Colour vision deficiency, commonly known as colour blindness, is a condition when people have difficulty identifying various shades of colours or cannot recognize colours at all.
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It is mostly caused by genes and it varies among sexes and races. While eight percent of Caucasian men have problems with red and green colour, only 0.5 percent of women have the same problem. The disorder is less common in Asia and Africa, but there are communities like Pingelap island where 10 percent of the population have that disorder. The complete colour blindness, achromatopsia, affects 1 in 40.000 people.
The retina is the part of the eye that is sensitive to light and deals with colours. In the retina there are rods and cones, two types of structures with different tasks: rods allow us to see in low light, while cones help us to see colours and details. Those structures contain chemicals sensitive to light: rods contain rhodopsin, cones contain photopigments. There are three kinds of cones and each of them is sensitive to a different wavelength of light. Because of those three types the normal vision is called trichromatic. People may have a range of problems regarding to colours, from mild to severe difficulties.
Those with a mild colour vision defect have anomalous trichromacy. That means that those people have all three types of cones but one of them is not functioning properly. There are people with deuteranomaly which have problems with the red cones, those with protanomaly have problems with green, and the rarest anomaly is called tritanomaly which causes problems with blue and yellow colour.
In the case of deuteranopia the red colour doesn't exist it appears greenish-gray, the purple is not there too, and green looks grayish. People with protanopia see very similar pictures as those with deuteranopia, except the red colour looks dark gray. In the case of tritanopia the yellow looks like pink, the orange doesn't exist, the blue is also changed, and everything is in shades of pink and blue.
The problem with red and green is linked to sex because that disorder is carried on the X chromosome. Since man has X and Y chromosome, if X carries the disorder his offspring will have the disorder. Since woman has two X chromosomes she needs both of them to be defective to get the colour vision deficiency. Some diseases can also cause problems with colour vision and those are diabetes, glaucoma, Alzheimer's, Parkinson's, alcoholism, leukaemia and multiple sclerosis.
Besides the people with defective cones, there are also people who have a missing cone. Those people have so called dichromatic vision, and there are three different types of it. When there are no green cones that condition is called deuteranopia, when there are no red cones that are protanopia, and people with no blue cones have tritanopia.
The most severe type of colour vision deficiency is monochromacy, a disorder which causes the complete absence of colours and people with that disorder see only white, black and shades of gray. There are two types of this disorder: rod monochromacy and cone monochromacy. Those who have rod monochromacy, or achromatopsia, along with defining colours problem, also have poor vision and are highly sensitive to light.
The colour vision deficiency can be detected with several tests. The well-known test is Ishihara plates and pseudoisochromatic plates (PIP). Those plates show the pictures made of colour dots with numbers in the middle. It's not a perfect test because it depends on the amount of light. Another test, mostly used in army, is Farnsworth Lantern test (FALANT). Two lights are shown at the same time and person must identify the colour which is the result of mixing of those two lights. Those lights are darkened so the person can't tell the colour by the brightness. Those two tests are used together to get more precisely result, which is important in certain professions such as flight control.
Since the cause of colour blindness lies in genes and today gene therapy is virtually nonexistent, colour vision deficiency is not a treatable condition. ■