Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Kings College London
Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Kings College London, UK, and University of Wisconsin at Madison, Canada
Correspondence: Dr Barbara Maughan, Box PO46, MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Kings College London, 16 De Crespigny Park, London SE5 8AF, UK. E-mail: b.maughan{at}iop.kcl.ac.uk
* This is one of a series of editorials being published in the
Journal to mark the 10th anniversary of the Social, Genetic and
Developmental Psychiatry Centre at the Institute of Psychiatry.
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INTRODUCTION |
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MAPPING CHILDHOODADULT CONTINUITIES |
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Behind headline findings of this kind, studies have also detailed psychopathological precursors to specific adult disorders. Some, as expected, reflect homotypic continuities: adult disorders (such as phobias) that are preceded by childhood and adolescent difficulties of a similar kind; but other developmental sequences emerging from longitudinal records are more complex. Early adult depression, for example, is commonly preceded by childhood anxiety, whereas adult anxiety is preceded by both depression and anxiety. anxiety. Less predictable still are sequences (now increasingly well replicated) that link apparently quite different disorders at different stages in the life course. In the Dunedin study, for example, conduct and oppositional disorders in childhood showed expected links with later substance misuse and antisocial personality disorder; in addition, however, they were associated with increased risk of adult depression, anxiety, eating disorders, schizophreniform disorders and even mania (Kim-Cohen et al, 2003). Understanding the processes involved in these heterotypic continuities, or patterns of sequential comorbidity, constitutes a key target for future research.
With the exception of severe early-onset disorders such as autism, continuities looking forwards from childhood are typically less strong. At most half of boys with conduct disorder, for example, go on to show antisocial personality disorder (Maughan & Rutter, 2001), and the majority of children with anxiety or depression will not have mood disorders in adult life (Wals & Verhulst, 2005). However, longitudinal evidence also suggests that to focus on categorically defined disorders alone is to take too narrow a view. Sub-threshold levels of childhood and adolescent symptoms can signal increased risk of adult disorder, and later psychopathology is by no means the only adverse consequence of poor childhood mental health. Studies have consistently shown, for example, that many young people with early histories of psychiatric disorder go on to face problems in other aspects of their adult lives: interpersonal relationships, educational attainments and occupational functioning seem especially likely to be compromised, as also may be physical health.
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HOW EARLY CAN WE TELL? |
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MECHANISMS FOR CONTINUITY AND DISCONTINUITY |
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Current thinking on risk mechanisms in schizophrenia illustrates the complexity of effects that may be involved (Walker et al, 2004). Largely as a consequence of insights from longitudinal studies, schizophrenia is now increasingly regarded as a developmental disorder. In part, this change of view was prompted by follow-back findings showing mild deficits in social, motor and cognitive functioning in children and adolescents, and even infants, who later went on to display psychotic symptoms. In addition, susceptibility to schizophrenia has been associated with a range of prenatal and perinatal risks (including obstetric complications, maternal stress and maternal exposure to infection in pregnancy) that have the potential to affect neurodevelopmental processes. Although direct evidence is still lacking, early insults of this kind perhaps in interaction with genetic predispositions are thought to lay the groundwork for vulnerable neuronal circuits whose effects can compromise brain structure and function. Not all individuals with these vulnerabilities go on to show disorder; instead, final illness expression is thought to depend on later developmental processes, associated with adolescent neuromaturation or enhanced sensitivity to the effects of later stress. The role of cannabis use as one element in this constellation of risks has attracted particular attention of late (Arseneault et al, 2004).
Developmental findings have also led to new thinking about the aetiology of depression. Historically, depression was rarely diagnosed before adulthood. Developmental evidence has made clear, however, that depressive disorders are manifest in childhood and adolescence, and that the marked increase in depressive phenomena (along with the emergence of the female predominance) occurs in the early teenage years (Angold & Costello, 2001). In addition, mood disorders are frequently associated with childhood adversity, in this case exposure to traumatic or abusive experiences in childhood, or lack of adequate parental care. Here, risks in genetically vulnerable individuals have been argued to stem from long-term effects of early stress on neuroendocrine functioning (Nemeroff, 2004), or from the psychological effects of early adversity on self-concepts or other psychological schemas.
