{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,18]],"date-time":"2026-05-18T23:48:02Z","timestamp":1779148082158,"version":"3.51.4"},"reference-count":59,"publisher":"Cambridge University Press (CUP)","issue":"1","license":[{"start":{"date-parts":[[2016,8,1]],"date-time":"2016-08-01T00:00:00Z","timestamp":1470009600000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Psychol. Med."],"published-print":{"date-parts":[[2017,1]]},"abstract":"<jats:sec id=\"S0033291716001574_sec_a1\">\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>There are no existing longitudinal studies of inflammatory markers and atopic disorders in childhood and risk of hypomanic symptoms in adulthood. This study examined if childhood: (1) serum interleukin-6 (IL-6) and C-reactive protein (CRP); and (2) asthma and\/or eczema are associated with features of hypomania in young adulthood.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"S0033291716001574_sec_a2\" sec-type=\"methods\">\n                    <jats:title>Method<\/jats:title>\n                    <jats:p>\n                      Participants in the Avon Longitudinal Study of Parents and Children, a prospective general population UK birth cohort, had non-fasting blood samples for IL-6 and CRP measurement at the age of 9 years (\n                      <jats:italic>n<\/jats:italic>\n                      = 4645), and parents answered a question about doctor-diagnosed atopic illness before the age of 10 years (\n                      <jats:italic>n<\/jats:italic>\n                      = 7809). These participants completed the Hypomania Checklist at age 22 years (\n                      <jats:italic>n<\/jats:italic>\n                      = 3361).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"S0033291716001574_sec_a3\" sec-type=\"results\">\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      After adjusting for age, sex, ethnicity, socio-economic status, past psychological and behavioural problems, body mass index and maternal postnatal depression, participants in the top third of IL-6 values at 9 years, compared with the bottom third, had an increased risk of hypomanic symptoms by age 22 years [adjusted odds ratio 1.77, 95% confidence interval (CI) 1.10\u20132.85,\n                      <jats:italic>p<\/jats:italic>\n                      &lt; 0.001]. Higher IL-6 levels in childhood were associated with adult hypomania features in a dose\u2013response fashion. After further adjustment for depression at the age of 18 years this association remained (adjusted odds ratio 1.70, 95% CI 1.03\u20132.81,\n                      <jats:italic>p<\/jats:italic>\n                      = 0.038). There was no evidence of an association of hypomanic symptoms with CRP levels, asthma or eczema in childhood.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"S0033291716001574_sec_a4\" sec-type=\"conclusion\">\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Higher levels of systemic inflammatory marker IL-6 in childhood were associated with hypomanic symptoms in young adulthood, suggesting that inflammation may play a role in the pathophysiology of mania. Inflammatory pathways may be suitable targets for the prevention and intervention for bipolar disorder.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1017\/s0033291716001574","type":"journal-article","created":{"date-parts":[[2016,8,1]],"date-time":"2016-08-01T07:34:52Z","timestamp":1470036892000},"page":"23-33","source":"Crossref","is-referenced-by-count":35,"title":["Childhood interleukin-6, C-reactive protein and atopic disorders as risk factors for hypomanic symptoms in young adulthood: a longitudinal birth cohort study"],"prefix":"10.1017","volume":"47","author":[{"given":"J. F.","family":"Hayes","sequence":"first","affiliation":[{"name":"UCL"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"G. 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