Health care for our bones: A practical nutritional approach to preventing osteoporosis

Abstract

elsewhere. 3-5 Vitamin D deficiency is epidemic in the United States and in other industrialized nations where dietary sources of vitamin D are inadequate and where people spend most of their time indoors and/or otherwise bprotectedQ from ultraviolet radiation by either clothes or sunscreen. Hypovitaminosis D impairs calcium absorption, increases calcium resorption from bone, and contributes significantly to a wide variety of common clinical disorders, including low back pain and generalized musculoskeletal pain. 6 Not surprisingly, subclinical vitamin D deficiency contributes significantly to the high prevalence of osteoporosis, and when left untreated, vitamin D deficiency impairs responsiveness to bone-building interventions, including bisphosphonate treatment 7 and nutritional-botanical interventions, as we have recently pointed out elsewhere. 5 In our recent review of the literature, 3 we concluded that optimal vitamin D status correlates with serum levels of 25-OHvitamin D in the range of 40 to 65 ng/mL (100-160 nmol/L). Serum levels of 25-OH-vitamin D must equal or exceed 40 ng/mL (100 nmol/L) to attain effective reduction of serum parathyroid hormone, and our optimal range for vitamin D is consistent with the serum levels seen in populations with adequate sun exposure and is not associated with adverse effects. To attain and maintain optimal vitamin D serum levels in the absence of frequent full-body sun exposure, oral supplementation at levels of 1000 IU/d for infants, 2000 IU/d for children, and 4000 IU/d for adults is required; these dosages are safe and are well supported by peer-reviewed research and clinical trials. Vitamin D toxicity is exceedingly rare at the physiological doses suggested here, provided that the patient does not have hypersensitivity to vitamin D (such as with sarcoi