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PRESENTED BY
Dr.Shyamsundar Lokhande
MPH (N) 2nd Semester
GMC Nanded
GUIDED BY
Dr.P.L.Gattani
Head of Department
Community Medicine
An Overview of Vitamin A
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
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.
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.
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
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
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.
Structure of Vitamin A
Where does it come from?
Animal Sources
• Eggs
• Meat
• Cheese
• Milk
• Liver
• Kidney
• Fish liver oils
Plant Sources
• Carrots
• Sweet Potatoes
• Apricots
• Broccoli
• Spinach
• Pumpkin
• Papaya
• Mango
GROUP RETINOL(mcg) ẞ CAROTENE(mcg)*
ADULTS
Man 600 4800
Woman 600 4800
Pregnancy 800 6400
Lactation 950 7600
INFANTS
0-6months 350 -
6-12months 350 2800
CHILDREN 400 3200
1-6yrs 600 4800
ADOLESCENTS
10-17yrs 600 4800
Recommended Dietary Allowances
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.
Conversion of b-carotene (provitamin)
to biologically active forms of vitamin A
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.
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 .
Wald’s visual cycle
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.
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.
Deficiency Manifestation
fundus
• XN Night blindness
• X1A Conjunctival Xerosis
• Conjunctival Xerosis
• X1B Bitot’s spot
• X2 Corneal Xerosiso
• Sis
• X3A Corneal ulceration/keratomalacia (< 1/3 corneal
surface) n
• X3B Corneal ulceration/keratomalacia (≥ 1/3 corneal
surface)
• XS Corneal scar C
• orneal scar
• XF Xerophthalmic fundus rophthalmic
Classification of xerophthalmia
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
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.
• 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
• 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
• Conjunctiva becomes
dry and non wettable.
• Instead of looking
smooth shiny it
appears muddy
&wrinkled.
Conjunctival Xerosis
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.
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
TREATMENT
• 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
• Large doses of Vit A orally.
• Quick organization.
• Minimum Infrastructure.
SHORT – TERM ACTION
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
• FORTIFICATION –
• Dalda
• Sugar
• Salt
• Tea
• Margarine
• Dried Skimmed
Milk
MEDIUM – TERM ACTION
• 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
• 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
National Vitamin A Prophylaxis Program
Aim : to decrease the prevalence of Vitamin A
deficiency.
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.
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.
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
Banglore •Chennai •Cochin •Guwahati •Hyderabad •Kolkata •Luckow •Mumbai
Wikipedia
Google
REFERENCES:
Any questions
THANK YOU

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Vitamin A

  • 1. PRESENTED BY Dr.Shyamsundar Lokhande MPH (N) 2nd Semester GMC Nanded GUIDED BY Dr.P.L.Gattani Head of Department Community Medicine An Overview of Vitamin A
  • 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.
  • 9. Where does it come from? Animal Sources • Eggs • Meat • Cheese • Milk • Liver • Kidney • Fish liver oils Plant Sources • Carrots • Sweet Potatoes • Apricots • Broccoli • Spinach • Pumpkin • Papaya • Mango
  • 10. GROUP RETINOL(mcg) ẞ CAROTENE(mcg)* ADULTS Man 600 4800 Woman 600 4800 Pregnancy 800 6400 Lactation 950 7600 INFANTS 0-6months 350 - 6-12months 350 2800 CHILDREN 400 3200 1-6yrs 600 4800 ADOLESCENTS 10-17yrs 600 4800 Recommended Dietary Allowances
  • 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.
  • 12. Conversion of b-carotene (provitamin) to biologically active forms of vitamin A
  • 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.
  • 19. fundus • XN Night blindness • X1A Conjunctival Xerosis • Conjunctival Xerosis • X1B Bitot’s spot • X2 Corneal Xerosiso • Sis • X3A Corneal ulceration/keratomalacia (< 1/3 corneal surface) n • X3B Corneal ulceration/keratomalacia (≥ 1/3 corneal surface) • XS Corneal scar C • orneal scar • XF Xerophthalmic fundus rophthalmic Classification of xerophthalmia
  • 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
  • 34. National Vitamin A Prophylaxis Program
  • 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 Banglore •Chennai •Cochin •Guwahati •Hyderabad •Kolkata •Luckow •Mumbai Wikipedia Google REFERENCES: