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Mental Health, Educational, and Social Role Outcomes of Adolescents With Depression
David M. Fergusson, PhD;
Lianne J. Woodward, PhD
Arch Gen Psychiatry. 2002;59:225-231.
ABSTRACT
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Background This study used longitudinal data to examine the extent to which young
people with depression in mid adolescence (ages 14-16) were at increased risk
of adverse psychosocial outcomes in later adolescence and young adulthood
(ages 16-21).
Methods Data were gathered during a 21-year longitudinal study of a birth cohort
of 1265 children. Measures included assessments of DSM-III-R major depression (at age 14-16); psychiatric disorders, educational
achievement, and social functioning (at age 16-21); social, familial, and
individual factors; and comorbid disorders.
Results Thirteen percent of the cohort developed depression between ages 14
and 16. Young people with depression in adolescence were at significantly
(P<.05) increased risk of later major depression,
anxiety disorders, nicotine dependence, alcohol abuse or dependence, suicide
attempt, educational underachievement, unemployment, and early parenthood.
These associations were similar for girls and boys. The results suggested
the presence of 2 major pathways linking early depression to later outcomes.
First, there was a direct linkage between early depression and increased risk
of later major depression or anxiety disorders. Second, the associations between
early depression and other outcomes were explained by the presence of confounding
social, familial, and individual factors.
Conclusions Young people having early depression were at increased risk of later
adverse psychosocial outcomes. There was a direct linkage in which early depression
was associated with increased risk of later major depression and anxiety disorders.
Linkages between early depression and other outcomes appeared to reflect the
effects of confounding factors.
INTRODUCTION
IN RECENT DECADES, there has been a growing awareness of depression
in childhood and adolescence.1-3
Although before the 1970s it was believed that depression did not occur in
young people, recent prevalence studies1, 4-7
have suggested that 2% to 8% of young people experience their first episode
of major depression by age 16. For example, Hankin et al5
found that almost 6% of young people in the Dunedin study cohort met DSM-III8 diagnostic criteria
for depression on at least one occasion by age 15. A similar rate was reported
by Fergusson et al,4 who found that almost
7% of 15-year-olds met DSM-III-R diagnostic criteria
for depression.
Increased recognition of the presence of depression in young people
has led to a growing interest in the etiology, comorbidities, and consequences
of early-onset depression. For example, there is emerging evidence to suggest
that young people showing early-onset depression or depressive tendencies
are at risk for several adverse outcomes, including a further depressive episode,9-11 impaired social functioning,9, 12-16
low academic achievement,9-10,12, 15, 17-18
and a range of other mental health problems, such as anxiety disorders, substance
abuse, and suicidal behaviors.12, 15, 19-21
These linkages between early depression and later outcomes are thought to
reflect the effects of early-onset depression on normal development and the
continuities of depressed mood across time.9
Although the linkages between later depression and later outcomes have
been well documented, less is known about the pathways linking early depression
to later outcomes. In general, there are 3 pathways that may explain linkages
between early depression and later outcomes. First, there may be a direct
effect of depression on later outcomes. Therefore, for example, depression
may lead to impaired educational achievement and reduced life opportunities.
Second, it is possible that the associations between early depression and
later outcomes are noncausal and reflect the presence of antecedent factors
that are associated with increased risk of depression and other adverse outcomes.
For example, early exposure to child abuse may be associated with increased
risk of depression and other adverse outcomes. Finally, it is possible that
the linkages between early depression and later outcomes are mediated by the
presence of comorbid disorders. Therefore, the associations between early
depression and later substance abuse may reflect the effects of conduct disorder
that is comorbid with early depression. To understand the role of early depression
in later disorders and adjustment, it is important to assess the various pathways
that link early depression to later outcomes.
In this article, we use data gathered during a 21-year longitudinal
study of a birth cohort of New Zealand children to examine the following questions:
(1) To what extent are young people who develop depression in mid adolescence
(age 14-16) at increased risk of subsequent mental disorders, academic underachievement,
and reduced life opportunities? and (2) What are the pathways that may link
adolescent depression to later outcomes?
More generally, the aims of the study were to examine the continuities
between adolescent depression and later outcomes and to explore the possible
routes by which these continuities may arise.
