Vitamin D and Aging

Abstract

Aging affects the formation of 1,25-dihydroxyvitamin D (1,25[OH]2D; calcitriol), the active form of vitamin D. Production of 1,25(OH)2D is reduced by 50% as a result of an age-related decline in renal function, although serum 1,25(OH)2D levels are maintained in part by secondary hyperparathyroidism. Aging also causes a decrease in calcium absorption that precedes the decrease in 1,25(OH)2D by 10 to 15 years. Because 1,25(OH)2D is dependent on an adequate supply of the substrate vitamin D, the development of vitamin D deficiency leads to further reduction in the formation of 1,25(OH)2D. Measurement of the metabolite 25OHD provides the most widely used assessment of vitamin D deficiency. A serum 25OHD level lower than 10 ng/mL (25 nmol/L) represents vitamin D deficiency and leads to a reduction in serum 1,25(OH)2D. Vitamin D deficiency, is uncommon in North America, probably because of supplementation of dairy products and other foods with vitamin D. Sunlight exposure increases serum 25OHD levels by about 10 ng/mL during the months of April through September, resulting in low serum 25OHD for about 3 to 4 months in winter, with 2 additional months of low levels in more northern latitudes, such as Canada, and 2 fewer months in the southern states. Vitamin D supplementation in the winter can prevent vitamin D deficiency. Vitamin D insufficiency has been defined by the Institute of Medicine as a serum 25OHD level lower than 20 ng/mL (and >10 ng/mL). A serum 25OHD level lower than 20 ng/mL is associated with an increased fracture rate and increased rate of bone loss and treatment. Although other diseases have been associated with low serum 25OHD levels, the evidence for a causative role has not yet been established. Treatment of elderly people with vitamin D 800 IU daily will increase serum 25OHD levels to higher than 20 ng/mL and reduce fractures; this is particularly important in institutionalized people.