.

 cereals cultivated are wheat, rice,

oats, barley, corn (maize), and
sorghum.
 PULSES
 Mung daal - split and skinned green gram.
 Hare mung daal - green gram.
 Chawli daal - black eyed beans.
 Masoor daal - split red lentils.
 Sabat masoor - Indian Brown lentils.
 Toor daal - yellow pigeon peas.
 Rajma - kidney beans.
 Hari matar - green peas.
.

 Polished rice is white and shiny, while

unpolished rice is brown.
VITAMIN B1 – THIAMINE
 CHEMISTRY

• Thiamine contains a pyrimidine ring

and a thiazole ring held by a methylene
bridge .
• Thiamine is the only natural compound
with thiazole ring.
• It is a sulphur containing vitamin.
• Synthesized by Plants, Yeast, Bacteria.
 COENZYME FORM
 Ithas a specific coenzyme, thiamine
pyrophosphate (TPP) which is mostly
associated with carbohydrate metabolism.
DIETARY SOURCES

 Plant sources
 Rich source : Cereals
 ( whole cereal grains, brans of cereals, nuts, whole wheat
flour and unpolished rice have better nutritive value than
polished refined foods ( 80 % removed ).
 Good source : Yeast
 Medium source : Flax seeds,
Vegetables(Cauliflower, Potato,Beans )
.

 Since , Thiamine is a water soluble vitamin, it

is extracted into water during cooking process
and hence such water should not be discarded.
Animal Sources

 Liver, Eggs, Milk.

RDA

• Adults:1-1.5 mg/day
• Children: 0.7-1.2 mg/day.
• Pregnancy , Lactation – 2 mg/day.
• Old Age And Alcoholism - 2 mg/day
ABSORPTION AND TRANSPORT

 Dietary thiamine is absorbed

readily from jejunum and
proximal ileum.

 Bindsto albumin and is

transported to tissues where it is
converted to the active form,
thiamine pyrophosphate.
 BIOCHEMICAL FUNCTIONS

1.OXIDATIVE-DECARBOXYLATION OF ALPHA-KETO ACIDS

• TPP is a component of mitochondrial

multienzyme complexes which bring about
oxidative-decarboxylation of alpha -keto
acids,
• Eg. pyruvate and alpha -ketoglutarate.
.
2. OXIDATIVE-DECARBOXYLATION OF
BRANCHED CHAIN AMINO ACIDS
• TPP serves as a coenzyme for
decarboxylation of branched chain amino
acids (valine, leucine and isoleucine) to the
respective keto acids.
3.TRANSKETOLASE
REACTIONS
 TPP actsas a coenzyme for
transketolase, in the pentose
phosphate pathway.
4. TPP plays an important role in
the transmission of nerve impulse,
as it is required for acetylcholine
synthesis and myelin sheath
formation.
 CAUSES FOR DEFICIENCY

 Staple diet is polished rice

 Malnutrition
 Starvation
 Malabsorption syndrome
 Chronic alcoholics ( Absorption of
Thiamine and its conversion TPP
is affected ).
.Thiamine deficiency leads to failure of
carbohydrate metabolism, resulting in
decreased production of ATP and thus
impaired cellular functions.

 Theneurological, cardiovascular and

gastrointestinal manifestations due to
thiamine deficiency is referred to as
Beri Beri
( Singhalese word meaning I cannot do ).
 Types of Beri Beri.

 1.Dry Beri Beri ( Neurological

Beri Beri )
 2.Wet Beri Beri (Cardiovascular
Beri Beri )
 3.Infantile Beri Beri
 4. Cerebral Beri Beri
1. DRY BERIBERI (NEUROLOGICAL BERI-BERI):

