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There has been ongoing uncertainty as to what level of circulating 25-hydroxy-vitamin D (25OHVitD) indicates vitamin D insufficiency. Vitamin D deficiency has been designated as a 25OHVitD level less than 30 nmol/l and insufficiency as less than 75 nmol/l [1, 2]. Please note that many laboratories give their results in ng/ml, and thus 30 nmol/l is equivalent to 12 ng/ml, and 75 nmol/l is equivalent to 30 ng/ml.

This would lead one to the expectation that treatment of a person with vitamin D insufficiency would be associated with adverse biochemical and morphological bone effects. Two recent publications should make us question the proposed 25OHVitD cut-off for vitamin D insufficiency [3, 4]. Shah and colleagues studied 11,855 people being assessed for 25OHVitD levels at a commercial laboratory and 150 people attending the Austin Hospital Melbourne [4]. Through a series of statistical analyses, they identified a ‘breakpoint’ of 30 nmol/l of vitamin D below which serum calcium was significantly lower, and parathyroid hormone (PTH) and alkaline phosphatase levels significantly higher. Although 34% of those with a 25OHVitD below 30 nmol/l had secondary hyperparathyroidism, the majority of people with a 25OHVitD below this level were biochemically normal. There was no signal of any biochemical abnormality amongst those with a 25OHVitD level between 30 and 75 nmol/l that justified a person being classified as vitamin D-insufficient. They also found no association between 25OHVitD and bone remodelling markers, bone mineral density (BMD) or matrix mineralization density in the subset of 150 people in which these parameters were measured. However, few people in this group had a 25OHVitD level below 30 nmol/l and this substudy may have been underpowered.

Reid and colleagues have concurrently reported the findings of a study in which 452 adults (mean age 69 years and two-thirds male) were randomly allocated to 100,000 IU of vitamin D3/month or placebo for 2 years [3]. No significant treatment effect was seen for BMD in the lumbar spine, which was the primary outcome. Although hip BMD declined in both groups, this was attenuated by 0.5% in the treated group. A treatment effect at the lumbar spine and hip was seen for the subset of 46 people who had a 25OHVitD level of 30 nmol/l or less at baseline.

The use of vitamin D supplementation is widespread across the developed world. However, contrary to prevailing practice, these studies indicate no bone health benefits of such supplementation for otherwise healthy adults when the serum 25OHVitD level is above 30 nmol/l. These recent findings should cause us strongly to question the validity of untargeted vitamin D supplementation for community-dwelling adults.


  • Susan R. Davis
    Chair of Women’s Health, Monash University, Melbourne, Australia


  1. Ross AC, Manson JE, Abrams SA, et al. The 2011 report on dietary reference intakes for calcium and vitamin D from the Institute of Medicine: what clinicians need to know. J Clin Endocrinol Metab 2011;96:53-8
  2. Holick MF, Binkley NC, Bischoff-Ferrari HA, et al. Evaluation, treatment, and prevention of vitamin D deficiency: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab 2011;96:1911-30
  3. Reid IR, Horne AM, Mihov B, et al. Effect of monthly high-dose vitamin D on bone density in community-dwelling older adults: sub-study of a randomized controlled trial. J Intern Med 2017 July 10. Epub ahead of print
  4. Shah S, Chiang C, Sikaris K, et al. Serum 25-hydroxyvitamin D insufficiency in search of a bone disease. J Clin Endocrinol Metab 2017 March 30. Epub ahead of print
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