Vitamin A is a fat soluble vitamin. Deficiency lead to many ocular and extra ocular manifestations.

1. Vitamin A deficiency and Control
Programme
Dr Soni Rani
PGT
Department Of Community medicine
Katihar medical College, Katihar

2. Introduction
• Vitamin A is a fat soluble vitamin Required for
vision, repair, reproduction, growth and tissue
differentiation
• This occurs in two forms, as retinol in animal
foods and as b-carotene in plant food.
• Carotene is converted into retinol in the
intestine, which is then absorbed and stored
in the liver as retinol-Palmitate.

3. Different Units of Vitamin A
• The international unit of vitamin A declared in
1954, which is equivalent to 0.3 microgram of
Retinol.
• 1 mcg of Retinaol= 1 RE ( Retinol Equivalent)
• 1 mcg of β carotene= 0.167 mcg of RE
• 1 mcg of other carotinoids=0.084 mcg of RE
• 1RE= 3.333 IU of Vitamin A.

4. Sources Of Vitamin A
A. Animal Foods (as Retinol):
• These are meat, liver,
fish, egg-yolk, milk,
cheese, butter, ghee.
• Richest source is fish
liver oil (Cod liver oil
and shark liver oil).

5. Sources Of Vitamin A
B. Vegetable Sources (as b-carotene)
Cheapest source is green leafy
vegetables, e.g. spinach,
amaranth.
Darker the green color of the
vegetables, higher the carotene
content.
Richest source is red palm oil.
Other sources are yellow fruits
like mango and papaya.
Some roots like carrots are also
rich in b-carotene.

6. Sources Of Vitamin A
• Fortified Foods: Food fortified with Vitamin A (e.g
Vanaspati , margarine, milk) can be an important
source.
• The human liver has enormous capacity to store
vitamin A in the form of retinol-Palmitate.
• Therefore, under normal conditions, a well-fed person
has sufficient reserve of vitamin A to meet his needs
for 6 to 9 months.
• But a newborn child is not having any reserve and it
depends upon vitamin A everyday.
• Thus, an young child is always at a risk of deficiency.

7. Retinol Content Of Selected Foods

8. Digestion, Absorption and Transportation

9. Functions Of Vitamin A
• Vitamin A helps in the synthesis of a pigment
called ‘Rhodopsin’ in the retina of the eye,
which is necessary for the normal vision,
especially in the dim-light for dark adoptation.
• Thus vitamin A is indispensable for normal
vision.
• It maintains the integrity of the skin and
mucous membrane of the conjunctiva, cornea,
respiratory, alimentary and urinary system.

10. Functions Of Vitamin A
• It promotes skeletal growth.
• It increases the immune response. Thus it is
anti-infective.
• It may protect some epithelial cancers such as
carcinoma of bronchus.

11. • Vitamin A is essential for vision (especially dark
adaptation),
• Immune response,
• Bone growth,
• Reproduction,
• Maintenance of the surface linings of the eyes,
epithelial cell growth and repair, and the epithelial
integrity of the respiratory, urinary, and intestinal tracts.
• Vitamin A is also important for embryonic development
and the regulation of adult genes.
Functions Of Vitamin A

12. Role In Vision
• In the retina, retinaldehyde functions as the
prosthetic group of the light-sensitive opsin
proteins, forming Rhodopsin (in rods) and
iodopsin (in cones).
• Any one cone cell contains only one type of
opsin, and is sensitive to only one color.

13. Role In Vision
• The absorption of light by Rhodopsin causes
isomerization of the retinaldehyde from 11-cis
to all-trans, and a conformational change in
opsin.
• This results in the release of retinaldehyde
from the protein, and the initiation of a nerve
impulse.

14. Wald’s visual cycle
• The formation of the initial excited form of
Rhodopsin, bathorhodopsin, occurs within
picoseconds of illumination.
• There are then a series of conformational
changes leading to the formation of
metarhodopsin II, which initiates a guanine
nucleotide amplification cascade and then
a nerve impulse.

15. Wald’s visual cycle
• The final step is hydrolysis to release all-
trans-retinaldehyde and opsin.
• The key to initiation of the visual cycle is
the availability of 11-cis-retinaldehyde,
and hence vitamin A.
• In deficiency, both the time taken to
adapt to darkness and the ability to see
in poor light are impaired.

16. Wald’s visual cycle

17. Role in the Regulation of Gene Expression and Tissue
Differentiation
• Retinoic acid is a ligand for certain nuclear
receptors that act as transcription factors.
• The retinoid receptors play an important role in
controlling cell proliferation and differentiation.
• Like vitamin D, retinoic acid interacts with nuclear
receptors that bind to control elements which are
specific regions on the DNA to regulate the
expression of specific genes.

18. Role in the Regulation of Gene Expression and Tissue
Differentiation
Two families of receptors (RAR and RXR receptors) are active in
retinoid-mediated gene transcription. RAR binds all-trans
retinoic acid and 9-cis retinoic acid, whereas RXR binds only 9-
cis retinoic acid.

19. Role in the Regulation of Gene Expression
and Tissue Differentiation
• All-trans-RA and 9-cis-RA are transported to the
nucleus of the cell bound to cytoplasmic retinoic
acid-binding proteins.
• Within the nucleus, all-trans-RA binds to retinoic acid
receptors (RAR) and 9-cis-RA binds to retinoid
receptors (RXR).
• RAR and RXR form RAR/RXR heterodimer, which bind
to regulatory regions of the chromosome called
retinoic acid response elements (RARE).

20. Role in the Regulation of Gene Expression
and Tissue Differentiation
• Binding of all-trans-RA and 9-cis-RA to RAR
and RXR respectively allows the complex to
regulate the rate of gene transcription.
• Nuclear Receptors in the Gonads increase
gene expression and maintain reproductive
tissues while nuclear receptors in epithelial
cells regulate cell differentiation.

21. Role of vitamin A in Immunity
1) Vitamin A and retinoic acid (RA) play a central role in the
development and differentiation of white blood cells, such as
lymphocytes, which play critical role in the immune response.
2) The skin and mucosal cells (function as a barrier and form
the body's first line of defense against infections. Retinol and
its metabolites are required to maintain the integrity and
functioning of these cells. Keratinization of mucous
membranes in vitamin A deficiency add up to the risk to
infections.
3)Retinol binding protein (RBP) is a negative ‘Acute phase
protein’, that results in decreased circulatory concentration of
the vitamin with further deterioration of the immune system.

22. Role of vitamin A in growth
• Vitamin A is required for-
• General body growth
• Bone and
• Brain development

23. Vitamin A deficiency- Overview
 Vitamin A deficiency can result from inadequate
intake, fat malabsorption, or liver disorders.
 Deficiency impairs immunity and hematopoiesis and
causes skin rashes and typical ocular effects (e.g.,
xerophthalmia, night blindness).
 Diagnosis is based on typical ocular findings and low
vitamin A levels.
 Treatment consists of vitamin A given orally or, if
symptoms are severe or malabsorption is the cause,
parenterally.

24. Etiology of Vitamin A deficiency
• Primary vitamin A deficiency
o Prolonged dietary deprivation
o Vegetarians,
o Refugees, and
o Chronic alcoholics,
o Toddlers and
o Preschool children

25. Etiology of Vitamin A deficiency
• Secondary vitamin A deficiency
o Sprue,
o Cystic fibrosis,
o Pancreatic insufficiency,
o Duodenal bypass,
o Chronic diarrhea,
o Bile duct obstruction,
o Giardiasis, and cirrhosis.

26. Symptoms of vitamin A deficiency
• The signs and symptoms are grouped into
ocular and extraocular manifestations.

27. Ocular manifestations
• All the ocular manifestations are due to
decreased synthesis of rhodopsin in the retina
and due to dryness of conjunctiva and its
consequences.
• All the ophthalmic manifestations due to
vitamin A deficiency are included under the
term ‘Xerophthalmia’ (Xerosis = dryness; dry
eye).

28. Stages Of Ocular manifestation
• Night blindness (Nyctalopia): That means inability to
seen the dim light by an young child as the evening
sets in.
• This is because of failure in the dark adoptation
because of decreased synthesis of rhodopsin in the
retina.
• The classical complaint by the mother is that her child
cannot find her or dashes against the wall as the dark
sets in.
• Nyctalopia is the earliest clinical feature. If not
managed at this stage, it passes on to the next stage.

29. Stages Of Ocular manifestation
• Conjunctival xerosis:
The normal, smooth,
shiny conjunctiva over
the sclera becomes dry,
dull and wrinkled giving
a smoky appearance.
• Often this occurs
following chronic
exposure to dust and
smoke also, but among
adults.

30. Stages Of Ocular manifestation
• Bitot’s spots: These are
triangular, foamy,
pearly-white or
yellowish spots on the
bulbar conjunctiva,
usually lateral to cornea
and often bilateral.
• It is characteristic of
vitamin A deficiency.

31. Stages Of Ocular manifestation
• Corneal xerosis: The
smooth, shiny,
transparent cornea
looks dull and dry,
eventually it becomes
opaque. If not managed
at this stage, it leads on
to corneal ulceration.
• Thus the involvement of
cornea constitutes
medical emergency.

32. Stages Of Ocular manifestation
• Corneal ulcer: The ulcer
may be big or small,
which after healing
leaves behind a
permanent scar, which
affects vision.

33. Stages Of Ocular manifestation
• Keratomalacia: As the
deficiency of vitamin A
continues, the entire
cornea or a part of it
becomes soft and later it
is liquefied.
• This constitutes a grave
medical emergency,
because the soft cornea
may burst open, leading
on to prolapse of iris.
• If the eye collapses, vision
is lost.

34. Extraocular Manifestations
• Retardation of growth
• Follicular hyperkeratosis (Phrynoderma)
• Anorexia
• Increased incidence of respiratory and
alimentary infections
• Development of urinary calculi.

35. Assessment of Vitamin A Deficiency
• Since the ophthalmic manifestations are many
due to deficiency of vitamin A, WHO has
recommended to consider any one of the
following criteria as an evidence of
xerophthalmia problem in the community, as
per the surveys done among preschool
children, aged 6 months to 6 years.

36. Prevalence criteria for determining the
Xerophthalmia problem

37. Prevalence Of Vitamin A deficiency in SEAR
Country
Children <6 years
No. of deaths
perceived Subclinical VAD (%) Clinical VAD (%)
Afghanistan 50,000 53 -
Bangladesh 28,000 28 0.7
Bhutan 600 32 0.7
India 3,30,000 57 0.7
Nepal 6,900 33 1
Pakistan 56,000 35 -
South Asia region 4,71,500 - -
World total 11,50,000 - -
Source- UNICEF 2003 UNICEF and MI 2004 : WHO 2000

38. Prevalence of Vitamin A deficiency(
India)

39. Prevalence of Vitamin A deficiency(
India)

40. Treatment Of Vitamin A deficiency
• Vitamin A deficiency should be treated
urgently.
• Nearly all of the early stages of xerophthalmia
can be reversed by administration of a
massive dose (200,00Q IU or 110 mg of retinol
palmitate) orally on two successive days (30).
• All children with corneal ulcers should receive
vitamin A whether or not a deficiency is
suspected.

41. Prevention
• Prevention and/or control takes two forms
a) improvement of people's diet so as to ensure a
regular and adequate intake of foods rich in
vitamin A, and
b) reducing the frequency and severity of
contributory factors, e.g., PEM, respiratory tract
infections, diarrhoea and measles.
• Both are long term measures involving intensive
nutrition education of the public and community
participation.

42. Prevention
• Since vitamin A can be stored in the body for 6 to 9
months and liberated slowly, a short term, simple
technology had been evolved by the National Institute
of Nutrition at Hyderabad (India) for community- based
intervention against nutritional blindness, which has
subsequently been adopted by other countries .
• The strategy is to administer a single massive dose of
200,000 IU of vitamin A in oil (retinol palmitate) orally
every 6 months to preschool children (1 year to 6
years), and half that dose (100,000 IU) to children
between 6 months and one year of age.

