Colour blindness in humans

Published: Last Edited:

This essay has been submitted by a student. This is not an example of the work written by our professional essay writers.


Colour blindness is an inherited condition that affects a small percentage of humans. To understand how colour blindness is possible, how we see colours in the first place must be explained.

As humans we see the world in a variety of different colours. This kind of colour vision is known as trichromacy, due to the fact that there are three wavelengths of light that can be perceived by the eye and mixed to provide a wider range of colours, much like mixing paints. This is due to the rods and cones present on the retina of our eyes. Rods and Cones are present in the retina in a random pattern making up a mosaic; S (short wavelength) cones are arranged randomly in the retina, absent in the fovea and are also sparse. M (medium) to L (long) ratio varies a lot in males with normal colour vision and they appear to have random distribution in the fovea (Deeb, 2006). Rods cells do not detect colour, however they are highly sensitive to changes in light and aid vision when light levels are low. Cone cells are less sensitive to light but are the cells which can detect colour, and because of trichromacy there are three different types of cone cell. Cones are named after the wavelength of light to which the pigments contained within them are sensitive too. They are therefore known as the L (long wavelength), M (medium wavelength) or S (short wavelength) cones (ISB, 2004). The L pigments are sensitive to light that has a wavelength of 700nm and detects red light. The M pigments are sensitive to light that has a wavelength of 546nm and detects green light. The S pigments are sensitive to light that has a wavelength of 436nm and detects blue light (Wilson, 2003) (Fig.1).

The eye only contains green, red and blue receptors. This does not explain how all the rest of the colours in the visible light spectrum can be seen. To enable us to see more colours, more than one cone is stimulated and the resulting signals mixed to simulate the actual colour of the object. For example, when we perceive yellow light the red and green cones are stimulated (Colour Therapy Healing, 2007). The colour is not perceived in the eye, merely detected. Even so, without processing by the brain, the stimulations would still not lead to colour vision. Different areas of the brain are used in the recognition and perception of colours. Perception of a particular colour also depends on the colours surrounding the item being identified (e.chalk, no date) (Fig. 2).

In the above picture all the grey dots in the middle of the squares are the same shade as can be seen from the following picture (Fig.3).

Colour Perception

Everyone's eyes are different, and may therefore contain different numbers of each particular cone cell. This may then lead to differences in the way each individual perceives a particular colour (HealthyEyes, no date). A rare condition that can only affect women may involve them having more cone cells on their retina than normal, meaning that they are tetrachromats and can differentiate between colours that look the same to ‘normal' trichromates (Roth, 2006). Another condition affecting colour vision is commonly called colour blindness.


Colour blindness is a condition which leads to a reduced ability to match or discriminate between colours in the long-wavelength spectrum (Wissinger and Sharpe, 1998). It is more likely to affect men than women, with 10% of men affected and 0.67% of women (Martini 2001). This is because colour blindness is a recessive condition carried on the X chromosome, meaning that for a female to be affected they need to have both X chromosomes with the recessive gene. As males only have one X chromosome, they only need one recessive gene to have the condition. In most cases, if a male has the condition, they inherited it from their mother; if a female has the condition then they inherited it from both their mother and father. If a female only has one recessive gene then they are said to be a carrier of the condition as they can pass the gene on to their children. If a male is colour blind they cannot pass the gene on to their sons, only their daughters. The genotypes can be shown by writing superscripted symbols next to the allele symbol. The genotypes then result in phenotypes, as illustrated in the table (Fig 5).



Normal Vision






X+X+ X+Xo

Red and green cone pigment genes co-localize on the X chromosome at Xq28 in a head to tail tandem array (Deeb, 2006) and are found between exons 2 - 5 (Nathans, 1999). Red-green deficiencies seem to be linked to red-green hybrid genes and structural rearrangements on gene Xq28. The different types of colour vision deficiencies are caused by the location of the hybrid gene. Protanopia and protanomaly are caused by a 5'red-3'green hybrid at the first position whereas deuteranopia and deuteranomaly are caused by a 5'green-3'red hybrid in the second position and a normal red gene. The severity of colour blindness experienced and determined from the composition of the hybrid gene present (Wissinger and Sharpe, 1998). The hybrid genes are able to form as the red and green pigment genes are very similar with only 15 amino acids different, with only 7 thought to be responsible for the differences in the peaks of absorbance in the cone pigments. The presence of a hybrid gene does not always show the phenotype for colour blindness as it depends on its location on the chromosome. Hybrid genes in the distal position do not have any effect of normal colour vision (Deeb, 2002).

