One of the main reasons that vitamin D supplementation is routinely justified is that low levels of vitamin D are frequently detected in patients with a range of inflammatory diseases. To be specific, low levels of one form of vitamin D are often low in many patients – a form of vitamin D called 25-hydroxyvitamin-D or 25-D.

But there is a major issue with studies that demonstrate these low levels of 25-D in people who are ill. Two very different possibilities can explain the association. One is that low levels of 25-D somehow contribute to disease progression. The second explanation is that low levels of 25-D are actually a result of inflammatory disease processes; in other words, as a person becomes sick, their bodies naturally lower the amount of 25-D in the body.

My research suggests that this second possibility is correct. Several papers I have published with the non-profit foundation Autoimmunity Research Foundation delineate a number of pathways by which the body naturally lowers 25-D levels as a person becomes ill. Please read the longer article below for more detail.

Under the above conditions, patients with low levels of 25-D need not be given supplements to bring their vitamin D back into the “correct range.” Instead, this article describes why doing so may actually be counterproductive.

The following excerpt is taken from a book chapter I recently published in the 2015 textbook Infection and Autoimmunity. It describes my view of vitamin D “deficiency” in more detail:

Low blood concentrations of vitamin D likely result from the inflammatory disease process 

In the 2015 textbook, Infection and Immunity, I write the following:

Vitamin D supplementation is routinely justified based on a plethora of studies that report low concentrations of 25-D in the blood of patients with a wide variety of inflammatory conditions. Thus far, the consensus on these findings has been to assume that the low concentrations of 25-D are driving or contributing to the pathogenesis of these diseases. However, the low concentrations of 25-D often detected in patients with inflammatory conditions may be a result of the inflammatory disease process rather than the cause of the inflammation.

Indeed, our data suggest that under conditions of microbiome and interactome dysregulation, the body uses multiple mechanisms to naturally downregulate intracellular production of 25-D. Expression of the enzyme CYP24A1 normally controls excess concentrations of 1,25-D. However, if VDR activity is slowed by the intraphagocytic microbiome, the enzyme cannot be expressed as robustly. In addition, when 1,25-D increases, it downregulates the amount of previtamin D converted into 25-D. One of these mechanisms is antagonism of the PXR nuclear receptor and expression of the enzyme CYP27A1. The result is that blood concentrations of 25-D, the metabolite most commonly measured in the clinic, decrease.

The concept of vitamin D “deficiency” has been further complicated by the arbitrary ranges used to define insufficiency and deficiency. Vitamin D supplementation has become so prevalent that individuals who choose not to ingest extra amounts of the secosteroid may be deemed deficient simply because they eat non-fortified foods. Indeed, it is difficult to find unsupplemented populations to study. Nevertheless, studies of healthy individuals in populations that do not heavily supplement their food supplies with vitamin D have demonstrated that subjects’ 25-D concentrations are naturally found to be in the range we today have labeled as “deficient”.

Saudi Arabia does not yet add vitamin D to their food supply. It is not surprising, then, that one study found that 100% of Saudi medical students receiving standard amounts of sunlight and eating a normal diet were vitamin D insufficient or deficient according to conventional standards. Similarly, a study of healthy Bangladeshi women not supplementing with vitamin D found that approximately 80% had 25-D concentrations less than 16 ng/mL. A separate study of premenopausal Bangladeshi women came to a similar conclusion. A study of young healthy adults from the west of India, also not consuming supplemental vitamin D, found the average serum concentration of 25-D to be 17.4 ng/mL. In 1992, before vitamin D supplementation became more common in China, a study found that healthy full-term Chinese infants had serum concentrations of 25-D ranging from an average of 5 to 14 ng/mL, a level that would be regarded as “highly deficient” by current dogma.

It is tempting to argue that the individuals in these studies do not receive adequate exposure to sunlight. (Whether people require a certain amount of sunlight also remains a matter of debate.) Yet, in each instance, the authors clearly ascertain that their subjects are healthy and quite functional. Instead of assuming that these healthy subjects should be given extra vitamin D, as the current standard of care indicates, it may be prudent to consider whether the ranges we have created for vitamin D deficiency and insufficiency have a basis in human molecular science.