This presentation contains Importance of vitamin A, Sources of Vitamin A, Absorption,Transport and Excretion of Vitamin A, Vitamin A Deficiency, Vitamin A Toxicity, Required dose of Vitamin A, Nutrition, Nutrition deficiency

2. Introduction
• Vitamin A deficiency (VAD) is a major
nutritional concern in poor
societies, especially in lower income
countries like INDIA.
• 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.

3. VITAMIN A
• Exits in 3 forms:
• all trans-retinol
• long chain fatty acyl ester of retinol (main
storage form)
• retinal (the active form in the retina)
• Retinoic acid is also considered to be
physiologically active
• Pro vitamin A or carotene can be
converted to retinol in vivo

5. Sources

6. Absorption
• Retinoids
• Retinyl esters broken down to free retinol in small
intestine - requires bile, digestive
enzymes, integration into micelles
• Once absorbed, retinyl esters reformed in
intestinal cells
• 90% of retinoids can be absorbed
• Carotenoids
• Absorbed intact, absorption rate much lower
• Intestinal cells can convert carotenoids to retinoids

7. • Approximately 80% is absorbed.
• It is passed along with fat through the
lymphatic system into blood stream.
• Absorption is poor in case of
diarrhea, jaundice and abdominal
disorder.
• Absorption increases if taken with fat.
• Vitamin A which is not absorbed is
excreted within 1 or 2 days in feces .

8. Transport
• Transported via chylomicrons from
intestinal cells to the liver
• Transported from the liver to target
tissue as retinol via retinol-binding
protein, which is bound to transthyretin

9. STORAGE
• The liver has enormous capacity to
store in the form of retinolpalmitate.
• under normal conditions a well-fed
person has sufficient Vitamin A
reserves to meet his need for 6 to
9months or more.

10. Excretion of Vitamin A
• Not readily excreted
• Some lost in urine
• Kidney disease and aging increase risk
of toxicity because excretion is impaired

11. Functions of vitamin A
• Vision (night, day, colour)
• Epithelial cell integrity against
infections
• Immune response
• Haematopoiesis
• Skeletal growth
• Fertility (male and female)
• Embryogenesis

12. Functions of Vitamin A:
Growth and Differentiation of
Cells
• Retinoic acid is necessary for cellular
differentiation
• Important for embryo
development, gene expression
• Retinoic acid influences
production, structure, and function of
epithelial cells that line the outside
(skin) and external passages (mucus
forming cells) within the body

15. Functions of Vitamin A:
Immunity
• Deficiency leads to decreased resistance
to infections
• Supplementation may decrease severity
of infections in deficient person

16. Functions of Vitamin A:
Vision
• Retinal is a necessary structural
component of rhodopsin or visual
purple, the light sensitive pigment
within rod and cone cells of the retina.
• If inadequate quantities of vitamin A
are present, vision is impaired.

17. Vision Cycle

18. The Visual Cycle
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19. • Role in Prevention of cardiovascular disease
• Antioxidant capabilities
• ≥5 servings/day of fruits and vegetables
• Role in Cancer prevention
• Antioxidant capabilities
• Lung, oral, and prostate cancers
• Studies indicate that vitamin A-containing foods are
more protective than supplements
• Other Roles in
•
•
•
•
Age-related macular degeneration
Cataracts
Acne
AML

21. Recommended daily allowances
(RDAs) for Vitamin A

22. Units of measuring vitamin A
Each μg RAE corresponds to
• 1 μg retinol,
• 2 μg of β-carotene in oil,
• 12 μg of "dietary" beta-carotene,
One International Unit (I.U.)
• 0.3 mcg. of retinol
• 0.6 mcg. of beta-carotene
• 1.2 mcg. of other total mixed carotenoids

23. Deficiency of Vitamin A

24. High risk group
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Infancy
Childhood
Pregnancy
Lactation
Urban poor
Older adults
Alcoholism
Liver disease (limits storage)
Fat malabsorption
Increased excretion as in cancer & UTI
Low protein intake resulting in deficient carriers

25. • Usually, Vitamin A Deficiency (VAD)
develops in an environment of ecological
social and economical deprivation
• Synergism between deficient dietary intake of
vitamin A coexists with severe
infections, such as measles, and frequent
infections causing diarrhoea and respiratory
diseases that can lower intake through
depressed appetite and absorption, and
deplete body stores of vitamin A through
excessive metabolism and excretion

26. Health consequences
• Xerophthalmia is the most specific
VAD, and is the leading preventable cause
of blindness in children throughout the
world
• Night blindness
• Anaemia can result from VAD in children
and women, likely due to multiple
apparent roles of vitamin A in supporting
iron mobilization and transport, and
hematopoiesis

27. Classification of xerophthalmia
• XN Night blindness
• X1A Conjunctival Xerosis
• X1B Bitot’s spot
• X2 Corneal Xerosis
• X3A Corneal
ulceration/keratomalacia (< 1/3
corneal surface)
• X3B Corneal
ulceration/keratomalacia (≥ 1/3
corneal surface)
• XS Corneal scar
• XF Xerophthalmic fundus

28. Night Blindness
• Lack of vitamin A causes
night blindness or inability to
see in dim light.
• night blindness occurs as a
result of inadequate pigment
in the retina.
• It also called tunnel vision.
• 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.

