- Jan 22, 2013
If you do your homework you'll find why it doesn't look a very good idea taking d3 other than from uvb exposure. Specially if you have not calcitriol levels checked previously.
I hear you, but Peat made it very clear in this show that derangements of vitamin D metabolism are likely due to calcium and vitamin D deficiency, not due to supplementation. One caller said she was taking 8,000 IU daily and he said he has never heard of anybody has any issues with 10,000 IU daily. I think his rationale was that 15min exposure to the sun results in 15,000 IU vitamin D being synthesized so taking much smaller amounts than that (especially during the winter) is not likely to cause issues.
You think body adjust vitamin d production rate according to calcitriol?!
I know, I listened the show the other day and it called my attention when Peat approved what the caller said about the units he was taking. From what I've read its not about the units, but about the way they reach the system. 25OH and 1.25 don't always correlate each other in a linear way, and sometimes it's the opposite. Unlike pre-d3 formation from uvb, taking oral d3 when calcitriol is in the upper range can seriously mess with vdr, and that is no joke.
Yep, and that feedback becomes pointless when you load yourself with high amounts of d3 (I mean higher than what you'd get from a normal diet).
So I think its wise to check 1.25 levels to be on the safe side, before any oral d3.
The classic symptoms of vitamin D toxicity are entirely attributable to hypercalcemia, and they include nausea, dehydration, and lethargy. Without laboratory testing, these signs of hypercalcemia have been mistaken for gastroenteritis.
Recent evidence in men shows that 8 wk of supplementation with 275 μg (12,500 IU)/d of vitamin D does not affect circulating calcium concentration (urine results were not reported). In other words, the dose is noncalcemic and safe by the criteria applied both to drug studies of vitamin D analogs and to nutrient recommendations.
Concentrations of 1,25(OH)2D are not increased much by vitamin D intoxication. This reflects the high level of regulation of the circulating concentrations of this hormone through both synthesis and catabolism. Nonetheless, vitamin D toxicity is the result of excessive levels of “free” 1,25(OH)2D displaced from its carrier protein, vitamin D–binding protein (DBP), when there is a vast excess of other vitamin D metabolites.
People with abundant exposure to sunlight can easily exhibit a serum 25(OH)D >150 nM (60 ng/ml), which would be a physiologic presupplement input of vitamin D equivalent to >100 μg (4000 IU)/d. An additional oral intake of 100 μg/d of vitamin D would still be less than the dose of 1250 μg (50,000 IU)/d vitamin D shown to be noncalcemic.
The absence of hypercalcemia and hypercalciuria in well-conducted trials of vitamin D leads to the conclusion that the current UL of 50 μg (2000 IU)/d has been excessively conservative. The overwhelming bulk of clinical trial evidence supports the conclusion that a prolonged intake of 250 μg (10,000 IU)/d of vitamin D3 likely poses no risk of adverse effects in almost all individuals in the general population. These conclusions are more fully supported in a formal risk assessment for vitamin D by Hathcock et al.
As shown in Fig. 3, lower serum 25(OH)D levels were associated with higher levels of PTH. Based on mathematical modelling using a quadratic fit, PTH reached a plateau at 33.9 ng mL−1; that is, serum PTH increased as serum 25(OH)D levels declined below 33.9 ng mL−1, but remained stable for serum 25(OH)D levels above that value.
Seriously. She wanted the whole show to be dedicated to her personal health profile as well.First caller didn't want to give her weight. Wow.
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