Neruological symptoms.
In longstanding deficiency, there is
degeneration of myelin sheath of sensory
and motor nerves .
Muscle wasting, difficulty in walking,
neuritis, sensory disturbances all leads to
paralysis
( neuritis – inflammation of nerve )
( Paralysis - loss of the ability to move)
2. WET BERI-BERI (CARDIOVASCULAR )
• Severe deficiency of Thiamine.
• Cardiovascular symptoms
• Characterized by edema of legs, face.
• Breathlessness and palpitation.
• Fast and bouncing pulse.
• Heart becomes weak and leads to cardiac
problems & death occurs due to cardiac failure.
• ( Edema is swelling caused by too much
fluid trapped in the body's tissues. Edema
can affect any part of the body.)
 3. INFANTILE BERIBERI

• Seen in infants born to mothers suffering from

thiamine deficiency.
• The breast milk of these mothers contains low
thiamine content.
• Characterized by sleeplessness, restlessness,
vomiting, convulsions and bouts of screaming
• Infants : 2 – 10 months.
• These problems are due to cardiac dilatation.
Death may occur suddenly due to cardiac failure.
4. CEREBRAL BERI BERI

• Wernike Korsakoff Syndrome

• Wernicke Syndrome
• Seen in Chronic alcoholism.
• Acute Thiamine Deficiency .
• Insufficient intake .
• Alcohol impairs intestinal absorption
of thiamine results CNS symptoms.
.

 Korsakoff Syndrome
 Chronic Thiamine Deficincy
 Characters – Psychosis, Loss of
memory, paralysis of limbs.
VITAMIN B3 - NIACIN
 SYNONYMS

Pellagra preventive
factor of Goldberger
Nicotinic acid
Nicotinamide
Niacinamide
 CHEMISTRY
 Niacin is pyridine-3-carboxylic acid. Amide form of Niacin is Niacinamide,
Nicotinamide.
 COENZYME FORM

Niacinis converted to its co-

enzyme forms,

Nicotinamide adenine
dinucleotide (NAD+) and
Nicotinamide adenine
dinucleotide phosphate
(NADP+).
Biochemical Reactions (Oxidation &
Reduction Reaction)

NAD + Dependent
Reactions
 Carbohydrate Metabolism,
 Lipid Metabolism
 Protein Metabolism
NADP+ Dependent Reactions

 Carbohydrate Metabolism ( HMP Shunt

Pathway)
NADPH Dependent Reactions

 Cholesterol Synthesis
 Protein Metabolism
 Folic Acid Metabolism
 RDA

 Adults: 15-20 mg/day

 Children: 10-15 mg/day
 Pregnancy: additional 2mg/day
 Lactation: additional 5mg/day
DIETARY SOURCES
 Plant Sources : Rice, Peanuts, Whole
cereals, sweet potatoes, spinach,
tomatoes, carrots, almonds, dates,
coffee, tea, dried yeast, mushrooms.
 Animal Sources : Eggs, Liver,
Kidney,Meat,Fish.
 DEFICIENCY MANIFESTATIONS

 Niacindeficiency results in a condition called

pellagra (Italian: rough skin).

 Thisdisease involves skin, gastrointestinal

tract and central nervous system.
 DIARRHOEA
 Inflammation of entire GI tract leading to
diarrhoea
with blood and mucus.

 Prolonged diarrhea leads to weight loss.

 Maybe associated with nausea, glossitis,

vomiting.
( Glossitis - inflammation of the
tongue.)
 DERMATITIS
 Bilateral and symmetrical bright red like
lesions found in the areas of the skin
exposed to sunlight (neck, dorsal part of
hand, feet, ankle and parts of face).
 Increasedpigmentation around the neck is
known as Casal’s necklace.
 DEMENTIA
Associated with degeneration
of nervous tissue.

The symptoms of dementia

include anxiety, delirium
( a disturbed state of mind),
irritability, poor memory,
insomnia (sleeplessness).
VITAMIN B6 - PYRIDOXINE
 .

 CHEMISTRY

 Vitamin B6 three compounds namely

pyridoxine, ( alcohol ) pyridoxal
( Aldehyde ) and pyridoxamine. ( amino
methyl group )
 Biologically active.
 COENZYME FORM
 The active form of vitamin B6 is the coenzyme
pyridoxal phosphate (PLP).
 PLP can be synthesized from the three
compounds pyridoxine, pyridoxal and
pyridoxamine.
 PLP is formed by action of pyridoxal kinase
using ATP.
 Human Brain is a rich source of pyridoxal
kinase
 B6 is excreted in urine as 4-pyridoxic acid.
BIOCHEMICAL FUNCTIONS
 PLP is closely associated with the metabolism of
amino acids.