29. Night blindness

30. Bitot’s Spot
• 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.

31. Conjunctival Xerosis
• Conjunctiva becomes
dry and non wettable.
• Instead of looking
smooth shiny it
appears muddy
&wrinkled.

32. Keratomalacia
• 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.

33. Other Symptoms of VAD
• Alteration of skin and mucous membrane
• Hepatic dysfunction
• Headache
• Drowsiness
• Peeling of skin about the mouth and
elsewhere

34. Follicular hyperkeratosis

35. Assessing vitamin A status and
deficiency
• Two sets of indicators of VAD are commonly
used for population surveys:
1. clinically assessed eye signs.
Term xerophthalmia encompasses the
clinical spectrum of ocular manifestations of
VAD, from milder stages of night blindness
and Bitot’s spots, to potentially blinding
stages of corneal xerosis, ulceration and
necrosis (keratomalacia)
1. biochemically determined concentrations of
retinol in plasma or serum

36. Serum retinol concentrations
• Serum retinol concentrations in a
population constitutes the second major
approach to assessing vitamin
• A status in a population, with values
below a cut-off of 0.70 μmol/l representing
VAD , and below 0.35 μmol/l representing
severe VAD.
• A serum retinol concentration below a
cutoff of 1.05 μmol/l has been proposed to
reflect low vitamin.

37. Criteria for assessing the public
health significance of
Xerophthalmia
Clinical (primary)
• Night blindness (XN)* 1.0%
• Bitot’s spot (X1B) 0.5%
• Corneal xerosis and/or
ulceration/keratomalacia (X2 + X3A + X3B)
0.01%
• Xerophthalmia-related corneal scars (XS)
0.05%
Biochemical (supportive)
• Serum retinol (vitaminA) < 0.35 μmol/L (10
μg/dL) 5.0%

38. Universal vitamin A distribution
schedule for preschool and
lactating mothers
• Children 1–6 years
200,000 IU of vitamin A orally every 3–6 months.
• Infants 6–11 months
100,000 IU of vitamin A orally every 3–6 months.
• Lactating mothers
200,000 IU of vitamin A orally once at delivery or
during the first 8 weeks postpartum if
breastfeeding or during the first 6 weeks if not
breast-feeding

39. Recommended Xerophthalmia
treatment schedule
6 -12 months
• Immediately 100,000 IU
• Next day
100,000 IU
• 2–4 weeks later 100,000 IU
> 1 yr
200,000 IU
200,000 lU
200,000 IU
• Severe Protein-Energy Malnutrition (PEM)
Monthly until PEM resolves
100,000 IU
200,000 IU
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40. Upper Level for Vitamin A
• 3000 μg retinol
• Hypervitaminosis A results from longterm supplement use (2 – 4 x RDA)
• Toxicity
• Fatal dose (12 g)
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41. Hypervitaminosis A
Acute Intoxication:
• Results when excessively large single
doses >300,000 IU ingested
• Infants: n/v, drowsiness or irritability
w/signs of increased ICP
• Adults:
drowsiness, irritability, headache &
vomiting
• Serum vitamin A values = 200-1000
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IU/dl (N: 50-100 IU/dl)

42. Toxicity of Vitamin A
Acute toxicity
short-term megadose (100 x RDA);
symptoms disappear when intake
stops
•GI effects
•Headaches
•Blurred vision
•Poor muscle coordination
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43. Chronic Intoxication
•
Results when >50,000 IU/day ingested for several
wks or more
• Signs & symptoms in infants:
• Early are anorexia, pruritus, irritability, tender
swollen bones w/motion limitation
• Alopecia, seborrhea, cheilosis & peeling of
palms & soles
• Hepatomegaly & hypercalcemia observed
• Craniotabes & hyperostosis of long bones
• Elevated serum vit A levels confirms diagnosis
• Reversible manifestations when vitamin A
discontinued
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44. Chronic Toxicity of Vitamin A
• long-term megadose; possible
permanent damage
•Bone and muscle pain
•Loss of appetite
•Skin disorders
•Headache
•Dry skin
•Hair loss
•Increased liver size
•Vomiting
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45. Toxicity of Vitamin A
• Teratogenic (may occur with as little as
3 x RDA of preformed vitamin A)
• Tends to produce physical defect on
developing fetus as a result of excess
vitamin A intake
• Spontaneous abortion
• Birth defects
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47. Thanking You