesterol undergoes a non-
enzymatic 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 & Contraction of blood

OSTEOMALACIA in vessels, high blood
adults. 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 TOXICITY

 May be seen in  Not documented.

patients with severe
fat malabsorption,
cystic fibrosis, chronic
liver disease and in
premature infants.
 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.