In the 21 September 2007 issue of the New Zealand Medical Journal, Livesey et al conclude that most Christchurch people are vitamin D deficient most of the time based upon a criteria for vitamin D deficiency as a serum 25-hydroxyvitamin D (25OHD) <75 nmol/L.1

In an accompanying editorial, Scragg and Bartley state that “defining vitamin D deficiency as a 25OHD level below 50 nmol/L is clearly not supported by the current evidence, optimum health occurs at much higher levels than this;” and conclude that optimum vitamin D status occurs with 25OHD levels >80 nmol/L.2

We have previously argued that there is no strong evidence to support the use of such high thresholds for vitamin D deficiency3 and that the widely used definitions of vitamin D deficiency (25OHD <25 nmol/L) and vitamin D insufficiency (25OHD < 50 nmol/L) remain appropriate.4

A recent panel of experts was not able to achieve a consensus definition of vitamin D sufficiency with recommendations ranging from 50–80 nmol/L,5 while other authors have suggested an even broader range from 25 to >100 nmol/L.5,6 The recommendations at the upper end of this range are based upon the measurement of surrogate endpoints such bone density or muscle strength in observational and cross-sectional studies. Such studies are potentially subject to confounding by frailty because people with poorer health are likely to spend less time outdoors, have less sun exposure, and have lower 25OHD levels than their healthy peers (rather than low vitamin D levels causing ill health).

In addition, people leading sedentary lives are at increased risk of obesity, and increased fat mass is inversely associated with 25OHD levels.7,8 This association may confound the reported relationships between low vitamin D status and conditions such as diabetes, ischaemic heart disease, hypertension, and cancer that occur more commonly in obesity.9 Confounding by health status can be powerful, as evidenced by the disparate results of randomised controlled trials and observational studies of postmenopausal hormone replacement therapy.

In contrast to the cross-sectional studies, intervention studies with clinically relevant endpoints such as fractures tend to give lower estimates of optimal 25OHD levels. For example, in a meta-regression analysis, the achieved 25OHD level associated with a reduction in all non-vertebral fractures was <50 nmol/L and for hip fractures was about 65 nmol/L,10 in agreement with four interventional studies suggesting that serum PTH is not further suppressed by increasing 25OHD levels above 40–60 nmol/L.6, 11-13

In order to achieve year-round serum 25OHD levels >75–80 nmol/L, vitamin D supplementation of most, if not all, of the population would be required. We suggest that implementation of population-based strategies to achieve such vitamin D levels are premature in the absence of clear evidence of benefit (and safety). Indeed, currently there is no clinical trial evidence that increasing vitamin D levels impacts favourably on non-skeletal outcomes. At present, the only convincing clinical trial evidence for beneficial skeletal effects of vitamin D supplementation is in institutionalised elderly women co-treated with calcium supplements.14