EyeTools_Question_of_the_Day_-_Video_(11)6.jpg

Welcome to question of the day #127

Eyetools question of the day #127

Vitamin A deficiency affects the cornea, conjunctiva and retina. Here I concentrate on the way it affects the retina.

A derivative of vitamin A is stored in the liver and is transported to the retinal pigment epithelium (RPE) through blood circulation when required.

This derivative of vitamin A is further processed in the RPE cells and eventually is transferred to rod photoreceptors where it plays a very important part in the chemical processes involved in generating an image in the brain. The chemical reactions which take place in the RPE and rods are known as the visual cycle.

Vitamin A deficiency has a direct effect on the ability of rod photoreceptors to function. Rod photoreceptors are specialised for vision in low light conditions and motion detection. It’s not surprising that vitamin A deficiency causes problems with poor vision at night or in dimly lit environments. This is also known as nyctalopia.

Although the term ‘night blindness’ implies no vision at all at night, this isn’t the case. People have difficulty seeing or driving in darkness but they are not blind.

The sole symptom of night blindness is difficulty seeing in the dark. People are more likely to experience night blindness when a person moves from a bright environment to an area of low light.

People who have pancreatic insufficiency, such as individuals with cystic fibrosis, have difficulty absorbing fat and are at a greater risk of having vitamin A deficiency because vitamin A is fat-soluble. This puts them at greater risk for developing night blindness.

Animal liver and dairy products are rich sources of vitamin A but this is of no use for those people who choose not to eat meat and other animal products.

The human body can produce vitamin A from carotenoids found in plants such as beta-carotene and alpha-carotene. These are collectively known as provitamin A. However, about 45% of people carry a genetic mutation that significantly reduces their ability to convert provitamin A into vitamin A. Vegetable sources of provitamin A are sweet potato, winter squash, kale and carrots. But people with the genetic mutation may still have vitamin A deficiency even if they consume these vegetables. Vitamin A supplements are useful for these people.