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The role of vitamin D in skeletal and mineral ion homeostasis has been long accepted. Dietary vitamin D and vitamin D endogenously synthesized in the skin are converted in the liver to 25-hydroxyvitamin D (25[OH]D). Serum 25(OH)D measurement estimates an individual’s vitamin D status. Studies suggesting the association of low vitamin D levels with increased risk of various diseases has led to extensive use of supplementation and laboratory testing of 25(OH)D in serum (1). However, there is a lack of knowledge on appropriate 25(OH)D levels needed to prevent disease and also a lack of causative evidence relating low 25(OH)D levels to increased disease risk. These gaps in knowledge have called into question the utility of 25(OH)D testing (2, 3). Because of the deficiency in knowledge surrounding the efficacy of vitamin D supplementation in disease prevention, an expert panel from the Endocrine Society produced Clinical Practice Guidelines to aid health care professionals in vitamin D supplementation and 25(OH)D testing (4). One major recent update from the previous 2011 guideline is that the Endocrine Society is no longer supporting specific serum levels of 25(OH)D in defining sufficiency, insufficiency, and deficiency due to lack of clinical trial evidence (3, 4).

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