This document provides an overview of vitamin A, including its classification, sources, functions, deficiency diseases, and national prevention programs in India. Vitamin A is a fat-soluble vitamin that exists in active forms of retinol, retinal, and retinoic acid. Major sources include animal foods like liver, eggs and dairy, and plant foods like carrots, sweet potatoes and dark leafy greens. Vitamin A plays an essential role in vision, cell growth and immune function. Deficiency can cause night blindness, xerophthalmia, and increased susceptibility to infection. India has implemented national programs to provide supplemental vitamin A to children and pregnant/lactating women to reduce deficiency.
2. CONTENTS
1. Introduction
2. What are vitamins?
3. Classification of vitamins
4. Active form of Vitamin A
5. Vitamin A & Its sources
6. Recommended Dietary Allowances
7. Absorption, Transport & Storage
8. Function of vitamin A
9. Deficiency diseases
10. Toxicity
11. Treatment
12. National Vitamin A Prophylaxis Program
11. Conclusion
13. References
3. Introduction
• Nutrients: are the constituents in food that must be supplied to the
body in suitable amounts. These include carbohydrates ,fat ,protein ,
minerals ,vitamins & water.
• Chemical substances obtained from food are used in the body to
provide energy, structural & regulating agents to support
growth,maintenance & repair of body tissue.
4. What are Vitamins ?
• Essential organic compounds that are required in small amounts for
normal growth, maintenance of good health and for the proper
utilization of other nutrients.
• Nutrients that our body does not make on its own. Thus we must
obtain them from the foods we eat, or via vitamin supplements.
5. Classification of Vitamins
• Fat soluble
• A
• D
• E
• K
• Water soluble
• B1 - Thiamine
• B2 - Riboflavin
• B3 – Niacin
• B5 – Pantothenic acid
• B6 – Pyridoxine
• B7 – Biotin
• B9 - Folic acid
• B12 - Cyanocobalamin
• C - Ascorbic acid
6. History: First described in 1909 and found to prevent night blindness in
1925. Vitamin –A activity of carotenoids was discovered by Stun Bocks.
The structure of Vit – A was determined by Karrer and its synthesis was
achieved in the laboratory by Kuhn & Morris.
• Vitamin A is an essential nutrient needed in small amounts for the
normal functioning of the visual system, and maintenance of cell
function for growth, epithelial integrity, red blood cell production,
immunity and reproduction.
• Vitamin A deficiency is a major nutritional concern in poor societies,
especially in lower income countries like India.
VITAMIN A
7. Active Form of Vitamin A
• Retinol:Primary alcohol (CH2OH) containing form
• Retinal: Aldehyde (CHO) containing form
• Retinoic acid: Carboxyl (COOH) containing form
• β-carotene: It is Provitamin found in plant.
• Retinyl ester: Found in Non-vegetarian sources.
11. Absorption, Transport and Storage
• Ingested β-carotene is cleaved in the intestine by β-carotene dioxygenase to yield
retinal. Retinal is reduced to retinol by retinaldehyde reductase, an NADPH
requiring enzyme within the intestine.
• Retinol is esterified with palmitic acid incorporated into chylomicrons together
with dietary lipid and delivered to the liver for storage.
• Transport of retinol from the liver to extrahepatic tissues, occurs by binding of
retinol to retinol binding protein (RBP).
• Transport of retinoic acid is accomplished by binding to albumin.
13. Functions of Vitamin A
• Vision
• Growth
• Reproduction
• Maintenance of epithelial cells
• β-carotene is an antioxidant and may play a role in trapping peroxy free radicals in
tissues.
• The antioxidant property of lipid soluble vitamin A may account for its possible
anticancer activity.
• High levels of dietary carotenoids have been associated with a decreased risk of
cardiovascular disease.
14. Role of Vitamin A in Vision
The cyclic events occur in the process of vision, known as Wald’s visual cycle Both rod and
cone cells of retina contain a photoreceptor pigment in their membrane and vitamin A is a
component of these pigments. Rhodopsin the visual pigment of rod cells in the retina
consists of 11-cis-retinal bound to protein opsin.
• When rhodopsin absorbs light, the 11-cis-retinal is converted to all-trans retinal.
• The isomerization is associated with a conformational change in the protein opsin.
• Conformational changes in opsin generates a nerve impulse that is transmitted by the optic
nerve to the brain.
• This is followed by dissociation of the all-trans retinal from opsin.
• The all-trans retinal is immediately isomerized by retinal isomerase to 11-cis-retinal.
• This combines with opsin to regenerate rhodopsin and complete the visual cycle.
The conversion of all-trans retinal to 11-cis-retinal is incomplete and therefore remaining all-
trans retinal which is not converted to 11-cis-retinal is converted to all-trans retinol by alcohol
dehydrogenase and is stored in the liver. When needed, retinol re-enters the circulation and
is taken up by the retina, where it is converted back to 11-cis-retinal which combines with
opsin again to form rhodopsin .
16. Dark adaptation time:
• When a person enters from bright light to dark there is
difficulty in seeing due to depletion of rhodopsin, but after
few minutes the vision improves. During these few minutes,
rhodopsin is resynthesized and vision is improved. The time
taken for regeneration of rhodopsin is known as dark
adaptation time. Dark adaptation time is increased in
vitamin A deficient individuals.
17. Color Vision:
• Color vision is mediated by three different retinal containing
pigments in the cone cells, the three pigments are called
porphyropsin, iodopsin and cyanopsin and are sensitive to the three
essential colors: red, green and blue respectively. All these pigments
consist of 11-cis-retinal bound to protein opsin.
