I am sure that you have either heard, seen or noticed about the existence of the special white animals on this earth.

White rabbit, white mouse, white hamster, white tiger are some examples of them.

But also there is some albinos that you may not know, among these albinos is white lion, white whale and more.

What?!!? WHITE LION!?!? Are you kidding mi?!

I think one of the reasons that we not know about this special animal is because we are Asians, if we are  Africans, we will surely know it.

Don't believe mi? Okay, look at these videos.

Here's some information about the cool white lion. (picked from wikipedia)

The white lion is occasionally found in wildlife reserves in South Africa and is a rare color mutation of the Kruger subspecies of lion (Panthera leo krugeri). It has been perpetuated by selective breeding in zoos around the world. White lions are not a separate subspecies and they have never been common in the wild. Regarded as divine by locals, white lions first came to public attention in the 1970s in Chris McBride's book The White Lions of Timbavati. The greatest population of white lions is in zoos where they are deliberately bred for color. The population of the white lion is unknown but the most recent count was in 2004 and 30 were alive. White lions are not albino lions. Instead, the white color is caused by a recessive gene known as chinchilla or color inhibitor. They vary from blonde through to near white, however some can also be red. This coloration gives white lions a distinct disadvantage in nature because they are highly visible. This gives them away to their prey and makes them an attractive target for hunters. According to Linda Tucker, in "Mystery of the White Lions - Children of the Sun God" they are bred in camps in South Africa as trophies for canned hunts.

The chinchilla mutation, a recessive gene, gives white lions their unusual colors. A similar gene also produces white tigers. White lions can therefore be selectively bred for zoos and animal shows. Such breeding involves inbreeding of close relatives and can result in inbreeding depression (genetic defects, reduced fertility, and physical defects) although this has not yet been recorded in white lions in zoos as it has in white tigers. According to Tucker, white lions in canned hunt camps have been found to have hind-limb paralysis and serious heart defects, indicating a severe level of inbreeding involved in mass-production although they are rare in the wild.People are concerned about the White Lions mating with regular lions.

White lions were first recorded in 1928 and in the early 1940s. In 1959, a pride with two white cubs was seen near Tshokwane in Kruger National Park, but later vanished. Albino lions had been recorded in the area according to David Alder ton's book "Wild Cats Of The World". In 1974, a light Grey lion cub was born at Birmingham Zoo, Alabama.

In 1975, two white cubs were seen at Timberland Game Reserve, adjacent to Kruger National Park. Their story is detailed by Chris McBride in his book "The White Lions of Timbavati". The two cubs, Temba (Zulu for "hope") and Tombi ("girl") had a tawny brother called Vela ('surprise'). In 1975, a white female cub called Phuma ("to be out of the ordinary") was sighted in the Timberland pride.

A few months later Temba, Tombi, and Vela (who carried the recessive white mutation) were taken to the National Zoo in Pretoria, South Africa. Temba sired several cubs. Tombi had a white cub in 1981, it was low in health but survived. Vela sired a litter, they grew up to be strong unusually one out of the 4 cubs was white while the rest were almost blonde. The white lions in the Ouwehands Dierenpark (Netherlands) and a private South African Zoo appear to be from Temba, or possibly Vela, lines. A few other white or blond cubs were born in Timberland after Temba, Tombi, and Vela were removed. Another white lion bloodline, possibly part of the Timbavati bloodline, comes from a white male captured in the Timberland area in the late 1980s and kept by a private reserve.

Temba has left descendants in captivity. A heterozygous tawny lion at Pretoria Zoo carries the mutation and most likely pass this on to his offspring. Two heterozygous tawny males from the Cincinnati Zoo are now at a private reserve in Africa. A white female and a heterozygous tawny male were sent to the Zoological Animal Reproduction Center in Indiana, USA. A second female was put together with another but didn't get along so they were separated for some time until they were comfortable in their surroundings.

In 1979, three litters containing white lions were recorded in Kruger National Park. In March, a female lion with three white cubs was observed near Tshokwane. In September, three white cubs (from two different lionesses) were seen. Another litter of white female cubs was captured from Kruger National Park and treated for sarcoptic mange. A white lion was od in the Hluhluwe-Umfolozi Game Reserve in Zululand.