SUBJECTS AND METHODS
SUBJECTS
The data reported herein were collected as part of the Christchurch
Health & Development Study, a longitudinal study of a birth cohort of
1265 children born in the Christchurch, New Zealand, urban region during mid
1977. These young people had been studied at birth, 4 months, 1 year, annual
intervals to age 16 years, and again at ages 18 and 21 years. The analyses
reported in this article were based on a sample of 964 young people for whom
complete data were available on the measures of adolescent depression and
later outcomes. This sample represented 76.2% of the initial birth cohort.
Losses to follow-up arose because of out-migration from New Zealand (50%),
failure to trace respondent (3%), subject refusal (37%), and mortality (10%).
To examine the effects of sample losses on the representativeness of
the sample, comparisons were made between the 964 young people included in
the analyses and the excluded 301 cohort members on a range of social background
measures collected at birth. This analysis suggested that losses to follow-up
were not associated with maternal age, family size, or sex of the child. However,
there were small but statistically detectable (P<.05)
tendencies for this sample to underrepresent children from Maori, New Zealand,
and from families with single parents or of lower socioeconomic status. Although
these results suggest some bias in the sample, it is unlikely that this bias
materially affects the results reported herein, because previous efforts to
correct for nonrandom sample loss in the cohort have shown these effects to
be negligible.22-23
ADOLESCENT DEPRESSION (AT AGE 14-16)
At ages 15 and 16, sample members and their parents were separately
interviewed about the extent to which a young person showed symptoms of depression
during the previous year. Fifteen was the earliest age at which depression
was assessed in the cohort. Self-reported depression was assessed between
ages 14 to 15 and 15 to 16 using the Diagnostic Interview
Schedule for Children,24 supplemented
by additional items based on DSM-III-R diagnostic
criteria.25 Parent-reported depression was
assessed for the same age intervals using the parent version of the Diagnostic Interview Schedule for Children and items from
the Diagnostic Interview Schedule.26
Sample members were classified as having experienced a depressive disorder
between ages 14 and 16 if, on the basis of parent- or self-report, they met DSM-III-R criteria for major depression during either of
the age intervals assessed.
PSYCHIATRIC, EDUCATIONAL, AND SOCIAL OUTCOMES (AT AGE 16-21)
At ages 18 and 21, sample members were interviewed on a range of measures
of personal and social functioning. On the basis of these 2 assessments, the
following outcome measures were developed.
Psychiatric Outcomes
At ages 18 and 21, sample members were interviewed about their mental
health and any substance abuse since the previous assessment using a questionnaire
based on the Composite International Diagnostic Interview,27 supplemented by custom-written survey
items. All interviews were conducted by trained lay interviewers. On the basis
of this information, DSM-IV28
symptom criteria were used to construct a series of psychiatric and substance
abuse diagnoses for each sample member.
Symptoms of major depression were assessed using Composite International Diagnostic Interview items. At age 18, subjects
were asked to report on symptoms occurring during the age intervals 16 to
17 and 17 to 18, and at age 21 for the age intervals 18 to 20 and 20 to 21.
At all interviews, subjects were also asked to report on the extent of impairment
caused by their symptoms. Subjects were classified as having major depression
if they met DSM-IV criteria for major depression
at any time between ages 16 and 21. Overall, 33.5% of subjects met DSM-IV criteria for major depression. This prevalence is similar to
the prevalence rate reported in the Dunedin Health and Development Study.5
Anxiety disorder symptoms were assessed using the Composite International Diagnostic Interview at ages 18 and 21. Subjects
were asked to report whether they had experienced a range of anxiety disorder
symptoms since the last assessment. Anxiety disorders assessed included generalized
anxiety, panic disorders, agoraphobia, social phobia, and specific phobia.
Subjects were classified as having an anxiety disorder if they met DSM-IV criteria for an anxiety disorder at either of the 2 assessments.
Symptoms of nicotine dependence were assessed using custom-written items
designed to reflect DSM-IV diagnostic criteria for
nicotine dependence. These items were assessed for the age intervals 17 to
18 and 20 to 21.