– Red if porphyropsin is split
– Green if iodopsin is split
– Blue if cyanopsin is split.
• If mixtures of the three are converted, the color read out in the
brain depends on the proportions of the three split.
20. Deficiency diseases due to Vitamin A:
• Failure of growth in children.
• Faulty bone modelling producing thick
cancellous (spongy) bones instead of thinner
and more compact ones.
• Abnormalities of reproduction, including
degeneration of the testes, abortion or the
production of malformed offspring
21. Night Blindness
• Lack of vitamin A causes night
blindness or inability to see in dim
light.
• Increased dark adaptation time.
• Night blindness occurs as a result of
inadequate pigment in the retina.
• Night blindness is also found in
pregnant women in some instances,
especially during the last trimester of
pregnancy when the vitamin A needs
are increased.
22. • These are foamy and
whitish cheese-like tissue
spots that develop
around the eye
ball, causing severe
dryness in the eyes.
• These spots do not affect
eye sight in the day light
Bitot Spot
23. • One of the major cause
for blindness in India.
• Cornea becomes soft
and may burst
• The process is rapid
• If the eye collapses
vision is lost
Keratomalacia
24. • Conjunctiva becomes
dry and non wettable.
• Instead of looking
smooth shiny it
appears muddy
&wrinkled.
Conjunctival Xerosis
25. Follicular Hyperkeratosis
Effect on Skin and Epithelial Cells:
• Vitamin A deficiency causes keratinization of
epithelial cells of skin which leads to keratosis of
hair follicles, and dry, rough and scaly skin.
• Keratinization of epithelial cells of respiratory,
urinary tract makes them susceptible to infections.
26. Hypervitaminosis A
• The symptoms of hypervitaminosis A include nausea, vomiting,
diarrhea, loss of hair (alopecia), scaly and rough skin, bone and joint
pain, enlargement of liver, loss of weight, etc.
• In pregnant women, the hypervitaminosis A may cause congenital
malformation in growing fetus .
TOXICITY
28. • Administration of large
doses of Vit.A
SHORT
TERM
• Fortification of food
MEDIUM
TERM
• Reduction or elimination
of factors contributing to
ocular disease
LONG
TERM
PREVENTION & CONTROL
29. • Large doses of Vit A orally.
• Quick organization.
• Minimum Infrastructure.
SHORT – TERM ACTION
30. Individual Oral dose of retinal
palmitate
Timing
Children < 12 months of
age
1 lakh I.U Once every 4-6 months
Children > 12 months of
age
2 lakh I.U Once every 4-6 months
Newborn 50,000 I.U At birth
Women of child bearing
age
3 lakh I.U Within one month of giving
birth
Pregnant and lactating
women
5000 IU
(OR)
20,000 I.U
Every day
(Or)
Once every week
VITAMIN A PROPHYLAXIS SCHEDULE
31. • FORTIFICATION –
• Dalda
• Sugar
• Salt
• Tea
• Margarine
• Dried Skimmed
Milk
MEDIUM – TERM ACTION
32. • Reduction or elimination of contributory factors.
• Consumption of Vit A rich foods.
• Promotion of breast feeding.
• Environmental hygiene.
• Immunization – Measles.
• Treatment- Diarrhoea, other infections.
• Health Services - Mother and children.
• Social & Health Education.
• Efficient Primary Health Care.
LONG – TERM ACTION
33. • It is a major controllable Public health and Nutritional problem in India.
• 5.7%of children suffer from eye signs of Vit.A deficiency.
• Even mild Vit.A deficiency probably increases morbidity and mortality in
children.
• In 1970, a national programme for prevention of nutritional blindness
was initiated to fight this deficiency.
• Vit.A supplementation is an integral part of RCH programme (now a
part of NRHM). It covers children upto 5yrs of age.
Vit.A deficiency in India
35. Aim : to decrease the prevalence of Vitamin A
deficiency.
36. Objectives:
1.Prevention of vitamin A deficiency:
i. Promoting consumption of Vitamin A rich food –promotion of regular dietary intake of
Vitamin A rich foods by all pregnant and lactating women and by children under 5 years of
age by increasing local production and consumption of green leafy vegetables and other
plant foods those are rich sources of carotenoids.
ii. Creating awareness about the importance of preventing Vitamin A deficiency– among
the women’s attending Antenatal clinics, immunization session, as well as women and
children registered under ICDS programme.
iii.Prophylactic Vitamin A as per the following dosage schedule:
100000 IU at 9 months with measles immunization
200000 IU at 16-18 months, with DPT booster
200000 IU every 6 months, up to the age of 5 years.
Thus, a total of 9 mega doses are to be given from 9 months of age up to 5 years.
2. Treatment of Vitamin A deficient children:
i. All children with xerophthalmia are to be treated at health facilities.
ii. All children having measles, to be given 1 dose of Vitamin A if they have not received it in the
previous month.
i. All cases of severe malnutrition to be given one additional dose of Vitamin A.
37. Conclusion
Today we got to know a vital information about vitamin A ,its sources,
structure , absorption, deficiency diseases, toxicity & their preventive
measures.
The vitamin A plays a prominent role in human vision ,immune
system & reproduction.
So its duty to spread awareness amongst the people of India about
importance of vitamin A & also make sure that no one else would
ever fall ill again due to vitamin A deficiency.
38. ESSENTIALS OF
BIOCHEMISTRY
Pankaja Naik 2nd Edition
JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD
New Delhi • Panama City • London
Nutrition Science Sixth Edition
B.Shrilakshmi
New Age International (p) Limited,Publishers
New Delhi •New Delhi •London
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REFERENCES: