This document discusses vitamin A deficiency and hypervitaminosis A. It begins by introducing vitamin A and its functions in vision, cell function, immunity and reproduction. It then describes the absorption, transport, storage and excretion of vitamin A in the body. The rest of the document details the causes and health effects of vitamin A deficiency, as well as strategies to assess and treat deficiency. It concludes by covering the potential toxicity risks from long-term high intake of vitamin A, such as birth defects and bone/skin issues.
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.
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3. Active forms are retinol, retinaldehyde, and retinoic
acid
Plants synthesize the more complex carotenoids
which are cleaved to retinol by most animals and
stored in the liver as retinyl palmitate
N retinol plasma values: 15-30 mcg/dl in infants &
30-90 mcg/dl in adults
Retinal is the prosthetic group of photosensitive
pigment in both rods (rhodopsin) & cones
(iodopsin), major difference lies in the nature of
protein bound
Needed in lysosomal membrane stability
Plays a role in keratinization, cornification, bone
development & cell growth & reproduction
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4. Absorption of Vitamin A
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
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5. Transport and Storage of
Vitamin A
Liver stores 90% of vitamin A in the body
Reserve is adequate for several months
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
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6. Excretion of Vitamin A
Not readily excreted
Some lost in urine
Kidney disease and aging increase risk of
toxicity because excretion is impaired
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7. Functions of vitamin A
Vision (night, day, colour)
Epithelial cell integrity against infections
Immune response
Haematopoiesis
Skeletal growth
Fertility (male and female)
Embryogenesis
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8. 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
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9. Functions of Vitamin A:
Immunity
Deficiency leads to decreased resistance to
infections
Supplementation may decrease severity of
infections in deficient person
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11. Prevention of cardiovascular disease
Antioxidant capabilities
≥5 servings/day of fruits and vegetables
Cancer prevention
Antioxidant capabilities
Lung, oral, and prostate cancers
Studies indicate that vitamin A-containing foods are more
protective than supplements
Age-related macular degeneration
Cataracts
Acne
AML
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12. Source of vitamin A
Colostrum
foods containing either preformed vitamin A
esters
- liver, milk,cheese,eggs or food products
fortified with vitamin A
or
carotenoid precursors (mainly beta-
carotene), such as green leaves, carrots, ripe
mangoes,eggs, and other orange-yellow
vegetables and fruits.
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13. Source of vitamin A
fruit carotenoid
sources(micrograms/100gm)
Mango (golden) 307
Papaya (solo) 124
Cucurbita (mature pulp) 862
Buriti palm (pulp) 3,000
Red palm oil 30,000
Carrot 2,000
Dark green leafy vegetables
685
Tomato 100
Apricot 250
Sweet potato, red and yellow
670
Animal (micrograms/100gm)
Fatty fish liver oils
Halibut 900,000
Cod 18,000
Shark 180,000
Dairy produce
Butter 830
Margarine, vitaminized 900
Eggs 140
Milk 40
Cheese, fatty type 320
Liver of sheep and ox 15,000
Beef, mutton, pork 0–4
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15. 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
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16. Prevalence of vitamin A
deficiency in South Asia (%)
Country sub clinical clinical
VAD (%) VAD (%)
Afghanistan 53 -
Bangladesh 28 0.7
Bhutan 32 0.7
INDIA 57 0.7
Nepal 33 1
Pakistan 35
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17. High risk group
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
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18. Usually,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
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19. Health consequences
Xerophthalmia is the most specificVADD,and
is the leading preventable cause of blindness
in children throughout the world
Night blindness
Anaemia can result fromVAD in children and
women,likely due to multiple apparent roles
of vitamin A in supporting iron mobilization
and transport, and hematopoiesis
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21. Assessing vitamin A status and
deficiency
Two sets of indicators ofVAD are commonly
used for population surveys:
1 clinically assessed eye signs.Term xerophthalmia
encompasses the clinical spectrum of ocular
manifestations ofVAD, from milder stages of
night blindness and Bitot’s spots, to potentially
blinding stages of corneal xerosis, ulceration and
necrosis (keratomalacia)
2 biochemically determined concentrations of
retinol in plasma or serum
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23. 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 severeVAD.
a serum retinol concentration below a cutoff
of 1.05 μmol/l has been proposed to reflect
low vitamin.
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24. 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%
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25. Universal vitamin A distribution
schedule for preschool and
lactating mothers
Children 1–6 years
200,000 IU of vitaminA orally every 3–6 months.
Infants 6–11 months
100,000 IU of vitaminA orally every 3–6 months.
Lactating mothers
200,000 IU of vitaminA orally once: at delivery or
during the first 8 weeks postpartum if
breastfeeding or during the first 6 weeks if not
breast-feeding
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26. Recommended xerophthalmia
treatment schedule
6 -12 months > 1 yr
Immediately 100,000 IU 200,000 IU
Next day 100,000 IU 200,000 lU
2–4 weeks later 100,000 IU 200,000 IU
Severe Protein-Energy Malnutrition (PEM)
Monthly until PEM resolves
100,000 IU 200,000 IU
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27. Upper Level for Vitamin A
3000 μg retinol
Hypervitaminosis A results from long-term
supplement use (2 – 4 x RDA)
Toxicity
Fatal dose (12 g)
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28. HypervitaminosisA
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 IU/dl (N:
50-100 IU/dl)
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29. Toxicity of Vitamin A
Acute – short-term megadose (100 x
RDA); symptoms disappear when intake
stops
GI effects
Headaches
Blurred vision
Poor muscle coordination
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30. ChronicIntoxication
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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31. 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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32. 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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