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The biopsychosocial model (BPSM) was proposed by George Engel in 1977 as an improvement to the biomedical model (BMM), to take account of psychological and social as well as biological factors relevant to health and disease. Since then the BPSM has had a mixed reputation, as the overarching framework for psychiatry, perhaps for medicine generally, while also being criticized for being theoretically and empirically vacuous. Over the past few decades, substantial evidence has accumulated supporting the BPSM but its theory remains less clear. The first part of this paper reviews recent well-known, general theories in the relevant sciences that can provide a theoretical framework of the model, constituting a revitalized BPSM capable of theorizing causal interactions within and between biological, psychological, and social domains. Fundamental concepts in this new framework include causation as regulation and dysfunction as dysregulation. Associated research paradigms are outlined in Part 2. Research in psychological therapies and social epidemiology are major examples of programs that have produced results anomalous for the BMM and consistent with the BPSM. Theorized models of causal mechanisms enrich empirical data and two biopsychosocial examples are models of chronic stress and pain perception. Clinical implications are reviewed in Part 3. The BPSM accommodates psychological and social as well as biological treatment effects evident in the clinical trials literature. Personal, interpersonal, and institutional aspects of clinical care are out of the scope of the BMM, assigned to the art of healthcare rather than the science, but can be accommodated and theorized in the BPSM. [ABSTRACT FROM AUTHOR]

Background: Reviews and practice guidelines for paediatric obsessive-compulsive disorder (OCD) recommend cognitive-behaviour therapy (CBT) as the psychological treatment of choice, but note that it has not been sufficiently evaluated for children and adolescents and that more randomized controlled trials are needed. The aim of this trial was to evaluate effectiveness and optimal delivery of CBT, emphasizing cognitive interventions. Methods: A total of 96 children and adolescents with OCD were randomly allocated to the three conditions each of approximately 12 weeks duration: full CBT (average therapist contact: 12 sessions) and brief CBT (average contact: 5 sessions, with use of therapist-guided workbooks), and wait-list/delayed treatment. The primary outcome measure was the child version of the semi-structured interviewer-based Yale-Brown Obsessive Compulsive Scale. Clinical Trial registration: http://www.controlled-trials.com/ISRCTN/; unique identifier: ISRCTN29092580. Results: There was statistically significant symptomatic improvement in both treatment groups compared with the wait-list group, with no significant differences in outcomes between the two treatment groups. Controlled treatment effect sizes in intention-to-treat analyses were 2.2 for full CBT and 1.6 for brief CBT. Improvements were maintained at follow-up an average of 14 weeks later. Conclusions: The findings demonstrate the benefits of CBT emphasizing cognitive interventions for children and adolescents with OCD and suggest that relatively lower therapist intensity delivery with use of therapist-guided workbooks is an efficient mode of delivery.

Background: To investigate the association between normative repetitive routines of childhood and paediatric obsessive compulsive symptom syndrome (OCSS) and the extent to which it is genetically mediated. Methods: In a two-phase design a community sample of 4,662 6-year-old twin-pairs were sampled and 854 pairs were assessed in the second phase for normative repetitive routines using the Childhood Routines Inventory (CRI) and for OCSS by maternal-informant diagnostic interview. The OCSS phenotype was defined using standard diagnostic criteria for obsessive compulsive disorder, though regardless of impairment. Results: In the bivariate model, correlation between the CRI defined phenotype and the OCSS phenotype was estimated to be 0.40 (95% CI 0.27-0.50), and this correlation was attributable wholly to additive genetic effects. The bivariate model also provided estimates of heritability of the two phenotypes separately: 55% (95% CI 80-89%) for the OCSS phenotype, with the remaining variance attributable mainly to non-shared environment, and 50% (95% CI 39-62%) for CRI assessed normative repetitive routines of childhood, with 36% of the remaining variance attributable to shared environment and 14% to non-shared. Conclusions: The moderate correlation between normative childhood repetitive routines and obsessive compulsive symptomatology, attributable to genetic factors, is consistent with the hypothesis that high levels of this trait in young children constitute a risk factor for the development of obsessive compulsive symptoms.

Background: Most studies of the effects of trauma on mental health have generally not separately assessed psychosocial functioning, and in those that have key issues have received little attention, such as the relation between the time courses of the two kinds of outcome, and detailed assessment of social functioning in a range of domains. The present study made separate assessments with a view to testing four hypotheses. First, that the experience of trauma itself (independently of effects on mental health) has a negative effect on psychosocial functioning; second, that psychopathology following trauma is associated with poorer psychosocial functioning; third, that psychosocial functioning recovers when psychiatric conditions remit; fourth, that post-traumatic stress and depression have different associations with impairments of psycho-social functioning. Method: One hundred and fifteen young adults who had survived a shipping disaster (the sinking of the Jupiter in 1988) between 5 and 8 years previously, and 50 control participants were assessed for psychopathology, and for psychosocial functioning using the Adolescent to Adult Personality Functioning Assessment (ADAPFA). Results: Results did not support the first hypothesis: survivors who, although experiencing a traumatic event, did not develop Post Traumatic Stress Disorder or other psychopathology warranting diagnosis, when compared with Controls who had no psychopathology since the time of the disaster, showed no significant differences on any ADAPFA domains or on total score. There was partial support for the second hypothesis: survivors with diagnosable disorder during the rating period showed poorer psychosocial functioning in total ADAPFA score and in the domains of "Education/Work, Love Relationships," and "Non-specific Social Contacts," though not in other domains. The third hypothesis was supported: recovered Survivors showed no psychosocial impairments compared with unaffected Controls. Results also supported the fourth hypothesis, showing differential effects of post traumatic stress and depression in relation to the extent and kind of psycho-social impairments. Conclusions: The results lend support to the general model that effects on psychosocial functioning following traumatic experience are mediated by psychopathology, though further research is needed to establish whether the present pattern of findings applies to other kinds of trauma.

This study investigated the PTSD symptoms of 37 mothers whose adolescent children had been directly involved in a disaster, the Jupiter sinking in 1988. This group included mothers whose children were (a) not diagnosed with Posttraumatic Stress Disorder and (b) were diagnosed with Posttraumatic Stress Disorder. The measure used was the Posttraumatic Stress Disorder Symptom Scale. Women whose children were involved in the disaster presented PTSD symptoms. 35% (n= 13) were diagnosed with PTSD 3 mo. after the disaster, and 8% (n=3) of them were diagnosed with PTSD 6 yr. afterward. This effect was greater in the subgroup whose children had developed traumatic stress disorder following the disaster.