Amelanism (also known as amelanosis) is a pigmentation abnormality characterized by the lack of pigments called melanins, commonly associated with a genetic loss of tyrosinase function. Amelanism can affect fish, amphibians, reptiles, birds, and mammals including humans. The appearance of an amelanistic animal depends on the remaining non-melanin pigments. The opposite of amelanism is melanism, a higher percentage of melanin.

A similar condition, albinism, is a hereditary condition characterised in animals by the absence of pigment in the eyes, skin, hair, scales, feathers or cuticle. This results in an all white animal, usually with pink or red eyes.

Melanism is a development of the dark-colored pigment melanin in the skin or its appendages and is the opposite of albinism. The word "melanism" is derived from the ("black pigment").

Pseudo-melanism, also called abundism, is another variant of pigmentation, characterized by dark spots or enlarged stripes, which cover a large part of the body of the animal, making it appear melanistic.

A deficiency in or total absence of melanin pigments is called amelanism.

The morbid deposition of black matter, often of a malignant character causing pigmented tumors, is called melanosis. For a description of melanin-related disorders, see melanin and ocular melanosis.

In humans, there are two principal types of albinism: oculocutaneous, affecting the eyes, skin and hair, and ocular affecting the eyes only.

There are different types of oculocutaneous albinism depending on which gene has undergone mutation. With some there is no pigment at all. The other end of the spectrum of albinism is "a form of albinism called rufous oculocutaneous albinism, which usually affects dark-skinned people".

According to the National Organization for Albinism and Hypopigmentation, "With ocular albinism, the color of the iris of the eye may vary from blue to green or even brown, and sometimes darkens with age. However, when an eye doctor examines the eye by shining a light from the side of the eye, the light shines back through the iris since very little pigment is present."

Because individuals with albinism have skin that entirely lacks the dark pigment melanin, which helps protect the skin from the sun's ultraviolet radiation, their skin can burn more easily from overexposure.

The human eye normally produces enough pigment to color the iris blue, green or brown and lend opacity to the eye. In photographs, those with albinism are more likely to demonstrate "red eye", due to the red of retina being visible through the iris. Lack of pigment in the eyes also results in problems with vision, both related and unrelated to photosensitivity.

Those afflicted with albinism are generally as healthy as the rest of the population (but see related disorders below), with growth and development occurring as normal, and albinism by itself does not cause mortality, although the lack of pigment blocking ultraviolet radiation increases the risk of melanomas (skin cancers) and other problems.

Development of the optical system is highly dependent on the presence of melanin. For this reason, the reduction or absence of this pigment in people with albinism may lead to:

- Misrouting of the retinogeniculate projections, resulting in abnormal decussation (crossing) of optic nerve fibres

- Photophobia and decreased visual acuity due to light scattering within the eye (ocular straylight) Photophobia is specifically when light enters the eye, unrestricted—with full force. It is painful and causes extreme sensitivity to light.

- Reduced visual acuity due to foveal hypoplasia and possibly light-induced retinal damage.

Eye conditions common in albinism include:

- Nystagmus, irregular rapid movement of the eyes back and forth, or in circular motion.

- Amblyopia, decrease in acuity of one or both eyes due to poor transmission to the brain, often due to other conditions such as strabismus.

- Optic nerve hypoplasia, underdevelopment of the optic nerve.

The improper development of the retinal pigment epithelium (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 discomfort in bright light, but this can be reduced by the use of sunglasses or brimmed hats.

Melanism, meaning a mutation that results in completely dark skin, does not exist in humans. Melanin is the primary determinant of the degree of skin pigmentation and protects the body from harmful ultraviolet radiation. The same ultraviolet radiation is essential for the synthesis of vitamin D in skin, so lighter color of skin - less melanin - is an adaptation for the prehistoric movement of humans away from equatorial regions, as there is less exposure to sunlight at higher latitudes. People from parts of Africa have very dark skin, but this is not melanism.

Melanocytes depend on the Melanocortin 1 receptor (MC1R) to signal the production of eumelanin. Loss of melanocortin 1 receptor function or high activity of the MC1R-antagonist, Agouti signalling peptide, can cause the widespread absence of eumelanin. Loss of MC1R function, a recessive trait, has been observed in many species. In humans, various mutations of the "MC1R" gene result in red hair, blond hair, fair skin, and susceptibility to sundamaged skin and melanoma. Aeumelanic hair coats, associated with mutations of the "MC1R" gene, have also been identified in mice, cattle, dogs, and horses. These coat colors are called "yellow" in mice and dogs, "red" in cattle and chestnut in horses. The loss of eumelanin in the coat is, in these species, harmless. The distinction between aeumelanism and hyperphaeomelanism – over abundance of phaeomelanin – is semantic.