Nina G. Jablonski ngi2 at psu.edu
George Chaplin
Department of Anthropology, The Pennsylvania State University, 409 Carpenter Building, University Park, PA 16802, USA
Phil. Trans. R. Soc. B 19 March 2012 vol. 367 no. 1590 785-792
Human skin pigmentation evolved as a compromise between the conflicting physiological demands of protection against the deleterious effects of ultraviolet radiation (UVR) and photosynthesis of UVB-dependent vitamin D3.
Living under high UVR near the equator, ancestral Homo sapiens had skin rich in protective eumelanin.
Dispersals outside of the tropics were associated with positive selection for depigmentation to maximize cutaneous biosynthesis of pre-vitamin D3 under low and highly seasonal UVB conditions.
In recent centuries, migrations and high-speed transportation have brought many people into UVR regimes different from those experienced by their ancestors and, accordingly, exposed them to new disease risks.
These have been increased by urbanization and changes in diet and lifestyle.
Three examples—
- nutritional rickets,
- multiple sclerosis (MS) and
- cutaneous malignant melanoma (CMM)—
are chosen to illustrate the serious health effects of mismatches between skin pigmentation and UVR.
The aetiology of MS in particular provides insight into complex and contingent interactions of genetic and environmental factors necessary to trigger lethal disease states.
Low UVB levels and vitamin D deficiencies produced by changes in location and lifestyle pose some of the most serious disease risks of the twenty-first century.
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Observation by Vitamin D Life
The most efficient form of selective evolution should be with diseases which strike before procreation.
The following graph shows that most of the selective evolution of dark skinned peoples living far from the equator happens later in life.
The dying off at this age reduces the grandparent benefit in evolution, that is, the fewer living grandparents a child has, the less likely he will survive.