Role of nutrition to prevent ocular disorders

1. Role of nutrition to prevent ocular
disorders
Sahibzada Hakim Anjum Nadeem
Co-Incharge OTTC, Optician, Refractionist, COAVS
CEO Anjum Eye Care & Optical Company
Optometrist, Al-Khair Eye Hospital Lahore
Phone:03344496480, Email: shanjum92@gmail.com

2. Role of nutrition to prevent ocular disorders

3. Nutrients
Chemical substances that constitute food
and are responsible for the functions of
food and also protect the body from
various disorders.

4. Types of nutrients
There are two types of nutrients.
I.Macronutrients
‐Proteins
‐carbohydrates
‐Fats
II.Micronutrients
‐Vitamins
‐Minerals

5. Introduction of Vitamins
Vitamins may be regarded as organic
compounds required in the diet in small
amounts to perform specific biological
functions for normal maintenance of
optimum growth and health of the
organism.

7. WHAT IS VITAMIN A?
• The term “vitamin A” makes it sound like there is one particular
nutrient called “vitamin A”, but this is not true. It is a broad group of
related nutrients.
• Vitamin A is a broad term for group of unsaturated nutritional
organic compounds, that includes retinol, retinal, retinoic acid, and
several provitamin A carotenoids, among which beta-carotene is the
most important.

8. Vitamin A is an Essential Fat soluble vitamin
occuring in the following forms:
Pre formed
Retinoids (retinal, retinol, retinoic acid)
Found in animal products
Pro vitamin A
Carotenoids
Must be converted to retinoid form
Found in plant products

9. HISTORY:
It is recorded in history that HIPPOCRATES
cured night blindness(about 500 B.C)
He prescribed to the patients Ox liver(in
honey)which is now known to contain high
quantity of vitamin A.
 By 1917, Elmer McCollum at the University of
Wisconsin–Madison, studied the role of fats in
the diet and discovered few accessory factors.
These "accessory factors" were termed "fat
soluble" in 1918 and later "vitamin A" in 1920.

10. In 1919, Harry Steenbock (University of
Wisconsin) proposed a relationship between
yellow plant pigments (beta-carotene) and
vitamin A.
In 1931, Swiss chemist Paul Karrer described
the chemical structure of vitamin A.
 Vitamin A was first synthesized in 1947 by
two Dutch chemists, David Adriaan van
Dorp and Jozef Ferdinand Arens.

11. Structure of vitamin A:
NOMENCLATURE:
PROVITAMIN A : β-Carotene
VITAMIN A1 : Retinol ( Vitamin A alcohol)
VITAMIN A2 : 3 -Dehydro-retinol
VITAMIN A ALDEHYDE : Retinal
VITAMIN A ACID : Retinoic acid
VITAMIN A ESTER : Retinyl ester
NEO VITAMIN A : Stereo isomer of Vitamin A1, has 70 –80% of
biological activity of Vitamin A1.

12. Sources of vitamin A:
• Animal : Fish Liver oil, Butter, Milk,
Cheese, Egg Yolk
• Plant : All Yellow –Orange –Red –Dark
Green fruits & vegetables like Tomatoes,
Carrots, Spinach, Papayas, Mangoes,
corn, sweet potatoes.

15. RECOMMENDED DIETARY ALLOWANCE
 Unit of activity is expressed as ‘RETINAL
EQUIVALENT’ (R.E.) / ‘INTERNATIONAL UNIT’
(I.U.)
1 Retinal Equivalent = 1μg of Retinol OR 6 μg
of β-carotene
1 I.U. = 0.3 μg of Retinol OR 0.34 μg of Retinyl
acetate OR 0.6 μg of β-carotene
Infants & Children : 400 t0 600 μg/day
Adults (Men & Women) : 600 to 800 μg/day
Pregnancy & Lactation : 1000 to 1200 μg/day

16. FUNCTIONS OF VITAMIN A:
 VISION
 GENE TRANSCRIPTION
 IMMUNE FUNCTION
 EMBRYONIC DEVELOPMENT AND REPRODUCTION
 BONE METABOLISM
 HAEMATOPOESIS
 SKIN AND CELLULAR HEALTH
 ANTIOXIDANT ACTIVITY
• Recent work suggests that, outside the retina, vitamin A is chiefly
concerned with mucopolysaccharide synthesis and stability of
lysozome membranes. Children aged three months to four years
are most commonly affected.

