Vitamin D and homeostasis

In my previous posts, I argued that a homeostatic mechanism keeps the level of vitamin D in our bloodstream within a certain range. When UV-B light is always intense, as in the tropics, the level seems to be 50-75 nmol/L in young adults and progressively lower in older age groups. The more sunlight varies seasonally, the more the body will produce vitamin D in summer in order to maintain at least 50 nmol/L in winter—a level well below the recommended minimum of 75 nmol/L and even further below the 150 nmol/L now being advocated by vitamin-D proponents.

This homeostatic mechanism breaks down if we daily ingest 10,000 IU of vitamin D or more (Vieth, 1999). It seems that the human body has never naturally encountered such intakes, at least not on a continual basis.

In a recent review article, Robins (2009) presents evidence for a second homeostatic mechanism. Even when the level of vitamin D varies in the bloodstream, the second mechanism ensures that these divergent levels will translate into the same concentration of the biologically active 1,25-(OH)2D metabolite.

Matsuoka et al. (1991) demonstrated that after single-dose, whole-body UVB exposure black subjects had distinctly lower serum vitamin D3 levels than whites, but differences between the two groups narrowed after liver hydroxylation to 25-OHD and disappeared after kidney hydroxylation to 1,25-(OH)2D. These findings suggest that there is a compensatory mechanism whereby, in the presence of vitamin D3 suppression by melanin, the liver and kidney hydroxylating enzymes are activated in tandem to ensure that the concentration of the biologically active 1,25-(OH)2D metabolite is normalized and kept constant regardless of ethnic pigmentation (Matsuoka et al., 1991, 1995).

Robins (2009) goes on to note that nearly half of all African Americans are vitamin-D deficient but show no signs of calcium 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 (McGillivray et al., 2007).

References

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.

Vieth, R. (1999). Vitamin D supplementation, 25-hydroxyvitamin D concentrations, and safety, American Journal of Clinical Nutrition, 69, 842-856.