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Where do we come from and where do we go? The future agenda

Where do we come from and where do we go? The future agenda. Deutscher Suchtkongress 11. - 14. Juni 2008, Mannheim. Basic questions. Why do some people develop substance use disorders and some not, given similar availability, access and exposure to substances?.

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Where do we come from and where do we go? The future agenda

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  1. Where do we come from and where do we go? The future agenda Deutscher Suchtkongress 11. - 14. Juni 2008, Mannheim

  2. Basic questions • Why do some people develop substance use disorders and some not, given similar availability, access and exposure to substances? • Why do some people change their substance use disorder behaviour and some not, given similar availability, access and exposure to interventions, and some even change without any formal intervention?  Mechanisms behind onset, course and reduction of substance use disorders

  3. Where do we come from (1) ? • Early treatment outcome studies 1) • Treatment shows positive outcome • Early meta analyses of treatment and outcome studies 2) • Treatment outcome differs between interventions • Superiority of BT-based interventions • Traditional analyses of treatment outcome related factors • Post-hoc analyses of factors related to outcome • Patient and disorder factors, treatment factors, setting variables, social context conditions (low predictive power) • Puzzling number of factors: (1) impact of single aspects unknown, (2) how these factors affect course and reduction/cessation of SUDs unknown, (3) trial data do not inform about the predictive power of these moderators • Polich, Armor & Braiker, 1980; Küfner & Feuerlein, 1989 • Miller & Heather, 1986; 1998; Miller & Wilbourne, 2002

  4. Where do we come from (2) ? • Mechanisms of change of standard interventions (CBT) 1) • No proof for hypothesised mechanisms of action • RCT treatment allocation studies • MATCH, COMBINE • No proof of treatment matching criteria 1) Morgenstern and Longabaugh, 2000

  5. Where do we come from (3) ? • Knowledge on substance-specific onset and course • EDSP • Analyses of incidence and prevalence figures, transition probabilities, critical time windows and risk and protective factors, interaction with comorbid disorders • The type of substance matters! • The time of exposure matters! • Prospective allocation of treatment interventions • ASAT projects: cannabis, tobacco, heroin • Major progress in developing targeted interventions for specific subgroups of SUDs or specific settings • No convincing results for individual allocation procedures • No one single pathway! No one single mechanism and process!

  6. What did we learn in the last years (1) ? 3.1 Onset

  7. What did we learn in the last years (2) ? 3.2 Reduction and cessation

  8. And now ? We need to understand what determines the inter-individual variability with regard to • Single exposure, regular use, abuse and dependence • Formal and informal interventions Core targets • Relationship to higher order cognitive functions • Relevance of cognitive impairments • Neural basis (functional imaging) • The role of affect and emotion (from traits to disorders) • Stress regulating processes • Family and genetic factors • Communalities / differences between exposure to psychotropic substances and “impulsive” behaviour (e.g., gambling)

  9. Where do we want to go (1) ? • The relevance of cognitive-affective control and attentional processes for onset and reduction of (problematic) substance use (SU) and other problematic “impulsive” behaviour (NSU) • Impairments of higher order executive functions (e. g., goal maintenance, intertemporal choice and impulse control, error- and conflict monitoring) • Variations in specifity of impaired control functions for different substances or different severity degrees of SU • Type and degree of impaired cognitive dysfunctions and related brain activities as predictors for onset and reduction of SU • Relationship between affect / emotions (comorbid disorders) and impaired control functions • Neuronal correlates of cognitive control deficits (PFC, OFC, ACC) • Interactions over time (developmental; stress) • Interactions with genetic factors (i.e., genomic imaging)

  10. Where do we want to go (2) ? • New translational tools for basic and treatment research • Computer assisted self infusion of ethanol (CASE) as a new experimental method for the administration of alcohol without the influence of individual variations in the perception of related cues and the gastrointestinal alcohol reception • Tool for testing new agonist treatment agents • Tool for new approaches to study the relevance of different factors which influence the perception of alcohol effects • Reaching consensus about standardized paradigms

  11. Where do we want to go (3) ? • Determinants and mechanisms of treatment outcome for subjects with different severity of problematic SU • Multi centre studies like MATCH and COMBINE and many single studies have demonstrated positive treatment effects but did not explain mechanisms of change in formal treatment and interactions with (1) patient and disorder variables, (2) setting variables and (3) social influence factors • To study the allocation of abstinence vs. controlled drinking for subjects with different degrees of problematic alcohol use based on cognitive control impairments and social support conditions • To study the relevance of CBT and additional social support conditions (community reinforcement approach) for the treatment of problematic cannabis use

  12. The ASAT Research Group Core PIs Hans-Ulrich Wittchen, Dresden (Speaker) Michael Bauer, Dresden Gerhard Bühringer, Dresden and Munich Thomas Goschke, Dresden Andreas Heinz, Berlin Michael Smolka, Dresden Ulrich Zimmermann, Dresden

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