Cognitive styles and future depressed mood in early adulthood:the importance of global attributions

BACKGROUND: Cognitive theories of depression suggest that beliefs of low self-worth and the tendency to attribute negative events to causes that are global (widespread rather than specific) and stable (will persist rather than change in the future) are associated with the development of depressed mood. Such theories are supported by evidence from prospective studies and have guided the development of successful treatment and prevention strategies such as CBT. However, the relative importance of different psychological constructs within cognitive theories is unknown. This is important to refine cognitive theories and develop more efficient prevention strategies.METHOD: We used prospective data from over 3500 young adults from the Avon Longitudinal Study for Parents and Children (ALSPAC) cohort in the UK to investigate the association between cognitive style, measured by short forms of the Dysfunctional Attitudes Scale (DAS) and Cognitive Styles Questionnaire-Short Form (CSQ-SF) at age 18, and future depressed mood at age 19. Structural equation modelling techniques were used to separate cognitive style constructs.RESULTS: Cognitive styles were associated with future depressed mood, independently of baseline mood, both as measured by the DAS-SF and the CSQ-SF. Of the different CSQ-SF constructs, only global attributions were associated with both baseline and future mood independently of other constructs.LIMITATIONS: The study was subject to attrition and the follow-up was relatively short (10 months).CONCLUSION: The findings suggest that the tendency to attribute negative events specifically to global causes could be particularly important for depression. Reducing global attributions is potentially important in the prevention and treatment of depression.</p

Common versus psychopathology-specific risk factors for psychotic experiences and depression during adolescence

Background. An argument often used to support the view that psychotic experiences (PEs) in general population samples are a valid phenotype for studying the aetiology of schizophrenia is that risk factors for schizophrenia show similar patterns of association with PEs. However, PEs often co-occur with depression, and no study has explicitly tested whether risk factors for schizophrenia are shared between PEs and depression, or are psychopathology specific, while jointly modelling both outcomes. Method. We used data from 7030 subjects from a birth cohort study. Depression and PEs at age 18 years were assessed using self-report questionnaires and semi-structured interviews. We compared the extent to which risk factors for schizophrenia across sociodemographic, familial, neurodevelopmental, stress-adversity, emotional-behavioural and substance use domains showed different associations with PEs and depression within bivariate models that allowed for their correlation. Results. Most of the exposures examined were associated, to a similar degree, with an increased risk of both outcomes. However, whereas female sex and family history of depression showed some discrimination as potential risk factors for depression and PEs, with stronger associations in the former, markers of abnormal neurodevelopment showed stronger associations with PEs. Conclusions. The argument that PEs are valid markers for studying the aetiology of schizophrenia, made simply on the basis that they share risk factors in common, is not well supported. PEs seem to be a weak index of genetic and environmental risk for schizophrenia; however, studies disentangling aetiological pathways to PEs from those impacting upon co-morbid psychopathology might provide important insights into the aetiology of psychotic disorders

Common versus psychopathology-specific risk factors for psychotic experiences and depression during adolescence

Background An argument often used to support the view that psychotic experiences (PEs) in general population samples are a valid phenotype for studying the aetiology of schizophrenia is that risk factors for schizophrenia show similar patterns of association with PEs. However, PEs often co-occur with depression, and no study has explicitly tested whether risk factors for schizophrenia are shared between PEs and depression, or are psychopathology specific, while jointly modelling both outcomes. Method We used data from 7030 subjects from a birth cohort study. Depression and PEs at age 18 years were assessed using self-report questionnaires and semi-structured interviews. We compared the extent to which risk factors for schizophrenia across sociodemographic, familial, neurodevelopmental, stress–adversity, emotional–behavioural and substance use domains showed different associations with PEs and depression within bivariate models that allowed for their correlation. Results Most of the exposures examined were associated, to a similar degree, with an increased risk of both outcomes. However, whereas female sex and family history of depression showed some discrimination as potential risk factors for depression and PEs, with stronger associations in the former, markers of abnormal neurodevelopment showed stronger associations with PEs. Conclusions The argument that PEs are valid markers for studying the aetiology of schizophrenia, made simply on the basis that they share risk factors in common, is not well supported. PEs seem to be a weak index of genetic and environmental risk for schizophrenia; however, studies disentangling aetiological pathways to PEs from those impacting upon co-morbid psychopathology might provide important insights into the aetiology of psychotic disorders