title: Cortisol levels in response to starting school in children at increased risk for social phobia.
abstract: BACKGROUND
  Research on depression has identified hyperactivity of the HPA axis as a potential contributory factor to the intergenerational transmission of affective symptoms. This has not yet been examined in the context of social phobia. The current study compared HPA axis activity in response to a universal social stressor (starting school) in children of 2 groups of women: one with social phobia and one with no history of anxiety (comparison group). To determine specificity of effects of maternal social phobia, a third group of children were also examined whose mothers had generalised anxiety disorder (GAD).
  
  
  METHODS
  Children provided salivary cortisol samples in the morning, afternoon and at bedtime across 3 time-blocks surrounding the school start: a month before starting school (baseline), the first week at school (stress response), and the end of the first school term (stress recovery). Child behavioural inhibition at 14 months was assessed to explore the influence of early temperament on later stress responses.
  
  
  RESULTS
  All children displayed an elevation in morning and afternoon cortisol from baseline during the first week at school, which remained elevated until the end of the first term. Children in the social phobia group, however, also displayed an equivalent elevation in bedtime cortisol, which was not observed for comparison children or for children of mothers with GAD. Children in the social phobia group who were classified as 'inhibited' at 14 months displayed significantly higher afternoon cortisol levels overall.
  
  
  CONCLUSIONS
  A persistent stress response to school in the morning and afternoon is typical for all children, but children of mothers with social phobia also display atypical elevations in evening cortisol levels when at school--signalling longer-term disruption of the circadian rhythm in HPA axis activity. This is the first study to report HPA axis disruption in children at increased risk of developing social phobia. Future research should determine whether this represents a pathway for symptom development, taking early temperament into account.
authors.affiliation: Winnicott Research Unit, School of Psychology and Clinical Language Science, University of Reading, UK.
authors.forename: Stephanie J
authors.initials: SJ
authors.lastname: Russ
authors.forename: Joe
authors.initials: J
authors.lastname: Herbert
authors.forename: Peter
authors.initials: P
authors.lastname: Cooper
authors.forename: Megan R
authors.initials: MR
authors.lastname: Gunnar
authors.forename: Ian
authors.initials: I
authors.lastname: Goodyer
authors.forename: Tim
authors.initials: T
authors.lastname: Croudace
authors.forename: Lynne
authors.initials: L
authors.lastname: Murray
mesh_terms: D000328:Adult; D001008:Anxiety Disorders / Q000378:metabolism*; D002675:Child, Preschool; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000032:analysis*; D007030:Hypothalamo-Hypophyseal System / Q000378:metabolism; D007266:Inhibition, Psychological; D008297:Male; D009035:Mothers / Q000523:psychology; D010698:Phobic Disorders / Q000175:diagnosis / Q000378:metabolism*; D010913:Pituitary-Adrenal System / Q000378:metabolism; D012463:Saliva / Q000737:chemistry; D012574:Schools; D013315:Stress, Psychological / Q000378:metabolism; D013997:Time Factors
chemical_list: D006854:Hydrocortisone