Developmental Psychopathology: A Paradigm Shift or Just A Relabeling?

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Development and Psychopathology 25 (2013), 1201–1213

# Cambridge University Press 2013


doi:10.1017/S0954579413000564

Developmental psychopathology: A paradigm shift


or just a relabeling?

MICHAEL RUTTER
King’s College London

Abstract
Developmental psychopathology is described as a conceptual approach that involves a set of research methods that capitalize on developmental and
psychopathological variations to ask questions about mechanisms and processes. Achievements are described in relation to attachment and attachment
disorders, autism, schizophrenia, childhood antecedents of adult psychopathology, testing for environmental mediation of risk effects, gene–environment
interplay, intellectual and language functioning, effects of mentally ill parents on the children, stress and vulnerability to depression, ethnicity and
schizophrenia, and drug response. Continuities and discontinuities over the course of development are discussed in relation to attention-deficit/hyperactivity
disorder, antisocial behavior, eating disorders, substance abuse and dependency, pharmacological and behavioral addictions, and a range of other disorders.
Research challenges are considered in relation to spectrum concepts, the adolescent development of a female preponderance for depression, the mechanisms
involved in age differences in response to drugs and to lateralized brain injury, the processing of experiences, the biological embedding of experiences,
individual differences in response to environmental hazards, nature–nurture integration, and brain plasticity.

Developmental psychopathology (DP) has been described as & Uher, 2012). There was much more overlap among diag-
a conceptual approach that involves a set of research methods nostic categories than had previously been appreciated and,
that capitalize on developmental and psychopathological var- in particular, there was no “clear water” between categories.
iations to ask questions about mechanisms and processes Moreover, not only the risks for mental disorders were largely
(Rutter, 2008; Sroufe & Rutter, 1984). There are several dis- dimensional but also the disorders themselves were mainly
tinctive features that are crucial: there is an expectation of dimensional (Rutter, 2003, 2011; Rutter & Uher, 2012;
both continuities and discontinuities; a recognition that it is Uher & Rutter, 2012a). Developmental psychology had be-
not a theory or a discipline; there is a focus on individual dif- come focused too exclusively on universals in development
ferences and not universals; a focus on mediating processes rather than on individual differences in development, and it
and not just risks; a recognition that age is an ambiguous vari- had also been concerned with quantification of trait stabilities
able that reflects both biological maturation and the accumu- over time, without any explicit recognition of both continu-
lation of experiences (Rutter, 1989); a focus on indirect and ities and discontinuities (Rutter & Rutter, 1993).
direct causal changes; and a recognition that indirect change For all of these reasons, it is clear that DP did involve a para-
may involve a complex mixture of both transformation and digm shift and not just a relabeling. Almost all people working
coherence (Rutter, 2008; Sroufe & Rutter, 1984). The reasons in the field would agree on that. In contrast, there has been some
why a concept of DP was needed is that the “life” theories of disagreement on the breadth of the DP approach. Thus, for ex-
systematizers (such as Freud, Piaget, and Erikson) had proved ample, Cicchetti and Toth (2009), two outstanding leaders in
seriously inadequate, and it was clearly most unlikely that any this field, have emphasized interdisciplinarity and the need
one type of mechanism could explain everything. for multiple levels of analysis; the need to integrate DP with
Child psychiatry, like DP, was concerned with individual biology, neuroscience, and genetics; the need to apply knowl-
differences and mediating mechanisms, but it had become edge to prevention and to intervention and to undertake trans-
much too preoccupied with narrowly defined and conceptual- lational research; and the need to consider culture and social
ized diagnostic issues. Research findings had made it all too context. All of those features are highly desirable, but they
clear that the concepts underlying the official diagnostic clas- should apply to the whole of science and not just to DP. In ad-
sification, such as DSM-IV and ICD-10 (World Health Orga- dition, the notion of this degree of generalization needs to apply
nization, 1992), needed radical revision (Rutter, 2011; Rutter across studies and not necessarily within any one single study.

Address correspondence and reprint requests to: Michael Rutter, MRC So- Achievements of DP
cial, Genetic & Developmental Psychiatry Centre, Institute of Psychiatry,
King’s College London, PO Box 080, De Crespigny Park, Denmark Hill, In considering the achievements of DP approaches, it is impor-
London SE5 8AF, UK; E-mail: [email protected]. tant to recognize that many of these are derived from research-
1201
1202 M. Rutter