 The synthesis of certain specialized products such as

serotonin, histamine, niacin coenzymes, heme,
GABA.

 Pyridoxal phosphate participates in reactions like

 TRANSAMINATION,
 DECARBOXYLATION,
 DEAMINATION,
 TRANS SULFURATION
.

 PLP is needed for the absorption

of amino acids from the intestine.

 Synthesis of sphingolipids and

formation of myelin sheath.
 DIETARY SOURCES
 AnimalSources : Liver, Kidney,
Meat,Fish,Egg yolk,Milk.
 PlantSources: Dried yeast,
Polished rice, Germinal portion of
Cereals & Pulses , Cabbage,
Banana, Tubers, Roots.
 RDA

Adult: 2 - 2.2 mg/day.

Pregnancy, Lactation And Old
Age: 2.5mg/day
 DEFICIENCY MANIFESTATIONS

1. NEUROLOGICAL MANIFESTATIONS
NEUROLOGICAL SYMPTOMS

 Depression,
 Irritability,
 Nervousness
 Mental confusion.
 Convulsions and peripheral neuropathy
 2. HEMATOLOGICAL
MANIFESTATIONS

Decrease in hemoglobin levels,

associated with hypochromic
microcytic anaemia. This is due to a
reduction in heme production.
3. DERMATOLOGICAL
MANIFESTATIONS
Pellagra – occurs due to involvement of
PLP in formation of Niacin and its co
enzymes from tryptophan.
 4. DRUG INDUCED B6
DEFICIENCY

Isoniazid and penicillamine combines

with pyridoxal phosphate to form
inactive hydrazone derivatives which
inhibit PLP dependent enzymes.
VITAMIN B9 - FOLIC ACID
  CHEMISTRY

 Folic acid consists of three components–

pteridine ring, p-amino benzoic acid
(PABA) and glutamate

 Folic acid mostly has one glutamic acid

residue and is known as pteroyl-glutamic
acid (PGA) or Folic acid.
 COENZYME FORM

The active form of folic acid is

Tetra Hydro
Folic Acid
(THFA ).
BIOCHEMICAL FUNCTIONS

1. Tetrahydrofolate is
actively involved in the one
carbon metabolism &
Histidine metabolism.
 BIOCHEMICAL
FUNCTIONS
 2.Purines (carbon 2, 8) which are
incorporated into DNA and RNA.
( Purine Synthesis )

3. Synthesis of Glycine, Methionine,

Thymidylic acid.
 DIETARY SOURCES

 Folic acid is widely distributed in nature.

 Plant Sources : Green Leafy Vegetables,
Whole Grains, Cereals, Beans, Yeast,
Pulses, Roots, Tubers, Oil Seeds.
 Animal Sources : Liver, Kidney, And Eggs.

 Milk is a poor source.

 RDA
Adults: 200 ug/day
Pregnancy: 400 ug/day
Lactation: 300 ug/day
 CAUSES FOR FOLATE DEFICIENCY

1. Pregnancy: Commonly seen in

pregnancy, where requirement is
increased.
2. Defective absorption: Resection
of jejunum absorption is defective.
3. Drugs: Anticonvulsant drugs
(phenytoin, phenobarbitone) will
inhibit the intestinal enzyme, so
that folate absorption is reduced.
CAUSES FOR FOLATE
DEFICIENCY
 4. Hemolytic anemias: As requirement of folic acid
becomes more, deficiency is manifested.

 5. Dietary deficiency: Absence of vegetables in food

for prolonged periods may lead to deficiency.

