Vitamin D and Health

5. Relationship between vitamin D exposure (from diet & skin
synthesis) and serum 25(OH)D concentration
5.1 Humans have two routes of exposure to vitamin D:
i. Vitamin D 3 derived from synthesis in human skin on exposure to UVB containing sunlight.
ii.
Dietary exposure through consumption of vitamin D 2 and D 3 in the form of naturally occurring
foods, fortified foods and dietary supplements. Some animal derived foods may contain small
amounts of 25(OH)D 3 in addition to vitamin D 3 .
Relationship between vitamin D intake and serum/plasma 25(OH)D concentration
5.2 The relationship between dietary exposure to vitamin D and serum 25(OH)D concentration could be
considered as the response of serum ‘total’ 25(OH)D concentration (i.e., summation of 25(OH)D 2 and
25(OH)D 3 ) to altered intake of vitamin D 2 and/or D 3 (plus 25(OH)D 3 in some cases). There are a
number of considerations which may impact on this relationship.
5.3 Vitamin D 2 and D 3 differ only in their side chain structure and both elevate serum total 25(OH)D
concentration (Seamans & Cashman, 2009). However, there is disagreement on whether both
vitamers are equally effective in raising and maintaining serum total 25(OH)D concentration (see
paragraphs 2.60-2.62).
5.4 Data indicate that per g of vitamin D compound consumed, 25(OH)D 3 (a minor dietary form) is
approximately 5-times as effective as vitamin D 3 in elevating serum 25(OH)D 3 concentration (Cashman
et al., 2012). This needs to be accounted for when deriving total vitamin D activity estimates for some
foods of animal origin (particularly in meats and eggs). It may also be of relevance to the vitamin D
content of breast milk.
5.5 It has been suggested that efficient absorption of vitamin D is dependent upon the presence of fat in
the intestinal lumen (Weber, 1981). Some physiological factors may also impact on the response of
serum 25(OH)D concentration to vitamin D intake. For example, in a study of healthy young adult
men (n=116; age, 28y), Barger-Lux et al. (1998) reported that the larger the BMI, the smaller the rise in
serum 25(OH)D concentration for any given dose of vitamin D. Forsythe et al. (2012), using data from
RCTs (Cashman et al., 2008; Cashman et al., 2009), reported that BMI was negatively associated with
change in serum 25(OH)D concentration following supplementation in older (n=109; age, ≥ 64y) but
not younger (n=118; age, 20-40y) adults. Barger-Lux et al. (1998) also observed that the higher the
baseline serum 25(OH)D concentration, the smaller the achieved concentration in response to a given
dose of vitamin D. However, a meta-regression analysis reported that baseline serum 25(OH)D
concentration did not influence the response of serum 25(OH)D concentration to vitamin D (IOM,
2011).
5.6 Despite these considerations, the relationship between vitamin D (not distinguishing between vitamin
D 2 and D 3 ) intake and serum 25(OH)D has been described. While a number of RCTs have reported the
response of serum 25(OH)D concentration to increased vitamin D intake (by supplementation), there
was great variability and many were not dose-response trials. Exploratory meta-regression analyses of
RCT data, 16 trials in adults (Cranney et al., 2007) and 36 trials in children and adults (Seamans &
Cashman, 2009), reported that for each additional 1 g (40 IU) of vitamin D consumed, serum
34