{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T23:10:38Z","timestamp":1791846638065,"version":"4.3.4"},"reference-count":63,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2014,11,29]],"date-time":"2014-11-29T00:00:00Z","timestamp":1417219200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Intl J Eating Disorders"],"published-print":{"date-parts":[[2015,11]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>In anorexia nervosa (AN), osteoporosis and osteopenia are common, which have been associated with low circulating levels of vitamin D (VitD) in other settings. We aimed to meta\u2010analyze cross\u2010sectional studies reporting on VitD parameters in patients with AN and healthy controls (HCs).<\/jats:p><\/jats:sec><jats:sec><jats:title>Method<\/jats:title><jats:p>Electronic PubMed search from database inception until December 31, 2013 and meta\u2010analysis of cross\u2010sectional studies comparing serum levels of 25\u2010hydroxyvitamin D (25OH\u2010D), 1,25\u2010dihydroxyvitamin D (1,25OH\u2010D) and dietary VitD between patients with AN and HCs, before or after VitD supplementation. We calculated random effects standardized mean differences (SMDs) \u00b195% confidence intervals (CIs) as effect size measures.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Out of 1,739 initial hits, 15 studies with a total of 927 participants (AN\u2009=\u2009408 and HCs\u2009=\u2009519) were meta\u2010analyzed. In the unsupplemented state, both serum 25OH\u2010D (studies\u2009=\u20094; <jats:italic>n<\/jats:italic>\u2009=\u2009168; SMD\u2009=\u2009\u22120.43; 95%CI: \u22120.83 to \u22120.03; <jats:italic>p<\/jats:italic>\u2009=\u2009.03) and 1,25OH\u2010D levels (studies\u2009=\u20094; <jats:italic>n<\/jats:italic>\u2009=\u2009113; SMD\u2009=\u2009\u22121.06; 95%CI: \u22121.47 to \u22120.66; <jats:italic>p<\/jats:italic>\u2009&lt;\u2009.00001) were significantly lower in AN than HCs. In AN patients treated with cholecalciferol supplementation, serum 25OH\u2010D levels were significantly higher than in HCs (studies\u2009=\u20095; <jats:italic>n<\/jats:italic>\u2009=\u2009449; SMD\u2009=\u20090.66; 95%CI: 0.01\u20131.31; <jats:italic>p<\/jats:italic>\u2009=\u2009.05). Paradoxically, despite lower 25OH\u2010D and 1,25OH\u2010D levels, AN patients reported similar intake of VitD compared to HCs (studies\u2009=\u20096; <jats:italic>n<\/jats:italic>\u2009=\u2009314; SMD\u2009=\u20090.33; 95%CI: \u22120.16, 0.81; <jats:italic>p<\/jats:italic>\u2009=\u2009.19).<\/jats:p><\/jats:sec><jats:sec><jats:title>Discussion<\/jats:title><jats:p>Although AN patients reported similar dietary VitD intake compared to HCs, AN patients had significantly lower 25OH\u2010D and 1,25OH\u2010D levels without supplementation. Conversely, supplementation with cholecalciferol fully normalized VitD serum levels. Future studies are needed to clarify the role of VitD supplementation in AN for improving bone health. \u00a9 2014 Wiley Periodicals, Inc. 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