page_title: Color blindness
section_title: Red–green color blindness
hierarchical_section_title: Color blindness / Diagnosis / Classification / Red–green color blindness
caption_attribution_description: English: Illustration of the distribution of cone cells in the fovea of a individual with normal color vision (left), and a color blind (protanopic) retina. Note that the center of the fovea holds very few blue-sensitive cones.
context_page_description: Color blindness, also known as color vision deficiency, is the decreased ability to see color or differences in color. Simple tasks such as selecting ripe fruit, choosing clothing, and reading traffic lights can be more challenging. Color blindness may also make some educational activities more difficult. However, problems are generally minor, and most people find that they can adapt. People with total color blindness may also have decreased visual acuity and be uncomfortable in bright environments.
  The most common cause of color blindness is an inherited problem in the development of one or more of the three sets of color-sensing cones in the eye. Males are more likely to be color blind than females, as the genes responsible for the most common forms of color blindness are on the X chromosome. As females have two X chromosomes, a defect in one is typically compensated for by the other, therefore non-colorblind females can still be carriers. Males only have one X chromosome and therefore always express the genetic disorder when possessing the recessive gene. Color blindness can also result from physical or chemical damage to the eye, optic nerve or parts of the brain.
context_section_description: Protanopia, deuteranopia, protanomaly, and deuteranomaly are commonly inherited forms of red–green color blindness which affect a substantial portion of the human population. Those affected have difficulty with discriminating red and green hues due to the absence or mutation of the red or green retinal photoreceptors. It is sex-linked: genetic red–green color blindness affects males much more often than females, because the genes for the red and green color receptors are located on the X chromosome, of which males have only one and females have two. Females (XX) are red–green color blind only if both their X chromosomes are defective with a similar deficiency, whereas males (XY) are color blind if their single X chromosome is defective.
  The gene for red–green color blindness is transmitted from a color blind male to all his daughters, who are usually heterozygote carriers and are thus unaffected. In turn, a carrier woman has a 50% chance of passing on a mutated X chromosome region to each of her male offspring. The sons of an affected male will not inherit the trait from him, since they receive his Y chromosome and not his (defective) X chromosome. Should an affected male have children with a carrier or colorblind woman, their daughters may be colorblind by inheriting an affected X chromosome from each parent.
  Because one X chromosome is inactivated at random in each cell during a woman's development, deuteranomalous heterozygotes (i.e. female carriers of deuteranomaly) may be tetrachromats, because they will have the normal long wave (red) receptors, the normal medium wave (green) receptors, the abnormal medium wave (deuteranomalous) receptors and the normal autosomal short wave (blue) receptors in their retinas. The same applies to the carriers of protanomaly (who have two types of long wave receptors, normal medium wave receptors, and normal autosomal short wave receptors in their retinas). If, by rare chance, a woman is heterozygous for both protanomaly and deuteranomaly, she could be pentachromatic. This situation could arise if, for instance, she inherited the X chromosome with the abnormal long wave gene (but normal medium wave gene) from her mother who is a carrier of protanomaly, and her other X chromosome from a deuteranomalous father. Such a woman would have a normal and an abnormal long wave receptor, a normal and abnormal medium wave receptor, and a normal autosomal short wave receptor—5 different types of color receptors in all. The degree to which women who are carriers of either protanomaly or deuteranomaly are demonstrably tetrachromatic and require a mixture of four spectral lights to match an arbitrary light is very variable. In many cases it is almost unnoticeable, but in a minority the tetrachromacy is very pronounced. However, Jameson et al. have shown that with appropriate and sufficiently sensitive equipment it can be demonstrated that any female carrier of red–green color blindness (i.e. heterozygous protanomaly, or heterozygous deuteranomaly) is a tetrachromat to a greater or lesser extent.  People in whom deuteranopia or deuteranomaly manifest are sometimes referred to as deutans, those with protanopia or protanomaly as protans.
  Since deuteranomaly is by far the most common form of red–green blindness among men of northwestern European descent (with an incidence of 8%) it follows that the proportion of carriers (and of potential deuteranomalous tetrachromats) among the females of that genetic stock is 14.7% (i.e. 92% × 8% × 2), based on the Hardy–Weinberg principle.
  Protanopia (1% of males): Lacking the red cones for long-wavelength sensitive retinal cones, those with this condition are unable to distinguish between colors in the green–yellow–red section of the spectrum. They have a neutral point at a cyan-like wavelength around 492 nm (see spectral color for comparison)—that is, they cannot discriminate light of this wavelength from white. For a protanope, the brightness of red, orange, and yellow are much reduced compared to normal. This dimming can be so pronounced that reds may be confused 
caption: Illustration of the distribution of cone cells in the fovea of an individual with normal color vision (left), and a color blind (protanopic) retina. The center of the fovea holds very few blue-sensitive cones.
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