ers who would not have identified themselves as DP research- the continuities between autism and normality, this was an in-
ers. For example, many of the advances came from adult psy- dication that there might be important discontinuities as well.
chiatrists and from genetics researchers (Rutter, 2010). This was apparent, too, in the finding that the rate of epilepsy
was not only raised in autism but was distinctive in having a
later age of onset than was usually the case (Bolton et al.,
Attachment and attachment disorders
2011).
The first area of achievement lies in the field of attachment
and attachment disorders (Rutter, Kreppner, & Sonuga-Barke,
Schizophrenia
2009; Rutter & Sroufe, 2000). Attachment research undoubt-
edly had its beginning in a theoretical approach about the Schizophrenia provides the third domain where there have
meaning of attachment (Ainsworth, Blehar, Waters, & Wall, been major achievements of DP approaches. Probably, this
1978; Bowlby, 1969). The DP qualities were shown in the rec- began in the 1970s when Johnstone, Frith, Crow, Husband,
ognition of the need to extend measurement to “disorganiza- and Kreel (1976) showed that schizophrenia was associated
tion” as well as insecurity (Main & Solomon, 1986) and to use with enlarged ventricles, a finding carrying the inference
a mixture of qualitative and quantitative approaches. Much that it was not just a functional psychosis. This provided evi-
more recently there was the demonstration that the pattern dence of discontinuity from normality. The second finding
of social disinhibition more crucially involved social dysreg- came from long-term, general-population, longitudinal stud-
ulation than insecure attachment (Bruce, Tarullo, & Gunnar, ies showing that schizophrenia (but not bipolar disorder or de-
2010; Rutter et al., 2009). Moreover, it is evident that the pat- pression/anxiety) was associated with impairments in lan-
tern is mainly a consequence of an institutional upbringing guage and/or motor function in the preschool years and
(Zeanah & Gleason, 2011). Finally, there was the finding with impairments in intelligence over the whole period
that problems of social relationships in early childhood were from early childhood onward (Cannon et al., 2002). The im-
highly predictive of adult mental health outcomes, but there plication was that schizophrenia had its beginnings in early
was very weak prediction from strange situation measure- onset neurodevelopmental impairment. At that time it was
ments in infancy (Grossman, Grossman, & Waters, 2005). not clear whether this was an impairment that was part of
the liability for schizophrenia or something independent
from it that nevertheless carried a risk for the onset of a schi-
Autism
zophreniform psychosis. The next finding was that schizo-
A second area of achievement concerned the very different phrenia was associated with minor psychotic-like features
psychopathological domain of autism. The DP feature here in late childhood/early adolescence (Poulton et al., 2000). Al-
that was distinctive was the recognition of the need to move though these were surprisingly common in the general popu-
from a diagnostic approach to a study of the possible under- lation (Laurens, Hobbs, Sunderland, Green, & Mould, 2011),
lying mentalizing deficits (Hermelin & O’Connor, 1970). they were associated with a substantially increased risk for the
The term theory of mind came to the forefront, which was first later development of schizophrenia. The fourth finding de-
studied in chimpanzees (Premack & Woodruff, 1978) and rived from a genetic, high family risk study in which abnor-
then in humans with normal children (Wimmer & Perner, malities akin to schizotypy, as manifest in late adolescence,
1983) and extended to children with autism (Baron-Cohen, were associated with the development of schizophrenia in
Leslie, & Frith, 1985). In short, there was a focus on continu- about half of the cases (Johnstone, Ebmeier, Miller, Owens,
ities and discontinuities between normality and disorder and a & Lawrie, 2005). In addition to all of these findings, Wein-
focus on possible mediating mechanisms. Both genetic and berger (1987) and Murray and Lewis (1987) argued that, de-
epidemiological evidence later showed that the genetic liabil- spite overt psychosis usually not being manifest until early
ity for autism extended far beyond the traditional diagnosis adult life, research findings indicated that schizophrenia
(LeCouteur et al., 1996; Rutter, 2000). Twin and family stud- should be considered to have arisen on the basis of an early
ies showed that there was a broader autism phenotype (BAP) neurodevelopmental impairment. Later findings suggested
that had a raised rate among the family members of those fam- that, although this was the case, in some cases there were fur-
ilies with an autistic individual as compared with controls ther neurodevelopmental changes that arose after the onset of
(Bailey, Palferman, Heavey, & Le Couteur, 1998). Imaging the psychosis (Andreasen, 2010; Rapoport & Gogtay, 2011).
and other neural studies showed that physiological brain dif- However, there are still uncertainties regarding the extent to
ferences were detectable by 12 months of age before the which the postonset changes reflect drug effects (Thompson
clinical manifestations had become evident (Bosl, Tierney, et al., 2009).
Tager-Flusberg, & Nelson, 2011; Luyster, Wagner, Vogel-
Farley, Tager-Flusberg, & Nelson, 2011). A rather different
Childhood antecedents of adult psychopathology
sort of finding was that social and language regression,
usually evident about the age of 2 years, seemed to be The fourth DP area of achievement lay in the evidence of the
much more common in autism than in other neurodevelop- childhood antecedents of serious adult mental disorder. Find-
mental disorders (Pickles et al., 2009). Having demonstrated ings from the Dunedin longitudinal study showed that over
DP: A paradigm shift or just a relabeling? 1203

half of mental disorders that were diagnosed when the indi- vided just the sort of natural experiment that would be valu-
viduals were aged in their 20s and which had resulted in able for this purpose (Rice et al., 2009; Thapar & Rutter,
the receipt of treatment had been manifest in childhood/early 2009). Thus, some forms (such as sperm donation) maintain
adolescence (Kim-Cohen et al., 2003). Although there was the genetic link between mother and child, whereas others
substantial (but minority) continuity in the type of disorder, (such as egg donation) disrupt that link. They used this ap-
oppositional defiant and conduct disorders were the most fre- proach to test the hypothesis that maternal smoking in preg-
quent antecedents of adult disorders (Kim-Cohen et al., nancy had a prenatal effect that predisposed to later atten-
2003). That is to say, as would be expected from any devel- tion-deficit/hyperactivity disorder (ADHD) and antisocial
opmental perspective, homotypic continuity was frequent, behavior. The assisted-conception design confirmed that
but what was new was the evidence of heterotypic continuity. there was a prenatal effect on low birth weight (as shown
That is, the problems in childhood were often disruptive be- also by both observational studies and animal models), but
havior, but the adult outcome lay in rather different phenom- there was not an effect on either ADHD or antisocial behav-
ena, such as eating disorders. ior. It was clear that statistical controls for confounding failed
to provide what was needed in the absence of the natural ex-
periment. The same finding that fetal exposure to maternal
Testing for Environmental Mediation of Risk Effects
smoking led to an increased likelihood of a low birth weight
The fifth area of DP achievements lay in the multiple different but no causal effect on either ADHD or antisocial behavior
approaches to the testing of hypotheses of environmental me- has also come from other types of natural experiment
diation of risks for psychopathology. All researchers and (D’Onofrio, Rathouz, & Lahey, 2011; D’Onofrio, Van Hulle,
clinicians will have been taught that statistical associations, Goodnight, Rathouz, & Lahey, 2011; Obel et al., 2011) such
however strong, do not necessarily mean a causal effect. as sibling comparisons (Obel et al., 2011).
Nevertheless, neither developmental psychologists nor child A different design is to focus on situations in which there
psychiatrists had paid much attention to the possible ways in is a radical, sudden and easily dated change of environment.
which the causal inference of environmental mediation might The longitudinal study of children from profoundly depriving
be tested. The situation changed with the recognition of the Romanian institutions who were adopted into UK families
ways in which “natural experiments” that pulled apart vari- constitutes just such an example (Rutter, Kumsta, Schlotz,
ables that ordinarily went together could do much to strengthen & Sonuga-Barke, 2012; Rutter & Sonuga-Barke, 2010).
or weaken the causal inference (Rutter, 2007, 2012b). There were many features that made this a clear-cut natural
Alongside this recognition, but also part of it, was the ap- experiment. The first was the massive improvement in func-
preciation that genetically sensitive designs could be enor- tioning that followed the adoption and departure from the in-
mously informative. For example, Kendler and Prescott stitution. However, what was of greater interest was not the
(2006) used the discordant twin design, in which one twin immediate situation but what happened with respect to later
had experienced sexual abuse and the other had not, to test development. The findings showed that a substantial minority
whether such abuse was associated with the later develop- of the young people did show deficits and that these took an
ment of psychopathology. The findings provided strong con- unusual and distinctive form (such as quasiautism and disin-
firmation of a likely environmental mediation of such effects. hibited attachment). The environmental mediation inference
Jaffee and colleagues (2004) used a multivariate twin analysis was strongly supported by the association with the duration
to compare the effects of physical abuse and of corporal pun- of institutional deprivation applied to those who did not
ishment on psychopathology. The findings were striking in have measurable subnutrition (Rutter et al., 2012) and the def-
showing that most of the effects of physical abuse were envi- icits persisted right up to the time of the most recent follow-up
ronmentally mediated, but most of the effects of corporal pun- at age 15 years.
ishment were not. The implication was that the association be- Another confounder in most studies is the possibility of so-
tween corporal punishment and mental disorders arose from cial selection, namely, that the association derived from the
the evocative effects of disruptive behavior in eliciting paren- opportunity of people to shape and select their own experi-
tal punishment. However, the findings also indicated that, al- ences. A natural experiment in this case is a situation in which
though corporal punishment and physical abuse functioned all people are exposed to the same experience without the op-
rather differently, nevertheless, the extensive use of physical portunity for any kind of selection or shaping. One such ex-
punishment carried an increased risk that this would later es- ample is provided by the Dutch famine in World War II (Sus-
calate into abuse. ser et al., 1996) and a similar famine in China (St. Clair et al.,
One of the issues that needs tackling in testing for environ- 2005). The findings in both cases showed that a prenatal ex-
mental mediation is the possibility that, although the risk fac- posure to famine conditions was associated with an increased
tor is manifestly and rightly labeled an environment (e.g., as risk of the development of schizophrenia many years later.
would be the case with parental discord or family poverty), A rather different example is provided by the study of the
risks may nevertheless be at least partially genetically medi- effects of a casino set up on a Native American reservation.
ated (Plomin & Bergeman, 1991). Thapar and Rice (Rice This was a natural experiment because, by Federal regulations
et al., 2009) had the creative idea that assisted conception pro- in the United States, the setting up of a casino on a reservation
1204 M. Rutter