The genes for Long and Medium pigments are OPN1LW (opsin 1 long wave) and OPNLW1MW (OPNLW middle wave). The arrangement of the genes on the X chromosome is 1 long wave pigment (red) followed by one or more medium (green) wave pigments (Deeb, 2002). The short gene pigment is OPN1SW and is found on chromosome 7 not on the X chromosome (Deeb, 2006).

A rare cause of colour blindness was found in 1 - 2% of Caucasian Northern Europeans and was due to a mutation in the gene, Cys203Arg, which means the proteins encoded are less stable (Deeb, 2006). Cones are thought to form S pigments which become altered into M or L pigments during development due to the presence of thyroid hormone (Deeb, 2006).


There are different types of colour blindness, the most common being Red-Green colour blindness. In reality, it is unlikely for a person to be able to see no colour at all, though it is possible and is called monochromacy (Reese, 2008). For this reason some people argue that the condition should not be called colour blindness, but colour vision deficiency (Archimedes' Lab, no date). The other types of colour vision deficiency (CVD) are called dichromacy, where one cone cell type is missing, and anomalous trichromacy, where all three cone types are present but at least one is altered in some way.

Dichromacy can be split into three varieties, protanopia, deuteranopia and tritanopia. Protanopia and deuteranopia are the defects which cause red-green colour vision deficiency. Protanopia and deuteranopia are the kinds more likely to occur in males than females. This can lead to problems distinguishing between yellows, greens, and reds but does not cause problems with blues and yellows. Protanopia is where the red cone has a loss of function and protanomaly is where it has an altered function (Deeb, 2002). Deuteranopia is where the green cone has a loss of function and deuteranomaly is where it has an altered function (Deeb, 2002). People with protanopia may be able to distinguish between green and red because green seems lighter than red. Tritanopia is blue-yellow CVD and is a lot rarer than red-green CVD; however it affects male and female in equal proportions. In this case people have trouble distinguishing between blues and yellows but have no problems with reds and greens. This means they often have fewer problems in everyday life.

In anomalous trichromacy people can distinguish between colours better than dichromats but not as well as true trichromats. Anomalous trichromats have an anomalous red or green hybrid pigment (Deeb, 2002). Anomalous trichromacy is also split into two varieties - protanomaly or deuteranomaly which are inherited in the same way as red-green dichromacy. This type of CVD can range from mild to severe, and in some cases be so mild that a person doesn't realise they have it. A third kind of anomalous trichromacy is tritanomaly but tends to be acquired more often than it is inherited (Reese, 2008). Tritanomaly is caused by weakened/mutated S cones and causes difficulties distinguishing blues and yellows (Flück, 2006).


Red-green colour blindness can be tested for using Ishihara test plates. These are special plates where a number is formed out of a series of coloured dots. These dots are then surrounded by a background of other coloured dots. Colour blind people will have trouble finding the number within the dots (Reese, 2008). In some cases, colour blind individuals will be able to identify patterns that people with ‘normal' colour vision will not be able to. Pseudoisochromatic plates were first invented in 1876 by Professor J Stilling from Strassburg. Professor Ishihara Shinobu from the Imperial University of Tokyo developed the famous testing plates, which then spread to the west and have been published in books. There are 5 groups of plates which help to decide which form of CVD a person has, group 1 can be seen by all (Fig. 7), group 2 shows differences between normal and colour blind individuals with colour blind people misreading the number present (Fig. 8), group 3 can only be seen by people with ‘normal' colour vision, group 4 should only be seen by people with CVD (Fig. 9) and group 5 differentiates between protanopia and deuteranopia (Fig.10) (The College of Optometrists, 2010). People with normal vision and all kinds of CVD should be able to see the number present on this plate.

It can be seen from these plates that people with red-green CVD have problems distinguishing colours, which can lead to problems in everyday life when having to decide on whether meat is properly cooked, whether fruit is ripe, whether clothes match or even as young children on deciding which crayon to pick to colour in water. CVD can mean that people cannot enter certain jobs, for example when entering arts or fashion. Individuals with CVD are also unable to fly in the Air Force, or some forms of engineering such as in the army (, no date). CVD can cause problems in science, for example when looking at cells and having to label different structures present (Fig. 11).


There is no cure for colour blindness. However pictures can be altered by a process called Daltonization which combines the processes of increasing the red-green contrast in pictures and changing variations of red and green to changes in brightness. The process is called Daltonization after John Dalton who was one of the first British Scientist to look into colour blindness (Vischeck, 2005). This process means that people with CVD can see the information present in pictures which would normally be invisible to them.