Alcohol abuse or dependence was assessed for annual intervals between
ages 16 and 21 using items from the Composite International
Diagnostic Interview. Subjects were classified as showing alcohol dependence
if they reported experiencing at least 3 of the following: increased tolerance
for alcohol, withdrawal symptoms when alcohol consumption was ceased, heavy
drinking and overuse of alcohol, unsuccessful attempts to quit or limit drinking,
spending large amounts of time in alcohol-related activities, restriction
of social and other activities as a result of drinking, and psychological
problems caused by heavy and prolonged drinking. Subjects were classified
as showing alcohol abuse if they did not meet criteria for alcohol dependence
but reported at least one of the following: alcohol misuse leading to successive
difficulties at school or neglect of schoolwork; difficulties at work or failure
to attend work; alcohol use that placed them at physical hazard from drunk
driving, crashes, falls, or other unintentional injury as a result of drinking;
being arrested or stopped by police for alcohol-related offenses on at least
2 occasions; continued alcohol use despite objections from family or friends;
and alcohol use causing legal, financial, or personal problems.
In addition to these measures, sample members were also interviewed
about any suicidal behavior between ages 16 and 21. On the basis of answers
to this questioning, a measure of whether a respondent had attempted suicide
during this interval was obtained.
Educational and Social Role Outcomes
To describe the subjects' educational achievement up to age 21 years,
the following 3 measures were used. First, a measure of whether respondents
had left school without formal qualifications was created using information
provided by them concerning their school-leaving age and performance on the
national school certificate examination. The second and third measures were
concerned with sample members' involvement in tertiary education and were
based on assessments of young people's educational and occupational histories
between ages 16 and 21 years. These measures included whether an individual
had enrolled in a trade- or skill-based tertiary or other technical training
course and whether he or she had enrolled in a university-level or equivalent
program by age 21 years.
Two measures of social role functioning were identified. First, a measure
of young people's exposure to multiple ( 2) periods of prolonged (>3 months')
unemployment was created. This measure was based on subjects' reports of the
frequency and duration of all periods of unemployment between ages 16 and
21. Second, a measure of the subjects' parenting status was created based
on their reports of any births between ages 16 and 21. The youngest subject
to become a parent was 16.
CONFOUNDING FACTORS
To assess the extent to which associations between adolescent depression
and later outcomes could be explained by the effects of confounding factors,
the following variables were included as covariates in the analysis.
Two measures of family social background were considered. First, maternal
educational achievement at the time of a subject's birth was coded on a 3-point
scale, ranging from no formal educational qualifications (1 point) to tertiary-level
qualifications (3 points). Second, family socioeconomic status at birth was
assessed using the Elley and Irving29 scale
of socioeconomic status for New Zealand. This scale categorizes families into
6 classes on the basis of paternal occupation.
Two measures of family functioning were included. First, a measure of
young people's exposure to sexual abuse was based on subjects' reports of
their experience of childhood sexual abuse before age 16.30
Subjects were classified into 4 groups, ranging from no childhood sexual abuse
reported (group 1) to childhood sexual abuse involving completed or attempted
oral, anal, or vaginal intercourse (group 4). The second measure assessed
the extent to which young people were exposed to parental change as a result
of parental separation or divorce, death, remarriage, and reconciliation31 between birth and age 14.
Three measures of individual functioning were included in the analysis.
At age 14, neuroticism was assessed using a short form of the Eysenck Personality
Inventory.32 The reliability of this scale,
assessed using coefficient  , was .80. Second, at age 9, as part of
a comprehensive school-based evaluation, the subject's intellectual ability
was assessed using the Wechsler Intelligence Scale for Children—Revised.33 The reliability of this scale, assessed using split-half
methods, was .93. Finally, at ages 15 and 16, young people were questioned
about the extent to which they associated with delinquent or substance-abusing
peers. Specifically, young people were asked to report the involvement of
their best friend and other friends in a range of behaviors, including the
use of tobacco, alcohol, or other substances and criminal offenses and related
behaviors. These items were then summed to provide an overall measure of the
extent to which each subject affiliated with delinquent or substance-abusing
peers between ages 14 and 16.34 The reliability
of this scale, assessed using coefficient , was .76.
COMORBID PSYCHIATRIC DISORDERS AND BEHAVIOR
Four measures of young people's psychiatric adjustment and behavior
between ages 14 and 16 were also included in the analysis. Specifically, at
ages 15 and 16, young people and their parents were interviewed separately
using items from the Diagnostic Interview Schedule for Children,24
Early Self-Report Delinquency Inventory,35
Rutgers Alcohol Problems Index,36 and other
custom-written items based on DSM-III-R criteria.
