Vitamin D deficiency may in children lead to rickets and in adults to osteomalacia. However, there is no consensus as to what can be considered an adequate or optimal serum 25(OH)D level. The serum level of 25(OH)D is generally considered as the best marker of a subjects vitamin D status, due to its ease of measurement, long half-life and correlation with known vitamin D effects.

If the serum calcium level falls, the serum PTH level increase stimulating secretion of 1,25(OH) 2D and thereby restoration of the serum calcium level. The 25-hydroxylation is substrate driven, whereas the 1-hydroxylation is tightly regulated by parathyroid hormone (PTH). The main biological effect of 1,25(OH) 2D is to increase the intestinal calcium absorption. Vitamin D is first hydroxylated in the liver to 25-hydroxyvitamin D (25(OH)D), and then in the kidneys to 1,25-dihydroxyvitamin D (1,25(OH) 2D) which is the active form of the vitamin. Vitamin D is obtained from the diet or supplements and also from production in the skin upon sun exposure.

There is, at least in subjects with an adequate vitamin D intake, a negative association between calcium intake and serum 25(OH)D. In females with higher vitamin D intakes, increasing calcium intake was associated with lower serum 25(OH)D levels. In the females, there was in subjects with low vitamin D intake (< 7 μg/d) a significant increase in serum 25(OH)D with increasing calcium intake, which could not be explained by secondary hyperparathyroidism. The difference in serum 25(OH)D between those with the highest and lowest calcium intakes was approximately 10%. In males there was, regardless of vitamin D intake, a significant decrease in serum 25(OH)D with increasing calcium intake. The analyses were therefore done stratified. There were significant interactions between sex, calcium and vitamin D intakes regarding serum 25(OH)D level. In the seventh survey of the Tromsø study, serum 25(OH)D and parathyroid hormone were measured, and questionnaires on calcium and vitamin D intakes filled in. However, there are only a few studies where this has been examined. There are indications that an increased intake of calcium has a vitamin D sparing effect, which might be explained by a decreased catabolism of 25-hydroxyvitamin D (25(OH)D).

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