The Use of Vitamins and Minerals in Skeletal Health

American Association of Clinical Endocrinologists and the American College of Endocrinology Position Statement

Daniel L. Hurley, MD, FACE; Neil Binkley, MD, FACE; Pauline M. Camacho, MD, FACE; Dima L. Diab, MD, FACE, FACP, CCD; Kurt A. Kennel, MD, FACE; Alan Malabanan, MD, FACE, CCD; Vin Tangpricha, MD, PhD, FACE

Disclosures

Endocr Pract. 2018;24(10):915-924. 

In This Article

Vitamin D

Vitamin D is present only in small amounts in food, and it is primarily produced in the skin upon exposure to ultraviolet B radiation.[47] Hypovitaminosis D is common when dietary intake is low or poorly absorbed and sun exposure is limited. Vitamin D plays a major role in active GI transport of calcium and may improve muscle function and balance, thereby reducing fall risk,[48] which is important for patients with osteoporosis, as falls cause ≥90% of hip fractures. Furthermore, vitamin D might also improve the BMD response to bisphosphonates.[49,50] As a result of all these skeletal effects, multiple medical organizations recommend optimizing vitamin D status as a core component in the treatment of osteoporosis. Defining "vitamin D inadequacy" is extremely controversial. RCTs evaluating nutrients are often confounded when "low" nutrient status is not established, since nutrients reach a threshold effect in which greater amounts do not provide enhanced physiologic effects.[51] As such, providing vitamin D to volunteers who are vitamin D replete should not be expected to demonstrate beneficial effects. Another major confounder is variability of the 25-hydroxyvitamin D (25[OH]D) assay. Despite being the best determinate of bodily vitamin D status,[52] substantial variability between 25(OH)D assays and laboratories persists.[53] The Office of Dietary Supplements Vitamin D Standardization Program (VDSP) facilitates standardization of the intra-assay variability and bias of 25(OH)D measurements, recommending a 10% coefficient of variation (CV) for clinical laboratories.[54] It is important to appreciate this assay variability. For example, a 25(OH)D laboratory result of 30 ng/mL meeting the 10% CV VDSP recommendation means that the "true" value is between 24 and 36 ng/mL.[55] Such variability in 25(OH)D results represents a major challenge to meta-analyses of RCTs.[56]

Based on this background of uncertainty, systematic reviews find vitamin D supplementation with daily doses of ≥800 IU to reduce hip and nonvertebral fractures.[57,58] A reasonable clinical approach is a vitamin D intake of ≥1,000 IU/day for adults ≥50 years of age, as vitamin D inadequacy is common in those with a low BMD or prior fragility fracture. AACE/ACE clinical practice guidelines recommend vitamin D sufficiency be defined as serum 25(OH)D ≥30 ng/mL, based on an increased prevalence of secondary hyperparathyroidism below this level.[22] The IOM reviewed virtually the same evidence base and recommended 25(OH)D ≥20 ng/mL to define vitamin D sufficiency.[52]

The level that constitutes "high" vitamin D status is similarly controversial. A conservative upper level, based upon 25(OH)D values achieved by highly sun-exposed young adults, is 50 to 60 ng/mL.[59] Reasonable approaches to vitamin D assessment and treatment include an initial measurement of 25(OH)D in patients at risk of deficiency, or alternatively, vitamin D supplementation and subsequent 25(OH)D measurement 3 to 4 months later to assess dose adequacy. The amount of vitamin D required to correct deficiency and reach target levels varies among individuals due to as yet poorly understood factors, to include obesity and ethnicity.[60] Use of huge single doses of vitamin D is not recommended, as limited data find this approach to paradoxically increase falls and fracture risk.[61] It is essential that vitamin D replacement of deficient states be followed by maintenance dosing (e.g., 1,000 to 2,000 IU/day), recognizing that higher doses may be needed in patients with obesity or malabsorption.

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