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monotonic association between melatonin suppression and circadian phase resetting induced by light exposure.<\/jats:p>\n <\/jats:list-item>\n \n We tested the association between melatonin suppression and phase resetting in humans.<\/jats:p>\n <\/jats:list-item>\n \n Sixteen young healthy participants received nocturnal bright light (\u223c9500\u00a0lux) exposure of continuous or intermittent patterns, and different durations ranging from 12\u00a0min to 6.5\u00a0h.<\/jats:p>\n <\/jats:list-item>\n \n Intermittent exposure patterns showed significant phase shifts with disproportionately less melatonin suppression.<\/jats:p>\n <\/jats:list-item>\n \n Each and every bright light stimulus in an intermittent exposure pattern induced a similar degree of melatonin suppression, but did not appear to cause an equal magnitude of phase shift.<\/jats:p>\n <\/jats:list-item>\n \n These results suggest that phase shifts and melatonin suppression are functionally independent such that one cannot be used as a proxy measure of the other.<\/jats:p>\n <\/jats:list-item>\n <\/jats:list>\n <\/jats:p>\n <\/jats:sec>\n \n Abstract<\/jats:title>\n \n Continuous experimental light exposures show that, in general, the conditions that produce greater melatonin suppression also produce greater phase shift, leading to the assumption that one can be used as a proxy for the other. We tested this association in 16 healthy individuals who participated in a 9\u2010day inpatient protocol by assessing melatonin suppression and phase resetting in response to a nocturnal light exposure (LE) of different patterns: (i) dim\u2010light control (<3\u00a0lux;\n n\u00a0=\u00a0<\/jats:italic>\n 6) or (ii) two 12\u2010min intermittent bright light pulses (IBL) separated by 36\u00a0min of darkness (\u223c9500\u00a0lux;\n n<\/jats:italic>\n \u00a0=\u00a010). We compared these results with historical data from additional LE patterns: (i) dim\u2010light control (<3\u00a0lux;\n n<\/jats:italic>\n \u00a0=\u00a011); (ii) single continuous bright light exposure of 12\u00a0min (\n n<\/jats:italic>\n \u00a0=\u00a09), 1.0\u00a0h (\n n<\/jats:italic>\n \u00a0=\u00a010) or 6.5\u00a0h (\n n<\/jats:italic>\n \u00a0=\u00a06); or (iii) an IBL light pattern consisting of six 15\u2010min pulses with 1.0\u00a0h dim\u2010light recovery intervals between them during a total of 6.5\u00a0h (\n n<\/jats:italic>\n \u00a0=\u00a07). All light exposure groups had significantly greater phase\u2010delay shifts than the dim\u2010light control condition (\n P<\/jats:italic>\n \u00a0<\u00a00.0001). While a monotonic association between melatonin suppression and circadian phase shift was observed, intermittent exposure patterns showed significant phase shifts with disproportionately less melatonin suppression. Each and every IBL stimulus induced a similar degree of melatonin suppression, but did not appear to cause an equal magnitude of phase shift. These results suggest unique specificities in how light\u2010induced phase shifts and melatonin suppression are mediated such that one cannot be used as a proxy measure of the other.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1113\/jp275501","type":"journal-article","created":{"date-parts":[[2018,4,29]],"date-time":"2018-04-29T20:05:52Z","timestamp":1525032352000},"page":"2147-2157","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":56,"title":["Functional decoupling of melatonin suppression and circadian phase resetting in humans"],"prefix":"10.1113","volume":"596","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8729-0500","authenticated-orcid":false,"given":"Shadab A.","family":"Rahman","sequence":"first","affiliation":[{"name":"Division of Sleep and Circadian Disorders, Departments of Medicine and Neurology Brigham & Women's Hospital Boston MA USA"},{"name":"Division of Sleep Medicine Harvard Medical School Boston MA 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