Using this information, young people were classified as meeting criteria for
anxiety disorders, conduct disorders, or alcohol abuse if they met DSM-III-R diagnostic criteria for these disorders on the basis of parent-
or self-report. In addition to these measures, a measure of early cigarette
smoking was obtained at age 15. Early cigarette smoking was defined as having
smoked a cigarette on at least one occasion during the past year.
STATISTICAL METHODS
The analysis was conducted in 4 stages. In the first stage, bivariate
associations were estimated describing the linkages between adolescent depression
and later outcomes (Table 1).
In all cases, data were stratified by sex, and tests of sex by adolescent
depression interactions were conducted using logistic regression analysis.
In the second stage of the analysis, associations between adolescent depression
and social, familial, and individual factors assessed up to age 16 were estimated
(Table 2). Associations were described
by the odds ratios (ORs) and 95% confidence intervals (CIs). In the third
stage of the analysis, associations between adolescent depression and later
outcomes were adjusted for confounding, social, familial, and individual factors.
The model fitted was: Logit (Yi) = B0 + B1 X1 +  Bj Zj, where Logit
(Yi) indicates the log odds of the ith outcome measure; X1, the measure of
adolescent depression; and Zj, the set of confounding, social, familial, and
individual factors. In fitting this model, all confounding factors were entered
into the initial model, and the model was successively refined to identify
significant (P<.05) covariates. From this model,
estimates of the ORs between X1 and Yi, adjusted for the confounding factors
Zj, were obtained (Table 3). Finally,
the logistic regression model was extended to consider factors that were comorbid
with depression in addition to the confounding factors Zj. The model fitted
was: Logit (Yi) = B0 + B1 X1 + Bj Zj + Bk Wk, where Wk indicates
the set of measures of disorders that were comorbid with adolescent depression.
In fitting this model, the significant covariate factors identified in the
third-stage analysis were retained in the model, and all measures of comorbid
disorders were included in the analysis. This baseline model was then successively
refined to identify significant covariates. From this model, estimates of
the ORs between X1 and Yi, adjusted for confounding factors Zj and comorbid
disorders Wk, were obtained.
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Table 1. Psychiatric, Educational, and Social Role Outcomes Associated
With Major Depression During Early Adolescence (Ages 14-16 y)*
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Table 2. Social Background, Family Functioning, and Individual Characteristics
of Young People With Major Depression During Early Adolescence (Ages 14-16
y)*
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Table 3. Psychiatric, Educational, and Social Role Outcomes Associated
With Major Depression During Early Adolescence After Adjustments (N = 964)*
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RESULTS
RELATIONSHIPS BETWEEN ADOLESCENT DEPRESSION AND LATER OUTCOMES
Adolescents with depression were at increased risk of a range of subsequent
outcomes between ages 16 and 21 (Table 1). These outcomes included later depression (OR, 4.5; 95% CI, 3.0-6.6),
anxiety disorders (OR, 3.9; 95% CI, 2.7-5.8), nicotine dependence (OR, 2.1;
95% CI, 1.5-3.2), alcohol abuse or dependence (OR, 1.5; 95% CI, 1.0-2.2),
suicidal behavior (OR, 2.9; 95% CI, 1.6-5.3), school failure (OR, 1.8; 95%
CI, 1.1-2.7), and a reduced likelihood of entering a university (OR, 0.6;
95% CI, 0.4-0.8) or pursuing another form of tertiary education (OR, 0.6;
95% CI, 0.4-0.9). In addition, at age 21, adolescents with depression were
characterized by higher rates of recurrent unemployment (OR, 1.8; 95% CI,
1.2-2.7) and early parenthood (OR, 3.7; 95% CI, 2.2-6.2).
Furthermore, the relationship between adolescent depression and later
outcomes was similar for girls and boys. The similarity of these associations
was confirmed by tests of sex by adolescent depression interactions, which
showed that, across all outcomes, no significant interactions between depression
and sex were found. However, for most outcomes, there was a significant (P<.05) main effect of sex, reflecting the fact that
rates of subsequent psychiatric, educational, and social role outcomes varied
in sex-specific ways.