People are worried that the White Lions will mate with regular Lions.

In May 2007 four white lion cubs were born at Jurques Zoo in France. The cubs consisted of one male and three females. Each cub weighed approximately 1.5 kilograms (3.3 pounds) at birth, and all four were in good health. However, they needed to be hand fed because their mother was not taking proper care of them.

White lions are not albinos but are leucistic. They have pigment visible in the eyes (which may be the normal hazel or golden color, blue-gray, or green-gray), paw pads and lips. Blue-eyed white lions exist and may be selectively bred. The leucistic trait is due to the chinchilla mutation that inhibits the deposition of pigment along the hair shaft, restricting it to the tips. The less pigment there is along the hair shaft, the paler the lion. As a result "white" lions range from blonde through to near white. The males have pale manes and tail tips instead of the usual dark tawny or black.

In 2003, the Global White Lion Protection Trust (WLT) initiated the first ever reintroduction of white lions to their natural endemic range - the Greater Timbavati region in South Africa. Preliminary results have shown that the hunting success of the white lion pride was comparable to or higher than the wild prides ('normal' coloured / tawny) of the Timbavati itself (Turner 2005, Turner in prep.). This pride of "all" white lions has shattered the misperception that white lions cannot hunt successfully (within their natural endemic habitat) due to a perceived lack of camouflage. The long-term objective of the WLT is to restore the natural balance by reintroducing an integrated pride/s of white and tawny lions within their endemic range. White lions are a unique contribution to the biodiversity of the region and are revered by the local communities that hold them sacred.

Oh ya.. just in case some of you don't know what is albinos that I've mentioned earlier, I paste some information about albinism below here. (reference from wikipedia)

Albinism (from Latin albus, "white"; see extended etymology, also called achromia, achromasia, or achromatosis) is a form of hypopigmentary congenital disorder, characterized by a partial (in hypomelanism, also known as hypomelanosis) or total (amelanism or amelanosis) lack of melanin pigment in the eyes, skin and hair, or more rarely in the eyes alone. Albinism results from inheritance of recessive alleles. The condition is known to affect mammals (including humans), fish, birds, reptiles and amphibians. While the most common term for an organism affected by albinism is "albino" (noun and adjective), the word is sometimes used in derogatory ways towards people; more neutral terms are "albinistic" (adjective) and "person with albinism" (noun). Additional clinical adjectives sometimes used to refer to animals are "albinoid" and "albinic".

It is not the same as leucism, where all integumental pigment is absent at least in patches but the eyes have their usual color.

Albinism is hereditary; it is not an infectious disease and cannot be transmitted through contact, blood transfusions, or other vectors. The principal gene which results in albinism prevents the body from making the usual amounts of the pigment melanin. Most forms of albinism are the result of the biological inheritance of genetically recessive alleles (genes) passed from both parents of an individual, though some rare forms are inherited from only one parent. There are other genetic mutations which are proven to be associated with albinism. All alterations, however, lead to changes in melanin production in the body.

Albinism was formerly categorized as tyrosinase-positive or -negative. In cases of tyrosinase-positive albinism, the enzyme tyrosinase is present. The melanocytes (pigment cells) are unable to produce melanin for any one of a variety of reasons that do not directly involve the tyrosinase enzyme. In tyrosinase-negative cases, either the tyrosinase enzyme is not produced or a nonfunctional version is produced. This classification has been rendered obsolete by recent research.

The chance of offspring with albinism resulting from the pairing of an organism with albinism and one without albinism is low, as discussed in more detail below. However, because organisms can be carriers of genes for albinism without exhibiting any traits, albinistic offspring can be produced by two non-albinistic parents. Albinism usually occurs with equal frequency in both genders. An exception to this is ocular albinism, because it is passed on to offspring through X-linked inheritance. Thus, males more frequently have ocular albinism as they do not have a second X chromosome.

Because organisms with albinism have skin that lacks (sufficiently or entirely) the dark pigment melanin, which helps protect the skin from ultraviolet radiation coming from the sun, they can sunburn easily from overexposure. (See human skin color for more information). Lack of melanin in the eye also results in problems with vision, related and unrelated to photosensitivity, which are discussed further below.

