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Differences in Early Childhood Risk Factors for Juvenile-Onset and Adult-Onset Depression
Sara R. Jaffee, PhD;
Terrie E. Moffitt, PhD;
Avshalom Caspi, PhD;
Eric Fombonne, MD;
Richie Poulton, PhD;
Judith Martin, MA
Arch Gen Psychiatry. 2002;59:215-222.
ABSTRACT
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Background Family and twin studies suggest that juvenile-onset major depressive
disorder (MDD) may be etiologically distinct from adult-onset MDD. This study
is the first to distinguish prospectively between juvenile- and adult-onset
cases of MDD in a representative birth cohort followed up from childhood into
adulthood.
Method The study followed a representative birth cohort prospectively from
birth to age 26 years. Early childhood risk factors covered the period from
birth to age 9 years. Diagnoses of MDD were made according to DSM criteria at 3 points prior to adulthood (ages 11, 13, and 15 years)
and 3 points during adulthood (ages 18, 21, and 26 years). Four groups were
defined as (1) individuals first diagnosed as having MDD in childhood, but
not in adulthood (n = 21); (2) individuals first diagnosed as having MDD in
adulthood (n = 314); (3) individuals first diagnosed in childhood whose depression
recurred in adulthood by age 26 years (n = 34); and (4) never-depressed individuals
(n = 629).
Results The 2 juvenile-onset groups had similar high-risk profiles on the childhood
measures. Compared with the adult-depressed group, the juvenile-onset groups
experienced more perinatal insults and motor skill deficits, caretaker instability,
criminality, and psychopathology in their family-of-origin, and behavioral
and socioemotional problems. The adult-onset group's risk profile was similar
to that of the never-depressed group with the exception of elevated childhood
sexual abuse.
Conclusions Heterogeneity within groups of psychiatric patients poses problems for
theory, research, and treatment. The present study illustrates that the distinction
between juvenile vs adult-onset MDD is important for understanding heterogeneity
within depression.
INTRODUCTION
SEVERAL FINDINGS suggest that juvenile- and adult-onset major depressive
disorder (MDD) have distinct origins.1 First,
although a significant proportion of depressed children become depressed adults,2-3 most individuals who experience depression
in adulthood were not depressed as children.4
Second, juvenile-onset MDD is associated with increased risk for MDD among
the first-degree relatives of depressed probands in clinical and community
samples.4-8
Third, the children of depressed parents are at high risk for juvenile-onset
MDD compared with the children of nondepressed parents, and this association
is explained by early parental age at onset of MDD.9
These findings implicate genetic risk factors in juvenile-onset MDD.
However, depressed children and adolescents may also experience unique psychosocial
risks, such as poor parenting or family discord, especially if these risks
are genetically mediated.10-11
Additional support for the hypothesis that juvenile- and adult-onset MDD are
distinct subtypes would be demonstrated if early childhood psychosocial risks
were differentially associated with juvenile vs adult-onset MDD.
A range of childhood psychosocial risk factors have been associated
with depression, including characteristics of the child (eg, behavioral and
socioemotional problems, poor school performance), characteristics of the
parents (eg, parent psychopathology, rejecting or intrusive behavior), and
family circumstances (eg, the loss of a parent, physical or sexual violence,
family discord).12-15
However, it has not been shown decisively whether these risks distinguish
juvenile from adult-onset MDD. To our knowledge, the only study to have assessed
the impact of a wide range of childhood risk factors on juvenile vs adult-onset
MDD14 found that family violence, parental
psychopathology, and the early death of a parent increased the risk for early
onset of depressive symptoms (by age 20 years) but not for later onset. However,
these results were limited by the use of a single screening question to assess
depression and retrospective recall of age of onset.
Despite increasing evidence for an early vs late-onset distinction,
a small body of research suggests there is also heterogeneity within juvenile-onset
groups as a function of whether the child was prepubertal or postpubertal
at onset. Prepubertal onset has been associated with lower risk of recurrence16-17; higher risk of bipolar disorder,
suicide attempts, alcohol dependence, and conduct disorder17;
and lower heritability.18-19 Results
from family studies have been inconsistent. Some results have shown higher
rates of criminality and family discord and lower rates of depressive disorder
among relatives of prepubertal vs postpubertal-onset MDD probands,20 and others have shown no significant differences
in rates of disorder among relatives in these 2 groups.21
Although the findings are not entirely consistent, they do suggest heterogeneity
within early-onset MDD.