had to be associated with the distribution of a proportion of Intellectual and Language Functioning
the funds to all members living on the reservation without
The seventh DP achievement concerns the effects in relation
their needing to either ask for it or to “deserve” it. Costello,
to intellectual and language functioning. Two findings re-
Compton, Keeler, and Angold (2003) had the ingenious
quire particular emphasis. The first is that unilateral brain
idea to use their own Smoky Mountains longitudinal study
damage in the dominant hemisphere leads to aphasia in adults
to examine the effect of the setting up of the casino in the mid-
but generalized intellectual impairment in infancy (Rutter,
dle of a period of data collection. The findings showed that
1993; Vargha-Khadem, Issacs, Van Der Werf, Robb, & Wil-
the relief of poverty was associated with a significant improve-
son, 1992). That is to say, unilateral brain damage has a
ment in the children’s behavioral functioning. It is striking that,
marked effect in all age groups, but the pattern is quite differ-
despite the obvious need, very few developmental studies of
ent in infancy compared with later childhood, adolescence,
social development have tested for environmental mediation
and adult life. The second finding is that severe intellectual
(Rutter, 2012c). The need for such testing is the key feature
disability is frequently associated with major pathogenic
of resilience research, but it is also a key feature of DP.
genes, but mild disability is not to the same extent (Einfeld
& Emerson, 2008). Thus, Down syndrome is a major cause
Gene–Environment Interplay of severe intellectual disability, but it is much less often asso-
ciated with mild intellectual disability. Pathogenic genetic
The sixth achievement of DP concerns gene–environment in-
mutations do account for a small proportion of cases of
terplay (Rutter, 2012a). This involves at least three different
mild intellectual disability, but for the most part, mild disabil-
types of interplay that are important. First, there are the effects
ity operates at the extreme end of a normal distribution. That
of epigenetic mechanisms in the biological embedding of ex-
is not the case with severe intellectual disability. The implica-
periences (Meaney, 2010). Many questions remain about epi-
tion is that there is almost complete discontinuity between se-
genetic effects, but what has been really exciting and impor-
vere intellectual disability and normality, whereas continu-
tant is the recognition that genes can only have effects if the
ities are relatively strong in the case of mild disability.
genes are “expressed,” and the expression of genes involves
several DNA elements, stochastic (random) effects, and ex-
periences. What this means is that although the environment
Effects of Mentally Ill Parents on the Children
cannot alter gene sequences, it can alter the effects of genes
through affecting gene expression. That is directly relevant The eighth DP achievement concerns the effects of mentally
for DP because it concerns a key mediating mechanism, a ill parents on the children. Using an extended children of
central role of DP research. Second, another type of interplay twins design to study the genetic environmental mediation
concerns gene–environment correlations (rGE; Kendler & of transgenerational transmission, Silberg, Maes and Eaves
Baker, 2007). These are important because they constitute (2012) found that parental antisocial disorder had an envi-
the mechanism by which environments can have genetically ronmentally mediated effect on child depression, a geneti-
mediated effects (Plomin & Bergeman, 1991). However, they cally mediated effect on ADHD, and an effect on child con-
are also important because they point to the various ways in duct disorder that involved both genetic and environmental
which people’s behavior shapes and selects environments. mediation (Silberg et al., 2012). A somewhat similar pattern
Once more, the DP significance lies in the highlighting of me- applied to parental depression (Silberg, Maes, & Eaves,
diating mechanisms. 2010). Parental depression had a direct, environmentally
The third type of interplay concerns gene–environment in- mediated effect in increasing the risk that the children devel-
teraction (G  E). The initial reports of epidemiological evi- oped depression. There was also an increased risk of conduct
dence showing G  E in humans emphasized the environ- disorder in the children, but this involved a mixture of genetic
mental role of life events. As it has turned out, however, the and environmental effects. This research made it abundantly
evidence for G  E is much stronger in relation to maltreat- clear that a general answer on whether the effects were envi-
ment than it is for acute life events (Karg, Burmeister, Shed- ronmentally or genetically mediated was going to be com-
den, & Sen, 2011). This means that the causal path begins pletely wrong. The mode of mediation varied according to
with maltreatment in early childhood with the effect being the child outcome.
evident in psychopathology only manifest in late adolescence A rather different approach concerned looking at the ef-
or early adult life. In other words, the biological pathway in- fects of intervention on the treatment of mentally ill parents
volves very substantial continuity over the developmental with respect to the benefits for the children. A meta-analysis
course. The second G  E finding that is crucial for DP is showed that preventive interventions (with cognitive, behav-
that human experimental studies utilizing structural and func- ioral, and psychoeducational components) were effective for
tional brain imaging have shown that the GE neural effects preventing both behavioral and emotional problems in the
are evident in individuals who have already been screened for children (Siegenthaler, Munder, & Egger, 2012). Using lon-
an absence of psychopathology (Hyde, Bogden, & Hariri, gitudinal analyses, other research showed that changes in the
2011; Meyer-Lindenberg & Weinberger, 2006). This shows level of maternal depression were accompanied by parallel
a continuity between normality and disorder. trajectories with respect to child symptoms, with the main ef-
DP: A paradigm shift or just a relabeling? 1205

