Intended for healthcare professionals

Letters Perspective on vitamin D

Hypovitaminosis D and disease: consequence rather than cause?

BMJ 2012; 345 doi: (Published 24 August 2012) Cite this as: BMJ 2012;345:e5706
  1. Rousseau Gama, chemical pathologist and honorary professor of laboratory medicine1,
  2. Jenna L Waldron, senior clinical scientist1,
  3. Helen L Ashby, specialist registrar in chemical pathology and metabolic medicine1,
  4. Michael P Cornes, senior clinical scientist1,
  5. Julia Bechervaise, academic FY21,
  6. Cyrus Razavi, academic FY21,
  7. Osmond L Thomas, consultant orthopaedic surgeon1,
  8. Sanjiv Chugh, consultant orthopaedic surgeon1,
  9. Shreeram Deshpande, consultant orthopaedic surgeon1,
  10. Clare Ford, consultant clinical scientist1
  1. 1New Cross Hospital, Wolverhampton WV10 0QP, UK
  1. rousseau.gama{at}

In their editorial calling for vitamin D to be put into perspective Harvey and Cooper do not consider the possibility, supportive to their view, that hypovitaminosis D is the consequence rather than the cause of disease.1 We recently completed a study showing unequivocally that serum 25-hydroxyvitamin D is a negative acute phase reactant.

We measured serum C reactive protein and 25-hydroxyvitamin D concentrations before and two days after elective knee or hip surgery in 30 patients. After surgery the mean serum concentration of C reactive protein increased (5.0 (SD 5.5) v 116.0 (81.2) mg/L; P <0.0001), whereas serum 25-hydroxyvitamin D decreased (56.2 (30.3) v 46.0 (27.6) nmol/L; P <0.0006).

These results are consistent with those of two other studies reporting a rapid and noticeable fall in serum 25-hydroxyvitamin D concentration during a systemic inflammatory response.2 3 They seem, however, to contradict the results of two other studies reporting no change in serum 25-hydroxyvitamin D concentration for up to 90 days after an inflammatory insult.4 5 The initial serum samples in these last two studies were, however, all collected after the inflammatory insult,4 5 when serum 25-hydroxyvitamin D is already likely to be at a nadir.2 3 A unifying explanation for the apparently conflicting results of these four studies is that serum 25-hydroxyvitamin D concentration decreases rapidly and dramatically after an inflammatory insult and persists for at least three months.

That serum 25-hydroxyvitamin D is a negative acute phase reactant has implications for acute and chronic diseases. Firstly, serum 25-hydroxyvitamin D is an unreliable biomarker of vitamin D status after an acute inflammatory insult. Secondly, hypovitaminosis D may be the consequence rather than the widely purported cause of a myriad of chronic diseases.1


Cite this as: BMJ 2012;345 :e5706


  • Competing interests: None declared.


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