Vitamin D is a hormone that controls phosphorus, calcium, and bone metabolism and neuromuscular function. Vitamin D synthesis is a process in which the skin, liver, and kidney are sequentially involved. The vitamin D pool is completed by the amount taken with food and supplements. Vitamin D deficiency causes osteopenia, precipitates and exacerbates osteoporosis, causes a painful disease, osteomalacia, and increases muscle weakness, which worsens the risk of falls and fractures. A high prevalence of vitamin D insufficiency exists in the apparently healthy population, osteoporotic patients, and patients with prior fractures. Factors contributing to low vitamin D levels include low sunlight exposure, decreased skin synthesis and intestinal absorption, and inadequate diet. The simplest way to correct hypovitaminosis is adequate nutrition and supplements. However, few patients with osteoporosis and/or fractures, receive adequate supplements. Vitamin D insufficiency may alter the regulatory mechanisms of parathyroid hormone and may induce a secondary hyperparathyroidism that increases the risk of osteoporosis and fractures, although the necessary degree of this is not established. Monitoring of serum 25-hydroxyvitamin D levels is the only way to assess vitamin D status. The ideal healthy blood levels of 25-hydroxyvitamin D are controversial, although a range from 30 to 60ng/mL is widely accepted. The role of vitamin D supplementation is to provide humans with the nutrient in an amount closer to the biological norm for our species. This amount of vitamin D results in optimal function of many aspects of health, including balance and muscle strength, thus reducing the risk of fracture beyond what is possible via the quality and quantity of bone itself.