The pictures above give people with normal colour vision some idea of how it is to be colour blind (Fig. 12). A lot of the pictures available on the internet are not a true representation of colour blindness because differences between the colours in the two pictures can be seen, whereas in the pictures above the first two do not look any different to those with CVD. The differences in how the world is seen by those with normal colour vision and CVD were discovered and explained by people with both types of vision - where one eye has a CVD and the other eye is ‘normal'. This condition is extremely rare but allowed comparisons that would otherwise be impossible (Wasserman, 1978).

Colour vision in animals

In terms of humans not being able to see a ‘normal' colour spectrum is counted as colour vision deficiency, however for some other animals this is a normal state of vision. For example dogs and bulls, in human terms, would be considered colour vision deficient. Dogs see in mostly greys with some blues and yellows. Likewise bulls do not see in colour and they charge at the matador because the cape is moving not because it is red (Morton, 2008). Some animals such as primates also have trichromatic vision, but others, such as the insects' bees and butterflies can also see UV helping them to see the nectar on flowers. Birds and fish may also have good colour vision as they live and move in a relatively blue environment so need to identify food and potential predators against a blue background (Causes of colour, no date).


So in conclusion, it can be see that colour blindness, or more accurately colour vision deficiency can is not a ‘normal' state of vision for humans. However it is not necessarily an uncommon state of vision amongst other animals. The most common form of colour vision deficiency is red-green deficiency which is split further into protanopia - red deficiency, and deuteranopia - green deficiency. Colour vision deficiencies can lead to problems in everyday life, some which could cause illness - undercooking meat and others which are just embarrassing - wearing mismatched clothes. Colour vision deficiencies are most often an inherited condition but in some cases can be acquired. CVD cannot be cured, but pictures can be altered so all visual information is visible; this process is called Daltonizing, after the British scientist John Dalton who investigated his own colour vision deficiency.


ADELSON, E (no date). Colour Perception 2, illusion 1. [Online] Accessed 3 March 2010 at:

Archimedes' Laboratory (no date). Ishihara Color Blindness Test, All You Need To Know About Color Deficiency. [Online] Accessed 3 March 2010 at:

ARMSTRONG, W.P (no date). Color Blindness & Baldness in People. [Online] Accessed 3 March 2010 at:

Causes of Color (no date). What colors do animals see? [Online] Accessed 5 March 2010 at: (no date). Ishihara Test for Color Blindness. [Online] Accessed 3 March 2010 at: (no date). Living with Color Blindness. [Online] Accessed 3 March 2010 at:

Colour Therapy Healing. (2007). Colour Perception. [Online] Accessed 3 March 2010 at:

DEEB, S.S (2002). The molecular basis of dichromatic color vision in males with multiple red and green visual pigment genes. Human Molecular Genetics. Volume 11 (1), pages 23 - 32.

DEEB, S.S (2006). Genetics of variation in human color vision and the retinal cone mosaic. Current Opinion in Genetics & Development. Volume 16, pages 301 - 307.

DOUGHERTY, B. WADE, A. (2005). Color blind image correction. [Online] Accessed 3 March 2010 at:

e.chalk (no date). Colour Perception 2, illusion 4. [Online] Accessed 3 March 2010 at:

FLÜCK, D (2008). Probability of Color Blindness. [Online] Accessed 3 March 2010

FLÜCK, D (2006). Tritanopia - Blue-Yellow Color Blindness. [Online] Accessed 3 March 2010 at:

Institute of Structural Biology and Biophysics. (2004). [Online] Accessed 2 March 2010 at:

MARTINI, F.H. (2001). Fundamentals of Anatomy & Physiology, Chapter 17, Sensory Function, Vision, pg 555. 5th ed. Prentice Hall, New Jersey.

MORTON, J.L (2008). How Animals See Color. [Online] Accessed 5 March 2010 at:

mrothery (no date). Genetic Diagram [Online] Accessed 3 March 2010 at:

NATHANS, J (1999). The Evolution and Physiology of Human Color Vision: Insights from Molecular Genetic Studies of Visual Pigments. Neuron. Volume 24, page 305.

REESE, M (2008). Color Blindness. [Online] Accessed 3 March 2010 at:

ROTH, M (2006). Some women may see 100 million colors, thanks to their genes. [Online] Accessed 3 March at:

The College of Optometrists (2010) Ishihara & other Colour Vision Tests. [Online] Accessed 3 March 2010 at:

WASSERMAN, G.S. (1978). Color Vision: AN HISTORICAL INTRODUCTION, Color Blindness, pg.63. New York, John Wiley & Sons.

WILSON, D (2003). Color Vision, Color Deficiency. [Online] Accessed 2 March 2010 at:

WISSINGER, B. SHARPE, L.T. (1998). GENETICS OF PERCEPTION '98. New Aspects of an Old Theme: The Genetic Basis of Human Color Vision. The American Society of Human Genetics. Volume 63, pages 1257 - 1262.