Vitamin D insufficiency is more prevalent among African Americans (blacks) than other Americans and, in North America, most young, healthy blacks do not achieve optimal 25-hydroxyvitamin D [25(OH)D] concentrations at any time of year. This is primarily due to the fact that pigmentation reduces vitamin D production in the skin. Also, from about puberty and onward, median vitamin D intakes of American blacks are below recommended intakes in every age group, with or without the inclusion of vitamin D from supplements. (Harris, 2006)
It’s well known that African Americans have low levels of vitamin D in their blood. In fact, this seems to be generally true for humans of tropical origin. In a study from Hawaii, vitamin D status was assessed in healthy, visibly tanned young adults who averaged 22.4 hours per week of unprotected sun exposure. Yet 51% had levels below the current recommended minimum of 75 nmol/L (Binkley et al., 2007). In a study from south India, levels below 50 nmol/L were found in 44% of the men and 70% of the women. The subjects are described as “agricultural workers starting their day at 0800 and working outdoors until 1700 with their face, chest, back, legs, arms, and forearms exposed to sunlight” (Harinarayan et al., 2007). In a study from Saudi Arabia, levels below 25 nmol/L were found in respectively 35%, 45%, 53%, and 50% of normal male university students of Saudi, Jordanian, Egyptian, and other origins (Sedrani, 1984).
These low levels are usually blamed on the darker skin of tropical humans, i.e., melanin blocks the UV-B component of sunlight, which the skin needs to make vitamin D. Actually, dark skin is not a serious constraint on vitamin D production. While it is true that a single UV-B exposure of moderate intensity will produce less vitamin D in black skin than in white skin, this difference narrows with longer exposure times, since white skin cuts back vitamin D production after only 20 minutes in the sun (Holick, 1995). Even in England, where sunlight is relatively weak, Asian, West Indian, and European adolescents show similar increases in vitamin D levels during the spring and summer (Ellis et al., 1977).
Another possible reason why tropical humans make less vitamin D is that there is no need to build up a reserve for the winter, when this vitamin cannot be produced. In contrast, such a reserve is necessary in the temperate zone. This seasonal variation is shown by a study of Nebraskan men after a summer of landscaping, construction, farming, and recreation. Their mean vitamin D level was initially 122 nmol/L. By late winter, it had fallen to 74 nmol/L (Barger-Lux & Heaney, 2002). Tropical humans may thus produce less of this vitamin because their skin doesn’t have to ‘make hay while the sun shines.’ This adaptation would then persist in those groups, like African Americans, that now inhabit the temperate zone.
Whatever the reason for this lower rate of production, tropical humans seem to compensate by converting more vitamin D into its active form. Although a single UV-B exposure produces less vitamin D3 in black subjects than in whites, the difference narrows after liver hydroxylation to 25-OHD and disappears after kidney hydroxylation to 1,25-(OH)2D. The active form of vitamin D is thus kept at a constant level, regardless of skin color (Matsuoka et al., 1991, 1995).
Robins (2009) notes that nearly half of all African Americans are classified as vitamin-D deficient and yet show no signs of calcium deficiency, which would be a logical result of vitamin D deficiency. Indeed, they “have a lower prevalence of osteoporosis, a lower incidence of fractures and a higher bone mineral density than white Americans, who generally exhibit a much more favourable vitamin D status.” He also cites a survey of 232 black (East African) immigrant children in Melbourne, Australia, among whom 87% had levels below 50 nmol/L and 44% below 25 nmol/L. None had rickets—the usual sign of vitamin-D deficiency in children (McGillivray et al., 2007).
In short, low vitamin D levels seem to be normal for African Americans and nothing to worry about. Such contrary evidence, however, doesn’t deter the vitamin D worrywarts:
Despite their low 25(OH)D levels, blacks have lower rates of osteoporotic fractures. This may result in part from bone-protective adaptations that include an intestinal resistance to the actions of 1,25(OH)2D and a skeletal resistance to the actions of parathyroid hormone (PTH). However, these mechanisms may not fully mitigate the harmful skeletal effects of low 25(OH)D and elevated PTH in blacks, at least among older individuals. Furthermore, it is becoming increasingly apparent that vitamin D protects against other chronic conditions, including cardiovascular disease, diabetes, and some cancers, all of which are as prevalent or more prevalent among blacks than whites. Clinicians and educators should be encouraged to promote improved vitamin D status among blacks (and others) because of the low risk and low cost of vitamin D supplementation and its potentially broad health benefits. (Harris, 2006)
The National Institute of Health is now studying the benefits of giving African Americans mega-doses of vitamin D, in the hope of bringing their disease rates down to those of other Americans. "We're excited about the potential of vitamin D to reduce this health gap," says the study co-leader. "But it is important to get answers from clinical trials before recommending megadoses of this supplement." (see article)
Yes, it might be best to get a few answers first. Unfortunately, there are millions of people out there who are now taking mega-doses of vitamin D every day. The mass experiment has already begun and the results should be ready in a decade or so, particularly among African Americans.
But why wait? The same experiment was performed from the mid-1980s to 2009 on an African American. The results are now in …
Was MJ done in by the D men?
A local journalist recalled interviewing Michael Jackson three years ago and noted that this man, then in his mid-40s, had the withered look of someone much older—like a vieillard.