 6. Folate trap: When B12 is deficient, this reaction

cannot take place, leading to folate deficiency .
 Deficiency Manifestations

 Megaloblastic Anemia – Most important feature of

folic acid deficiency.
 In peripheral circulation, RBC are mostly
macrocytic and also megaloblastic.
 Nuclear remnants such as Howell Jolly Bodies &
Cabot rings are seen.
 Abnormal RBC are destroyed in spleen.
 Reduced RBC production & Increased RBC
destruction leads to Anemia.
 Leucopenia . ( Low WBC count )
 Thromobocytopenia. ( Low Platelet count ).
.

 Neural Tube Defects – Folic acid

deficiency in pregnancy leads to
Neural tube defects in foetus 7
Down Syndrome.
 Folic acid supplementation in
pregnancy prevents these defects.
 Homocystinuria
 HPV infecytion : Cervical cancer.
.

 The term macrocytosis refers to a blood

condition in which red blood cells (RBC)
are larger than normal.

Megaloblastic anemia is a form of anemia
characterized by very large red blood
cells and a decrease in the number of
those cells.
.

 Howell–Jolly bodies: These are usually

single peripheral bodies within red cells
representing DNA material.
.
.

 Cabot rings are rare, threadlike

strands found in red blood cells.
.
 TREATMENT

 Therapeutic dose is 1 mg of folic

acid per day orally.
VITAMIN B12
 CHEMISTRY

The structure of vitamin B12

consists of a corrin ring with a
central cobalt atom.
 COENZYME

(a) De oxy adenosyl

cobalamin
(b) Methyl cobalamin
 BIOCHEMICAL FUNCTIONS
1. Synthesis of methionine from
homocysteine.
2. Isomerization of L - methyl
malonyl CoA to succinyl CoA.
 DIETARY SOURCES

 Foods of animal origin are the only

sources for vitamin B12.
 Rich Sources: Liver, Kidney, Milk,
Curd, Eggs, Fish, Pork And Chicken.
 Vitamin B12 is synthesized only by
anaerobic microorganisms.
 RDA
Adults: 1-2 ug/day
 Pregnancy and lactation: 3 ug/day
CAUSES FOR VITAMIN B12 DEFICIENCY

Dietary Intake is low.

Decrease in Absorption:
Strict Vegetarians.
Pancreatic deficiency
Fish tapeworm
Diphyllobothrium latum
infections
.
Pernicious Anemia
It is manifested usually in persons over 40
years. It is an autoimmune disease

 Pregnancy
Increased requirement of vitamin in
pregnancy is another common cause for
vitamin B 12 deficiency.
 Gastric Atrophy
 Deficiency Manifestations
 1. Megaloblastic anemia
 2.Degeneration of spinal cord
 3. Homocystinuria - Homocysteine is
not converted to methionine.
( deficiency of methyl cobalamin –
form of cobalamin ).
 Serum Homocysteine Level increases.
 Homocysteine is a risk factor for
Coronary Heart Diseases.
.

 4. Glossitis: Inflammation of
tongue.
 Beefy red tongue
( painful, burning, loss of taste
sensation ).
 TREATMENT

 Vitamin B12 is administered

in therapeutic doses
(100-1000 ug) intramuscularly.
VITAMIN C - ASCORBIC ACID
 CHEMISTRY
• Pure Vitamin C is white, crystalline,
odourless substance with acid taste.
( odour – smell )
• Ascorbic acid is structurally similar to
carbohydrates (Hexoses)
• Acidic property is due to the enolic
hydroxyl groups.
• Strong reducing agent.
 BIOCHEMICAL
FUNCTIONS

1. COLLAGEN FORMATION

Vitamin C plays the role of a

coenzyme in hydroxylation of
proline and lysine.
 2. Healing Process :
Necessary for process of
wound healing.
 3. IRON METABOLISM

• Vitamin C enhances iron absorption in

intestine keeping iron in the ferrous
form.
4. HEMOGLOBIN METABOLISM

• Vitamin C is useful in the

reconversion of methemoglobin
to hemoglobin.
• The degradation of
hemoglobin to bile pigments
requires ascorbic acid.
4. TRYPTOPHAN METABOLISM

