title: Hypothalamic-pituitary-adrenal axis dysregulation in dysphoric children and adolescents: cortisol reactivity to psychosocial stress from preschool through middle adolescence.
abstract: BACKGROUND
  Most depressed adults exhibit dysregulation of the hypothalamic-pituitary-adrenal axis, including cortisol hyperreactivity to psychosocial challenge. In contrast, remarkably little is known about hypothalamic-pituitary-adrenal axis activity in response to psychosocial challenge among at-risk children and adolescents. This study examined cortisol response to psychosocial challenge in nondepressed, at-risk, dysphoric and nondysphoric control youth across different developmentally salient age groups (preschool, third-, sixth-, and ninth-graders).
  
  
  METHODS
  Two samples of youth (Study 1-preschoolers; Study 2-third-, sixth-, and ninth-graders) without a history of clinical depression were administered developmentally appropriate psychosocial challenges. Of these nondepressed children, we examined youth at high-risk (n = 60) and low-risk (n = 223) status, as defined by elevated but subthreshold dysphoric symptoms according to multiple informants. Cortisol levels were assessed before and after a psychosocial stressor.
  
  
  RESULTS
  Nondysphoric control youth at all ages displayed the expected cortisol rise to challenge followed by return to baseline. However, prepubertal, at-risk, dysphoric children--specifically preschoolers and third-graders--exhibited cortisol hyporeactivity to challenge, whereas postpubertal dysphoric adolescents (ninth-graders) displayed hyperreactivity to the stressor. Additional analyses revealed that this switch from cortisol hyporeactivity to hyperreactivity among at-risk, dysphoric youth occurred as a function of pubertal development.
  
  
  CONCLUSIONS
  Findings suggest a developmental switch in cortisol response for at-risk, dysphoric youth from preschool through adolescence and have implications for a developmental pathophysiological understanding of how at-risk youth across the lifespan might develop depressive disorder.
authors.affiliation: Department of Psychology, University of Denver, Denver, Colorado 80208, USA. ben.hankin@psy.du.edu
authors.forename: Benjamin L
authors.initials: BL
authors.lastname: Hankin
authors.forename: Lisa S
authors.initials: LS
authors.lastname: Badanes
authors.forename: John R Z
authors.initials: JR
authors.lastname: Abela
authors.forename: Sarah E
authors.initials: SE
authors.lastname: Watamura
mesh_terms: D000293:Adolescent; D000328:Adult; D000342:Affective Symptoms / Q000503:physiopathology / Q000523:psychology; D000818:Animals; D002648:Child; D002675:Child, Preschool; D006801:Humans; D006854:Hydrocortisone / Q000097:blood / Q000378:metabolism; D007030:Hypothalamo-Hypophyseal System / Q000502:physiology / Q000503:physiopathology; D019964:Mood Disorders / Q000503:physiopathology / Q000523:psychology; D010913:Pituitary-Adrenal System / Q000502:physiology / Q000503:physiopathology; D011627:Puberty / Q000502:physiology / Q000523:psychology*; D051381:Rats; D013315:Stress, Psychological / Q000503:physiopathology / Q000523:psychology
chemical_list: D006854:Hydrocortisone