Continuities between childhood and adult life

The child, said the poet, is father of the man. As findingsfrom long-term studies of psychopathology proliferate, so thetruth of that dictum becomes ever more apparent in the mentalhealth field. Many childhood disorders – once thoughtto resolve with age – are now known to cast long shadowsover later development. Equally importantly, many adult disordersare now recognised as having roots in childhood vulnerabilities,traceable in some instances to the very earliest stages ofdevelopment. These developmental findings have shed new lighton the aetiology and course of many disorders, and underscoredthe usefulness of a life-span perspective on psychopathology for researchers and clinicians alike. We focus here on threethemes emerging from this rapidly expanding literature: first,evidence on the extent and complexity of childhood–adultcontinuities; second, some of the mechanisms proposed as mediatingthose links; and third, the implications that follow for nosologyand clinical practice.

MAPPING CHILDHOOD–ADULT CONTINUITIES

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MAPPING CHILDHOOD-ADULT...

Although hinted at for many years, the most persuasive evidencefor childhood–adult continuities has come from prospectivestudies of unselected birth cohorts, set up by far-sightedinvestigators many years ago (Coleman & Jones, 2004). As cohorts of this kind mature into adulthood, their findingsoffer two contrasting perspectives on links between psychopathologyin childhood and in adult life. First, looking forwards fromchildhood, longitudinal data provide estimates of the extentto which children and adolescents with mental health problemsare at risk of disorder later in the life course. Second, looking backwards from adulthood, they highlight early roots of adultvulnerability. Probably the most striking evidence for continuitiescomes from this second approach. Recent reports from the Dunedinlongitudinal cohort, for example, have shown that most youngadults with a psychiatric disorder had diagnosable problemsmuch earlier in life (Kim-Cohen et al, 2003). Of those withmental health problems at age 26 years, half had first metcriteria for disorder by age 15 years; by the late teens, thatfigure approached 75%. On this evidence, many adult disorders could be re-framed as extensions of juvenile difficulties.

Behind ‘headline’ findings of this kind, studieshave also detailed psychopathological precursors to specificadult disorders. Some, as expected, reflect homotypic continuities:adult disorders (such as phobias) that are preceded by childhoodand adolescent difficulties of a similar kind; but other developmentalsequences emerging from longitudinal records are more complex.Early adult depression, for example, is commonly preceded by childhood anxiety, whereas adult anxiety is preceded by bothdepression and anxiety. anxiety. Less predictable still aresequences (now increasingly well replicated) that link apparentlyquite different disorders at different stages in the life course.In the Dunedin study, for example, conduct and oppositionaldisorders 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 evenmania (Kim-Cohen et al, 2003). Understanding the processesinvolved in these heterotypic continuities, or patterns ofsequential comorbidity, constitutes a key target for futureresearch.

With the exception of severe early-onset disorders such as autism, continuities looking forwards from childhood are typicallyless strong. At most half of boys with conduct disorder, forexample, go on to show antisocial personality disorder (Maughan & Rutter, 2001),and the majority of children with anxietyor depression will not have mood disorders in adult life (Wals & Verhulst, 2005).However, longitudinal evidence alsosuggests that to focus on categorically defined disorders aloneis to take too narrow a view. Sub-threshold levels of childhoodand adolescent symptoms can signal increased risk of adult disorder, and later psychopathology is by no means the only adverse consequenceof poor childhood mental health. Studies have consistentlyshown, for example, that many young people with early historiesof psychiatric disorder go on to face problems in other aspectsof their adult lives: interpersonal relationships, educationalattainments and occupational functioning seem especially likelyto be compromised, as also may be physical health.

HOW EARLY CAN WE TELL?

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HOW EARLY CAN WE...

To date, most studies tracking links between childhood and adultdisorders have ‘begun’ in middle to late childhood.However, individual differences in children’s temperaments,and in behavioural styles, are evident much earlier in development:one key question thus centres on the extent to which earlybehaviours of this kind are also implicated in risk. Usingtheir observations of 3-year-old children, Caspi et al (1996)documented modest but none the less conceptually meaningfulassociations with psychopathology at age 21 years. Behaviourallyinhibited toddlers were more likely than other young childrento show mood disorders in their early 20s, and undercontrolled 3-year-olds were at increased risk of antisocial personalitydisorder and persistent violent offending; both groups showedhigher rates of suicide attempts. Prior to age 3 years, datareaching forward to adulthood are still rare. Tracked intochildhood and adolescence, however, early temperamental difficultiesdo show coherent associations with later mental health, although again the links are modest (Sanson et al, 2004). Many commentatorsconclude that very early temperamental features represent predispositionsor vulnerabilities to disorder, but that later developmentalprocesses are required to transform them more directly intorisk (Rothbart & Bates, 1998).

MECHANISMS FOR CONTINUITY AND DISCONTINUITY

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MECHANISMS FOR CONTINUITY AND...