Vitamin C is essential for the

hydroxylation of tryptophan to
hydroxy tryptophan in the
synthesis of serotonin.
 5. LIPID METABOLISM

Formation of Carnitine
Synthesis of Bile acids
 6. PEPTIDE HORMONE SYNTHESIS

• Vitamin C is necessary for the hydroxylation

reactions in the synthesis of peptide
hormones.
 8. SYNTHESIS OF
CORTI COSTEROID HORMONES
• Adrenal gland possesses high
levels of ascorbic acid,
particularly in periods of stress.
• Vitamin C is necessary for the
hydroxylation reactions in the
synthesis of corticosteroid
hormones.
 7. AS AN ANTIOXIDANT
• Serve as an antioxidant in several non
enzymatic reactions.
• It decreases oxidation of DNA and arrests
protein damage,
• Reduces lipid peroxidation
• Reduces oxidation of low-density
lipoproteins
• Decreases production of extracellular
oxidants from neutrophils.
• Prevention of atherosclerosis and coronary
heart disease.
8. IMMUNOLOGICAL FUNCTION

• Enhances the synthesis of

immunoglobulins (antibodies)

•Increases the phagocytic

action of leucocytes.
 9. PREVENTIVE ACTION ON
CATARACT

• Reduces the risk of cataract

formation.
• Concentrated in the lens of eye.
•Regular intake of ascorbic acid
reduces the risk of cataract
formation
 10. PREVENTIVE ACTION ON
CHRONIC DISEASES

•As an antioxidant, vitamin

C reduces the risk of
cancer, cataract, and
coronary heart diseases.
..

11.
Cellular Respiration :
Essential for ETC in
Mitochondria.
.

 Necessary for maintenance of

normal connective tissue
.
 Normal Plasma level: 0.7 – 1.2 mg/dl
 DIETARY SOURCES
• Rich Sources : Amla ( Indian
Gooseberry)
• Good Sources : Citrus fruits , guava,
papaya
green vegetables (cabbage, spinach),
tomatoes, potatoes (particularly skin) .
• Milk is a poor source of ascorbic acid.
High content of vitamin C is found in
adrenal gland.
 RDA
• Adult: 60-75 mg/day
• Pregnancy and lactation: 100 mg/day
• Smokers, chronic alcoholics and on oral
contraceptives: 125 mg/day
 DEFICIENCY
MANIFESTATIONS

• The deficiency of ascorbic acid results

in Scurvy.

• Symptoms are related to

impairment in the synthesis of
collagen and/or the antioxidant
property of vitamin C.
 1. Biochemical Basis of
Haemorrhagic Tendency :
 Vitamin C is required for post translational modification
of pro to collagen to collagen , where vitamin C acts as
a Co enzyme for hydroxylation of hydroxy proline to
proline & hydroxy lysine to lysine.
 In Deficiency, Collagen is abnormal and the intracellular
cement is brittle. ( breakable ).
 Capillaries are fragile ( soft ) leading to bleed.
 2. Skin Changes :

 Skin becomes dry & rough.

 3. BONES

• Failure of the osteoblasts to form the intercellular

substance, osteoid.

• Demineralisation of bone

• Deposition of bone is arrested.

• Results in scorbutic bone is weak and fractures easily.

• There may be hemorrhage into joint cavities.

• Painful swelling of joints may prevent locomotion of

 4. INFANTILE SCURVY
(BARLOW'S DISEASE)

•In infants between 6 to 12

months of age, (period in
which weaning from breast
milk) – Vitamin C is not given
in diet.
 5. Anemia

 Leads
to microcytic hypochromic
anemia.
 Weakness, Irritation, Loss of weight
is seen.
 Decreased RBC production ( Folic
acid metabolism – Decreased
availability of THFA ).
Therapeutic Uses of Vitamin C

 Vitamin C supplementation of ( 500

mg / day ) appears to have benefit in
treatment of conditions such as
Common cold, Diabetes Mellitus,
Hypertension, High Cholesterol level,
Cancer, Proper wound healing, Stroke,
Cardiovascular diseases, Alzheimers
disease.