Ten Reasons Everything We Thought We Knew About Vitamin D Is Wrong: Part 3

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Incomplete Research: testing for 25-D rather than 1,25-D

When combing through the research on “Vitamin D” you will find an overwhelming failure to test for 1,25-D, the biologically active metabolite, in subjects with chronic diseases.  Results continue to be accepted that simply do not bother to measure 1,25-D.  Why is this a problem? ALL, repeat, ALL of the biological actions attributed to “vitamin D” is the sole responsibility of 1,25-D.  Yet the research measures only 25-D and can only produce correlations based on these inaccurate findings. 

“Vitamin D” deficiency has been reported in 57% of 290 medical inpatients in Massachusetts, 93% of 150 patients with overt musculoskeletal pain in Minnesota, 48% of patients with multiple sclerosis, 50% of patients with lupus and fibromyalgia, 62% of the morbidly obese African American Women, 83% of 360 patients with low back pain in Saudi Arabia, 73% of Austrian patients with Ankylosing Spondylitis, 58% of Japanese girls with Graves‘ Disease, and 40- 70% of all Finnish medical patients. On the surface, this sounds conclusive, but a complete picture has not been painted from these results.  As stated in previous writings; down-regulation is not a deficiency.  When we take into consideration the relationship between 25-D and 1,25-D it becomes very clear that this is NOT a “vitamin D” deficiency, but rather just the opposite.  You see, an elevated 1,25-D is actually what is responsible for a low level of 25-D.  Low 25-D is a consequence, rather than a cause, of the disease process.

The extent of low levels of 25-D amongst the US population is indisputable. In fairness, this research is well-intended, yet it has missed the mark.  There is simply a failure of researchers and even physicians to question the level of not just 25-D but 1,25-D in subjects and patients. The roles and fates of these two molecules are wholly intertwined.  To measure one without the other is simply uninformative and woefully incomplete. 

The relationship between low 25-D and high 1,25-D is often written off as hyperparathyroidism.  Here, the kidneys produce more 1,25-D to compensate for inadequate calcium intake. Rather than addressing this issue with increased calcium intake, clinicians generally recommend more “vitamin D” in supplement form.  However, secondary hyperparathyroidism can be ruled out by measuring the parathyroid hormones.  Thorough research on several inflammatory diseases has specifically ruled out secondary hyperparathyroidism as a cause for high levels of 1,25D relative to 25D. The testing and assessment of 1,25-D is not a simple task.  Further adding to this conundrum, for the testing of 1,25-D to be accurate, the sample must be frozen.

Robert C Jacobs

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