Aetiological models for disruptive behaviour disorders illustrate yet other insights deriving from developmental findings. Here, one long-standing puzzle centred on the heterogeneity of outcomes for antisocial young people: some face lives of continued antisocial involvement, while others achieve much better adjustment in adulthood. Developmental studies concurred with genetic findings in highlighting age at onset as a key differentiating factor here. This in turn led to the formulation of a developmental taxonomy, involving distinct aetiological models for childhood- and adolescent-onset groups (Moffitt, 1993). Adolescent-onset delinquency is in many ways normative, and is largely prompted by affiliations with deviant peers. Severe early-onset disruptiveness, in contrast, is thought to stem from interactions between early neurocognitive deficits and adverse parenting that set in train negative interactional patterns, and possibly cognitive sets, that in turn evoke reinforcing responses from others. In part, later continuities in antisocial behaviour rest on indirect chain effects, whereby poor outcomes at one stage of development elevate risks for functioning at the immediately succeeding stage. By the same token, links in the chain of risk can be broken if environmental reinforcements are disrupted. Turning point experiences life-course changes that offer opportunities for pro-social pro-social engagements, and provide appropriate social controls have attracted particular attention here (Rutter, 1996). Importantly, studies have shown that processes of this kind are not confined to early stages in development, but can arise well into adult life.
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IMPLICATIONS |
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REFERENCES |
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Arseneault, L., Cannon, M., Witton, J., et al
(2004) Causal association between cannabis and psychosis:
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Caspi, A., Moffitt, T. E., Newman, D. L., et al (1996) Behavioral observations at age 3 years predict adult psychiatric disorders longitudinal evidence from a birth cohort. Archives of General Psychiatry, 53, 1033 1039.[Abstract]
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Kim-Cohen, J., Caspi, A., Moffitt, T. E., et al
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Kraepelin, E. (1919) Dementia Praecox and Paraphrenia (transl. R. M. Barclay). Edinburgh: Livingstone.
Maughan, B. & Rutter, M. (2001) Antisocial children grown up. In Conduct Disorders in Childhood and Adolescence (eds J. Hill & B. Maughan), pp. 507 552. Cambridge: Cambridge University Press.
Moffitt, T. E. (1993) Adolescence-limited and life-course-persistent antisocial behavior a developmental taxonomy. Psychological Review, 100, 674 701.[CrossRef][Medline]
Nemeroff, C. B. (2004) Neurobiological consequences of childhood trauma. Journal of Clinical Psychiatry, 65 (suppl. 1), 18 28.[Medline]
Rothbart, M. K. & Bates, J. E. (1998) Temperament. In Handbook of Child Psychology, vol. 3: Social, Emotional and Personality Development (eds W. Damon & N. Eisenberg), pp. 105 176. New York: John Wiley.
Rutter, M. (1996) Transitions and turning points in developmental psychopathology: as applied to the age span between childhood and mid-adulthood. International Journal of Behavioural Development, 19, 603 626.
Sanson, A., Hemphill, S. A. & Smart, D. (2004) Connections between temperament and social development: a review. Social Development, 13, 142 170.[CrossRef]
Walker, E., Kestler, L., Bollini, A., et al (2004) Schizophrenia: etiology and course. Annual Review of Psychology, 55, 401 430.[CrossRef][Medline]
Wals, M. & Verhulst, F. (2005) Child and adolescent antecedents of adult mood disorders. Current Opinion in Psychiatry, 18, 15 19.
Widiger, T. A. & Clark, L. A. (2000) Toward DSMV and the classification of psychopathology. Psychological Bulletin, 126, 946 963.[CrossRef][Medline]
Received for publication February 14, 2005. Accepted for publication February 17, 2005.
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