Vitamin D plays a critical role in bone metabolism and many cellular and immunological processes [1–4]. Low levels of vitamin D have been associated with various chronic and infectious diseases including cancer, multiple sclerosis, diabetes, rheumatoid arthritis, osteoporosis, cardiovascular disease, and microbial infections [5–13]. Vitamin D is synthesized in the skin upon exposure to the sun's ultraviolet B radiation (UVB) . Vitamin D can also be acquired from the diet from sources where it occurs naturally (such as fatty fish, fish oil and eggs), from fortified products (such as milk and orange juice) and from supplements . For many people, exposure of their skin to UVB is the primary source of their vitamin D [4, 14]. However, at latitudes far from the equator, such as Canada, the amount of UVB available from sunlight during the winter months is inadequate to allow cutaneous vitamin D synthesis [4, 15].
Several other factors can affect vitamin D concentrations, including: skin pigmentation (melanin, the major natural pigment in the skin, interferes with cutaneous production of vitamin D) [16, 17]; age (the skin loses the ability to synthesize vitamin D with increased age) [14, 18]; weight (higher adiposity has been associated with lower vitamin D levels) [19–22]; deliberate avoidance of sun exposure and/or use of sunblock (due to sun safety or cultural reasons) [12, 23]; malabsorption disorders which affect the body's ability to absorb vitamin D (including celiac disease, Crohn's disease, cystic fibrosis) ; diseases and disorders of the kidneys and/or liver that affect vitamin D metabolism  and use of certain medications (including anticonvulsants, anti-rejection medications, corticosteroids) [12, 25].
The standard method for the determination of vitamin D status tests the circulating concentration of serum 25-hydroxyvitamin D [25(OH)D], which measures the amount of vitamin D coming into the body from all sources (cutaneous synthesis, diet or supplements) . Previous efforts to assess optimal serum 25(OH)D levels focused on the role of vitamin D in bone health, and the optimal 25(OH)D concentration was defined as the concentration that maximally suppressed serum parathyroid hormone (PTH) and promoted maximum calcium absorption . In general, vitamin D "deficiency" was classified as concentrations below 25–27.5 nmol/L [28, 29]. Levels below these cutoffs are associated with calcium malabsorption, severe hyperparathyroidism and vitamin D rickets or osteomalacia . Some past studies have considered serum 25(OH)D levels of 40–50 nmol/L as the low end of the normal range [31, 32]. However, other studies have shown that PTH levels [33, 34] and calcium absorption  are not optimized until serum 25(OH)D levels reach approximately 80 nmol/L. Most vitamin D researchers now recognize that concentrations of serum 25(OH)D should be in excess of 75 nmol/L for multiple health outcomes, not only bone health [27, 36]. Accordingly, recent reports refer to serum 25(OH)D levels > 75 nmol/L as "optimal", between 75 nmol/L and 50 nmol/L as "insufficient" and < 50 nmol/L as "deficient" . In our study, we report the percentage of the individuals in our sample under three widely used cutoffs, 25 nmol/L, 50 nmol/L and 75 nmol/L, and we consider 25(OH)D levels > 75 nmol/L as optimal.
Previous research indicates that vitamin D concentrations are low in many otherwise healthy Canadian adults, particularly during the winter months [28, 38]. Vieth et al.  studied a sample of young women (18–35 years old) in Toronto and found that 21% of white women, 31.9% of non-white women (a group which combined women of First Nations, South Asian, Indo-Asian and East Asian ancestries) and 25% of black women had serum concentrations below 40 nmol/L during the winter months. Rucker et al.  examined a group of men and women of mostly European ancestry living in western Canada and observed that 20% had serum concentrations below 40 nmol/L, 39% had serum concentrations below 50 nmol/L and 86% had serum concentrations below 80 nmol/L.
Past studies examining the vitamin D status of Canadians have focused primarily on individuals of European ancestry and have included few or no individuals of other ancestries, who constitute a large proportion of the population of Canadian metropolitan areas . Individuals of European ancestry have a lower risk of vitamin D insufficiency because they have low cutaneous melanin levels. It is well known that melanin interferes with the production of vitamin D in the skin and that individuals with darker skin pigmentation are at increased risk of vitamin D insufficiency . Therefore, it is likely that the prevalence of insufficiency among all Canadians exceeds currently reported estimates [28, 38]. Additionally, previous studies in Canada have failed to measure pigmentation quantitatively. Therefore, it is critical to expand the existing research to explore how differences in skin pigmentation  or other factors potentially associated with vitamin D levels, such as vitamin D dietary intake, supplementation or sun exposure, affect the vitamin D status of broadly defined population groups. Results of such studies will be important to inform public health policies regarding fortification and recommendation of intakes in order to ensure that all Canadians have sufficient vitamin D levels.
The aim of this study is to evaluate the wintertime vitamin D status and dietary vitamin D intake of young adults of diverse ancestry in Canada, and to assess the impact of quantitatively measured skin pigmentation and dietary intake on serum 25(OH)D levels.