Any recessive genetic characteristic that persists at a level as high as 5% is generally regarded as possibly having some advantage over the long term. In World War II it was discovered that analysis of color aerial photos yielded more information if at least one team member was color blind. Humans are the only trichromatic primates with such a high percentage of color blindness.
Another possible advantage might result from the presence of a tetrachromic female. Owing to X-chromosome inactivation, women who are heterozygous for anomalous trichromacy ought to have at least four types of cone in their retinae. It is possible that this affords them an extra dimension of color vision, by analogy to New World monkeys where heterozygous females gain trichromacy in a basically dichromatic species.
Genetic modes of inheritance
Color blindness can be inherited genetically. It is most commonly inherited from mutations on the X chromosome but the mapping of the human genome has shown there are many causative mutations – mutations capable of causing color blindness originate from at least 19 different chromosomes and many different genes (as shown online at the Online Mendelian Inheritance in Man (OMIM) database at Johns Hopkins University). These are some of the inherited diseases known to cause color blindness: Cone dystrophy, Cone-rod dystrophy, Achromatopsia (aka Rod Monochromatism, aka Stationery Cone Dystrophy, aka Cone Dysfunction Syndrome), Blue cone monochromatism, Retinitis pigmentosa (initially affects rods but can later progress to cones and therefore color blindness), Diabetes, Age-Related Macular degeneration, Retinoblastoma, and Leber's congenital amaurosis.
Inherited color blindness can be congenital (from birth), or it can commence in childhood or adulthood. Depending on the mutation, it can be stationary, that is, remain the same throughout a person's lifetime, or progressive. As progressive phenotypes involve deterioration of the retina and other parts of the eye, certain forms of color blindness can progress to legal blindness, i.e., an acuity of 6/60 or worse, and often leave a person with complete blindness.
Color blindness always pertains to the cone photoreceptors in retinas as the cones are capable of detecting the color frequencies of light.
About 5–8 percent of males, but less than 1 percent of females, are color blind in some way or another, whether it be one color, a color combination, or another mutation. The reason males are at a greater risk of inheriting an X linked mutation is because males only have one X chromosome (XY, with the Y chromosome being significantly shorter than the X chromosome), and females have two (XX); if a woman inherits a normal X chromosome in addition to the one which carries the mutation, she will not display the mutation. Men do not have a second X chromosome to override the chromosome which carries the mutation. If 5% of variants of a given gene are defective, the probability of a single copy being defective is 5%, but the probability that two copies are both defective is 0.05 × 0.05 = 0.0025, or just 0.25%.
Other causes of color blindness include Shaken Baby Syndrome (this can cause retina and brain damage and therefore can cause color blindness), accidents and other trauma (swelling of the brain in the occipital lobe), and UV damage to the retina (from not wearing appropriate protection). Most UV damage is caused during childhood and this form of retinal degeneration is the leading cause of blindness in the world. Damage often presents itself later on in life.
There are many types of color blindness. The most common are red-green hereditary (genetic) photoreceptor disorders, but it is also possible to acquire color blindness through damage to the retina, optic nerve, or higher brain areas. Higher brain areas implicated in color processing include the parvocellular pathway of the lateral geniculate nucleus of the thalamus, and visual area V4 of the visual cortex. Acquired color blindness is generally unlike the more typical genetic disorders. For example, it is possible to acquire color blindness only in a portion of the visual field but maintain normal color vision elsewhere. Some forms of acquired color blindness are reversible. Transient color blindness also occurs (very rarely) in the aura of some migraine sufferers.
The different kinds of inherited color blindness result from partial or complete loss of function of one or more of the different cone systems. When one cone system is compromised, dichromacy results. The most frequent forms of human color blindness result from problems with either the middle or long wavelength sensitive cone systems, and involve difficulties in discriminating reds, yellows, and greens from one another. They are collectively referred to as "red-green color blindness", though the term is an over-simplification and is somewhat misleading. Other forms of color blindness are much more rare. They include problems in discriminating blues from yellows, and the rarest forms of all, complete color blindness or ''monochromacy'', where one cannot distinguish any color from grey, as in a black-and-white movie or photograph.
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