Vitamin-D deficiency rickets in Jamaican children.

Miller, Colin G.; Chutkan, Winston B

doi:10.1136/adc.51.3.214

Cited by 9 publications

(2 citation statements)

References 14 publications

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“…Congolese living in Belgium have much lower 25(OH)D levels compared to those in Africa or to native Belgians (M'Buyamba- Kabangu et al, 1987). Later studies contradict Robins's (2008) suggestion that Caribbean people do not have 25(OH)D deficiency in the UK (Hannam et al, 2004); it occurs even in Jamaica (Miller and Chutkan, 1976). Children of Pacific Islander ancestry compared to those of European ancestry living in New Zealand had much lower 25(OH)D status, with 56% exhibiting deficiency (Rockell et al, 2005).…”

Section: Questioning Cutaneous Vitamin D Production As a Mechanism Fomentioning

confidence: 86%

Vitamin D and the evolution of human depigmentation

Chaplin

Jablonski

2009

American J Phys Anthropol

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In his recent commentary, Robins (2009) disputed the role played by ultraviolet radiation (UVR), namely, the vitamin-D-producing wavelengths of ultraviolet B (UVB), in the evolution of human skin. He questioned the theory that reduced levels of pigmentation in human skin were selected to facilitate absorption of UVB. He provided evidence to support his idea that people can produce enough vitamin D in their skin, regardless of pigmentation, if they are not pursuing a modern lifestyle. He asserted that, within his framework, rickets was the only selective force that could have influenced the evolution of light pigmentation because other detrimental effects of vitamin D deficiency are unproven. As rickets is increased by industrialization, Robins concluded that ''. . . vitamin D status could not have constituted the fitness differential between lightly pigmented and darkly pigmented individuals at high latitudes that favored the evolutionary selection of the former' ' (Robins, 2009).In this article, we examine the current evidence for what has been termed the ''vitamin D theory,'' and highlight the importance of UVB penetration in the evolution of human skin. We begin with an overview of the solar processes involved in cutaneous vitamin D synthesis, followed by a discussion of causal arguments and causation in the context of the vitamin D theory, and conclude with a review of physiological mechanisms and their evolutionary significance. SOLAR PROCESSES OUT OF AFRICAThe emergence of the human lineage and of Homo sapiens both occurred in equatorial Africa. The solar regimes at the equator and within the tropics are very different from those outside of the tropics. Within the tropics, the sun is directly overhead twice each year and creates two annual peaks of solar radiation. The solar flux is more intense and less variable, and it exhibits a different mixture of wavelengths. Levels of serum vitamin D [25-hydroxyvitamin D or 25(OH)D] in the human body are highly dependent on solar processes because UVB initiates vitamin D production in the skin. The amount of UVB that reaches a human body at any particular location is determined by global and local atmospheric parameters, by the amount of reflection from the substrate, by the posture and amount and type of clothing worn, and by personal behavior.Humans living at the earth's surface manufacture previtamin D 3 in their skin directly from UVB, optimally at 297 nm, but up to wavelengths of 310-315 nm. This radiation transforms 7-dehydrocholesterol (7-DHC or pro-vitamin D 3 ) in the skin into pre-vitamin D 3 (precholecalciferol). Pre-vitamin D 3 is unstable and is transformed in the skin into vitamin D 3 (cholecalciferol or calciol) within hours (Holick, 1987(Holick, , 1995. Vitamin D 3 is itself biologically inactive, and exits the skin into the circulation bound to vitamin-D-binding protein. It is then converted into its biologically active form, 1,25(OH)2D, by two successive hydroxylation steps that take place in the liver and kidneys in the hours following UVB exposure...

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Section: Questioning Cutaneous Vitamin D Production As a Mechanism Fomentioning

confidence: 86%

Vitamin D and the evolution of human depigmentation

Chaplin

Jablonski

2009

American J Phys Anthropol

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“…132 Children in a rural area of Jamaica were also found to have rickets, and both dietary factors and limited sun exposure were thought to be relevant. 133 Around the 1990s, nutritional rickets experienced a 'wave' of resurgence and was increasingly reported from around North America in breastfed, (almost universally) darkly pigmented babies who received no supplemental vitamin D. Eighteen such children were reported from Washington, 134 three in Michigan, 135 nine from New Jersey, 136 four in New York, 137 19 mostly immigrant children without significant sun exposure in Toronto, 138 five in Alaska, 139 nine in Texas, 140 30 in North Carolina, 141 four in Arizona, 142 five in Georgia, 143 51 in Wisconsin, the 'dairy state', 144 and others elsewhere. 145 Almost without exception, the affected children were breastfed without receiving vitamin supplementation and were darkly pigmented (mostly black, some Hispanic, only rarely Caucasians); some were kept out of the sun for religious reasons, and a few had been weaned to restrictive diets.…”

Section: Rickets In North Americamentioning

confidence: 99%