What mechanisms underlie these longterm developmental linkages– and what contributes to discontinuities when they arise?As yet, answers to these questions are more speculative, althoughknowledge is increasing at a rapid pace. Key pointers havecome not only from studies of individual characteristics, butalso from longitudinal findings on potential risks. Here, developmentalstudies have highlighted associations between ‘adult’disorders and both prenatal and postnatal factors that may influenceneurological or psychological development. As a result, aetiological models now frequently posit interactions between individualvulnerabilities (genetic or acquired) and prenatal or postnatalenvironmental insults; these in turn are thought to set intrain biological or psychological processes whose effects cumulateacross development, or are activated by later developmentalchallenges. We illustrate possible pathways of this kind in relation to three disorders: schizophrenia, depression andantisocial behaviour.

Current thinking on risk mechanisms in schizophrenia illustratesthe complexity of effects that may be involved (Walker etal, 2004). Largely as a consequence of insights from longitudinalstudies, schizophrenia is now increasingly regarded as a developmentaldisorder. In part, this change of view was prompted by follow-backfindings showing mild deficits in social, motor and cognitivefunctioning in children and adolescents, and even infants, wholater went on to display psychotic symptoms. In addition, susceptibility to schizophrenia has been associated with a range of prenataland perinatal risks (including obstetric complications, maternalstress and maternal exposure to infection in pregnancy) thathave the potential to affect neurodevelopmental processes.Although direct evidence is still lacking, early insults ofthis kind – perhaps in interaction with genetic predispositions– are thought to lay the groundwork for vulnerable neuronalcircuits whose effects can compromise brain structure and function. Not all individuals with these vulnerabilities go on to showdisorder; instead, final illness expression is thought to dependon later developmental processes, associated with adolescentneuromaturation or enhanced sensitivity to the effects of laterstress. The role of cannabis use as one element in this constellationof risks has attracted particular attention of late (Arseneault et al, 2004).

Developmental findings have also led to new thinking about theaetiology of depression. Historically, depression was rarelydiagnosed before adulthood. Developmental evidence has madeclear, however, that depressive disorders are manifest in childhoodand adolescence, and that the marked increase in depressivephenomena (along with the emergence of the female predominance) occurs in the early teenage years (Angold & Costello, 2001).In addition, mood disorders are frequently associatedwith childhood adversity, in this case exposure to traumaticor abusive experiences in childhood, or lack of adequate parentalcare. Here, risks in genetically vulnerable individuals havebeen argued to stem from long-term effects of early stresson neuroendocrine functioning (Nemeroff, 2004), or from the psychological effects of early adversity on self-concepts orother psychological schemas.

Aetiological models for disruptive behaviour disorders illustrateyet other insights deriving from developmental findings. Here,one long-standing puzzle centred on the heterogeneity of outcomesfor antisocial young people: some face lives of continued antisocialinvolvement, while others achieve much better adjustment inadulthood. Developmental studies concurred with genetic findingsin highlighting age at onset as a key differentiating factorhere. This in turn led to the formulation of a developmentaltaxonomy, involving distinct aetiological models for childhood-and adolescent-onset groups (Moffitt, 1993). Adolescent-onsetdelinquency is in many ways normative, and is largely promptedby affiliations with deviant peers. Severe early-onset disruptiveness,in contrast, is thought to stem from interactions between earlyneurocognitive deficits and adverse parenting that set in trainnegative interactional patterns, and possibly cognitive sets,that in turn evoke reinforcing responses from others. In part,later continuities in antisocial behaviour rest on indirectchain effects, whereby poor outcomes at one stage of developmentelevate risks for functioning at the immediately succeeding stage. By the same token, links in the chain of risk can bebroken if environmental reinforcements are disrupted. ‘Turningpoint’ experiences – life-course changes that offeropportunities for pro-social pro-social engagements, and provideappropriate social controls – have attracted particularattention here (Rutter, 1996). Importantly, studies have shownthat processes of this kind are not confined to early stagesin development, but can arise well into adult life.

IMPLICATIONS

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IMPLICATIONS

As this brief overview suggests, developmental perspectiveshave led to important reconceptualisations of disorder in anumber of domains. At this stage, however, these insights haveyet to be incorporated into classification systems, and diagnosticcriteria continue to place most weight on current symptomatology.Yet for Kraepelin (1919), information on the overall courseof a disorder was at least as important for diagnostic decision-makingas the presence of specific behavioural indicators. Evidence from longitudinal studies increasingly supports the view thatfuture revisions of the diagnostic criteria should includeinformation on individuals’ lifetime experience of psychopathologyalongside details of current symptoms (Widiger & Clark, 2000).For the clinician, these findings also underscore theusefulness of a developmental perspective. Many patients seenin adult services will already have experienced episodes ofdisorder, or been subject to early stress; many child and adolescentpatients will face long-term vulnerabilities. Setting patients’current difficulties in the context of a longer-term view offersthe promise of both more accurate diagnosis and more appropriately tailored treatments.

REFERENCES

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