Role of nutrition to prevent ocular disorders

Primary Eye Care OD-104

Sahibzada Hakim Anjum NadeemDepartmental Coordinator,Department of Optometry and Vision Sciences CEO Anjum Eye Care & Optical CompanyOptometrist, Al-Khair Eye Hospital LahoreCo-Incharge OTTC, Optician, Refractionist, COAVSPhone:03344496480, Email: shanjum92@gmail.com

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

Types of nutrientsThere are two types of nutrients.I.Macronutrients ‐Proteins ‐carbohydrates‐Fats

II.Micronutrients‐Vitamins‐Minerals

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.

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.

Vitamin A is an Essential Fat soluble vitamin occuring in the following forms:

Pre formedRetinoids (retinal, retinol, retinoic acid)Found in animal products

Pro vitamin ACarotenoids Must be converted to retinoid formFound in plant products

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.

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.

Structure of vitamin A:

NOMENCLATURE:PROVITAMIN A : β-CaroteneVITAMIN A1 : Retinol ( Vitamin A alcohol)VITAMIN A2 : 3 –Dehydro-retinolVITAMIN A ALDEHYDE : RetinalVITAMIN A ACID : Retinoic acidVITAMIN A ESTER : Retinyl esterNEO VITAMIN A : Stereo isomer of Vitamin A1, has 70 –80% of

biological activity of Vitamin A1.

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.

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-caroteneInfants & Children : 400 t0 600 μg/dayAdults (Men & Women) : 600 to 800 μg/dayPregnancy & Lactation : 1000 to 1200 μg/day

FUNCTIONS OF VITAMIN A:VISIONGENE TRANSCRIPTIONIMMUNE FUNCTIONEMBRYONIC DEVELOPMENT AND REPRODUCTIONBONE METABOLISMHAEMATOPOESISSKIN AND CELLULAR HEALTHANTIOXIDANT 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.

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

VITAMIN A DEFICIENCY:Most susceptible populations:Preschool childrenOlder adultsAlcoholismLiver disease (limits storage)Fat malabsorption

Vitamin A deficiency may result from :Dietary insufficiency of Vitamin A /

PrecursorsInterference with absorption from

intestineseg: diarrhoea, malabsorption syndrome,

bile salt deficiencyDefect in the transport due to protein

malnutrition –‘Kwashiorkar’Defect in the storage due to diseases of

liver

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.

OCULAR MANIFESTATIONS OF VITAMIN A DEFICIENCYXEROPHTHALMIA 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.

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

XN :NIGHT BLINDNESS(Nyctalopia)Earliest symptom of xerophthalmia in

childrenDiminished visual acuity in ‘dim

light’(Insufficient adaptation to darkness)Defective rhodopsin function.

•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.

X1A CONJUNCTIVAL XEROSISCharacterised by:One or more patches of dry,

lustreless,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 cryCan lead to conjunctival thickening,wrinkling and

pigmentation.

X1B BITOT’S SPOTSBilateralBulbar conjunctiva in the interpalpebral areaCommonly in temporal quadrant.Raised triangular greyish/silvery white spots/plaques.Firmly adherent to conjunctivaFoamy keratinised epithelium(corynebacterium

xerosis)

X2 CORNEAL XEROSISDry lustreless appearance of corneaEarliest change is punctate keratopathyBegins in the lower nasal quadrantBilateral punctate corneal epithelial erosions Can progress to epithelial defects Reversible on treatment

X3A & X3B CORNEAL ULCERATIONStromal 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.

Small ulcers 1-3mmOccur peripherallyCircularSteep margins and

sharply demarcated

Large ulcersMore than 3mmOccur centrallyInvolve entire cornea

XS CORNEAL SCARHealing of stromal defects results in corneal

scarringSize of the corneal scar depends on the size

and density of corneal defect.

XF XEROPHTHALMIC FUNDUSUncommon in occurenceTypical seed like lesionsWhitish/yellow in colourRaised lesionsScattered uniformly over fundusAt 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 involvementRespond to vitamin A therapy with scotoma disappearing

in 1-2 weeks and retinal lesions fading in 1-4 months

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 preparationDose – 1,00,000 IU(Half the oral dose)

PROPHYLAXIS AGAINST XEROPHTHALMIA1.Short term approach:

-Periodic administration of vitamin A supplements-WHO recommended,universal distribution schedule of vit A for

prevention is as follows:

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 child birth

- Other measures like nutritional education,social marketing, home or community garden programs and measures to improve food security.

HYPERVITAMINOSIS AIngestion of large amounts of preformed vitamin A from the diet,

supplement intake or medications;I.Acute:Single doses of >3,00,000 IUHeadache ,Blurred vision,nausea ,vomiting, drowsiness,irritability i.e

signs of raised ICP(Benign intracranial hypertension)Serum Vit A values-200-1000 IU/dlII.Chronic – long-term megadose; possible permanent damage ( >50,000 IU/day for several weeks)

Bone and muscle pain,Loss of appetite,Skin disordersHeadacheDry skinHair lossIncreased liver sizeManifestations reversible when vitamin A discontinued

DEFICIENCY OF VITAMIN B1{THIAMINE}

•Can result in Corneal anaesthesia•Conjunctival dystrophy•Corneal Dystrophy•Acute Retrobulbar neuritis

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

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

DEFICIENCY OF VITAMIN D

•It may be associated with Zonular Cataract•Papilledema•Increased lacrimation

VITAMIN EI.FUNCTIONS •Potent anti-oxidant•Prevents Age related macular degeneration (ARMD)

II.SOURCES•Broccoli •Carrot•Spinach•Fish

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

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

SELENIUMI.Helps in treating :•Retro-bulbar pain•Oedema•Grave’s disease

II.Sources:•Turkey•Brazel nuts•Tuna