Predictors of vitamin D status in New Zealand adults and the effect of vitamin D2 and vitamin D3 supplementation on 25-hydroxyvitamin D and parathyroid hormone concentrations

Vitamin D deficiency is associated with impaired calcium absorption leading to compensatory hyperparathyroidism, increased bone resorption and decreased bone integrity. The prevalence of low vitamin D status among New Zealanders is increasingly documented, and food fortification and/or supplementation strategies to meet physiological needs may be required. To this end, an examination of demographic, and lifestyle influences on vitamin D status are important for the development of population-specific health recommendations as is the determination of dose, frequency and form of vitamin D used for supplementation and/or food fortification. There are two forms of vitamin D commonly used, ergocalciferol (vitamin D2) and cholecalciferol (vitamin D3). Although public health recommendations do not discriminate between vitamin D2 and vitamin D3, a number of studies using large, single oral dose preparations ranging from 50,000 to 300,000 IU have suggested that vitamin D2 is less effective than vitamin D3. Lower dose clinical trials comparing daily administration of vitamin D2 and vitamin D3 have yielded inconsistent results and have been limited by short study duration, small participant numbers, the effects of cutaneous production of vitamin D3, background dietary and supplemental vitamin D intake and body mass index. In an attempt to address some of these limitations, the goal of this thesis was to evaluate the effectiveness of a daily physiological dose of vitamin D2 and vitamin D3 on serum 25(OH)D levels in healthy adults living in Dunedin, New Zealand (latitude 45°S). In addition, possible predictors of serum 25(OH)D status among this group of healthy adults were examined along with the relationship between serum 25 (OH)D and serum PTH concentrations. To achieve the overall study goals, a placebo-controlled, double-blinded intervention trial was conducted in 95 participants, aged 18–50 y, who were randomly assigned to receive either 1000 IU vitamin D3/d (n = 32), 1000 IU vitamin D2/d (n = 31) or placebo (n = 32) for 24 wk period beginning at the end of summer (March). Total serum 25(OH)D, as 25(OH)D3 and 25(OH)D2, and PTH were measured at baseline and at 4, 8, 12 and 24 wk. Baseline measurements of 25(OH)D and PTH concentrations (n = 95) were used to determine predictors of serum 25(OH)D status among participants, and to assess the relationship between serum 25(OH)D and PTH concentrations. Change over time in serum 25(OH)D and PTH concentrations were used to compare the potencies of vitamin D2 and vitamin D3 supplementation over the winter. At baseline, serum 25(OH)D concentrations ranged from 27.9 to 141.0 nmol/L with the geometric mean serum total 25(OH)D of 74.9 nmol/L. Seven (7.4%) participants had 25(OH)D concentrations below 50 nmol/L, six (6.3%) participants had a serum 25(OH)D concentration ranging between 30–50 nmol/L and one (1.1%) had a serum 25(OH)D < 30 nmol/L. None of the known predictors of vitamin D status such as age, body mass index (BMI), constitutive or facultative skin colour were significantly associated with serum 25(OH)D concentrations; however, mean serum 25(OH)D concentrations were 17 nmol/L higher in those participants taking a vitamin-D containing supplement in the 3 months prior to study commencement (P = 0.035). In terms of the bone effects, serum PTH decreased as serum 25(OH)D concentrations increased with evidence of a plateau in PTH concentrations at a serum 25(OH)D of ~70 nmol/L. Following 24 wk of supplementation, the vitamin D3-supplemented group demonstrated no significant change (t-test; P = 0.879) in serum 25(OH)D concentration over the winter time course of the study, whereas mean (95% CI) 25(OH)D significantly decreased by 43 (35, 50) nmol/L (P < 0.001) in the placebo group and by 22 (14, 30) nmol/L in the vitamin D2-supplemented group (P < 0.001). There was no evidence of a statistically significant change in serum PTH concentrations observed between the groups (P = 0.646), nor was there a change in 25(OH)D3 throughout the study in Vitamin D3 treated participants. As expected, participants assigned to both the vitamin D2 and placebo groups experienced a significant decline in 25(OH)D3 concentration over the winter months relative to the vitamin D3 supplemented group; however, baseline adjusted serum 25(OH)D3 was significantly lower [7.1 (0.8, 13.3) nmol/L] in the vitamin D2 group compared to the placebo group (P = 0.028). In conclusion, vitamin D3 is more effective than vitamin D2 in maintaining summertime 25(OH)D concentration over the winter period. This difference may be partly explained by the negative effect of vitamin D2 ingestion on serum 25(OH)D3 levels. The assumption of vitamin D2 and D3 equivalence from not only a physiological but also a therapeutic basis should be reconsidered, particularly in light that the dose employed in our study is commonly used in over-the-counter dietary supplements. Furthermore, the use of vitamin D-containing supplements significantly impacts vitamin D status, even when UV synthesis is high