fect appearing to be from parent to child but also including but are not so in children. Children with ADHD benefit from
some bidirectional effects (Garber, Ciesla, McCauley, Dia- taking stimulants, but they do not actually like the sensation
mond, & Schloredt, 2011; Garber & Cole, 2010; Kouros & that the drug provides. Another age effect is that the adverse ef-
Garber, 2010). fects of psychotropic drugs, such as risperidone, are much
more common in children than in adults (Fedorowicz & Fom-
bonne, 2005; Stigler, Potenza, Posey, & McDougle, 2004). Fi-
Stress and Vulnerability to Depression
nally, depression in childhood does not respond to tricyclics,
The ninth DP achievement concerns research seeking to ex- whereas depression in adult life usually does. This is not a
amine mediation effects in relation to the associations be- question of resistance to antidepressant medication, because
tween the experience of stress and vulnerability to depression. depression in young people does respond to selective serotonin
There is a good deal of evidence from many studies that stress reuptake inhibitors; it is just that it does not seem to respond to
is associated with depression, but the suggested mechanisms tricyclics (Hazell, O’Connell, Heathcote, Robertson, & Henry,
are very variable. Thus, three main models have been pro- 1995).
posed. First, there is stress sensitization, meaning that a sen-
sitivity to stressors increases with the number of stress experi-
Continuities and Discontinuities Over the Course
ences. Second, there is the stress inoculation model, that is,
of Development
stress experiences have a diminishing effect over the course
of repeated stress experiences. Third, there is diathesis–stress The 12th achievement concerns a better understanding of con-
model, that is, a vulnerability to stress associated with con- tinuities and discontinuities over the course of development.
tinuing biological features. Using longitudinal data, Garber
and colleagues found little support for the stress inoculation
ADHD
model but evidence in favor of both the stress sensitization
and diathesis–stress models (Morris, Ciesla, & Garber, ADHD is ordinarily thought of as a clinical disorder, but it is
2010). This is an important topic, but it is one in which defin- evident that the genetic liability operates across a dimensional
itive answers are hard to come by. Thus, animal models have range and not just on an extreme representing disorder (Tha-
shown that, provided the stress is mild and manageable, there par, Harrington, Ross, & McGuffin, 2000). Classification has
are stress inoculation effects in the sense that they lead to an traditionally dealt with subcategories in terms of whether it is
increased resistance to later stressors (Rutter, 2012c, 2013). predominantly inattention or predominantly hyperactivity/
impulsivity or some combined pattern. At any one point in
time these appear rather different, but it is clear that the differ-
Ethnicity and Schizophrenia
ences among them are not stable over time and there are sys-
The tenth DP achievement concerns the association between tematic changes in pattern with increasing age. Attention def-
ethnicity and schizophrenia. There is good evidence that the icits tend to increase and hyperactivity/impulsivity tends to
incidence of schizophrenia (and other psychoses) is substan- decrease (Larsson, Dilshad, Lichtenstein, & Barker, 2011).
tially elevated in individuals of Black Caribbean or Black It has also been found that inattention/overactivity is a con-
African origin living in the United Kingdom as compared sequence of an institutional upbringing (Rutter & Sonuga-
with that of individuals of similar ethnicity living in the Ca- Barke, 2010; Vorria & Ntouma, 2012). This need not be a
ribbean and that of indigenous, White individuals living in surprise, because ADHD is a multifactorial disorder and, de-
the United Kingdom (Fearon et al., 2006; Jones & Fung, spite high heritability, clearly environmental factors will play
2005). The findings showed that the effects were particularly a part. However, this cannot be the usual way in which envi-
mediated by social disadvantage in adult life and separation ronmental factors operate because an institutional upbringing
from parents (Morgan et al., 2009). Other research (Schäfer has an infrequent association with ADHD. Moreover, the in-
& Fisher, 2011) has shown the role of childhood trauma in attention/overactivity found following institutional depriva-
psychosis and the DP relevance lies in the focus on both con- tion is somewhat unusual in its association with quasiautism
tinuities across diverse social risks and the importance of and/or disinhibited attachment.
these in an illness that involves strong genetic influences.
Antisocial behavior
Drug Response
It has long been realized that antisocial behavior is heteroge-
The eleventh achievement concerns drug responses. Rapo- neous. At one extreme, the majority of people commit antiso-
port showed more than 30 years ago that the response to stim- cial acts at some time, although they are generally well func-
ulants was very similar in the general population and in patients tioning (Rutter, Giller, & Hagell, 1998). At the other extreme,
with ADHD (Rapoport et al., 1980). It was previously consid- some antisocial behavior persists into adult life in association
ered a paradoxical response, but stimulants improve attention with substantial social dysfunction. Moffitt’s (1993) paper
in everyone to some degree. In contrast, there is a difference ac- brought clarity through its differentiation of life-course-per-
cording to age in that stimulants are recreational drugs in adults sistent (LCP) and adolescence-limited (AL) antisocial behav-
1206 M. Rutter

