The Myth of chronic Black Vitamin D deficiency

Eumelanin is essential for protection against UV radiation which causes skin cancer by damaging DNA. Black skin blocks out twice as much UV radiation as White skin. The melanocytes in black skin are more resistant to damage and also give more durable supplies of melanin.

Dark skin, which contains more eumelanin than fair skin is better protected against UV-induced damage, and eumelanin is thought to be superior to pheomelanin in its photoprotective properties. As discussed by Gloster and Neal melanin in Black skin is twice as effective compared to White skin in inhibiting UVB radiation from penetrating. While Black epidermis allows only 7.4% of UVB and 17.5% of UVA to penetrate, 24% UVB and 55% UVA passes through White skin. Further, melanosomes in dark skin are resistant to degradation by lysosomal enzymes, remain intact throughout the epidermal layers and form supranuclear caps in keratinocytes and melanocytes which contribute considerably to photoprotection against UV-induced damage. In contrast, in lightly pigmented skin, melanosomes are degraded and only persist as “melanin dust” in the suprabasal layers. This reduction of melanosomes in the upper epidermis is considered to be an important factor in carcinogenesis, as it compromises the photoprotection of the skin. Other important properties of eumelanin are its functions as a free radical scavenger and superoxide dismutase that reduce ROS.” (Brenner and Hearing, 2008:541-542)

The number of melanocytes in skin is about the same between ethnic groups. The differences are in the number, size and dispersal of melanosomes.

At the same time, the skin depends on UV light to synthesise vitamin D which is essential for healthy and strong bones. Vitamin D deficiency is associated with a number of problems, most notably weak bones. Because of this, a commonly-held belief is that people with darker skin struggle to get enough vitamin D from the minimal sunshine in the northern hemisphere. But this is problematic as the following demonstrates:

“Skin pigmentation influences the effectiveness of vitamin D3 synthesis in the skin as melanin absorbs UVB photons and competes for them with 7-dehydrocholesterol. However, available data about the relationship between solar UVR, skin pigmentation and vitamin D status show contradictory results. On the one hand, it was reported that skin pigmentation greatly reduces the UVR-mediated synthesis of vitamin D3 as those with Black skin require at least a 6-fold greater UVR dose to increase circulating levels of vitamin D3 than do those with White skin. It was also reported that many African Americans who live in northern parts of the US suffer severe vitamin D deficiencies in spite of supplementing foods with vitamin D. In contrast, Matsuoka found no difference in 1,25-(OH)2-vitamin D3 levels in the sera of different ethnic groups, although there was a significant association between skin color and vitamin D3 synthesis. This view was supported by Nelson et al. who reported that there is no difference in the disposition for calcium deficiency in dark-skinned compared to fair-skinned individuals and in that report they further emphasized that African women have the same bone mass as Caucasian women.” (Brenner and Hearing 2008:540-541)

In addition, studies show that black people have bones that have a stronger density and are at less of breaking (O’connor et al., 2003:263) which shouldn’t be the case if we are generally Vitamin D deficient.

Vitamin D plays a crucial role in calcium absorption


The key to understanding this apparently contradictory picture is to firstly recognise that the body needs to convert vitamin D into a different form before it can use it:

In the liver D2 and D3 become hydroxlyated at the 25-carbon position leading to the formation of the biochemically stable compound, 25-hydroxyvitamin D (25(OH)D). Even though 25(OH)D is used clinically as a marker of vitamin D sufficiency, it is not biologically active. To become biologically active, 25(OH)D must undergo a second hydrox-ylation by 1α-hydroxylase to form 1,25-dihydroxyvitamin D (1,25(OH)2D)” (O’connor et al. 2013:262)

Because levels of total 25-hydroxyvitamin D are consistently lower in black Americans than in white Americans, blacks are frequently classified as being vitamin D–deficient. In our study involving community-dwelling adults, we found that levels of vitamin D–binding protein are also lower in blacks, probably because of the high prevalence of a common genetic variant. Lower levels of vitamin D–binding protein in blacks appear to result in levels of bioavailable 25-hydroxyvitamin D that are equivalent to those in whites. These data, combined with previous data from our group, suggest that low total 25- hydroxyvitamin D levels do not uniformly indicate vitamin D deficiency and call into question routine supplementation in persons with low levels of both total 25-hydroxyvitamin D and vitamin D– binding protein who lack other traditional manifestations of this condition.” (Powe et al. 2013:7)

This is a great example of why it is important to factor in race and ethnicity into the study of the human body and medicine. If you simply take a 'race-blind' approach which assume that everybody is the same, you will inevitably come up with erroneous concepts and practices. The same biological indicator (in this case, circulating levels of 25(OH)D) can mean different things depending on the race/ethnicity of the person in question.


Brenner, M and Hearing, V. (2008). The Protective Role of Melanin Against UV Damage in Human Skin. Photochemistry and Photobiology, Volume 84 (3), pp.539-549. [Full text: accessed 21/08/18]

O’Connor, M. et al (2013). The Uncertain Significance of Low Vitamin D Levels in African Descent Populations: A Review of the Bone and Cardiometabolic Literature. Prog Cardiovasc Dis, Volume 56(3), pp.261–269 [Full text: accessed 22/08/18]

Powe, C. et al (2013). Vitamin D–Binding Protein and Vitamin D Status of Black Americans and White Americans. New England Journal of Medicine, Volume 369(21), pp.1991-2000. [Full text: accessed 21/08/18]


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