43. Prevention
• In this way, the child would be, as it were
"immunized" against xerophthalmia.
• The protection afforded by six-monthly dosing
seems very adequate as measured by clinical
signs of deficiency .

44. Recommended Daily Allowances

45. Hypervitaminoses A (Toxicity)
• An excess intake of retinol causes anorexia,
vomiting followed by sleep disorders and skin
desquamation.
• Other features are hepatomegaly,
papilledema, bony exostoses (swelling over
the long bones), brittleness of the bones and
often fractures.
• The teratogenic effects of massive doses of
vitamin A is the most recent focus of interest.

46. Vitamin A supplementation (VAS)
programme in India
• The National Prophylaxis Programme against
Nutritional Blindness due to Vitamin A Deficiency
(NPPNB) was initiated in 1970 with the specific aim
of preventing nutritional blindness due to
keratomalacia.
• The Programme was started as a 100 per cent
centrally sponsored programme.
• It was launched as an urgent remedial measure to
combat the unacceptably high magnitude of
xerophthalmic blindness in the country reported in
the 1950s and 1960s.

47. • To begin with, this Programme was initiated in
11 States of the country.
• Evaluation studies conducted by the National
Institute of Nutrition (NIN), Hyderabad in 1976
in two States revealed positive results of the
Programme.
• In subsequent years, the Programme was
extended to all States in the country.
Vitamin A supplementation (VAS)
programme in India

48. • In 1994, under the National Child Survival and
Safe Motherhood (CSSM) Programme, the
NPPNB due to VAD was modified keeping in
view of the vulnerability of VA deficiency in
young children.
• The age group of eligible children for coverage
was restricted to 9 to 36 months of age.
Vitamin A supplementation (VAS)
programme in India

49. • Accordingly, each child was to receive five
doses of VA before her/his 3rd birthday
(children age 6-11 months, 1 dose of 100,000
IU of VA and in age 12- 36 months of age one
dose of 200,000 IU of VA every six months).
• In view of operational feasibility, the
administration of first dose of VA was linked to
measles immunization.
Vitamin A supplementation (VAS)
programme in India

50. • In 2006, the age group of eligible children was
revised as 6-59 months.
• This was done after reconsidering the
recommendations of WHO, UNICEF and
Ministry of Women and Child Development.
• This was despite the evidence that clinical VAD
was limited to a few isolated geographical
pockets in the country.
Vitamin A supplementation (VAS)
programme in India

51. • Presently, vitamin A supplementation (VAS) is
implemented through the existing network of
primary health centres and sub-centres.
• The female multipurpose worker and other
paramedics at the village level sub-health
centres are responsible for administering
vitamin A solution.
Vitamin A supplementation (VAS)
programme in India

52. • The services of Integrated Child Development
Services (ICDS) functionaries are also utilized
for the implementation of the Programme.
• Monthly intensive drives are undertaken every
six months to achieve universal coverage of
those children who could not be covered
during the routine visits of health
functionaries.
Vitamin A supplementation (VAS)
programme in India

53. • However, with disappearance of Bitot’s spot, now
the subclinical deficiency of VA, as assessed by
serum retinol (SR) levels is being advocated and
utilized as a marker of VAD.
• Serum retinol may not be an operationally
feasible indicator to be utilized in communities to
establish the prevalence of VAD.
• Estimation of SR requires collection of blood
samples of children and sophisticated laboratory
equipment.
Vitamin A supplementation (VAS)
programme in India

54. Reasons for decline in VAD in India
• The prevalence of severe undernutrition has
come down significantly.
• Immunization coverage for measles and other
vaccine preventable diseases has improved
from 5-7 per cent in early seventies to
currently 60-90 per cent, in different States.
• There has been a significant improvement in
the overall dietary intake of young children.

55. • The ICDS which covers 80 per cent of rural
India provides nutritional supplements to
children less than six years of age, nutrition
education to mothers and also facilitates the
distribution of vitamin A supplements.
• Improvements in infrastructure have led to
better access to health care facilities.
• Food availability in India has improved in the
last 30 years
Reasons for decline in VAD in India

56. Problem with current Policy
1) Unjustified claims of benefit.
2) Indiscriminate Mega Dosing.
3) Possible Adverse Effects ( Bulging fontanel,
Vitamin D Antagonism, Potential Zinc
deficiency, Risk Of Acute respiratory
Infections)
4) Cost Of Vitamin A Coverage.

57. Need for targeting VAS ..!
• According to WHO guidelines, vitamin A
supplementation in children 6-59 months of age
is recommended in settings where vitamin A
deficiency is a public health problem.
• In the Indian context, it would, therefore, be
prudent to restrict massive dose prophylaxis in
isolated geographical pockets or areas where
clinical vitamin A deficiency is a significant public
health problem rather than continuing universal
prophylaxis.

58. Approach for VA supplementation
• At this stage, we should focus our efforts on
sustainable food based approaches to combat
vitamin A deficiency.
• The solution is to increase local production and
consumption of green leafy vegetables and other
plant foods that are rich sources of carotenoids.
• Green leafy vegetables, many fruits and other
plant foods are also good sources of folate,
vitamin C, Fe, Ca and many other micronutrients
and bioactive compounds.

59. • A food-based approach to combat VAD in non-
clinically deficient areas would be a
sustainable and cost effective solution.
• States of Bihar, Uttar Pradesh and Madhya
Pradesh with poor intake of food providing all
micronutrients, may have targeted approach
of VAS in areas endemic for clinical VAD.
Approach for VA supplementation

60. • In India, for cost-effective utilization of limited
resources available to the health sector, the `Triple A’
(Assessment, Analysis and Action) strategy should be
adopted; first, assess the problem of VAD, then
undertake the detailed analysis of causes of VAD, and
then decide the combination of approaches to be
adopted for prevention and control in the community.
• Countries with limited financial resources and
competing health priorities cannot afford the luxury of
initiating interventions to raise serum biochemistry
alone.
Approach for VA supplementation

61. References
1. Government of India, Ministry of Health and Family Welfare, Department of Family Welfare, Child
Health Division, Order no. Z.28020/30/2003-CH dated 2 November 2006 Available from:
http://www.poshan.nic.in/jspui/bitstream/DL/389/1/mcn-vitamin-a-ifa-supplementation.pdf,
accessed on September 12, 2013.
2. National Nutrition Monitoring Bureau (NNMB). 9. Prevalence of vitamin A deficiency among rural
preschool children. Report No 23. Hyderabad, India: National Institute of Nutrition, Indian Council
of Medical Research; 2006.
3. World Health Organization (WHO). 1. Human vitamin and mineral requirements, World Health
Organization, Food and Agriculture Organization of the United Nations, Rome. Geneva: WHO
Press; 2002. p. 22-8.
4. Maternal and child health scheme for prophylaxis against nutritional blindness in children caused
by vitamin A deficiency. Family Planning Programme, Fourth Five-Year Plan Technical Information:
MCH
5. Vitamin A prophylaxis. In:National child survival and safe motherhood programme, MCH Division,
Department of Family Welfare, Ministry of Health and Family Welfare, Government of India. New
Delhi: Government Press; 1994. p. 88-93
6. USAID. Cost analysis of the national vitamin A supplementation 40. programs in Ghana, Nepal,
and Zambia: a synthesis of three studies. Arlington, VA, USAID, 2004. Available from:
httpf/www.mostproject.org/IVACG/GhanaNepalZambiaSythesis.pdf, accessed on May 20, 2011
7. World Health Organization. Guidelines for Vitamin A 41. supplementation in Infants and Children
6-59 months of age. Geneva: WHO; 2011. Available from: www.who.int/entity/nutrition/,
accessed on January 20, 2011.