The present study is the first to trace prospectively the course of
depression in a representative birth cohort from childhood to adulthood, using DSM diagnoses of MDD. The longitudinal design allowed us
to determine whether early childhood risk factors were differentially associated
with juvenile vs adult-onset MDD and to assess heterogeneity within the juvenile-onset
group.
SUBJECTS AND METHODS
SUBJECTS
Participants are part of the Dunedin Multidisciplinary Health and Development
Study, a longitudinal investigation of health and behavior in a complete birth
cohort.22 The study members were born between
April 1, 1972, and March 31, 1973, in Dunedin, New Zealand. Of these, 1037
children (91% of eligible births; 52% male) participated in the first follow-up
at age 3 years, forming the base sample for the longitudinal study. Cohort
families are primarily white and represent the full range of socioeconomic
status in the general population of New Zealand's South Island.
The Dunedin sample has been assessed with a diverse battery of psychological,
medical, and sociological measures with high rates of participation at age
3 (n = 1037), 5 (n = 991), 7 (n = 954), 9 (n = 955), 11 (n = 925), 13 (n =
850), 15 (n = 976), 18 (n = 993), 21 (n = 992), and, most recently, 26 years
(n = 980; 96% of the living cohort members). The research procedure involves
bringing 4 study members per day (including emigrants living overseas) to
the research unit within 60 days of their birthday for a full day of individual
data collection. Each research topic is presented, in private, as a standardized
module by a different trained examiner in counterbalanced order throughout
the day. In addition, data are gathered from sources such as parents, partners,
and courts.
At ages 11, 13, and 15 years, study members were administered the Diagnostic
Interview Schedule for Children.23 Major depressive
disorder was diagnosed according to DSM-III criteria.
The Diagnostic Interview Schedule for Children has shown good interrater reliability
in this cohort ( >0.86). The modifications and descriptive epidemiology
of the Diagnostic Interview Schedule for Children in this sample have been
described by McGee et al.24 At ages 18, 21,
and 26 years, study members were administered the Diagnostic Interview Schedule.25 Major depressive disorder was diagnosed according
to DSM-III-R criteria at ages 18 and 21 years and DSM-IV criteria at age 26 years. The Diagnostic Interview
Schedule demonstrates good interrater reliability (>0.85) and validity
in this cohort, as demonstrated by the disordered group who sought treatment
frequently and had high levels of functional impairment.26
For both the Diagnostic Interview Schedule for Children and the Diagnostic
Interview Schedule, the reporting period was 12 months prior to the interview
(eg, at age 11 years [hereafter, age-11] interviews assessed depression while
the child was age 10 years). Interviewers were blind to the study members'
psychiatric history and had tertiary degrees and experience in social work,
medicine, and clinical psychology.
To be included in the analyses, study members must have completed psychiatric
interviews in both childhood (at ages 11, 13, or 15 years) and adulthood (at
ages 18, 21, or 26 years); 998 study members (96% of the birth cohort) met
this criterion. Of the 998, 66% completed all 6 psychiatric interviews, 24%
completed 5 interviews, 6.4% completed 4 interviews, 2.4% completed 3 interviews,
and 0.8% completed 2 interviews (ie, 1 child and 1 adult interview). Here
we report findings based on the full study cohort (N = 998). In addition,
all analyses were rerun on the subsample that had all 6 interviews.
The juvenile-depressed group comprised study members who were first
diagnosed as having MDD at age 10, 12, or 14 years but who had no subsequent
episode (n = 21; 8 women [38%]). The adult-depressed group comprised those
who were first diagnosed as having MDD at age 17, 20, or 25 years (n = 314;
201 women [64%]). The juvenile/adult–depressed group comprised those
who were first diagnosed as having MDD at age 10, 12, or 14 years and whose
depression recurred in adulthood by age 26 years (n = 34; 22 women [65%]),
and the never-depressed group comprised those who were never diagnosed as
having MDD (n = 629; 252 women [40%]). A  2 analysis revealed
that the sex distribution across the 4 groups was not equal because depressed
adults were more likely to be women (23 = 53.92; P .001).
We defined adult-onset MDD as a first diagnosis at 17 years or older
because (1) this cutoff was consistent with the definition of adult-onset
MDD used by Harrington et al2 and (2) the incidence
of new cases of depression in this sample spiked between the ages of 15 and
18 years and declined thereafter, suggesting that onset of depression at or
before age 15 years is unique (Figure 1). 27
The juvenile-depressed group had a significantly earlier age of MDD
onset (mean [SD], 12 [1.84] years) compared with the juvenile/adult–depressed
group (13 [1.47] years; t366 = 2.93; P.01). The juvenile-onset and juvenile/adult–onset
groups had a significantly earlier age of onset compared with the adult-depressed
group (20 [3.12] years; t366 = 24.22; P.001). The mean age at menarche in this sample was
13 years (range, 8.5-15 years), and 46% of the adolescent boys had their growth
spurt from ages 13 to 15 years. On this basis, a significant proportion of
the juvenile-depressed group was prepubertal and the juvenile/adult–depressed
group was pubertal or postpubertal at MDD onset.
EARLY CHILDHOOD RISK FACTORS FOR DEPRESSION
Early childhood risk factors for depression included many of those identified
in the literature, such as neurodevelopmental characteristics, parental characteristics,
family circumstances, and child behavior and temperament. The risk factors
associated with the diagnosis of depression covered the period before age
9 years so as to be temporally nonoverlapping with the period covered by the
age-11 diagnosis of depression. Although a review of these risk factors and
their links to depression would be beyond the scope of this article, excellent
reviews are available.10-12,28
Neurodevelopmental characteristics encompassed a count of perinatal
insults, which included any of 12 prenatal or 12 neonatal problems recorded
by physicians during the mother's pregnancy.29
Gross motor skills (eg, standing long jump, balance) were measured with the
Bayley Motor Scale30 at age 3 years, the McCarthy
Motor Scales31 at age 5 years, and the Basic
Motor Ability Test32 at ages 7 and 9 years.
Scores on these measures were standardized and summed ( = .71). Intelligence
quotient was measured with the Wechsler Intelligence Scale for Children (Revised)33 at ages 7 and 9 years and was averaged (r = .79).
Parental characteristics included mother's internalizing symptoms, which
were assessed with the Rutter Malaise Inventory34
when the study members were ages 5, 7, and 9 years. This includes 23 items
measuring physical and psychological symptoms of depression and anxiety. The
total number of symptoms endorsed by mothers was summed, and scores were averaged
across the 3 assessments ( = .90). At age 3 years, mother-child interactions
were observed and rated across 8 categories during a 1-hour testing session
and during the child's physical examination. To construct the rejecting behavior
composite, 1 point was awarded for each behavior that was rated by psychometricians
and physicians as hostile or rejecting (eg, if the mother's expression of
affect was consistently negative or if she was unresponsive to her child's
needs; = .71).35 Parents'criminal conviction
history was assessed via a questionnaire posted to parents who were asked
to report if they had ever been convicted of a crime; 3% of the mothers and
12% of the fathers reported that they had been. Parental disagreement about
discipline was reported by mothers when the study children were ages 5, 7,
and 9 years as part of an interview about how parents dealt with misbehavior.
Mothers indicated whether they and their partners disagreed about how to discipline
the child and how often they disagreed in front of the child. Scores were
standardized and averaged across ages 5 to 9 years ( = .62).
Family circumstances included the number of residence changes and parent-figure
changes that each study member experienced from birth to age 9 years. Socioeconomic
status was measured with a 6-point scale that places each occupation into
1 of 6 categories based on the educational level and income associated with
that occupation in the data from the New Zealand census.36
Measures of socioeconomic status were averaged from birth to age 9 years (
= .79). Unwanted sexual contact by age 11 years (having one's genitals touched,
touching another's genitals, and sexual intercourse)13
was assessed retrospectively at age 26 years as part of an interview about
sexual behavior and reproductive health. Eighteen percent of females and 7%
of males reported having experienced unwanted sexual contact, which is consistent
with rates reported elsewhere.37 Finally, it
was recorded whether study members lost a parent by age 9 years because of
death, divorce, or separation (12.6%).
Child behavior and temperament were measured from ages 3 to 9 years.
When the study members were aged 3 years, mothers reported on a 3-point scale
whether their child had been difficult to manage as a baby (0, "easy all of
the time" to 2, "very difficult to manage"). At age 3 years, children were
observed during a 1-hour psychological examination, and their behavior was
rated across 15 categories. Three factors emerged from these ratings and these
were cluster analyzed, yielding temperament profiles.38
Of interest are the inhibited and undercontrolled temperament profiles. Inhibited
children were shy, fearful, and passive; engaged in little verbal communication;
exhibited flat affect; and were distractible. Undercontrolled children were
irritable, distractible, emotionally labile, and rough and uncontrolled in
their behavior. From ages 5 to 9 years, teachers completed the Rutter Child
Behavior Scale,39 which assesses children's
worried/fearful, hyperactive, and antisocial behavior. Children were scored
on a 3-point scale (0, "does not apply" to 2, "certainly applies"). Teachers'
reports were chosen instead of parents' reports, which may be biased by their
own psychopathology.40-41 Scores
on these 3 scales were averaged over time (all,  .70). In addition,
2 items from the Rutter Scale were chosen to measure peer problems ("Not much
liked by other children" and "Tends to do things on his own. Rather solitary.").
Scores on these items were summed across ages 7 and 9 years ( = .60).
Finally, at age 9 years, study members completed an interviewer-administered
depression checklist. A total score was created by summing positive responses
to the items. Because the checklist did not show acceptable criterion validity
against clinical judgment,42 it is included
as a measure of depressive symptomatology and not clinical depression.
STATISTICAL ANALYSIS
2 Analyses were conducted to show associations between
depression-onset status and other juvenile and adulthood diagnoses of mental
disorder. A second set of analyses evaluated group differences on the childhood
risk factors within a regression framework. To test specific predictions about
group differences, orthogonal-planned contrasts were conducted.43
The first contrast tested the prediction that the juvenile-depressed and juvenile/adult–depressed
groups would differ from the adult-depressed group because a growing body
of research suggests that juvenile-onset MDD is distinct from adult-onset
MDD. The second contrast tested the prediction that the adult-depressed and
never-depressed groups would not differ significantly on the early childhood
risk factors because the effects of childhood adversity on depression onset
decline with age.14 The third contrast compared
the juvenile-depressed and juvenile/adult–depressed groups on the early
childhood risk factors. Given the inconsistent findings in the literature
regarding heterogeneity within juvenile-onset MDD, no predictions were made
regarding the direction of effects. All comparisons were adjusted for sex
because of its unequal distribution across groups. Group differences were
considered statistically significant at P.05,
2-tailed. The magnitude of the effect size for group differences was also
evaluated. An effect size of 0.2 is small; 0.5, moderate; and 0.8, large.44
RESULTS
PATTERNS OF COMORBIDITY
Juvenile-onset MDD was highly comorbid, with 33% to 62% of the juvenile-depressed
group and 27% to 47% of the juvenile/adult–depressed group having a
diagnosis of conduct disorder, attention deficit disorder, or anxiety disorder
by age 15 years (Table 1). The
combined juvenile-depressed and juvenile/adult–depressed groups did
not differ from the adult-depressed group in rates of comorbid disorder at
age 26 years, except in the case of schizophreniform disorder (Table 1, column 7). However, the adult-depressed group had elevated
rates of disorder at age 26 years compared with the never-depressed group
(Table 1, column 8).
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Table 1. Depressed and Never-Depressed Groups With Juvenile (DISC-C
Report) and Adult Diagnoses (DIS Report) of Other Mental Disorders*
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EARLY CHILDHOOD RISK FACTORS FOR DEPRESSION
Comparison of the combined juvenile-depressed and juvenile/adult–depressed
vs the adult-depressed groups shows that juvenile-onset MDD is associated
with worse risk across a range of variables (Table 2). Compared with the adult-depressed group, the combined
juvenile-depressed and juvenile/adult–depressed groups experienced more
perinatal insults and had poorer motor skills. Their mothers reported more
symptoms of depression and anxiety and their parents were more likely to have
a criminal conviction. The juvenile-depressed and juvenile/adult–depressed
groups experienced more parent figure changes and were more likely to have
lost a parent because of death, divorce, or separation. They had more peer
problems; and were more worried/fearful, hyperactive, and antisocial, as reported
by teachers. Finally, the juvenile-depressed and juvenile/adult–depressed
groups reported more symptoms of depression at age 9 years and were more temperamentally
inhibited compared with the adult-depressed group. Additional analyses were
conducted to determine whether these effects remained statistically significant
after controlling for juvenile conduct disorder, attention deficit disorder,
and anxiety. Compared with the adult-depressed group, the juvenile-depressed
and juvenile/adult–depressed groups' risk profile remained significantly
worse except in the case of mothers' internalizing symptoms, the likelihood
of having lost a parent, teacher ratings of antisocial and hyperactive behavior,
and self-reports of depression symptoms at age 9 years.
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Table 2. Group Differences on Continuous and Categorical Early Childhood
Risk Factors*
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Comparison of the adult-depressed vs never-depressed groups (Table 2) shows an overall pattern of similarity,
although the adult-depressed group experienced more residence changes and
unwanted sexual contact. Lastly, comparison of the juvenile-depressed vs juvenile/adult–depressed
groups (Table 2) shows an overall
pattern of similarity, although the juvenile-depressed group had more perinatal
problems. The small sample sizes of these 2 groups may have hindered our ability
to detect significant differences, and nonsignificant trends will be discussed
herein.
Finally, all analyses were rerun on the subsample of study members having
data from all 6 psychiatric interviews (66% of the sample). The results regarding
group differences on childhood risk factors were unchanged (Table 2). Findings regarding adult comorbidity (Table 1) showed 1 change: group differences on alcohol dependency
at age 26 years were no longer statistically significant.
COMMENT
This study is the first to our knowledge to distinguish prospectively
between juvenile- and adult-onset MDD in a representative birth cohort that
has been followed up from childhood into adulthood. These findings replicate
and extend the work of Kessler and Magee14
by showing that early childhood risks differentiate juvenile from adult-onset
cases. With few exceptions, the adult-depressed group resembled the never-depressed
group in having experienced low levels of early childhood risk factors. In
contrast, the combined juvenile-depressed and juvenile/adult–depressed
groups experienced significant risk factors: neurodevelopmental problems in
the form of perinatal and motor skill problems, more psychopathology and instability
in their family of origin, and more behavioral and socioemotional problems.
Many of these group differences were specific to childhood depression because
they remained statistically significant after controlling for comorbidity
with other childhood disorders. It is also important to highlight that the
early childhood risk factors we measured were specifically associated with
MDD onset and not simply recurrence. That is, regardless of whether MDD persisted
beyond childhood, the early childhood risk factors distinguished the juvenile-onset
groups from the adult-onset group.
Several limitations to these findings must be noted. First, these results
are limited to a single, contemporary cohort of New Zealand young adults.
Although current prevalence rates of psychiatric disorder in New Zealand match
rates from national US surveys,26, 46
further studies are required to determine whether our results will extend
to other times and places. Moreover, studies with larger samples of juvenile-onset
cases are needed.
Second, because diagnoses of MDD covered the year prior to the scheduled
assessment periods and assessments were separated by a year or more, it is
possible that we failed to detect episodes of MDD that emerged between interviews.
Moreover, at age 26 years, the sample had not passed completely through the
age of risk for MDD and study members will experience more episodes of MDD
in the future. Thus, individuals in each of the 4 groups might have been misclassified.
However, misidentification would have exerted a conservative effect on our
analyses by making it more difficult to detect group differences. Misclassification
may also have occurred because we included in the analyses study members who
did not complete psychiatric interviews at all 6 assessments. However, excluding
these study members did not change the results.
Third, the identification of risk factors for juvenile-onset MDD in
no way ensures their causal status.47 Although
the early childhood risk factors (except childhood sexual abuse) covered the
period prior to the first diagnosis of MDD (and could thus be ruled out as
consequences of depression), future research is needed to determine whether
changes in any of the childhood risk factors would decrease the likelihood
of MDD, thus implying their causal status. Moreover, our list of early childhood
risk factors was not exhaustive. For example, although we assessed mothers'
symptoms of depression and anxiety, parental history of psychiatric disorder
is an important risk factor for depression that was not measured.
With these limitations in mind, the strengths of the study can be noted.
Because of its unique prospective, longitudinal design, this study makes several
improvements over the existing literature. First, despite the possibility
that we failed to detect episodes of MDD, there were opportunities for MDD
to be observed at 3 points in childhood and in adulthood. Second, diagnoses
of MDD were made prospectively, thus eliminating problems associated with
long-term retrospective recall.48 Third, diagnoses
of MDD were made in a birth cohort as opposed to a clinical sample. Thus,
the observed associations between juvenile-onset and early childhood risk
factors were not caused by high-risk families selectively coming to clinical
attention. Lastly, the predicted group differences were observed and were
consistent with the extant literature on the distinction between juvenile
vs adult-onset MDD.
The findings differentiating juvenile- and adult-onset MDD are consistent
with results from family studies, suggesting that juvenile-onset MDD may be
a distinct subtype associated with both genetic and early childhood psychosocial
risk factors. Future research is needed to determine whether these early childhood
risk factors are genetically mediated49 and
how these risks may be causally implicated in the origins of depression.
With the exception of having experienced unwanted sexual contact (which
was measured retrospectively), adult-onset MDD does not seem to have an early
developmental diathesis. This finding calls for renewed vigor in the search
for adolescent and early-adult life events that trigger adult-onset MDD. A
question for future research is whether risk factors exert their effects for
only a limited period (suggesting that the same risk factors we measured in
early childhood, such as losing a parent, would predict adult-onset MDD if
they occurred in late adolescence) or whether risk factors are developmentally
sensitive, and those that predict juvenile-onset MDD are qualitatively different
from those that predict adult-onset MDD. A history of depression should be
included as a control variable in analyses that assess the relationship between
childhood risk factors and adult depression. Otherwise it is unclear whether
the risk variables are related to the current episode or whether they exert
their effect via past episodes of depression.14
A developmental perspective on psychopathology illustrates how the course
and correlates of disorder vary as a function of age at onset. Thus, findings
from longitudinal studies have important nosological implications.50 Although our findings differentiated juvenile- and
adult-depressed groups, we also draw attention to a pattern of nonsignificant
findings that suggest heterogeneity within juvenile-depressed groups. The
juvenile-depressed group had a higher proportion of males and exhibited a
pattern reminiscent of externalizing behavior, characterized by more perinatal
problems and somewhat higher rates of comorbid conduct disorder, attention
deficit-disorder, crime by parents, and temperamentally undercontrolled behavior.
In contrast, the juvenile/adult–depressed group had a higher proportion
of girls and exhibited a pattern reminiscent of internalizing behavior, characterized
by somewhat more temperamentally inhibited behavior, adult anxiety, and parental
loss (but also more antisocial behavior). However, given the small size of
our juvenile-depressed groups, the small effect sizes, and the statistical
nonsignificance of the estimates, studies with larger samples of juvenile-onset
cases are needed to determine whether there is meaningful heterogeneity within
juvenile-onset MDD.
Heterogeneity within groups of psychiatric patients who present with
the same symptom profile poses problems for theory, research, and treatment.
Distinctions based on age of onset have proven important for understanding
heterogeneity within attention-deficit/hyperactivity disorder51
and antisocial disorder,52-53
in which childhood onset has worse implications for course, recurrence, familial
transmission, and treatment resistance.54 Research
on schizophrenia is also benefiting from a focus on childhood neurodevelopmental
processes55 and juvenile-onset symptoms.56 The present study and others1
illustrate that the distinction between juvenile vs adult-onset MDD is important
for understanding heterogeneity within depression as well.
AUTHOR INFORMATION
Accepted for publication August 13, 2001.
The Dunedin Multidisciplinary Health and Development Study is supported
by the Health Research Council of New Zealand. This study was supported by
grants MH45070 and MH49414 from the National Institute of Mental Health, Bethesda,
Md; by fellowships from the University of Wisconsin and the Dolores Liebmann
Trust, Madison; and by the UK Medical Research Council.
We thank Michael Rutter, MD, for his valuable comments on earlier drafts
of the manuscript; Air New Zealand; HonaLee Harrington, BA; Phil Silva, MD;
and the Dunedin study members and staff.
Corresponding author and reprints: Sara R. Jaffee, PhD, Institute
of Psychiatry, Social, Genetic, and Developmental Psychiatry Research Centre,
111 Denmark Hill, London, SE5 8AF, England (e-mail: s.jaffee{at}iop.kcl.ac.uk).
From the Social, Genetic, and Developmental Psychiatry Research Centre,
Institute of Psychiatry (Drs Jaffee, Moffitt, and Caspi) and Department of
Child and Adolescent Psychiatry, Institute of Psychiatry (Dr Fombonne), King's
College, London, England; Department of Psychology, University of Wisconsin,
Madison (Drs Jaffee, Moffitt, and Caspi); and Dunedin Multidisciplinary Health
and Development Research Unit (Dr Poulton) and Department of Psychological
Medicine (Ms Martin), University of Otago, Dunedin, New Zealand.
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