Most humans and many animals with albinism appear white or very pale; the multiple types of melanin pigment are responsible for brown, black, gray, and some yellow colorations. In some humans and animals there can be single a patch or patches of skin, displaying Albinism. Especially albinistic birds and reptiles, ruddy and yellow hues or other colors may be present on the entire body or in patches (as is common among pigeons), due to the presence of other pigments unaffected by albinism such as porphyrins, pteridines and psittacins, as well as carotenoid pigments derived from the diet. Some animals are white or pale due to chromatophore (pigment cell) defects, and do not lack melanin production, and have normal eyes; they are referred to as leucistic. The direct opposite of albinism, an unusually high level of melanin pigmentation (and sometimes absence of other types of pigment in species that have more than one), is known as melanism, and results in an appearance darker than non-melanistic specimens from the same genepool. Albinism-like conditions may affect other pigments or pigment-production mechanisms in some animals (e.g. "whiteface", a lack of psittacins that can affect some parrot species.). Another is common in reptiles and amphibians: axanthism, in which xanthophore metabolism, instead of synthesis of melanin, is affected, resuling in reduction or absence of red and yellow pteridine pigments. Of all these conditions, only albinism and melanism affect humans.

The eyes of an animal with albinism occasionally appear red due to the underlying retinal blood vessels showing through where there is not enough pigment to cover them. In humans this is rarely the case, as a human eye is quite large and thus produces enough pigment to lend opacity to the eye, often colouring the iris pale blue. However, there are cases in which the eyes of an albinistic person appear red or purple, depending on the amount of pigment present.

The albinistic are generally (but see related disorders below) as healthy as the rest of their species, with

growth and development occurring as normal, and albinism by itself does not cause mortality (though the lack of pigment is an elevated risk for skin cancer and other problems.) Many animals with albinism lack their protective camouflage and are unable to conceal themselves from their predators or prey; the survival rate of animals with albinism in the wild is usually quite low. However the novelty of albino animals has occasionally led to their protection by groups such as the Albino Squirrel Preservation Society.

Intentionally-bred albinistic strains of some animal species are commonly used as model organisms in biomedical study and experimentation. Examples include the BALB/c mouse and Wistar and Sprague Dawley rat strains, while albino rabbits were historically used for Draize toxicity testing. Albino axolotls, zebrafish, medaka and frogs are other common laboratory animals. The yellow mutation in fruit flies is their version of albinism.

The incidence of albinism can be artificially increased in fish by exposing the eggs to heavy metals.

About 1 in 17,000 human beings has some type of albinism, although up to 1 in 70 is a carrier of albinism genes.

There are two main categories of albinism in humans:

Other conditions include albinism as part of their presentation. These include Hermansky-Pudlak syndrome, Chediak-Higashi syndrome, Griscelli syndrome, Waardenburg syndrome, and Tietz syndrome. These conditions are sometimes classified with albinism. Several have sub-types. Some are easily distinguished by appearance, but in most cases genetic testing is the only way to be certain.

Genetic testing can confirm albinism and what variety it is, but offers no medical benefits except in the cases of non-OCA disorders (see below) that cause albinism along with other medical problems which may be treatable. The symptoms of albinism can be treated by various methods detailed below.

Eye conditions common in albinism may include:

Organisms with albinism usually have impaired vision due to one or more of the listed conditions. While a person with albinism may suffer from common refractive errors like nearsightedness or farsightedness, the visual problems particularly associated with albinism arise from a poorly-developed retinal pigment epithelium (RPE) due to the lack of melanin. This degenerate RPE causes foveal hypoplasia (a failure in the development of normal foveae), which results in eccentric fixation and lower visual acuity, and often a minor level of strabismus. Nystagmus is usually seen, as is photophobia or light sensitivity (see below).