ior. The former was said to be characterized by a childhood the span of behavioral variation and over developmental
onset, individual neurodevelopmental deficits, and chronic course. The existing classification in ICD-10 has as its prime
family adversity. In contrast, the latter was viewed as largely feature the specific drug or substance that is involved. That
developmentally normative and associated with an antisocial seems all back to front, as it is the nature of the particular
peer group. Subsequent research has largely supported the problem that should constitute the prime basis and not the
LCP and AL distinction, but it has indicated the need for three drug. That would be so in any case, but the argument is
main modifications. First, as shown earlier by Robins (1966, greatly strengthened by the universal observation that it is
1978) and confirmed by Odgers and colleagues (2008), about usual for substance abuse to involve several, often many, dif-
half of those with an early onset do not continue their antiso- ferent substances (Weinberg, Harper, & Brumback, 2008).
cial behavior into adult life, pointing to the need to recognize The notion that typically it is just one substance is simply
a substantial childhood-limited (CL) group. Second, adoles- wrong. At one time, it was assumed that there was a hierarchy
cent-onset antisocial behavior often constitutes a precursor wherein “softer” drugs were always taken first before pro-
of more severe, long-term social malfunction (Odgers et al., ceeding to “harder” drugs, such as opiates or cocaine. Robins’
2007). Third, the adolescent-onset group differed from non- pioneering studies of soldiers in Vietnam indicated how mis-
antisocial youth in showing both individual and family adver- taken this was (Robins, 1993; Robins, Davis, & Goodwin,
sity, albeit less than that associated with LCP (Roisman, 1974). The soldiers tended to start with hard drugs, and she
Monahan, Campbell, Steinberg, & Cauffman, 2010). In sum- concluded that this was because they were more readily avail-
mary, in line with a DP perspective, antisocial behavior able in Vietnam than were some of the softer drugs (which, of
should be conceptualized as showing both continuities and course, is not the case in the general population). A particular
discontinuities across the twin spans of behavioral variation continuity issue concerned the question of whether the use of
and life span development. certain drugs constitutes a “gateway” to the use of other, more
serious substances. Clearly there is no necessary progression
of this kind, but careful studies have indicated that marijuana
Eating disorders
does have this gateway function in some instances (Lynskey,
The strictness of the criteria for anorexia and bulimia nervosa Vink, & Boomsma, 2006; Stenbacka, Allebeck, & Romels-
in DSM-IV and ICD-10 meant that the great majority of eat- joe, 1993). It is highly unlikely that the gateway constitutes
ing disorders could not be included and had to be put in a re- any pharmacological pathway for the reasons already given.
sidual category of eating disorders not otherwise specified. It is probably a question of attitudes, availability, or peer
The evidence clearly indicated that these were part of the group pressures.
same group of disorders and that the boundaries needed to A further continuity/discontinuity question concerns the
be altered to respond to that recognition (Uher & Rutter, links between occasional experimental use of substances
2012b). In contrast, there is much more uncertainty over the and gross dependence on or abuse of them. For obvious rea-
continuity between the dieting and weight preoccupations sons, experimental use is likely to be the starting point, but the
of a high proportion of adolescent girls and anorexia nervosa. evidence also suggests that environmental factors play a ma-
It is also clear that there are important differences, as well as jor role in occasional, experimental use, whereas genetic fac-
strong similarities, between anorexia nervosa and bulimia tors have a more substantial role with respect to abuse and de-
nervosa. The former has a substantially earlier age of onset pendency (Goldman & Ducci, 2007).
and the latter usually does not begin until late adolescence Another key issue concerns possible discontinuities ac-
or early adult life. However, it is not at all uncommon to find cording to age. The best documented example of this kind
clinical pictures in which, over the course of time, one is fol- concerns the effects of cannabis in increasing the liability
lowed by the other and then returns to the previous pattern. to schizophreniform disorders (Arseneault et al., 2002; Casa-
The greatest uncertainty concerns the possible continuities dio, Fernandes, Murray, & Di Forti, 2011; Rutter, in press).
and discontinuities between what used to be called eating dis- Cannabis taken only for the first time in adult life is not asso-
orders of childhood (such as pica, regurgitation, and extreme ciated with any substantial increase in risk. By contrast, can-
faddiness) and anorexia/bulimia nervosa. It is highly likely nabis use that begins in childhood or adolescence, particu-
that, although these will be treated as separate diagnoses, larly if it is heavy regular use, is associated with a
they will be put in the same cluster in DSM-5 and ICD-11. substantial increase in liability. This does not seem to be a
There are few longitudinal data that provide a good answer purely social phenomenon, because the same does not apply
on continuities and discontinuities, but the existing evidence to other substances, but it does apply to animal models (Rut-
suggests that there is a complex mixture of both (Uher & Rut- ter, in press) when cognitive functioning is treated as a depen-
ter, 2012b). dent variable (as there is not a satisfactory rodent model of
schizophrenia).
It used to be said that the early use of alcohol was associ-
Substance abuse and dependency
ated with an increased risk of alcoholism in later life (Grant,
This is another group of disorders that seem to show a com- Stinson, & Harford, 2001). General population studies do
plex mixture of continuities and discontinuities over both show such a statistical association, but the evidence indicates
DP: A paradigm shift or just a relabeling? 1207

that this is likely to be a function of shared liability rather than flects a shared underlying liability. There is some evidence
a causal effect (McGue, Iacono, Legrand, & Elkins, 2001). that there may be qualitative differences between tic-related
Thus, for example, if early use is associated with an earlier forms of OCD and causes of OCD without a personal or fam-
age of puberty, leading to an increase in drunkenness in ado- ily history of tics (Hounie et al., 2006).
lescence, it is not associated with an increase in alcoholism in Similar issues apply to tic disorders, which span simple
adult life (Stattin & Magnusson, 1990). motor tics that are common in the general population and
are associated with little social impairment, and the much
less common, severe disorder usually referred to as Tourette
Pharmacological and behavioral addictions
syndrome, which involves a combination of vocal and multi-
A further continuity question concerns the continuities or dis- ple motor tics (Leckman & Bloch, 2008; Walkup, Ferrão,
continuities between the abuse of substances and behavioral Leckman, Stein, & Singer, 2010). Once again, uncertainty re-
addictions. Thus, should problematic gambling or gross in- mains on whether the difference in severity and frequency re-
ternet dependency be viewed as part of the same group of flects quantitative or qualitative differences.
problems as exemplified by the abuse or dependency of sub- It may seem that elimination disorders should constitute
stances? The evidence suggests that there are commonalities, the prototype of disorders that represent a quantitative rather
but there are equal differences (Grant, Potenza, Weinstein, & than qualitative variation from normality. No babies are con-
Gorelick, 2010; Petry, 2007; Potenza, 2006). The value of a tinent at birth, but almost all gain continence with increasing
DP perspective is that it forces one to ask questions rather age, although there is substantial individual variation in the
than fall back on some theoretical position that it must be age when continence is achieved (Butler, 2008). It may be
the one or it must be another. that nighttime wetting fits the normal variations model; but,
even with that phenomenon, there is likely heterogeneity,
with a sex difference between nighttime wetting and daytime
Continuities and discontinuities with other disorders
wetting and variations in both according to the presence or ab-
It is beyond the scope of this paper to provide an exhaustive sence of bladder dysfunction (Butler, 2008). Fecal soiling is
summary of the evidence on all mental disorders. However, it both different and more complicated, with some varieties fit-
is clear that very similar questions arise with respect to, for ting the normal variation model and others (such as the de-
example, obsessive–compulsive disorder (OCD), tics, elimi- position of feces in inappropriate places) obviously not. As
nation disorders, sleep disorders, and posttraumatic stress dis- with other disorders, there appear to be both continuities
order (PTSD). Thus, OCD is a distinctive syndrome charac- and discontinuities across the span of behavioral variation
terized by obsessional thoughts or compulsive acts. Such (Butler, 2008).
thoughts comprise ideas, images, or impulses that enter the Much the same applies to sleep disorders (American
individual’s mind again and again in a stereotyped form. Academy of Sleep Medicine, 2005; Dahl & Harvey, 2008).
Compulsive acts are similarly rituals of stereotyped behaviors Thus, behavioral insomnia and nightmares are so common
that the individual feels compelled to perform repeatedly, al- that, although they may be problematic, it is not obvious
though they are not particularly enjoyable, nor do they result that they constitute a disorder. Sleep walking is less common
in the completion of inherently useful tasks (Leckman et al., and is not ordinarily part of normal development. Narcolepsy
2010; Rapoport & Shaw, 2008). Such features are extremely (which involves sleep attacks, sudden loss of muscle tone
common in the general population and many ritualistic and without change in consciousness, an inability to move after
supposedly “magical” behaviors are part of normal develop- waking up, and dreamlike imagery before falling asleep) is
ment, as well as part of normal adult behavior (e.g., the ritual- the most clearly abnormal sleep phenomenon, and it is
ized behaviors of many top tennis stars). Thus, OCD appears usually considered a chronic neurological disorder.
to be a continuously distributed trait with biological continu- PTSD (probably better termed hyperarousal/hypervigi-
ity between normality and psychopathology. However, the lance syndrome) is a behavioral pattern that is characterized
normal ritualistic/magical behaviors seen in many young by specific features and that follows an exceptionally severe
children do not seem to predict overt OCD when they are traumatic event that involves actual physical injury or the
older. A further continuity issue concerns the possible links threat of actual violence or injury (Brewin, Andrews, &
between OCD and other apparently similar disorders such Rose, 2003; Zohar et al., 2009). It is not a developmental phe-
as hoarding (Mataix-Cols et al., 2010; Pertusa, Frost, & Ma- nomenon, but it does arise in children as well as adults. In a
taix-Cols, 2010; Phillips, Stein, et al., 2010), hair-pulling sense, PTSD represents an understandable response to an ex-
(Stein et al., 2010), and body dysmorphic disorder (Phillips, treme circumstance, but it is not a normal phenomenon out-
Wilhelm, et al., 2010). A DP perspective requires that ques- side of that situation. The pattern involves a mixture of per-
tions about continuities/discontinuities be posed, but unfortu- sonal liabilities and unusual experiences.
nately, the empirical research findings do not provide any de- In short, in line with DP perspectives, each of these disor-
finitive answer. OCD features commonly co-occur with ders includes a varied mixture of both continuities and dis-
anxiety disorders and with tic disorders, and there is continu- continuities across the span of behavioral variation. Questions
ing uncertainty on the extent to which this co-occurrence re- come up most obviously in relation to classification issues,
1208 M. Rutter

