Vitamin D insufficiency in a population of healthy western Canadians

BackgroundPeople with low levels of vitamin D and its metabolites are at increased risk for osteoporotic fractures. We wished to ascertain levels of vitamin D in a representative sample of adult western Canadians, to help assess the level of risk. We evaluated the prevalence of vitamin D insufficiency, defined as 25-hydroxyvitamin D 25(OH)D] less than 40 nmol/L, and seasonal variations in 25(OH)D, parathyroid hormone and related biochemical indices in a community-dwelling population of healthy Canadians living in Calgary (lati- tude 51°07''N).MethodsDuring calendar year 1999, we collected fasting overnight blood samples every 3 months from 60 men and 128 women (age range 27 to 89 years) who had volunteered to participate in another study. We used commercial radioimmunoassay kits to measure calciotrophic hormones and other biochemical indices. Regression models for longitudinal data were used to assess the effect of season and other potential predictors on individual parameters.ResultsFor a total of 64 participants (34%), vitamin D insufficiency, defined as 25(OH)D less than 40 nmol/L, was recorded at least once out of the 4 sampling times. After adjustment for age, body mass index and holiday travel, we observed the anticipated rise in serum 25(OH)D from a mean of 57.3 (standard deviation SD] 21.3) nmol/L in the winter to 62.9 (SD 28.8) nmol/L in spring (p = 0.001) and 71.6 (SD 23.6) nmol/L in summer (p < 0.001), with a subsequent decline to 52.9 (SD 17.2) nmol/L in the fall (p = 0.008). The anticipated inverse relation between 25(OH)D and parathyroid hormone was not consistently observed: after adjustment for age, sex, body mass index and serum calcium, serum levels of parathyroid hormone did decrease significantly, from 39.5 (SD 18.8) ng/L in winter to 36.3 (SD 17.8) ng/L in summer (p = 0.001), but they continued to decline to 34.5 (SD 17.3) ng/L in the fall (p < 0.001). There was no association between 25(OH)D and parathyroid hormone (p = 0.21).InterpretationWe documented a high prevalence of vitamin D insufficiency, which warrants consideration of dietary vitamin D supplementation.Vitamin D deficiency has long been recognized as a cause of rickets in children and osteomalacia in adults. More recent is the awareness of a preclinical phase of vitamin D deficiency, known as vitamin D insufficiency, which increases the risk of osteoporotic fractures.^1,2,3 Low levels of vitamin D metabolites are associated with malabsorption of calcium, which results in bone loss.^4,5 Vitamin D can be obtained through the diet or it is synthesized in the skin after exposure to the sun. However, because few foods provide a natural source of vitamin D⁶ and because fortification of foods with vitamin D is often unreliable,^7,8 skin synthesis is thought to constitute the major source. People living in countries at higher latitudes are more prone to seasonal vitamin D insufficiency because wintertime sunlight does not promote conversion of the vitamin D precursor in the skin.⁹ Levels of vitamin D and its main circulating metabolite, 25-hydroxy vitamin D 25(OH)D], are under the predominant influence of solar ultraviolet B radiation (wavelength 290 to 315 nm). Webb and colleagues⁹ have shown that in Boston (latitude 42°N), sun irradiation is inadequate to generate previtamin D in vitro from November through February; in Edmonton (latitude 53°3$\acute{0}$N), this period extends from October through March.The vitamin D hormone system and parathyroid hormone are the principal regulators of serum concentrations of calcium and therefore influence skeletal calcium reserves. Because of the health risks associated with low levels of vitamin D, our objective was to determine patterns of seasonal variation in 25(OH)D, as well as the prevalence of vitamin D insufficiency, defined as 25(OH)D less than 40 nmol/L,¹⁰ in a population of healthy men and women living in western Canada. Although 1,25-dihydroxy vitamin D 1,25-(OH)₂D] is the most potent form of vitamin D, 25(OH)D is the main circulating metabolite of vitamin D and is considered the correct functional indicator of vitamin D stores in humans.^11,12 We also examined associations between 25(OH)D and serum concentrations of 1,25-(OH)₂D, parathyroid hormone and other related biochemical markers.