What was responsible? His repeated plastic surgeries? His starvation diet? His abuse of painkillers and tranquillizers? These are the usual suspects. In the shadows, however, lurks another suspect who will never be questioned.
Michael Jackson had probably been taking mega-doses of vitamin D. This regimen would have started when he began bleaching his skin in the mid-1980s to even out blotchy pigmentation due to vitiligo. Since this bleaching made his skin highly sensitive to UV light, his dermatologist told him to avoid the sun and use a parasol. At that point, his medical entourage would have recommended vitamin D supplements. How high a dose? We’ll probably never know, but there are certainly many doctors who recommend mega-doses for people who get no sun exposure.
Such a recommendation would have dovetailed nicely with Michael’s fondness for vitamins. A 2005 news release mentions vitamin therapy as part of his health program:
“He’s getting vitamin nutrients and supplements,” the source said.
This source would not elaborate on the type of supplements or the way in which they are being administered.
There is also an interview with his former producer Tarak Ben Ammar:
C'était un hypocondriaque et on savait jamais vraiment s'il était malade car il a été entouré de médecins charlatans qui vivaient de cette maladie, qui lui facturaient des milliers et des milliers de dollars de médicaments, de vitamines…
[He was a hypochondriac and one never really knew whether he was sick because he was surrounded by charlatan doctors who lived from this sickness, who billed him for thousands and thousands of dollars of medication, of vitamins …]
It’s known that Michael Jackson was receiving injections of the ‘Myers cocktail’ (a mix of vitamins and nutrients), but this mix doesn’t normally contain vitamin D. He was probably taking the vitamin in tablet form.
What effects can we expect from long-term use of vitamin D at high doses? Keep in mind that we are really talking about a hormone, not a vitamin. This hormone interacts with the chromosomes and will gradually shorten their telomeres if concentrations are either too low or too high. Tuohimaa (2009) argues that optimal levels may lie in the range of 40-60 nmol/L. This is well below the current recommended minimum of 75 nmol/L. Furthermore, compliance with this optimal range may matter even more for populations of tropical origin, like African Americans, since their bodies have not adapted to the wide seasonal variation of non-tropical humans.
If this optimal range is continually exceeded, the long-term effects may look like those of aging:
Recent studies using genetically modified mice, such as FGF23-/- and Klotho-/- mice that exhibit altered mineral homeostasis due to a high vitamin D activity showed features of premature aging that include retarded growth, osteoporosis, atherosclerosis, ectopic calcification, immunological deficiency, skin and general organ atrophy, hypogonadism and short lifespan.
… after the Second World War in Europe especially in Germany and DDR, children received extremely high oral doses of vitamin D and suffered hypercalcemia, early aging, cardiovascular complications and early death suggesting that hypervitaminosis D can accelerate aging. (Tuohimaa 2009)
Have we opened a Pandora’s box? Far from being a panacea, vitamin D could be an angel of death that will make millions of people old before their time.
Poor Michael. He looked to his doctors for eternal youth and they gave him premature old age.
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Binkley N, Novotny R, Krueger D, et al. (2007). Low vitamin D status despite abundant sun exposure. Journal of Clinical Endocrinology & Metabolism, 92, 2130 –2135.
Ellis, G., Woodhead, J.S., & Cooke, W.T. (1977). Serum-25-hydroxyvitamin-D concentrations in adolescent boys, Lancet, 1, 825-828.
Harinarayan, C.V., Ramalakshmi, T., Prasad, U.V., Sudhakar, D., Srinivasarao, P.V.L.N., Sarma, K.V.S., & Kumar, E.G.T. (2007). High prevalence of low dietary calcium, high phytate consumption, and vitamin D deficiency in healthy south Indians, American Journal of Clinical Nutrition, 85, 1062-1067.
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Holick, M.F. (1995). Noncalcemic actions of 1,25-dihydroxyvitamin D3 and clinical applications, Bone, 17, 107S-111S.
Matsuoka, L.Y., Wortsman, J., Chen, T.C., & Holick, M.F. (1995). Compensation for the interracial variance in the cutaneous synthesis of vitamin D, Journal of Laboratory and Clinical Medicine, 126, 452-457.
Matsuoka, L.Y., Wortsman, J., Haddad, J.G., Kolm, P., & Hollis, B.W. (1991). Racial pigmentation and the cutaneous synthesis of vitamin D. Archives of Dermatology, 127, 536-538.
McGillivray, G., Skull, S.A., Davie, G., Kofoed, S., Frydenberg, L., Rice, J., Cooke, R., & Carapetis, J.R. (2007). High prevalence of asymptomatic vitamin-D and iron deficiency in East African immigrant children and adolescents living in a temperate climate. Archives of Disease in Childhood, 92, 1088-1093.
Robins, A.H. (2009). The evolution of light skin color: role of vitamin D disputed, American Journal of Physical Anthropology, early view.
Sedrani, S.H. (1984). Low 25-hydroxyvitamin D and normal serum calcium concentrations in Saudi Arabia: Riyadh region, Annals of Nutrition & Metabolism, 28, 181-185.
Tuohimaa, P. (2009). Vitamin D and aging, Journal of Steroid Biochemistry and Molecular Biology, 114, 78-84.