Vitamin A Deficiency

Author: Fabio Finocchiaro
Date: 27/01/2013



Vitamin A deficiency is a lack of vitamin A in humans. Night blindness is one of the first signs of vitamin A deficiency. Xerophthalmia (medical condition in which the eye fails to produce tears), Keratomalacia (eye disorder that leads to a dry cornea), and complete blindness can also occur since Vitamin A has a major role in phototransduction

WikipediaVitamin A deficiency
The Diseases DatabaseVitamin A deficiency
MedScapeVitamin A deficiency


As a World Health Organization (WHO) research reveals people most likely to have Vitamin A deficiency are children under 5 years old and pregnant women in developing or poor countries.

Deficiency prevalence (%):

  • Africa
    • Children <5 years: 41,6
    • Pregnant women: 14,3
  • Asia
    • Children <5 years: 33,5
    • Pregnant women: 18,4
  • Global
    • Children <5 years: 33,3
    • Pregnant women: 15,3

The fact that global VAD has a 33% prevalence means that one third off under 5 years are likely to develop diseases.

Global prevalence of Vitamin A deficiency, WHO Report


  • Reduced night vision
  • Night blindness
  • Dry eyes (Keratomalacia, Xerophthalmia)
  • Eye inflammation
  • Corneal inflammation


  • Blood analysis: Vitamin A levels <0,35 umol/L
  • Functional indicator: night blindness
  • Biochemical indicators: serum retinol; breast-milk VitA; serum-rethinol binding protein,
  • Histological indicators: conjunctival impression citology (CIC); Impression citology with transfer (ICT)

Indicator for assessing Vitamin A deficiency, WHO Report


VAD affects vision by inhibiting the production of rhodopsin, the eye pigment responsible for sensing low light situations. Rhodopsin is found in the retina and is composed of retinal (an active form of vitamin A) and opsin (a protein). Because the body cannot create retinal in sufficient amounts, a diet low in vitamin A will lead to a decreased amount of rhodopsin in the eye, as there is inadequate retinal to bind with opsin. Night blindness results.

Night blindness caused by VAD has been associated with the loss of goblet cells in the conjunctiva, a membrane covering the outer surface of the eye. Goblet cells are responsible for secretion of mucus, and their absence results in xerophthalmia, a condition where the eyes fail to produce tears. Dead epithelial and microbial cells accumulate on the conjunctiva and form debris that can lead to infection and possibly blindness.

Rhodopsin consists of the protein moiety opsin and a reversibly covalently bound cofactor, retinal.
Isomerization of 11-cis-retinal into all-trans-retinal by light induces a conformational change (bleaching) in opsin, continuing with metarhodopsin II, which activates the associated G protein transducin and triggers a second messenger cascade.
Rods deal with low light level and do not mediate color vision. Rhodopsin of the rods is responsible for monochromatic vision in the dark.

It is clear that lack of Vitamin A interrupts this pathway as there is no retinal to be hit by light waves.

More about
Photoreceptor cell
Visual photorasduction


  • Pregnancy
  • Excessive alcohol consumption
  • Low fat absorption: Vitamin A is a fat soluble vitamin and depends on micellar solubilization for dispersion into the small intestine, which results in poor use of vitamin A from low-fat diets.
  • Zinc deficiency can also impair absorption, transport, and metabolism of vitamin A because it is essential for the synthesis of the vitamin A transport proteins and as the cofactor in conversion of retinol to retinal


Adequate supply, but not excess vitamin A, is especially important for pregnant and breastfeeding women for normal fetal development. Deficiencies cannot be compensated by postnatal supplementation. Excess vitamin A, which is most common with high dose vitamin supplements, can cause birth defects and therefore should not exceed recommended daily value.


Treatment of vitamin A deficiency can be undertaken with both oral and injectable forms, generally as vitamin A palmitate.

It was made up a genetic modified rice called Golden Rice: it was engineered to produce Vitamin A under form of beta-cartone and for that reason it has the reddish colour after which it is named. The probelm was due to absorption as the population needed to ingest fat as well to absorb the vitamin. Also patent and ethicalt problems came up so the idea was abandoned.

More about Golden rice

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