EDIT: I feel I should just add that a number of factors came together for these last two posts. Vieth's article from Ted crystalised it. I'd been thinking about JK and vitamin D for some time and Ken supplied, years ago, several interesting papers and ideas on D3 and skin colour. I think he's talking sense.
I discussed in my last post how Dr Vieth has a model of tissue 1,25(OH)2D synthesis and degradation in which the level of active substance is pretty well independent of blood vitamin D level, provided the level is either rising or stable. I think it is also worth pointing out that he is talking, hypothetically, about tissue 1,25(OH)2D, not plasma level... As we know, almost nothing is known about tissue 1,25(OH)2D control.
By Vieth's hypothesis tissue 1,25(OH)2D is OK so long as there is at least SOME vitamin D present in plasma and the level dose not vary too much. Obviously there is a level below which you can have as much of the enzyme for converting vitamin D to the active form as you like, if there is no vitamin D in your blood you can't make any 1,25(OH)2D in your tissues, or in your kidneys for export to your blood to control calcium levels. At the lower extremes we have rickets and osteomalacia. These are clear cut, unarguable markers of vitamin D deficiency, in the absence of confounding factors (there are a few).
For reasons which will become clearer I am far more interested in what is happening at the lower levels of vitamin D availability, rather than any toxicity from high dosages.
There was a problem of clinical rickets and osteomalacia in children and women of Asian and Middle Eastern origin in Glasgow from the 1960s onwards. The problem centres around gross deficiency of vitamin D, with 25(OH)D in the plasma sitting around 20nmol/l. Some of these people develop full blown rickets or frank osteomalacia, some don't. Dunnigan appears to have spent most of his career on this problem. A simple vitamin D deficiency does not seem to be adequate for rickets, though it is required.
Here's what Dunnigan has to say on the subject:
"The discovery of late rickets and osteomalacia in the Glasgow Muslim community in 1961 (Dunnigan et al. 1962) was followed by a study of 7 d weighed dietary intakes in rachitic and normal Muslim schoolchildren and in a control group of white schoolchildren (Dunnigan & Smith, 1965). Surprisingly, the dietary vitamin D intakes of rachitic Asian children, normal Asian children and Glasgow white children were similar. The higher fibre and phytate intakes of the Asian children were not considered aetiologically significant. Studies of daylight outdoor exposure showed no significant differences between the summer and non-summer exposures of rachitic and normal Muslim schoolchildren or between Muslim and white schoolchildren (Dunnigan, 1977). These patterns of daylight outdoor exposure did not conform to the Muslim ‘purdah’ stereotype, although sunbathing was unknown in the Asian community. It was also evident that many Glasgow white schoolchildren went out relatively little, even in fine weather, in a form of ‘cultural purdah’. Similar patterns of apparently adequate daylight outdoor exposure were noted in Asian women with privational osteomalacia wearing Western dress in London (Compston, 1979). These observations did not support the hypothesis that Asian rickets and osteomalacia resulted from deficient exposure to UVR or from deficient dietary vitamin D intake relative to white women and children in whom privational rickets and osteomalacia were unknown outside infancy and old age."
What appears to make a difference in his book is meat:
"Where UVR is limited by latitude and urbanization, the prevalence of privational rickets and osteomalacia is determined by dietary factors. Limited UVR is necessary but insufficient to induce ‘cases’ of privational rickets or osteomalacia unless the diet deviates from the Western omnivore pattern. This diet is characterized by high intakes of meat, fish and eggs, and low intakes of high-extraction cereals. The Western omnivore diet provides complete protection from privational rickets and osteomalacia from infancy to old age at the low levels of dietary vitamin D intake which characterize the largely unfortified British diet and at the levels of casual exposure to UVR experienced in the high latitudes of the UK. An omnivore Western diet will not prevent hypovitaminosis D at very low or zero UVR exposure levels; by inducing mild secondary hyperparathyroidism this may contribute to the risk of type two osteoporosis in old age. As the dietary pattern moves from omnivore to vegetarian, rachitic and osteomalacic risk rise synergistically with falling exposure to UVR (Fig. 1). UVR exposure levels associated with Asian rickets and osteomalacia in the UK are similar to the casual daylight exposure levels of a substantial proportion of the urban white population. Dietary risk factors for privational rickets and osteomalacia are independent of the low vitamin D content of most foods and appear to result from interactions between constituents of animal foods (predominantly meat and meat products) and the intermediary metabolism of endogenously-synthesized vitamin D."
Dunnigan feels the evidence from Glasgow suggests that an animal based diet largely protects against bone based effects of gross 1,25(OH)2D deficiency in the plasma. Supplementary vitamin D does also work, but was only transiently taken up by the Asian community.
"The provision of free vitamin D supplements in 1979 in an effort to reduce the prevalence of Asian rickets in the city is not responsible for this trend (Dunnigan et al. 1985). Supplement uptake declined rapidly within a few years of the onset of the campaign and vitamin D supplements are now rarely consumed by Asian schoolchildren and women (Henderson et at. 1989)."
Omnivory was taken up with westernisation of the diet. Along with the disappearance of rickets there was noted the arrival of appendicitis, an excellent confirmation of the switch in diet pattern.
From all of this I would deduce that, under marginal levels of UVB in Glasgow, the primary determinant of gross clinical expression of deficiency of vitamin D is vegetarianism. There is a protective effect of meat consumption. McDonalds will do. So might reindeeer meat in the Magdalenian Basin 18,000 years ago.
Which brings me to human migration out of the tropics and in to temperate areas. We came out of Africa and across central Russia about 60,000 years ago. During/since that time we northerners have lost our bulk melanin pigment layer, except for a faint induced tinge after summer sun exposure, which presumably acts to blunt excessive vitamin D production. If we can lose our sunscreen, yet still put up a temporary sunshade of a tan, do we really need 10,000iu per day year round?
Vieth argues for generous supplementation. I cannot see any argument against maintaining modest yet minimally variable levels, based on his own hypothesis. Modest UVB exposure with a meat based diet might well be adequate.
I would then tend to leave the vitamin D paradox as a suggestion that the role of vitamin D in cancer might need re evaluating. I am quite well convinced from the Glasgow experience that catastrophic vitamin D deficiency can be largely be ameliorated by eating meat. Can "suboptimal" vitamin D deficiency relating to cancer and CVD also be optimised by eating meat? Supplementing just 100iu/d sorts out rickets but the same effect can be achieved with the occasional burger.
Most of us who have ended up on low carbohydrate eating did not think it up for ourselves. There are shoulders on which we still try to scramble. For me it was Atkins, Yudkin, Lutz, Groves and especially Kwasniewski. No one was or is advocating 10,000iu/d of vitamin D. They were/are all advocating a diet based on meat and animal fat. These pioneers did not have the EBCT tracking which is available to many of us nowadays, but their clinical experience, with all of the caveats that that needs, is that LC, animal fat based diets reverse CVD.
I can see that aiming for a middle to upper lab range is a reasonable hedging of bets. I'm not sure it is needed unless you come from a history of vegetarianism or persist in the consumption of whole meal flour, especially if coupled with near complete UV avoidance. Never forget that much of the data on vitamin D supplementation comes from a population crushed under the Food Pyramid or its derivatives, an eating plan which almost seems to have been designed to maximise disease. Vitamin D might well help under these situations, but what of those of us who eat Food?
It seems like humans can get away with vegetarianism in the tropics. Move north and you need to eat meat.