The iris is a sphincter with pigmented tissue (which makes up the color of the eyes) that contracts to limit the amount of light that can enter through the pupil and relaxes again to allow for better vision in darkness. This mechanism can be observed in humans and mammals (like in cat's eyes) and is needed because too much light is uncomfortable or even painful and decreases vision. In people with albinism, the iris does not have enough pigment to block the light, thus the decrease of pupil diameter is only partially successful in reducing the amount of light that enters the eye. Additionally, the improper development of the RPE, which in normal eyes absorbs most of the reflected sunlight, further increases glare due to light scattering within the eye. The resulting sensitivity (photophobia) generally leads to a dislike of and discomfort in bright light, but does not prevent people with albinism enjoying the outdoors, especially when using sunglasses and/or brimmed hats.

The lack of pigment also makes the skin unusually sensitive to sunlight and thus susceptible to sunburn, so people with albinism should either avoid prolonged exposure to bright sunlight or protect their skin.

Albinism is a condition that cannot be "cured", but small things can be done to improve the quality of life for those affected. Most importantly to improve vision, protect the eyes from bright lights, and avoid skin damage from sunlight. The extent and success rate of these measures depend on the type of albinism and severity of the symptoms; in particular, people with ocular albinism are likely to have normally-pigmented skin, and thus do not need to take special precautions against skin damage.

For the most part, treatment of the eye conditions consists of visual rehabilitation. Surgery is possible on the ocular muscles to decrease nystagmus, strabismus and common refractive errors like astigmatism. Strabismus surgery may improve the appearance of the eyes. Nystagmus-damping surgery can also be performed, to reduce the "shaking" of the eyes back and forth. The effectiveness of all these procedures varies greatly and depends on individual circumstances. More importantly, since surgery will not restore a normal RPE or foveae, surgery will not provide fine binocular vision. In the case of esotropia (the "crossed eyes" form of strabismus), surgery may help vision by expanding the visual field (the area that the eyes can see while looking at one point).

Glasses and other vision aids, large-print materials and closed captioning, as well as bright but angled reading lights, can help individuals with albinism, even though their vision cannot be corrected completely. Some albinistic people do well using bifocals (with a strong reading lens), prescription reading glasses, and/or hand-held devices such as magnifiers or monoculars. Contact lenses may be colored to block light transmission through the iris. Some use bioptics, glasses which have small telescopes mounted on, in, or behind their regular lenses, so that they can look through either the regular lens or the telescope. Newer designs of bioptics use smaller light-weight lenses. Some US states allow the use of bioptic telescopes for driving motor vehicles. (See also NOAH bulletin "Low Vision Aids".)

Although still disputed among the experts, many ophthalmologists recommend the use of glasses from early childhood onward to allow the eyes the best development possible.

Optometrists or ophthalmologists who are experienced in working with low vision patients can recommend various optical aids. Some low-vision clinics provide these aids on trial loan, with instruction in their use.

It is vital that people with albinism use sunscreen when exposed to sunlight to prevent premature skin aging or skin cancer. This poses a problem for those who cannot afford sunscreen, especially in regions with high exposure to sunlight, as in Africa.

Use of sunglasses and hats with wide brims can make the glare outside bearable. Other things that can help people with albinism are avoiding sudden changes of the lighting situation (switching the light on in complete darkness), using dimmable switches and adding tint to car windows or blinds to normal windows. Lights should be yellowish rather than white and not point towards the usual position of a person with albinism (like their seat at a table).

While some of the very rare albinism disorders that are coupled with deafness and immunodeficiency, like Chediak-Higashi Syndrome, appear to be linked with inbreeding, the vast majority of sufferers of common albinism are not the product of such unions; the more usual albinism genes are widespread enough that they can easily produce albinistic offspring from parents that are not related.

A common misconception is that albinistic individuals of a species are sterile; they are in fact fully capable of reproducing. It is also thought by many that people with albinism live short life spans. This is not true in general, but may be a distorted view of a more reasonable fact that people with albinism have a higher risk of skin cancer if they do not use proper skin protection when in the sun. (Some very rare variants of albinism are lethal by adulthood or sooner, but they are so little-known by the general public that they are unlikely to have contributed to this belief.)

It has also been misunderstood that a person or other animal with albinism will become blind halfway through life; this is incorrect. Not all albinos are photophobic.

