Neuropsychopharmacology (2013) 38, 259-274; doi:10 1038/npp 2012

Neuropsychopharmacology (2013) 38, 259-274; doi:10.1038/npp.2012.179; published online 5 September 2012″
“Background. Clinical depression involves persistent dysphoria, implicating impaired affect regulation or mood repair failure. Ulixertinib However, there is comparatively little information about the mood repair repertoires of individuals with histories of clinical depression, how their repertories differ from that of never-depressed people, and whether particular types of mood repair responses differentially contribute to depression risk.

Method. Adult probands who had childhood-onset

depressive disorder (n=215) and controls with no history of major mental disorder (n=122) reported which specific (cognitive, behavioral, interpersonal and soma

tic-sensory) responses they typically deploy when experiencing sad affect, including responses known to appropriately attenuate dysphoria (‘adaptive’ responses) and those known to exacerbate dysphoria in the short or long run (‘maladaptive’ responses). Subjects were longitudinally followed and evaluated.

Results. Remitted probands and probands in depressive episodes both reported a greater number of maladaptive responses and fewer adaptive responses to their own sadness PF-573228 than did controls, although probands did not have an absolute deficiency of adaptive responses. Maladaptive (but not adaptive) mood repair responses predicted future increases in depression symptoms and an increased probability of a recurrent depressive episode among probands (even after controlling for several clinical predictors

of course). Post-hoc analyses revealed that maladaptive non-cognitive and maladaptive cognitive mood repair response sets each predicted depression Outcomes.

Conclusions. Individuals with past and present episodes of depressive disorder report an array of cognitive and non-cognitive responses to their own sadness that are likely to exacerbate that affect, and this pattern predicts a worse course of ARN-509 molecular weight the disorder.”
“Adolescence and young adulthood off er opportunities for health gains both through prevention and early clinical intervention. Yet development of health information systems to support this work has been weak and so far lagged behind those for early childhood and adulthood. With falls in the number of deaths in earlier childhood in many countries and a shifting emphasis to non-communicable disease risks, injuries, and mental health, there are good reasons to assess the present sources of health information for young people. We derive indicators from the conceptual framework for the Series on adolescent health and assess the available data to describe them.

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