SS-01-01

The impact of childhood trauma on co-morbid symptoms in first episode psychosis

M. Birchwood. Early Intervention Service, Un, Birmingham, United Kingdom

Objective: To evaluate the impact of childhood trauma as a risk factor for the development of co-morbid disorders in individuals with first episode psychosis. Background evidence is accruing that levels of trauma and abuse are high in clinical populations but the effect of different types of abuse on co-morbid symptoms of psychosis remains unclear.

Methods: Clients of a first episode early intervention service (n=26) were compared with a non-clinical sample (n=54) employing the Childhood Trauma Questionnaire (CTQ); Dissasociative Experiences Scale (DES) and Hammarberg Scale for PTSD. Samples did not differ in age or gender.

Results: Significant differences were found between the samples for levels of emotional neglect (p<0.001) physical abuse (p>0.02) sexual abuse (19<0.04) and PTSD (p,0.02) with significant correlations between dissociation and childhood trauma sub-scales. Further analysis revealed patterns of substance use and positive symptoms associated with trauma sub-scales in the clinical sample.

Conclusion: A consideration of the role of early trauma on the development of co-morbid symptoms including PTSD and dissociative disorders may have implications for assessment and intervention approaches for individuals with psychosis.

SS-01-02

R. Murray. Institute of Psychiatry, London, United Kingdom

SS-01-03

Genes that make you feel blue in the flow of daily life: A momentary assessment study of gene-stress interaction

N. Jacobs. Maastricht University, Maastricht, Netherlands

Objective: Individual differences in stress-reactivity constitute a crucially important mechanism of risk for depression. As stress is better conceptualized as the continuous occurrence of minor daily hassles, this study focused on emotional reactivity to stress in the flow of daily life and examined to what degree individual differences in emotional reactivity could be explained by genetic and/or environmental factors.

Methods: 275 female twin pairs (170 monozygotie and 105 dizygotic) participated in this Experience Sampling study (ESM). ESM is a validated structured diary technique assessing stressors and mood in daily life. Individual emotional stress-reactivity was conceptualised as changes in negative affect in relation to minor daily life stressors. Structural equation modelling was used to fit univariate models. The best fitting model was chosen, based on likelihood and parsimony. In addition, saliva samples were collected for determination of functional polymorphims (such as 5- HTTLPR).

Results: Genetic factors (explaining 55 to 68% of individual differences) and individual-specific environmental factors (explaining 32 to 45% of individual differences) influenced daily life stress-reactivity. The best fitting model also incorporated negative sibling interaction.

Conclusion: The demonstration of a genetic influence on the dynamic relationship between minor stress and affective response in the flow of daily life sheds light on the gene-environment interactions that drive the risk to develop stress related disorders such as depression. Differences in stress-reactivity between children in the same family may result in part from compensatory sibling interactions. In addition, the role of functional polymorphisms, such as 5-HTTLPR, in moderating the individual response to minor daily life stress will be discussed.

SS-01-04

Abnormal response to metabolic stress in schizophrenia: Marker of vulnerability or acquired sensitisation?

M. C. Marcelis, E. Cavalier, J. Gielen, P. Delespaul, J. van Os. Dept. of Psychiatry Maastricht University, Maastricht, Netherlands

Objective: Previous work suggests that individuals with schizophrenia display an altered HVA-response to metabolic stress. The present study replicated and extended this paradigm, including individuals with elevated genetic risk for schizophrenia.

Methods: Patients with psychosis (n=50), non-psychotic firstdegree relatives of patients with psychosis (n-51) and controls without psychosis (n=50) underwent, in randomised order, doubleblind administration of placebo and the glucose analog 2-deoxy-Dglucose (2DG), which induces a mild, transient clinical state of glucoprivation. Plasma HVA and cortisol were assessed twice before the start of the 2DG/placebo infusion (baseline values), as well as four times post infusion. Data were analysed using multilevel random regression techniques.

Results: During the stress condition, significant increases in plasma HVA and cortisol were found. The increase in plasma HVA level during the stress condition was significantly stronger in patients than in controls, whereas this was not the case in relatives versus controls. The increase in plasma cortisol during the staess condition was significantly less in patients than controls, but no significant difference in the increase of plasma cortisol during stress was found in the comparison between relatives and controls.

Conclusion: Patients with psychosis, but not their nonpsychotic first-degree relatives, show an altered neurobiological response to metabolic stress, suggesting that this dysregulation is not a genetically transmitted vulnerability, but an illness-related effect, possibly reflecting acquired sensitisation ofcatecholamine systems by repeated environmental stressors or repeated stimulation with agonistic drugs.