I am sure that you have either heard, seen or noticed about the existence of the special white animals on this earth.

White rabbit, white mouse, white hamster, white tiger are some examples of them.

But also there is some albinos that you may not know, among these albinos is white lion, white whale and more.

What?!!? WHITE LION!?!? Are you kidding mi?!

I think one of the reasons that we not know about this special animal is because we are Asians, if we are  Africans, we will surely know it.

Don't believe mi? Okay, look at these videos.

Here's some information about the cool white lion. (picked from wikipedia)

The white lion is occasionally found in wildlife reserves in South Africa and is a rare color mutation of the Kruger subspecies of lion (Panthera leo krugeri). It has been perpetuated by selective breeding in zoos around the world. White lions are not a separate subspecies and they have never been common in the wild. Regarded as divine by locals, white lions first came to public attention in the 1970s in Chris McBride's book The White Lions of Timbavati. The greatest population of white lions is in zoos where they are deliberately bred for color. The population of the white lion is unknown but the most recent count was in 2004 and 30 were alive. White lions are not albino lions. Instead, the white color is caused by a recessive gene known as chinchilla or color inhibitor. They vary from blonde through to near white, however some can also be red. This coloration gives white lions a distinct disadvantage in nature because they are highly visible. This gives them away to their prey and makes them an attractive target for hunters. According to Linda Tucker, in "Mystery of the White Lions - Children of the Sun God" they are bred in camps in South Africa as trophies for canned hunts.

The chinchilla mutation, a recessive gene, gives white lions their unusual colors. A similar gene also produces white tigers. White lions can therefore be selectively bred for zoos and animal shows. Such breeding involves inbreeding of close relatives and can result in inbreeding depression (genetic defects, reduced fertility, and physical defects) although this has not yet been recorded in white lions in zoos as it has in white tigers. According to Tucker, white lions in canned hunt camps have been found to have hind-limb paralysis and serious heart defects, indicating a severe level of inbreeding involved in mass-production although they are rare in the wild.People are concerned about the White Lions mating with regular lions.

White lions were first recorded in 1928 and in the early 1940s. In 1959, a pride with two white cubs was seen near Tshokwane in Kruger National Park, but later vanished. Albino lions had been recorded in the area according to David Alder ton's book "Wild Cats Of The World". In 1974, a light Grey lion cub was born at Birmingham Zoo, Alabama.

In 1975, two white cubs were seen at Timberland Game Reserve, adjacent to Kruger National Park. Their story is detailed by Chris McBride in his book "The White Lions of Timbavati". The two cubs, Temba (Zulu for "hope") and Tombi ("girl") had a tawny brother called Vela ('surprise'). In 1975, a white female cub called Phuma ("to be out of the ordinary") was sighted in the Timberland pride.

A few months later Temba, Tombi, and Vela (who carried the recessive white mutation) were taken to the National Zoo in Pretoria, South Africa. Temba sired several cubs. Tombi had a white cub in 1981, it was low in health but survived. Vela sired a litter, they grew up to be strong unusually one out of the 4 cubs was white while the rest were almost blonde. The white lions in the Ouwehands Dierenpark (Netherlands) and a private South African Zoo appear to be from Temba, or possibly Vela, lines. A few other white or blond cubs were born in Timberland after Temba, Tombi, and Vela were removed. Another white lion bloodline, possibly part of the Timbavati bloodline, comes from a white male captured in the Timberland area in the late 1980s and kept by a private reserve.

Temba has left descendants in captivity. A heterozygous tawny lion at Pretoria Zoo carries the mutation and most likely pass this on to his offspring. Two heterozygous tawny males from the Cincinnati Zoo are now at a private reserve in Africa. A white female and a heterozygous tawny male were sent to the Zoological Animal Reproduction Center in Indiana, USA. A second female was put together with another but didn't get along so they were separated for some time until they were comfortable in their surroundings.

In 1979, three litters containing white lions were recorded in Kruger National Park. In March, a female lion with three white cubs was observed near Tshokwane. In September, three white cubs (from two different lionesses) were seen. Another litter of white female cubs was captured from Kruger National Park and treated for sarcoptic mange. A white lion was od in the Hluhluwe-Umfolozi Game Reserve in Zululand.

