{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,1]],"date-time":"2026-04-01T11:42:15Z","timestamp":1775043735141,"version":"3.50.1"},"reference-count":30,"publisher":"Oxford University Press (OUP)","issue":"5","content-domain":{"domain":["eje.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2011,11]]},"abstract":"<jats:sec><jats:title>Objective<\/jats:title><jats:p>Iodine deficiency has re-emerged in New Zealand, while selenium status has improved. The aim of this study was to investigate the effects of excess iodine intake as iodate on thyroid and selenium status.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>In a randomized controlled trial on older people (mean\u00b1<jats:sc>s.d<\/jats:sc>. 73\u00b14.8 years;<jats:italic>n<\/jats:italic>=143), two groups received &gt;50\u200amg iodine as iodate\/day for 8 weeks because of supplement formulation error, either with 100\u200a\u03bcg selenium (Se+highI) or without selenium (highI). Four other groups received 80\u200a\u03bcg iodine as iodate\/day with selenium (Se+lowI) or without selenium (lowI), selenium alone (Se+), or placebo. Thyroid hormones, selenium status, and median urinary iodine concentration (MUIC) were compared at weeks 0, 8, and 4 weeks post-supplementation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>MUIC increased nine- and six-fold in Se+highI and highI groups, decreasing to baseline by week 12. Plasma selenium increased in selenium-supplemented groups (<jats:italic>P<\/jats:italic>&lt;0.001). The level of increase in whole blood glutathione peroxidase (WBGPx) in the Se+highI group was smaller than Se+ (<jats:italic>P<\/jats:italic>=0.020) and Se+lowI (<jats:italic>P<\/jats:italic>=0.007) groups. The decrease in WBGPX in the highI group was greater than other non-selenium-supplemented groups, but differences were not significant. Ten of 43 participants exposed to excess iodate showed elevated TSH (hypothyroidism) at week 8. In all but two, TSH had returned to normal by week 12. In three participants, TSH decreased to &lt;0.10\u200amIU\/l (hyperthyroidism) at week 8, remaining low at week 12.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Excess iodate induced hypothyroidism in some participants and hyperthyroidism in others. Most abnormalities disappeared after 4 weeks. Excess iodate reduced WBGPx activity and resulted in smaller increases in WBGPx after selenium supplementation.<\/jats:p><\/jats:sec>","DOI":"10.1530\/eje-11-0575","type":"journal-article","created":{"date-parts":[[2011,8,31]],"date-time":"2011-08-31T02:21:20Z","timestamp":1314757280000},"page":"745-752","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-1","source":"Crossref","is-referenced-by-count":16,"title":["Minimal impact of excess iodate intake on thyroid hormones and selenium status in older New Zealanders"],"prefix":"10.1093","volume":"165","author":[{"given":"Christine D","family":"Thomson","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jennifer M","family":"Campbell","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jody","family":"Miller","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sheila A","family":"Skeaff","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","reference":[{"issue":"2","key":"1_31343035","doi-asserted-by":"publisher","first-page":"81","DOI":"10.1016\/j.jtemb.2008.03.001","volume":"22","author":"Zimmermann","year":"2008","journal-title":"Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS)","ISSN":"https:\/\/id.crossref.org\/issn\/0946-672X","issn-type":"print"},{"issue":"6","key":"2_10889906","doi-asserted-by":"crossref","first-page":"545","DOI":"10.1089\/thy.1999.9.545","volume":"9","author":"Delange","year":"1999","journal-title":"Thyroid : official journal of the American Thyroid Association","ISSN":"https:\/\/id.crossref.org\/issn\/1050-7256","issn-type":"print"},{"key":"3_40944689","first-page":"83","volume":"8","year":"1999","journal-title":"Thyroid : official journal of the American Thyroid Association","ISSN":"https:\/\/id.crossref.org\/issn\/1050-7256","issn-type":"print"},{"issue":"3","key":"4_11908185","doi-asserted-by":"crossref","first-page":"203","DOI":"10.1111\/j.1445-5994.1971.tb02290.x","volume":"1","author":"Stewart","year":"1971","journal-title":"Australian and New Zealand journal of medicine","ISSN":"https:\/\/id.crossref.org\/issn\/0004-8291","issn-type":"print"},{"issue":"3","key":"5_9463048","doi-asserted-by":"crossref","first-page":"179","DOI":"10.1111\/j.1365-2265.1991.tb00290.x","volume":"34","author":"Ford","year":"1991","journal-title":"Clinical endocrinology","ISSN":"https:\/\/id.crossref.org\/issn\/0300-0664","issn-type":"print"},{"issue":"2","key":"6_9205581","doi-asserted-by":"crossref","first-page":"249","DOI":"10.1111\/j.1365-2265.1990.tb00489.x","volume":"33","author":"Brownlie","year":"1990","journal-title":"Clinical endocrinology","ISSN":"https:\/\/id.crossref.org\/issn\/0300-0664","issn-type":"print"},{"issue":"8","key":"7_28633866","doi-asserted-by":"publisher","first-page":"3122","DOI":"10.1210\/jc.2007-0732","volume":"92","year":"2007","journal-title":"Journal of Clinical Endocrinology &amp; 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