Introduction to vitamin D deficiency

The main source of vitamin D (colecalciferol or vitamin D3) in humans is ultraviolet B radiation from the sun acting on 7-dehydrocholesterol in the skin. Vitamin D3 is converted in the liver to 25-hydroxyvitamin D, the form of vitamin D that is measured in the serum. 25-hydroxyvitamin D is converted in the kidneys to the active form of vitamin D, 1,25-dihydroxyvitamin D (calcitriol), which promotes absorption of calcium and phosphate from the gut, and assists bone mineralisation by interacting with parathyroid hormone. Dietary sources provide less than 10% of total requirements of vitamin D.

Adequate exposure to sunlight is the best way to prevent vitamin D deficiency. The amount of exposure required depends on the season, the location (ie distance from the equator) and the person’s skin tone. Suggested exposure times depending on location in Australia can be found on the Healthy Bones Australia website.

Vitamin D deficiency can be classified by severity, as shown in Classification of vitamin D deficiency by severity. Serum 25-hydroxyvitamin D concentration can vary seasonally by up to 20 nanomol/L, so measurements should always be interpreted in the context of the season.

Vitamin D deficiency is usually asymptomatic, but can present with mild bone pain and muscle weakness. Severe deficiency can cause defects in bone mineralisation leading to osteomalacia in adults or rickets in children.

Table 1. Classification of vitamin D deficiency by severity

[NB1]

Severity of vitamin D deficiency

Serum 25-hydroxyvitamin D concentration

mild

30 to 49 nanomol/L

moderate

12.5 to 29 nanomol/L

severe

lower than 12.5 nanomol/L

Note: NB1: Serum 25-hydroxyvitamin D concentration can vary seasonally by up to 20 nanomol/L, so measurements should always be interpreted in the context of the season.