Vitamin D Research
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Worst Science on Vitamin D
The Vitamin D Council reviews three studies which, due to their faulty science, we consider to have done a grave disservice to humanity by preventing adequate vitamin D nutrition.
Role of vitamin D in pulmonary tuberculosis
Narang, et al's, 1984 paper may have done the most damage to the most people of any paper on vitamin D in the world's literature. The authors wrote about groups of six subjects with hypercalcemia who reportedly consumed increasing amounts of vitamin D, with the highest dose at 3800 IU (95 µg) per day, for up to six months. A protocol involved 25 subjects per group and Heaney, et al, used doses as high as 10,000 IU (250 µg) per day. Vieth R, Chan PC, MacFarlane GD. Efficacy and safety of vitamin D3 intake exceeding the lowest observed adverse effect level Am J Clin Nutr. 2001 Feb;73(2):288–94. Heaney RP, Davies KM, Chen TC, Holick MF, Barger-Lux MJ. Human serum 25-hydroxycholecalciferol response to extended oral dosing with cholecalciferol. Am J Clin Nutr. 2003 Jan;77(1):204–10.
There was no hint of hypercalcemia in either of these modern studies. The old Narang data suggest error on technical grounds: i.e. the hypercalcemia suggests that Narang, et al, did not confirm the accuracy of vitamin D doses given, and the doses were probably many times higher than they thought—there is no other explanation for this.
But the real problem here is with the Food and Nutrition Board. For although several reports (dated prior to 1995) of the safety of higher, physiologic doses of vitamin D were available, the FNB instead chose to rely solely upon the data from the Narang study to support their current toxicity levels (LOAEL of 3800 IU). Those specious toxicity levels have prevented millions of people from obtaining adequate vitamin D3 nutrition ever since.
Gains in bone mineral density with resolution of vitamin D intoxication
Adams and Lee presented four patients with hypercalcuria in the prestigious Annals of Internal Medicine who were taking dietary supplements with an "unadvertised" high level of vitamin D. Their paper was accompanied by an editorial expressing "a word of caution" about vitamin D. Three of the four cases appeared to be industrial type poisoning with vitamin D, probably from errors in the manufacturing of the supplements. The fourth patient also had hypercalcuria but only had a 25(OH)D level of 140 nM/L (56 ng/mL). In addition, her calcium to creatinine urinary ratio remained unchanged even after her 25(OH)D levels fell to low, "normal" values, indicating that her hypercalcuria was from another cause.
Besides misdiagnosing the fourth patient, the main problem with the paper is the authors' definition of toxic 25(OH)D levels. The authors simply assumed that the upper limit of their reference lab (two standard deviations) meant toxic 25(OH)D levels. This is false and reflects the ignorance that surrounds vitamin D toxicity. The upper limit of Adams and Lee's reference lab (140 nM/L or 56 ng/mL) simply reflects the Normal or Gaussian distribution of 25(OH)D levels for that lab at that latitude and those levels are often achieved in sun–exposed populations. Except for the report of Adams and Lee, all toxicosis from vitamin D reported in the world literature has been associated with serum 25(OH)D levels of more than 200 nM/L (80 ng/mL).
The Adams and Lee paper and the accompanying editorial have both been critically assessed by Vieth and Heaney, et al.
The mistake made by Adams and Lee continues to be made today because 25(OH)D levels are still reported as Gaussian distributions instead of optimum or target levels. Remember, if fifty percent of a population is deficient in vitamin D based on PTH levels, then Gaussian reporting methods will only correctly pickup a small percentage of people with deficiency and who would benefit from the simple, cost-effective measure of taking vitamin D3 supplements. For this reason, the Vitamin D Council has asked the College of American Pathologists to immediately review reporting methodology for 25(OH)D levels.
Serum 25-hydroxyvitamin D3 levels are elevated in South Indian patients with ischemic heart disease
Rajasree and his colleagues published an alarming paper that could scare anybody away from sunshine, for fear of developing heart disease from the vitamin D it might produce. Rajasree, et al, reported a world record high for 25(OH)D levels (four times higher than the average reports from India) due to sun exposure in a country where low, not high, 25(OH)D levels are the problem. Besides the greatly elevated 25(OH)D levels, Rajasree reported unexplained high occurrences of both hypercalcemia and hyperphosphatemia, in subjects as well as controls, a finding that throws suspicion on their analytical methodology. The suspiciously elevated 25(OH)D levels are explained by Rajasree using an antiquated and inaccurate method for measuring them—a method never validated by any proficiency survey for 25(OH)D. [note, clinical laboratories should take part in such surveys to ensure quality results that match what the rest of the world is measuring.] The best survey is DEQAS. Rajasree and colleagues did a disservice to the people of India, who are in reality suffering from too little vitamin D. Ganapati Mudur New DelhiIndian endocrinologists warn of vitamin D deficiencyBMJ 2003;326:12 (4 January)
We think the Rajasree paper was published because it played into the irrational and near hysteric fear of vitamin D toxicity that pervades the medical profession. The European Journal of Epidemiology published a letter to the editor that explained the error but Rajasree, et al, choose not to respond—this amounted to a virtual acceptance of the critiques of the Rajasree paper.
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