People are worried that the White Lions will mate with regular Lions.

In May 2007 four white lion cubs were born at Jurques Zoo in France. The cubs consisted of one male and three females. Each cub weighed approximately 1.5 kilograms (3.3 pounds) at birth, and all four were in good health. However, they needed to be hand fed because their mother was not taking proper care of them.

White lions are not albinos but are leucistic. They have pigment visible in the eyes (which may be the normal hazel or golden color, blue-gray, or green-gray), paw pads and lips. Blue-eyed white lions exist and may be selectively bred. The leucistic trait is due to the chinchilla mutation that inhibits the deposition of pigment along the hair shaft, restricting it to the tips. The less pigment there is along the hair shaft, the paler the lion. As a result "white" lions range from blonde through to near white. The males have pale manes and tail tips instead of the usual dark tawny or black.

In 2003, the Global White Lion Protection Trust (WLT) initiated the first ever reintroduction of white lions to their natural endemic range - the Greater Timbavati region in South Africa. Preliminary results have shown that the hunting success of the white lion pride was comparable to or higher than the wild prides ('normal' coloured / tawny) of the Timbavati itself (Turner 2005, Turner in prep.). This pride of "all" white lions has shattered the misperception that white lions cannot hunt successfully (within their natural endemic habitat) due to a perceived lack of camouflage. The long-term objective of the WLT is to restore the natural balance by reintroducing an integrated pride/s of white and tawny lions within their endemic range. White lions are a unique contribution to the biodiversity of the region and are revered by the local communities that hold them sacred.

Oh ya.. just in case some of you don't know what is albinos that I've mentioned earlier, I paste some information about albinism below here. (reference from wikipedia)

Albinism (from Latin albus, "white"; see extended etymology, also called achromia, achromasia, or achromatosis) is a form of hypopigmentary congenital disorder, characterized by a partial (in hypomelanism, also known as hypomelanosis) or total (amelanism or amelanosis) lack of melanin pigment in the eyes, skin and hair, or more rarely in the eyes alone. Albinism results from inheritance of recessive alleles. The condition is known to affect mammals (including humans), fish, birds, reptiles and amphibians. While the most common term for an organism affected by albinism is "albino" (noun and adjective), the word is sometimes used in derogatory ways towards people; more neutral terms are "albinistic" (adjective) and "person with albinism" (noun). Additional clinical adjectives sometimes used to refer to animals are "albinoid" and "albinic".

It is not the same as leucism, where all integumental pigment is absent at least in patches but the eyes have their usual color.

Albinism is hereditary; it is not an infectious disease and cannot be transmitted through contact, blood transfusions, or other vectors. The principal gene which results in albinism prevents the body from making the usual amounts of the pigment melanin. Most forms of albinism are the result of the biological inheritance of genetically recessive alleles (genes) passed from both parents of an individual, though some rare forms are inherited from only one parent. There are other genetic mutations which are proven to be associated with albinism. All alterations, however, lead to changes in melanin production in the body.

Albinism was formerly categorized as tyrosinase-positive or -negative. In cases of tyrosinase-positive albinism, the enzyme tyrosinase is present. The melanocytes (pigment cells) are unable to produce melanin for any one of a variety of reasons that do not directly involve the tyrosinase enzyme. In tyrosinase-negative cases, either the tyrosinase enzyme is not produced or a nonfunctional version is produced. This classification has been rendered obsolete by recent research.

The chance of offspring with albinism resulting from the pairing of an organism with albinism and one without albinism is low, as discussed in more detail below. However, because organisms can be carriers of genes for albinism without exhibiting any traits, albinistic offspring can be produced by two non-albinistic parents. Albinism usually occurs with equal frequency in both genders. An exception to this is ocular albinism, because it is passed on to offspring through X-linked inheritance. Thus, males more frequently have ocular albinism as they do not have a second X chromosome.

Because organisms with albinism have skin that lacks (sufficiently or entirely) the dark pigment melanin, which helps protect the skin from ultraviolet radiation coming from the sun, they can sunburn easily from overexposure. (See human skin color for more information). Lack of melanin in the eye also results in problems with vision, related and unrelated to photosensitivity, which are discussed further below.

