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In this issue of the Journal, Hao et al. (1) report a secondary analysis of a multicenter study on a large cohort of patients who had a hip fracture requiring surgical intervention to determine the influence of vitamin D status and the Geriatric Nutritional Risk Index on mortality rates and ability to ambulate. They conclude that patients who had a serum 25-hydroxyvitamin D [25(OH)D] of ≥12 ng/mL had higher rates of self-reported walking at 30 and 60 d postoperatively compared with patients with a 25(OH)D <12 ng/mL. On the other hand, poor nutritional status was observed to have a marginal effect on reduced mobility at 30 d but not at 60 d. They also found no association of vitamin D status nor nutritional status on mortality at these 2 time points. This editorial begins with a brief summary of previous studies providing insight about the controversy associated with vitamin D supplementation recommendations for improving muscle function. It then discusses the merits of the study by Hao et al. (1) and its health implications not only for elderly with hip fractures but also for all children and adults. By the turn of the 20th century, rickets was a pandemic in most industrialized cities throughout the world (2). The most obvious clinical manifestations were skeletal deformities and growth retardation. However, it was also recognized that children with skeletal manifestations of rickets presented with proximal muscle weakness especially in the hip girdle region (2). Because severe vitamin D deficiency can cause hypocalcemia and hypophosphatemia, it was thought that the muscle weakness was associated with deficiencies of these minerals, which were considered to be essential for maximum skeletal muscle function. Correction of vitamin D deficiency in these children rapidly improved muscle function, whereas improvement in the skeletal abnormalities required a longer duration of therapy. What is the role of vitamin D for skeletal muscle function? Does it have a direct effect on maintaining maximum skeletal muscle function, or are the associated alterations in calcium and phosphate metabolism more likely to affect skeletal muscle function? Vitamin D deficiency results in a decrease in the efficiency of intestinal calcium and phosphorus absorption. In response to the decrease in the body’s ability for acquiring calcium from the diet, the parathyroid glands increase the production and release of parathyroid hormone (PTH) into the circulation. In the kidneys, PTH conserves calcium by increasing tubular reabsorption of calcium from the ultrafiltrate. PTH also causes the internalization of the sodium phosphate cotransporter, resulting in a loss of phosphate into the urine and a decrease in serum phosphate concentrations. PTH also takes advantage of the skeletal stores of calcium by stimulating the production of receptor activator of NF-κB ligand (RANKL) in osteoblasts. This ligand interacts with its receptor RANK on monocytes, inducing them to amalgamate into multinucleated osteoclasts. The mature osteoclasts release HCl and collagenases, causing the release of skeletal calcium into the circulation. PTH also stimulates the kidneys to convert 25(OH)D to 1,25-dihydroxyvitamin D [1,25(OH)2D]. 1,25(OH)2D interacts with its nuclear vitamin D receptor (VDR) in the intestine to increase the efficiency of intestinal calcium absorption. It interacts with its VDR in osteoblasts, resulting in the production of RANKL, which like PTH increases the production of osteoclasts. The net effect is for PTH to maintain a normal serum calcium while reducing serum phosphate concentrations. The consequence is a reduced calcium phosphate product, resulting in a mineralization defect of newly laid down collagen matrix and thus resulting in rickets in children and the painful muscle and bone disease, osteomalacia, in adults (2, 3). Vitamin D exerts multiple effects on skeletal muscle health. Evidence suggests that skeletal muscle has a VDR and the ability to convert 25(OH)D to 1,25(OH)2D (2, 3). It has been proposed that 1,25(OH)2D has both genomic and nongenomic effects, including calcium signaling in skeletal muscle cells (2). Previous studies illustrate that vitamin D plays a pivotal role in muscle cell proliferation and differentiation as well as improving muscle mitochondrial activity, functional capacity, and having a protective effect on muscle fat accumulation and mitochondrial dysfunctions (2, 4). Lower extremity function, proximal muscle strength, and physical performance have been

A call for action: standard of care guidelines to assess vitamin D status are needed for patients with hip fracture