but these are not just nosological matters, because the an- brain damage in the dominant hemisphere with respect to ef-
swers to the questions on continuities and discontinuities fects on language and intelligence. Mention has already been
are fundamental to an understanding of the meaning of the made of the change in sex ratio for depression in adolescence,
disorders and the mediating mechanisms for them. and there are also changes between childhood and adult life in
drug response.
Overview
Continuities between normality and pathology
Continuities and discontinuities over the course
There are at least some half a dozen disorders for which there
of development
is substantial evidence for continuities between normality and
Putting together the findings as already discussed, there is pathology. This has long been evident in depression and con-
reasonably consistent evidence for continuities between nor- duct disorder where the decision as to when a disorder pre-
mality and psychopathology with respect to depression, con- sents is arbitrary to some extent, because it is assessed on
duct disorder, autism, schizophrenia, mild intellectual dis- the basis of the overall level of functioning and persistence.
ability, and attention-deficit disorder. In contrast, there is Mild intellectual disability also shows substantial continuity
substantial evidence showing discontinuities with respect to in the great majority of cases, although there is a proportion
severe intellectual disability, social regulation disorder and at- (it remains uncertain how high a proportion this is) due to
tachment insecurity, autism (as possibly shown through brain some pathogenic mutation. Attention-deficit disorder also
imaging findings) and schizophrenia (also possibly shown largely functions as a dimension, although the possibility of
via imaging findings). In other words, there are several sorts an extreme variety that is qualitatively different cannot be
of psychopathology wherein there is evidence for both conti- firmly ruled out as yet.
nuities and discontinuities. This applies to both autism and Until fairly recently most people would have considered
schizophrenia. This underlines the importance of the DP per- autism a disorder that is distinct from normality, but the evi-
spective involving acceptance of both continuities and dis- dence of the validity of a BAP indicates that the diagnosis ex-
continuities and not an assumption that there will always be tends much more broadly than used to be thought. Moreover,
the one and not the other. at least some cases (perhaps most) of the BAPS share the
Much the same applies to continuities and discontinuities same genetic liability (LeCouteur et al., 1996). What remains
over the course of development. Continuities are strongly evi- uncertain is what it is that causes liability to lead to the overt
dent with respect to antisocial behavior, depression, and handicapping disorder rather than to the much milder prob-
ADHD, but even with these, there is also discontinuity. For lems of the broader phenotype. Is that simply a function of de-
example, distinctions have been shown between childhood gree of genetic liability or is there some kind of two-hit
restricted antisocial behavior, AL antisocial behavior, and mechanism, and if there is, what is the other hit that is in-
LCP behavior (Moffitt, Caspi, Harrington, & Milne, 2002). volved?
Several studies, including the Dunedin study, have shown Somewhat similar questions arise with respect to schizo-
that in childhood there is an equal sex ratio for depression phrenia. The psychosis due to manifest schizophrenia would
but during adolescence, a female preponderance develops seem to be quite different from normality, but the strong as-
and continues into adult life (Hankin et al., 1998). It is not sociation with schizotypal disorder indicates that this, too, ex-
quite clear why this occurs, and it is notable that this is the tends much more broadly than used to be thought. Moreover,
case despite a substantial continuity between depression in the risk factors in neurodevelopmental impairment evident in
childhood and depression in adult life (Harrington, Fudge, early life similarly raise questions about how the disorder de-
Rutter, Pickles, & Hill, 1990). The key issue here is whether velops. It certainly is not an inevitable progression because
change is a function of puberty as observed or hormonal even with the very high risk groups studied in adolescence/
changes as measured. Of course, the two are closely intercon- early adult life, only a proportion (albeit a sizeable propor-
nected, but they are not the same and the mechanisms will be tion) go on to show overt schizophrenia. Again, what are
different. The timing will also not be the same because the the factors that take it over that threshold?
hormonal changes begin well before the observed pubertal
changes. Angold, Costello, Erkanli, and Worthman (1999)
Discontinuities between normality and pathology
showed that it was the hormonal changes that were critical
and not puberty, each being controlled when looking at the Severe intellectual disability is the most obvious diagnosis
other. In contrast, it cannot be the direct effect of hormones that shows very little continuity with normality. Variations
because therapeutic administration of hormones does not in IQ within the normal range are not explicable in terms of
have much effect on mood. Rather, it seems that the hormonal the pathogenic mutations found with severe intellectual dis-
changes provide the necessary precondition for other mecha- ability. Of course, even within the severe disability range,
nisms to come into play (Angold, 2008). the degree of disability does have a prognostic value for the
The evidence for discontinuities over the course of devel- level of functional impairment in adult life, but for the most
opment is most obvious in relation to the effects of unilateral part, there is discontinuity with normality.
DP: A paradigm shift or just a relabeling? 1209