SOCIAL, FAMILIAL, AND INDIVIDUAL FACTORS ASSOCIATED WITH DEPRESSION
IN EARLY ADOLESCENCE (AGE 14-16)
Table 2 shows the relationship
between major depression in early adolescence and a range of measures of social
background, familial, and individual factors. Also shown are the associations
between depression and other comorbid psychiatric disorders and behaviors
in adolescence. For ease of data display, all measures have been presented
in dichotomous form. Results revealed that, although there was a tendency
for adolescents with depression to have been reared by a mother with educational
underachievement (P<.02), adolescents with and
without depression had similar socioeconomic backgrounds. In contrast, small
to moderate associations were found between adolescent depression and family
measures, individual factors, and comorbid psychiatric disorders, with ORs
ranging from 1.9 to 4.2 (median, 3.0). Specifically, adolescents with depression
were significantly (P<.001) more likely to have
been exposed to sexual abuse and parental change during childhood. They also
tended to have had lower IQ scores at age 9 (P<.01),
showed tendencies to neuroticism (P<.001), and
reported higher rates of deviant peer involvement in adolescence (P<.001). Finally, adolescents with depression had significantly
higher (P<.001) rates of comorbid anxiety disorders,
conduct disorders, and alcohol abuse and were more likely to smoke cigarettes.
RELATIONSHIPS BETWEEN DEPRESSION IN ADOLESCENCE AND LATER OUTCOMES,
ADJUSTED FOR CONFOUNDING FACTORS
As explained in the "Subjects and Methods" section, a logistic regression
analysis was used to examine the role of confounding factors and comorbid
disorders. The results of these analyses are shown in Table 3, which gives estimates of the ORs between adolescent depression
and later outcomes after adjustment for confounding factors and for confounding
factors and comorbid disorders. The results suggest 2 conclusions. First,
there was evidence of a clear and specific continuity from adolescent depression
to later depression (OR, 3.5; 95% CI, 1.9-6.4) and anxiety (OR, 2.2; 95% CI,
1.4-3.5), even after controlling for confounding factors and comorbid disorders.
Second, in all cases, the associations between adolescent depression and other
outcomes, including nicotine dependence, alcohol abuse or dependence, suicide
attempt, educational underachievement, unemployment, and early parenthood,
were explained by confoundingfactors (parental change, childhood sexual abuse,
IQ, neuroticism, involvement with deviant peers, and maternal educational
underachievement) associated with depression. Further controlling for comorbid
disorders did not change these associations. These results imply that the
elevated rates of these outcomes among teenagers with depression reflected
the antecedent social background, familial, and personal factors that were
associated with adolescent depression and increased risk of later adverse
outcomes, rather than the direct effects of depression on later adjustment
and life experiences.
COMMENT
In this study, we used data gathered during a 21-year longitudinal study
to examine the long-term consequences of depression in adolescence (age 14-16
years). This analysis leads to the following conclusions about the linkages
between adolescent depression and later outcomes. First, in confirmation of
previous studies,9-10,12, 15-16,19, 37
young people developing depression in adolescence were an at-risk group for
a range of adverse outcomes that included subsequent depression and anxiety,
suicidal behaviors, nicotine dependence, academic and employment difficulties,
and early parenthood. Odds ratios between adolescent depression and mental
health outcomes ranged from 1.2 to 4.5, while ORs for educational and social
role outcomes ranged from 0.6 to 1.8 and 1.8 to 3.7, respectively. There is
little doubt from this evidence that the onset of depression in adolescence
is a marker for long-term problems of adjustment in late adolescence and early
adulthood.
Second, also in confirmation of previous research,2, 38
depression in adolescence was associated with other adverse factors. These
factors included higher rates of exposure to adverse social and familial circumstances,
lower IQ, higher levels of neuroticism, and higher rates of comorbid adolescent
disorders, including anxiety, conduct disorders, and substance abuse.
These results raise an important question about the developmental pathways
that link depression in adolescence to later outcomes. There are 3 general
pathways that may explain these linkages. First, it is possible that there
are direct linkages in which depression in adolescence leads directly to increased
risk of later outcomes. Second, it is possible that the relationship between
depression and later outcomes is spurious and reflects the presence of confounding
factors that are related to early depression, but that also contribute to
later outcomes. Finally, it is possible that the linkages between adolescent
depression and later outcomes may be mediated by intervening variables. In
this study, we used methods of logistic regression analysis to identify the
likely pathways linking early depression to a range of later outcomes that
include mental disorders, suicidal behaviors, educational underachievement,
unemployment, and early parenthood. These analyses suggested the presence
of 2 routes by which adolescent depression was associated with later social
maladjustment.
