Vitamin D Deficiency

Causes

The main function of vitamin D is to maintain calcium homeostasis, which is essential for development, growth, and maintenance of a healthy skeleton. In vitamin D deficiency, calcium absorption cannot be increased enough to satisfy the body’s calcium needs(3). For efficient dietary calcium absorption from the intestine vitamin D is needed.

Infants who are exclusively breast-fed and do not receive vitamin D supplementation are at high risk of vitamin D deficiency, particularly if if the lactating mother has insufficient vitamin D levels, or they have dark skin and/or receive little sun exposure (65). Older infants and toddlers exclusively fed milk substitutes and weaning foods that are not vitamin D fortified are also at risk of vitamin D deficiency (70).

Health experts recommend that all infants be given a vitamin D supplement of 400 IU/day (65).

The elderly have reduced capacity to synthesize vitamin D in skin when exposed to ultraviolet-B (UVB) radiation. In addition, the elderly are more likely to stay indoors or use sunscreen, which blocks vitamin D synthesis.

People with dark-colored skin synthesize less vitamin D on exposure to sunlight than those with light-colored skin (1). The risk of vitamin D deficiency is particularly high in dark-skinned people who live far from the equator.

Soft bones (‘osteomalacia’) have been documented in women who cover all of their skin whenever they are outside for religious or cultural reasons.

The application of sunscreen with a sun protection factor of 8 reduces production of vitamin D by 95% (1).

In addition, air and clouds reduce cutaneous vitamin D production.

Moreover, people with obesity (77), cystic fibrosis, cholestatic liver disease (61), and inflammatory bowel disease (78) can show an impaired absorption of dietary vitamin D.

Symptoms

Rapidly growing bones in infants and children are most severely affected by ‘rickets’: the growth plates of bones continue to enlarge, but in the absence of adequate mineralization, weight-bearing limbs (arms and legs) become bowed, and the rib cage may become deformed. In severe cases, low blood calcium levels (‘hypocalcemia’) may cause seizures.

Although adult bones are no longer growing, they are in a constant state of turnover (‘remodeling’), a process that includes bone break down (‘resorption’) and bone formation. In adults with severe vitamin D deficiency, the bone’s protein (‘collagen’) matrix is preserved but bone mineral is progressively lost, resulting in bone pain and soft bones (‘osteomalacia’).

Vitamin D deficiency causes muscle weakness and pain in children and adults (79, 80). A randomized controlled trial found that supplementation of elderly women with 800 IU/day of vitamin D and 1,200 mg/day of calcium for three months increased muscle strength and decreased the risk of falling by almost 50% compared to supplementation with calcium alone (81). A randomized controlled trial in 124 nursing home residents (average age, 89 years) found that those taking 800 IU/day of supplemental vitamin D had a 72% lower fall rate than those taking a placebo (82).

Assessing vitamin D nutritional status

The 25(OH)D level in blood is the best indicator of vitamin D deficiency and sufficiency (83). In general, serum 25(OH)D values less than 20–25 nanomoles (nmol)/L (8–10 ng/mL) indicate severe deficiency associated with rickets and osteomalacia (84). Although 50 nmol/L (20 ng/mL) has been suggested as the low end of the normal range (85), more recent research suggests that calcium absorption (86) is not optimized until blood 25(OH)D levels reach approximately 80 nmol/L (32 ng/mL), and that consequently values less than 80 nmol/L should be considered insufficient (84). Others suggest that a healthy serum 25(OH)D value is between 75 nmol/L and 125 nmol/L (30 ng/mL and 50 ng/mL) (87).

Data from supplementation studies indicate that vitamin D intakes of at least 800–1,000 IU/day are required by adults living in temperate latitudes to achieve serum 25(OH)D levels of at least 75 nmol/L (88, 89).

Authored by Dr Peter Engel in 2010, reviewed and updated by Dr Igor Bendik-Falconnier on 18.06.2017