Most humans and many animals with albinism appear white or very pale; the multiple types of melanin pigment are responsible for brown, black, gray, and some yellow colorations. In some humans and animals there can be single a patch or patches of skin, displaying Albinism. Especially albinistic birds and reptiles, ruddy and yellow hues or other colors may be present on the entire body or in patches (as is common among pigeons), due to the presence of other pigments unaffected by albinism such as porphyrins, pteridines and psittacins, as well as carotenoid pigments derived from the diet. Some animals are white or pale due to chromatophore (pigment cell) defects, and do not lack melanin production, and have normal eyes; they are referred to as leucistic. The direct opposite of albinism, an unusually high level of melanin pigmentation (and sometimes absence of other types of pigment in species that have more than one), is known as melanism, and results in an appearance darker than non-melanistic specimens from the same genepool. Albinism-like conditions may affect other pigments or pigment-production mechanisms in some animals (e.g. "whiteface", a lack of psittacins that can affect some parrot species.). Another is common in reptiles and amphibians: axanthism, in which xanthophore metabolism, instead of synthesis of melanin, is affected, resuling in reduction or absence of red and yellow pteridine pigments. Of all these conditions, only albinism and melanism affect humans.

The eyes of an animal with albinism occasionally appear red due to the underlying retinal blood vessels showing through where there is not enough pigment to cover them. In humans this is rarely the case, as a human eye is quite large and thus produces enough pigment to lend opacity to the eye, often colouring the iris pale blue. However, there are cases in which the eyes of an albinistic person appear red or purple, depending on the amount of pigment present.

The albinistic are generally (but see related disorders below) as healthy as the rest of their species, with

growth and development occurring as normal, and albinism by itself does not cause mortality (though the lack of pigment is an elevated risk for skin cancer and other problems.) Many animals with albinism lack their protective camouflage and are unable to conceal themselves from their predators or prey; the survival rate of animals with albinism in the wild is usually quite low. However the novelty of albino animals has occasionally led to their protection by groups such as the Albino Squirrel Preservation Society.

Intentionally-bred albinistic strains of some animal species are commonly used as model organisms in biomedical study and experimentation. Examples include the BALB/c mouse and Wistar and Sprague Dawley rat strains, while albino rabbits were historically used for Draize toxicity testing. Albino axolotls, zebrafish, medaka and frogs are other common laboratory animals. The yellow mutation in fruit flies is their version of albinism.

The incidence of albinism can be artificially increased in fish by exposing the eggs to heavy metals.

About 1 in 17,000 human beings has some type of albinism, although up to 1 in 70 is a carrier of albinism genes.

There are two main categories of albinism in humans:

Other conditions include albinism as part of their presentation. These include Hermansky-Pudlak syndrome, Chediak-Higashi syndrome, Griscelli syndrome, Waardenburg syndrome, and Tietz syndrome. These conditions are sometimes classified with albinism. Several have sub-types. Some are easily distinguished by appearance, but in most cases genetic testing is the only way to be certain.

Genetic testing can confirm albinism and what variety it is, but offers no medical benefits except in the cases of non-OCA disorders (see below) that cause albinism along with other medical problems which may be treatable. The symptoms of albinism can be treated by various methods detailed below.

Eye conditions common in albinism may include:

Organisms with albinism usually have impaired vision due to one or more of the listed conditions. While a person with albinism may suffer from common refractive errors like nearsightedness or farsightedness, the visual problems particularly associated with albinism arise from a poorly-developed retinal pigment epithelium (RPE) due to the lack of melanin. This degenerate RPE causes foveal hypoplasia (a failure in the development of normal foveae), which results in eccentric fixation and lower visual acuity, and often a minor level of strabismus. Nystagmus is usually seen, as is photophobia or light sensitivity (see below).

