{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,22]],"date-time":"2026-07-22T20:39:18Z","timestamp":1784752758508,"version":"3.55.0"},"reference-count":52,"publisher":"MDPI AG","issue":"6","license":[{"start":{"date-parts":[[2016,6,3]],"date-time":"2016-06-03T00:00:00Z","timestamp":1464912000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Nutrients"],"abstract":"<jats:p>Inadequate dietary intake of vitamin C results in hypovitaminosis C, defined as a plasma ascorbate concentration \u226423 \u03bcmol\/L. Our objective was to carry out a retrospective analysis of two vitamin C supplementation studies to determine whether supplementation with 50 mg\/day vitamin C is sufficient to restore adequate ascorbate status (\u226550 \u03bcmol\/L) in individuals with hypovitaminosis C. Plasma ascorbate data from 70 young adult males, supplemented with 50 or 200 mg\/day vitamin C for up to six weeks, was analyzed. Hypovitaminosis C status was identified based on plasma ascorbate being \u226423 \u03bcmol\/L and the response of these individuals to vitamin C supplementation was examined. Of the participants consuming 50 mg\/day vitamin C for up to six weeks, those with hypovitaminosis C at baseline achieved plasma concentrations of only ~30 \u03bcmol\/L, whereas the remainder reached ~50 \u03bcmol\/L. Participants who consumed 200 mg\/day vitamin C typically reached saturating concentrations (&gt;65 \u03bcmol\/L) within one week, while those with hypovitaminosis C required two weeks to reach saturation. Regression modelling indicated that the participants\u2019 initial ascorbate status and body weight explained ~30% of the variability in the final ascorbate concentration. Overall, our analysis revealed that supplementation with 50 mg\/day vitamin C, which resulted in a total dietary vitamin C intake of 75 mg\/day, was insufficient to achieve adequate plasma ascorbate concentrations in individuals with hypovitaminosis C. Furthermore, increased body weight had a negative impact on ascorbate status.<\/jats:p>","DOI":"10.3390\/nu8060341","type":"journal-article","created":{"date-parts":[[2016,6,3]],"date-time":"2016-06-03T10:37:37Z","timestamp":1464950257000},"page":"341","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":31,"title":["Marginal Ascorbate Status (Hypovitaminosis C) Results in an Attenuated Response to Vitamin C Supplementation"],"prefix":"10.3390","volume":"8","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5890-2977","authenticated-orcid":false,"given":"Anitra","family":"Carr","sequence":"first","affiliation":[{"name":"Department of Pathology, University of Otago, Christchurch, P.O. Box 4345, Christchurch 8140, New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Juliet","family":"Pullar","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Otago, Christchurch, P.O. Box 4345, Christchurch 8140, New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephanie","family":"Bozonet","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Otago, Christchurch, P.O. Box 4345, Christchurch 8140, New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4261-0854","authenticated-orcid":false,"given":"Margreet","family":"Vissers","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Otago, Christchurch, P.O. Box 4345, Christchurch 8140, New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2016,6,3]]},"reference":[{"key":"ref_1","first-page":"443","article-title":"Ascorbic acid: Chemistry, biology and the treatment of cancer","volume":"1826","author":"Du","year":"2012","journal-title":"Biochim. Biophys. 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