Disinhibited social engagement disorder, previously manifest schizophrenia, and with respect to both autism and
termed social disinhibition disorder, seems qualitatively dif- schizophrenia, why does the progression occur in some indi-
ferent from the variations in attachment security/insecurity viduals but not in others? In much the same way, why does a
seen in the general population. Not only is there a strong as- childhood onset of antisocial behavior predispose to persis-
sociation with institutional deprivation but also the particular tence into adult life, yet this progression applies to less than
form of the disorder is evident more in the interactions with half of childhood-onset cases? Are genetic or environmental
strangers than with parents, the opposite of what is found or- influences largely concerned with LCP?
dinarily. It is clear that depressive disorders become more prevalent
Autism has been discussed in terms of continuities, but the in adolescence and that this increase is associated with the de-
imaging findings suggest that there may also be an important velopment of a female preponderance. Why does this hap-
degree of discontinuity. The imaging findings, to date, are not pen? What are the mechanisms that underlie the development
of a kind to enable a definitive answer one way or the other on of a female preponderance of emotional disorders in adoles-
this point but there may be a qualitative difference. The same cence but a male preponderance of most (but not all) neuro-
applies to schizophrenia. In summary, there are instances developmental disorders in early childhood? Theorizing has
where elements of a disorder may show continuity and yet tended to focus on the sex difference found in different disor-
there may also be elements of discontinuity. ders (such as the suggestion that autism represents extreme
Numerous examples have been given of discontinuities maleness), but DP findings suggest that this focus is too nar-
over the course of development. This applies, for example, row. Why does the male preponderance apply to syndromes
to the effects of unilateral brain damage in the dominant as seemingly diverse as dyslexia, ADHD, and autism?
hemisphere in relation to aphasia, the change in sex ratio The research world has thus far paid little attention to un-
for depression in adolescence, the changes between child- derstanding the mechanisms involved in age differences in re-
hood and adult life in drug response, the change in rate of sponse to drugs and to lateralized brain injury. Why do stimu-
side effects of psychotropic drugs, the change in pattern of lants have similar beneficial effects in both those with ADHD
ADHD, the risks for schizophreniform disorders stemming and normal individuals and have similar effects in both chil-
from heavy cannabis use, and several aspects of the course dren and adults yet show important differences in side ef-
of eating disorders. fects? Why are stimulants recreational drugs in adults but
Most of the topics considered have provided evidence on seemingly not so in children? Of course, one answer is that
mediating mechanisms. This is most obviously the case in children do not like the feelings brought on by stimulants,
the use of natural experiments to test for environmental me- but why is that so? Why do young people differ from adults
diation: the study of GE, rGE, epigenetics, and the biological in their response to tricyclic antidepressants but not to selec-
embedding of experiences. It has also been evident in the ef- tive serotonin reuptake inhibitors? Why are adverse side ef-
fects on children of parental mental disorder that differ ac- fects to psychotropic medication greater in children than in
cording to the child disorder being considered and the differ- adults?
ent models of reactivity distress. In many instances, the Although it has long been apparent that individuals of all
answers have not provided a definitive delineation of the ages actively process their experiences, the mechanisms in-
mechanisms involved; but the use of a DP perspective has volved have been very little explored with respect to either
meant that this is a major aim, and the research has given the processing or the effects of this on individual differences
rise to important findings. in behavioral outcomes. Similar questions arise on children’s
shaping and selecting of experiences and, especially, on the
ways in which their behavior has evocative effects. DP per-
Research Challenges
spectives indicate that the greatest need is to understand the
DP is characterized by using continuities and discontinuities behavioral mediation of these evocative effects.
across the span from normality to overt disorder, and the span A key issue with respect to the persistence of environ-
across the course of development in order to ask, and seek to mental effects beyond the duration of the risk experience con-
answer, questions about the mediating mechanisms and pro- cerns the biological embedding of experiences, in other
cesses involved in the continuities and discontinuities found. words, how environments “get under the skin.” It is clear
There is no shortage of reports describing continuities and that epigenetic changes represent one such possibility (Rutter,
discontinuities, but there is a paucity of investigations into 2012d) but so do changes in the neuroendocrine system (Gun-
the mediators of both. The first need, therefore, is to better de- nar & Vazquez, 2001, 2006), neural effects, and altered men-
lineate what needs explaining. For example, there is currently tal models. The first challenge is to determine which of these
much psychopathological interest in spectrum concepts (e.g., mainly accounts for the effects on behavior and the second is
with respect to autism, schizophrenia, OCDs, and eating dis- to determine whether the biological features account for indi-
orders), but there has been very little attempt to determine the vidual differences in response, for example, between the sen-
possible processes that may be involved. Thus, how does sitizing and steeling (strengthening) effects of stress.
BAP become transformed into autism “proper,” how do the In this connection, it is essential to investigate the huge in-
various developmental precursors of schizophrenia lead to dividual differences in people’s responses to all forms of
1210 M. Rutter