First, there was evidence of a direct pathway linking depression in
adolescence to increased risk of later depression and anxiety. Model estimates
suggested that young people who were depressed as adolescents had more than
3 times the risk of subsequent depression and more than twice the risk of
later anxiety than their peers without depression, independent of social background,
family circumstances, individual characteristics, and comorbid disorders.
These results suggest the presence of a direct and specific continuity in
which adolescent depression is a precursor of long-term depression and anxiety.
These findings are consistent with other studies9, 11-12,15
that have shown that depression and anxiety are disorders that often recur
over the life course.
However, for other outcomes, including substance abuse disorders (nicotine
and alcohol), suicide attempt, educational underachievement, unemployment,
and early parenthood, the relationship with depression appeared to be noncausal.
In particular, controlling for social, familial, and personal factors (parental
educational achievement, parental change, exposure to childhood sexual abuse,
IQ, neuroticism, and deviant peer involvement) suggested that the linkages
between depression and the other outcomes arose because adolescent depression
was associated with a range of adverse social, familial, and personal factors,
and because, in turn, these factors had linkages with a range of outcomes.
These results suggest that, when due allowance was made for social, familial,
and personal correlates of adolescent depression, there was no evidence to
suggest that those subject to adolescent depression were at significantly
increased risk of later substance abuse, suicide attempts, educational underachievement,
unemployment, or early parenthood. Rather, the results suggested that the
contextual factors that were associated with an increased risk of adolescent
depression were also associated with increased risk of these later adverse
outcomes.
There are 2 major clinical implications of these findings. First, the
results reinforce the growing consensus of evidence that depressive disorders
are frequently recurrent conditions, and it appears that this applies to disorders
developing in adolescence. The present study suggests that nearly two thirds
of those with depression between ages 14 and 16 will experience a further
episode of depression by age 21. Similarly, those with early depression also
are at increased risk of later anxiety disorders, with just under half of
adolescents with depression developing an anxiety disorder by age 21.
Second, although the evidence suggests that depression in adolescence
is associated with a range of later adverse outcomes, including suicidal behaviors,
educational underachievement, unemployment, and early parenthood, these outcomes
do not appear to be the consequences of early depression, but rather arise
as a result of common social, familial, and personal factors that contribute
to adolescent depression and later outcomes. These findings imply that adolescent
depression in combination with problematic social, familial, and personal
factors may be associated with a range of adverse outcomes. These results
emphasize the importance of placing an early episode of depression within
the context of a young person's life history and social and personal circumstances.
There are several limitations to the findings of this study. First,
the results are based on a specific New Zealand cohort studied, and it remains
open to examination whether similar findings will apply to other cohorts or
in other social contexts. Second, the assessment of depression during adolescence
and early adulthood relied on young people's retrospective reporting of depressive
symptoms. In addition, it is unclear how many of those reporting depressive
symptoms would have met clinical criteria for major depression. Inevitably,
there is likely to be some imprecision in reporting the extent and timing
of symptoms. Third, because the study is based on self-reported data, it is
open to question whether the episodes of depression described by subjects
would, in fact, meet clinical diagnostic criteria. This feature may explain
the high rate of depression reported between ages 16 and 21 years. Finally,
the analysis involves a large number of outcome variables and covariate factors.
Because of this, it is possible that some regression models may have overcontrolled
for the effects of confounding factors. Given this, the findings of this study
should be replicated on independent samples. These limitations notwithstanding,
the results of this study suggest that young people who develop depression
in adolescence are an at-risk population for a range of adverse outcomes.
These linkages appear to reflect the presence of specific continuities between
adolescent depression and later anxiety or depression and the effects of common
risk factors associated with adolescent depression and other outcomes.
AUTHOR INFORMATION
Submitted for publication November 1, 2000; final revision received
June 13, 2001; accepted June 26, 2001.
This research was funded by grant HRC 9705 from the Health Research
Council of New Zealand, Auckland; National Child Health Research Foundation,
Auckland; Canterbury Medical Research Foundation, Christchurch, New Zealand;
and New Zealand Lottery Grants Board, Wellington.
Corresponding author and reprints: David M. Fergusson, PhD, Christchurch
Health & Development Study, Christchurch School of Medicine, PO Box 4345,
Christchurch, New Zealand (e-mail: david.fergusson{at}chmeds.ac.nz).
From the Christchurch Health & Development Study, Christchurch
School of Medicine, Christchurch, New Zealand.
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