The iris is a sphincter with pigmented tissue (which makes up the color of the eyes) that contracts to limit the amount of light that can enter through the pupil and relaxes again to allow for better vision in darkness. This mechanism can be observed in humans and mammals (like in cat's eyes) and is needed because too much light is uncomfortable or even painful and decreases vision. In people with albinism, the iris does not have enough pigment to block the light, thus the decrease of pupil diameter is only partially successful in reducing the amount of light that enters the eye. Additionally, the improper development of the RPE, which in normal eyes absorbs most of the reflected sunlight, further increases glare due to light scattering within the eye. The resulting sensitivity (photophobia) generally leads to a dislike of and discomfort in bright light, but does not prevent people with albinism enjoying the outdoors, especially when using sunglasses and/or brimmed hats.

The lack of pigment also makes the skin unusually sensitive to sunlight and thus susceptible to sunburn, so people with albinism should either avoid prolonged exposure to bright sunlight or protect their skin.

Albinism is a condition that cannot be "cured", but small things can be done to improve the quality of life for those affected. Most importantly to improve vision, protect the eyes from bright lights, and avoid skin damage from sunlight. The extent and success rate of these measures depend on the type of albinism and severity of the symptoms; in particular, people with ocular albinism are likely to have normally-pigmented skin, and thus do not need to take special precautions against skin damage.

For the most part, treatment of the eye conditions consists of visual rehabilitation. Surgery is possible on the ocular muscles to decrease nystagmus, strabismus and common refractive errors like astigmatism. Strabismus surgery may improve the appearance of the eyes. Nystagmus-damping surgery can also be performed, to reduce the "shaking" of the eyes back and forth. The effectiveness of all these procedures varies greatly and depends on individual circumstances. More importantly, since surgery will not restore a normal RPE or foveae, surgery will not provide fine binocular vision. In the case of esotropia (the "crossed eyes" form of strabismus), surgery may help vision by expanding the visual field (the area that the eyes can see while looking at one point).

Glasses and other vision aids, large-print materials and closed captioning, as well as bright but angled reading lights, can help individuals with albinism, even though their vision cannot be corrected completely. Some albinistic people do well using bifocals (with a strong reading lens), prescription reading glasses, and/or hand-held devices such as magnifiers or monoculars. Contact lenses may be colored to block light transmission through the iris. Some use bioptics, glasses which have small telescopes mounted on, in, or behind their regular lenses, so that they can look through either the regular lens or the telescope. Newer designs of bioptics use smaller light-weight lenses. Some US states allow the use of bioptic telescopes for driving motor vehicles. (See also NOAH bulletin "Low Vision Aids".)

Although still disputed among the experts, many ophthalmologists recommend the use of glasses from early childhood onward to allow the eyes the best development possible.

Optometrists or ophthalmologists who are experienced in working with low vision patients can recommend various optical aids. Some low-vision clinics provide these aids on trial loan, with instruction in their use.

It is vital that people with albinism use sunscreen when exposed to sunlight to prevent premature skin aging or skin cancer. This poses a problem for those who cannot afford sunscreen, especially in regions with high exposure to sunlight, as in Africa.

Use of sunglasses and hats with wide brims can make the glare outside bearable. Other things that can help people with albinism are avoiding sudden changes of the lighting situation (switching the light on in complete darkness), using dimmable switches and adding tint to car windows or blinds to normal windows. Lights should be yellowish rather than white and not point towards the usual position of a person with albinism (like their seat at a table).

While some of the very rare albinism disorders that are coupled with deafness and immunodeficiency, like Chediak-Higashi Syndrome, appear to be linked with inbreeding, the vast majority of sufferers of common albinism are not the product of such unions; the more usual albinism genes are widespread enough that they can easily produce albinistic offspring from parents that are not related.

A common misconception is that albinistic individuals of a species are sterile; they are in fact fully capable of reproducing. It is also thought by many that people with albinism live short life spans. This is not true in general, but may be a distorted view of a more reasonable fact that people with albinism have a higher risk of skin cancer if they do not use proper skin protection when in the sun. (Some very rare variants of albinism are lethal by adulthood or sooner, but they are so little-known by the general public that they are unlikely to have contributed to this belief.)

It has also been misunderstood that a person or other animal with albinism will become blind halfway through life; this is incorrect. Not all albinos are photophobic.