environmental hazard. It is clear that, even with severe trauma tensive massed practice of the damaged limb led to improved
such as child abuse, some individuals are surprisingly resis- functioning in both brain-injured adults and children with ce-
tant to ill effects (Rutter, 2012c, 2013). Part of the explanation rebral palsy. The suggestion was that this might reflect neural
is to be found in the operation of GE (Rutter, in press) but changes, but did it? A recent experimental study with rodents
that is by no means the only mechanism (Rutter, 2013). In ad- (van den Brand et al., 2012) showed, following transaction of
dition, it seems that although the main focus has been on re- the spine, that there was new growth of neurons and increased
sponse to stress, the main GE is seen with maltreatment in synaptic connections. The DP challenge is to determine if
early childhood and not acute stress. This suggests a biolog- mediation of psychological change can be due to induced
ical pathway beginning early and extending into adult life brain changes. Of course, the answers will also have implica-
where the psychopathology becomes apparent. Moreover, al- tions for the lateralized brain injury effect differences accord-
though most research reports concern the response to adverse ing to age.
experiences, evolutionary concepts and a growing body of
evidence suggest that the phenomenon concerns a sensitivity
to positive and negative environments (Ellis, Boyce, Belsky,
Conclusions
Bakermans-Kranenburg, & van IJzendoorn, 2011). As al-
ready noted, the G  E findings apply to individuals without To return to the points made in the introductory section, DP is
psychopathology as well as to those with disorder. DP con- not a theory and it is not a discipline. It is not a theory because
cerns, to understand both continuities and discontinuities it does not propose an overall explanatory account. It is not a
over behavior and over the life course, come to the forefront. discipline because it does not refer to a definable body of
Similar issues arise with respect to the need to find out knowledge, and it does not involve a single profession. Ra-
whether the particular unusual responses to institutional dep- ther, it constitutes a conceptualization that leads to crucial
rivation (Rutter & Sonuga-Barke, 2010) also apply to depri- questions on continuities and discontinuities and which is
vation in family settings. dedicated to the discovery of mediating mechanisms. Much
The epidemiological/longitudinal study findings on GE has been achieved but many challenges remain.
with respect to psychopathology rightly received a lot of at- DP research employs both categorical and dimensional ap-
tention, but as the investigators themselves appreciated, the proaches, although the latter predominate. There are those
evidence does not show the biological pathways involved. who would like to argue that the distinction between categor-
Of course, G  E does suggest that the pathway for the gene ical and dimensional approaches is something that can be set-
effects and the pathway for the environment effects are likely tled by the appropriate statistical analyses. However, nearly
to be closely related. In order to determine the biological pro- half a century ago Zubin (1967) pointed out that nearly all
cesses, human experimental approaches and animal models categories can be transformed into dimensions, and con-
are needed and are being used (Rutter, in press-b). Natural ex- versely nearly all dimensions can be translated into categor-
periments also have an important role to play. The DP chal- ies. The question is not what is the reality in nature but, rather
lenge is to make maximal use of diverse, experimentally which is more useful in relation to the particular questions
oriented research strategies to understand the biology. being addressed. It will be appreciated that, although this ar-
Finally, there is the fundamental challenge of understand- ticle has been solely concerned with mental disorders, much
ing the neural underpinning of the workings of the mind. As- the same issues arise in relation to internal medicine when
pects of that issue have been noted in relation to G  E, but dealing with multifactorial disorders such as coronary artery
they apply most strikingly in relation to brain plasticity and disease, hypertension, and atopic disease. Each of these gives
the recovery of function after serious brain injury. Neuro- rise to similar questions about continuities and discontinuities
science findings (Bavelier, Levi, Li, Dan, & Hensch, 2010) and in many instances both are found. For example, hyperten-
have shown that plasticity continues into adult life, although sion is obviously a dimensional feature but once the changes
it diminishes with age. Most crucially, it has shown that there that are characterized by the label of malignant hypertension
are influences that can extend or curtail plasticity. The possi- arise, the course becomes a different one. DP is concerned
ble practical implications were highlighted by Taub’s finding with psychopathology, but the principles are likely to apply
(Taub, 2000; Taub, Ramey, DeLuca, & Echols, 2004) that in- across medicine and across biology.

References
Ainsworth, M. D. S., Blehar, M. C., Waters, E., & Wall, S. (1978). Patterns of Angold, A. (2008). Sex and developmental psychopathology. In J. J. Hudziak
attachment: A psychological study of the Strange Situation. Hillsdale, NJ: (Ed.), Developmental psychopathology and wellness: Genetic and envi-
Erlbaum. ronmental influences (pp. 109–138). New York: American Psychiatric
American Academy of Sleep Medicine. (2005). International classification Publications.
of sleep disorders (ICSD): Diagnostic and coding manual (2nd ed.). Angold, A., Costello, E. J., Erkanli, A., & Worthman, C. M. (1999). Pubertal
New York: Author. changes in hormone levels and depression in girls. Psychological Medi-
Andreasen, N. C. (2010). The lifetime trajectory of schizophrenia and the cine, 29, 1043–1053.
concept of neurodevelopment. Dialogues in Clinical Neuroscience, 12, Arseneault, L., Cannon, M., Poulton, R., Murray, R., Caspi, A., & Moffitt,
409–415. T. E. (2002). Cannabis use in adolescence and risk for adult psychosis:
DP: A paradigm shift or just a relabeling? 1211

Longitudinal prospective study. British Journal of Psychiatry, 325, 1212– Goldman, D., & Ducci, F. (2007). Addictive disorders. In D. L. Rimoin, J. M.
1213. Connor, R. E. Pyeritz, & B. R. Korf (Eds.), Emery & Rimoin’s principles
Bailey, A., Palferman, S., Heavey, L., & Le Couteur, A. (1998). Autism: The and practice of medical genetics (5th ed., Vol. 3, pp. 2629–2647). Phila-
phenotype in relatives. Journal of Autism and Developmental Disorders, delphia, PA: Elsevier Ltd.
28, 369–392. Grant, J. E., Potenza, M. N., Weinstein, A., & Gorelick, D. A. (2010). Intro-
Baron-Cohen, S., Leslie, A. M., & Frith, U. (1985). Does the autistic child duction to behavioral addictions. American Journal of Drug and Alcohol
have a “theory of mind”? Cognition, 21, 37–46. Abuse, 36, 233–241.
Bavelier, D., Levi, D. M., Li, R. W., Dan, Y., & Hensch, T. K. (2010). Re- Grant, B. F., Stinson, F. S., & Harford, T. C. (2001). Age at onset of alcohol
moving brakes on adult brain plasticity: From molecular to behavioral in- use and DSM-IV alcohol abuse and dependence: A 12-year follow-up.
terventions. Journal of Neuroscience, 30, 14964–14971. Journal of Substance Abuse, 13, 493–504.
Bolton, P. F., Carcani-Rathwell, I., Hutton, J., Goode, S., Howlin, P., & Rut- Grossman, K. E., Grossman, K., & Waters, E. (2005). Attachment from in-
ter, M. (2011). Epilepsy in autism: Features and correlates. British Jour- fancy to adulthood: The major longitudinal studies. New York: Guilford
nal of Psychiatry, 198, 289–294. Press.
Bosl, W., Tierney, A., Tager-Flusberg, H., & Nelson, C. (2011). EEG com- Gunnar, M. R., & Vazquez, D. M. (2001). Low cortisol and a flattening of
plexity as a biomarker for autism spectrum disorder risk. BMC Medicine, expected daytime rhythm: Potential indices of risk in human develop-
9, 18. ment. Development and Psychopathology, 13, 515–538.
Bowlby, J. (1969). Attachment and loss: Vol. 1. