Latest Insights into Skin Hyperpigmentation


Exposure to sun

Melanin in the skin protects the body by absorbing solar radiation. In general, the more melanin there is in the skin the more solar radiation can be absorbed. Excessive solar radiation causes direct and indirect DNA damage to the skin and the body naturally combats and seeks to repair the damage and protect the skin by creating and releasing further melanin into the skin's cells. With the production of the melanin, the skin color darkens or red blotches, but can also cause sunburn. The tanning process can also be created by artificial UV radiation.

There are two different mechanisms involved. Firstly, the UVA-radiation creates oxidative stress, which in turn oxidises existing melanin and leads to rapid redness or darkening of the melanin. Secondly, there is an increase in production of melanin (melanogenesis). Melanogenesis leads to delayed tanning and first becomes visible about 72 hours after exposure. The tan that is created by an increased melanogenesis lasts much longer than the one that is caused by oxidation of existing melanin.

A person's natural skin color has an impact on their reaction to exposure to the sun. The tone of human skin can vary from a dark brown to a nearly colorless pigmentation, which may appear reddish due to the blood in the skin. Europeans generally have lighter skin, hair, and eyes than any other group, although this is not always the case. Africans generally have darker skin, hair, and eyes, although this too is not universal.

Dark skin with large concentrations of melanin protects against exposure to ultraviolet light and skin cancers; light-skinned people have about a tenfold greater risk of skin cancer, compared with dark-skinned persons, under equal sunlight exposure. Furthermore, UV-A rays from sunlight are believed to interact with folic acid in ways which may damage health.

While dark skin offers better protection from intense ultraviolet light, it may be result in low vitamin D levels and has led to concern that darker skinned people living at relatively high latitude, such as African Americans, may have inadequate vitamin D levels. Research shows that dark-skinned people living in Western societies have lower vitamin D levels. The explanation for low vitamin D levels in dark-skinned people is thought to be that melanin in the skin hinders vitamin D synthesis. However, recent studies have found novel evidence that low vitamin D levels among people of African ancestry may be due to other reasons, such as that black women have an increase in serum parathyroid hormone – implicated in adverse cardiovascular outcomes – at a lower vitamin D level than white women. In a large scale association study of the genetic determinants of vitamin D insufficiency in Caucasians no links to pigmentation were found.


This hyperpigmentary disorder occurs typically as symmetrical lesions on the face, primarily in darker skin type females at puberty or later in life. Sunlight exposure is probably a factor in the development of melasma, as it occurs on the face (a sun-exposed body site) and as the condition worsens in the summer. Most melasma sufferers have a hypersensitivity to UV radiation, that is, they display a lower minimum erythemal dose, and even brief exposures to sunlight can stimulate hyperpigmentation. There is also a hormonal component, likely progesterone, as episodes of melasma are often associated with pregnancy and the use of hormonal birth control. In melasma lesions, there is excess melanin present in both the epidermis and upper dermis (associated with extravascular macrophages). As there is only a slight increase in number of melanocytes, the abnormality appears to be in function of the skin cells, in particular increased expression of -melanocyte-stimulating hormone in keratinocytes and overexpression of stem cell factor in fibroblasts of the involved skin (Imokawa, 2004, 2006; Kang et al., 2006). Additionally, there is more likely a genetic component that predisposes individuals to melasma, although the specific genetic basis for it is not defined.

A classic target is inhibition of tyrosinase, the first enzyme in the conversion of tyrosine to melanin. Agents such as mulbery, kojic acid, arbutin, ascorbic acid, bearberry extract and licorice are effective in interfering with this process. However, as several of these materials also have other effects, their mechanism to the observed effect on pigmentation have been exploit into our formulation. For example, licorice and hyaluronic compounds are also effective antioxidants. Overviews a short list of the many possible targets and a few agents effective against skin aging.


Article written by

Jean-Paul Ortonne and Donald L Bissett