17. METABOLISM
•LIVER STORES 90% OF VITAMIN A
•ACTIVE METABOLITES
•TRANS RETINOIC ACID
•CIS RETINOIC ACID
•REGULATES EXPRESSION OF KERATIN AND
MUCINS
•RHODOPSIN IN VISUAL CYCLE

19. VITAMIN A DEFICIENCY:
Most susceptible populations:
Preschool children
Older adults
Alcoholism
Liver disease (limits storage)
Fat malabsorption

20. Vitamin A deficiency may result from :
Dietary insufficiency of Vitamin A /
Precursors
Interference with absorption from intestines
eg: diarrhoea, malabsorption syndrome, bile
salt deficiency
Defect in the transport due to protein
malnutrition –‘Kwashiorkar’
Defect in the storage due to diseases of liver

21. Tissues chiefly affected –‘Epithelial’
principally which are not normally
keratinized.
Includes epithelium of respiratory tract,
gastrointestinal tract, genitourinary tract,
eye & paraocular glands, salivary glands,
accessory glands of tongue & buccal cavity
and pancreas.
Fundamental change: Metaplasia of normal
non-keratinised living cells into keratinising
type of epithelium.

22. OCULAR MANIFESTATIONS OF VITAMIN A
DEFICIENCY
XEROPHTHALMIA
The term Xerophthalmia was given by a
joint WHO and USAID committee in 1976 to
cover all the ocular manifestations of
vitamin A deficiency including the
structural changes affecting the
conjunctiva, cornea and retina and also the
biophysical disorders of retinal rods and
cones functions.

23. XEROPHTHALMIA CLASSIFICATION (modified)
(1982)
• WHO CLASSIFICATION:
• XN-NIGHT BLINDNESS
• X1A-CONJUNCTIVAL XEROSIS
• X1B-BITOT’S SPOT
• X2-CORNEAL XEROSIS
• X3A-CORNEAL ULCER<1/3RD OF CORNEAL SURFACE
• X3B-CORNEAL ULCER>1/3RD OF CORNEAL SURFACE
• XS-CORNEAL SCAR
• XF-XEROPHTHALMIC FUNDUS

24. XN :NIGHT BLINDNESS(Nyctalopia)
Earliest symptom of xerophthalmia in
children
Diminished visual acuity in ‘dim
light’(Insufficient adaptation to darkness)
Defective rhodopsin function.

25. •Night blindness,is not pathognomonic of
vitamin A deficiency, being also a feature
of various eye diseases e.g. retinitis
pigmentosa, Oguchi's disease,
choroideremia, gyrate atrophy of the
choroid and retina, onchocerciasis and
occasionally congenital.
• If nutritional in origin the symptom will
disappear after consumption of about
30,000 I.U. of vitamin A daily
administered as cod or halibut liver oil.

26. X1A CONJUNCTIVAL XEROSIS
Characterised by:
One or more patches of dry, lusterless ,
nonwettable conjunctiva.
Interpalpebral conjunctiva(commonly temporal
quadrants)
Severe cases involves the entire bulbar
conjunctiva.
Desribed as ‘emerging like sand banks at receding
tide’when child ceases to cry
Can lead to conjunctival thickening,wrinkling and
pigmentation.

28. X1B BITOT’S SPOTS
Bilateral
Bulbar conjunctiva in the interpalpebral area
Commonly in temporal quadrant.
Raised triangular greyish/silvery white spots/plaques.
Firmly adherent to conjunctiva
Foamy keratinised epithelium(corynebacterium
xerosis)

29. X2 CORNEAL XEROSIS
Dry lustreless appearance of cornea
Earliest change is punctate keratopathy
Begins in the lower nasal quadrant
Bilateral punctate corneal epithelial erosions
Can progress to epithelial defects
Reversible on treatment

30. X3A & X3B CORNEAL ULCERATION
Stromal defects occur in late
stages due to colliquative
necrosis leading to corneal
ulceration ,softening (melting)
and destruction of
cornea(keratomalacia)
Corneal ulcers may be small or
large
Stromal defects involving less
than 1/3rd cornea usually heal
leaving some useful vision
Large stromal defects
commonly result in blindness.

31. Small ulcers
1-3mm
Occur peripherally
Circular
Steep margins and
sharply demarcated
Large ulcers
More than 3mm
Occur centrally
Involve entire cornea

32. XS CORNEAL SCAR
Healing of stromal defects results in corneal
scarring
Size of the corneal scar depends on the size and
density of corneal defect.

33. XF XEROPHTHALMIC FUNDUS
Uncommon in occurence
Typical seed like lesions
Whitish/yellow in colour
Raised lesisions
Scattered uniformly over fundus
At the level of optic disc.
FFA reveals these dots to be focal retinal pigment epithelial
defects
 Rarely these patients can present with scotomas
corresponding to the area of retinal involvement
Respond to vitamin A therapy with scotoma disappearing in
1-2 weeks and retinal lesions fading in 1-4 months

35. 2. Parenteral therapy: IN CASES OF
• severe disease
• unable to take oral feeds
• Repeated vomiting and diarrhoea
• malabsorption
Intramuscular injections of water miscible
vitamin A preparation
Dose – 1,00,000 IU(Half the oral dose)

36. PROPHYLAXIS AGAINST XEROPHTHALMIA
1.Short term approach:
-Periodic administration of vitamin A supplements
-WHO recommended,universal distribution schedule of vit A for
prevention is as follows:

37. 2.Medium term approach:
- fortification of food with Vit A
3. Long term approach:
- Promotion of adequate intake of Vit A rich foods
in high risk groups particularly preschool aged
children on a periodic basis and to mothers within
6-8 weeks after childbirth
- Other measures like nutritional education,social
marketing, home or community garden programs
and measures to improve food security.

38. HYPERVITAMINOSIS A
 Ingestion of large amounts of preformed vitamin A from the diet,
supplement intake or medications;
I.Acute:
 Single doses of >3,00,000 IU
 Headache ,Blurred vision,nausea ,vomiting, drowsiness,irritability i.e
signs of raised ICP(Benign intracranial hypertension)
 Serum Vit A values-200-1000 IU/dl
II.Chronic – long-term megadose; possible permanent damage
( >50,000 IU/day for several weeks)
 Bone and muscle pain,Loss of appetite,Skin disorders
 Headache
 Dry skin
 Hair loss
 Increased liver size
 Manifestations reversible when vitamin A discontinued

39. DEFICIENCY OF VITAMIN B1{THIAMINE}
•Can result in Corneal anaesthesia
•Conjunctival dystrophy
•Corneal Dystrophy
•Acute Retrobulbar neuritis

40. DEFICIENCY OF VITAMIN B2{RIBOFLAVIN}
I.FUNCTIONS- plays an important role in cellular growth
• It acts as a co – factor for a number of enzymes involved in energy
metabolism.
II.SOURCES:
• Eggs , liver, green leafy vegetables
• Milk
III.Deficiency may cause;
• Keratitis
• Susceptibility of cataract
• Photophobia
• Burning Sensation
• Conjunctival irritation
• Vascularization of Cornea

41. DEFICIENCY OF VITAMIN C
• It may be associated with haemorrhages in the conjunctiva, lids, anterior
chamber, retina and orbit.
• It delays wound healing
• It causes bleeding of gum
• Effective anti-oxidant
• Protects eyes against u.v rays
• Delays cataract formation < more than 300 mg>
SOURCES:
• Citrus
• guava
• mango
• Amla
• Pineapple

42. DEFICIENCY OF VITAMIN D
•It may be associated with Zonular Cataract
•Papilledema
•Increased lacrimation

43. VITAMIN E
I.FUNCTIONS
•Potent anti-oxidant
•Prevents Age related macular degeneration
(ARMD)
II.SOURCES
•Broccoli
•Carrot
•Spinach
•Fish

44. OMEGA -3- FATTY ACID
I.Functions:
•Essential fatty acid used to produce new cells ,
muscle, nerves and organs
•Protects against ARMD, dry eye syndrome
II.Sources:
•Fish
• walnut
• flax seeds

45. ZINC
•This trace mineral has a protective effect on early
ARMD
•Acutely concentrated in the eye and hence very
important
Sources:
•Almonds
•Wheat germs
•Dairy

46. SELENIUM
I.Helps in treating :
•Retro-bulbar pain
•Oedema
•Grave’s disease
II.Sources:
•Turkey
•Brazel nuts
•Tuna