Tot mijn grote verbazing en blijdschap in de nieuwste Wise Traditions het volgende stukje over de mythe van de 'naakte aap':
Problems With the “Naked Ape” Hypothesis of Optimal Serum 25(OH)D Concentrations
One of the most widely influential perspectives about 25(OH )D that appears in the scientific literature and pervades the alternative health literature is the “naked ape” hypothesis of optimal serum 25(OH )D. This hypothesis holds that humans evolved as “naked apes” in the tropical savannahs of Africa where they were exposed to maximal sunshine and when the requirement for 25(OH )D was indelibly fixed into our genome. Now that we have invented modern clothing, indoor living, and migrated far from the tropics, most of us have far lower 25(OH )D than we had "back when we evolved," as shown by the much higher levels of 25(OH )D found in lifeguards working in Missouri and Israel. Reinhold Vieth promoted this view in a popular 1999 article.29 At the time of this writing, Google Scholar reports that this article has been cited 1,159 times.
While it may seem compelling on the surface, the argument is deeply problematic. The hypothesis assumes that at some point between the loss of body hair and the gain of clothing we existed as naked sunbathers, and it was at just this very point where the requirement for serum 25(OH )D was indelibly fixed into our genome. If we take “molecular clock” estimates at face value, the loss of body hair and the gain of dark skin pigmention both occurred 1.2 million years ago,30,31 indicating we were never truly “naked” since both hair and pigment protect the skin from ultraviolet light. Evidence for hide scrapers likely used to make leather, either for clothing or some other form of shelter from the sun such as housing, goes back almost eight hundred thousand years.30 Clothing was certainly in widespread use by the time clothing lice diverged from head lice, which scientists estimate occurred some one hundred seventy thousand years ago.30 Colored pigments appear in the African archeological record over a quarter million years ago and remain a constant feature of African culture through the present.32 These may have been used to paint the skin, as commonly occurs in Africa today. Weston Price wrote in Nutrition and Physical Degeneration that it was a universal tradition in the Pacific Islands to use coconut oil as a sunscreen, and there is no particular reason to doubt the premise that prehistoric humans used botanical sunscreens as well. African primates and traditionally living African humans seek shade from the hot sun at mid-day.33,34 Prehistoric humans living in the African savannah were thus likely to be neither “naked” nor sunbathers.
Most of prehistoric human life was dominated by glacial periods in which the earth was substantially colder and aerosolized dust and salt were much higher.35 The lower exposure of the earth to solar radiation and the higher aerosols during these times probably made the average UV-B exposure considerably lower, suggesting that no living human beings provide a proxy for prehistoric 25(OH )D levels. The worst example we could possibly use for such a purpose, however, are modern lifeguards. The Israeli lifeguards whose high 25(OH )D Vieth cited in his 1999 paper as the closest approximation to the vitamin D status of our “naked ape” ancestors had evidence of sun damage and twenty times the risk of kidney stones as the general population. The lifeguards had a mean 25(OH )D higher than 50 ng/mL, and their increased risk of soft tissue calcification is consistent with the increased risk of cardiovascular disease that occurs above 40 ng/mL (see Figure 2).
Additionally, certain populations seem adapted to a lower “normal” 25(OH )D. Greenland Inuit on their traditional diet have a mean serum 25(OH )D of only 20 ng/mL, but appear to convert 25(OH )D to the more active 1,25(OH )2D at a higher rate.36 Similarly, African Americans have lower 25(OH )D than white Americans, but higher 1,25(OH )2D and higher bone density.37 It seems that these groups have lower 25(OH )D but higher total biological activity of vitamin D, creating the illusion of a “deficiency” that does not actually exist. If different groups are adapted to different optimal levels of 25(OH )D, moreover, this suggests that the requirement for 25(OH )D has continued to evolve over time and was never indelibly fixed into the human genome at any point, certainly not in some fictitious era of the “naked ape.”
The very concept of an optimal 25(OH )D may itself be flawed. The total biological activity of vitamin D is determined by both 25(OH )D and the much more active 1,25(OH )2D. The conversion of 25(OH )D to 1,25(OH )2D is, like many other steps in vitamin D metabolism, partly determined by genetics.38 Many other factors can influence either the demand for or the supply of 1,25(OH )2D. Calcium deficiency increases the demand for it and lowers 25(OH )D status independently of vitamin D exposure.39 Vitamin A, by contrast, seems to increase the supply of 25(OH )D to the kidney, making it easier to convert it to 1,25(OH )2D.40 Acute inflammation41 and cancer42 also increase the conversion. If we only measure 25(OH )D and it is low, we have no idea whether total biological activity of vitamin D is increased or decreased, nor do we know why it is altered or whether this is a concern. The fact that crisis states such as acute inflammation and disease states such as cancer can influence the conversion raises an additional problem: are associations between 25(OH )D and disease risk cause or effect? Until these questions are resolved, we should place much less emphasis on using vitamin D supplements to achieve a desired 25(OH )D and much more emphasis on improving the nutrient density and nutrient balance of the diet.
http://www.westonaprice.org/cardiovascular-disease/beyond-cholesterol#problem
Mike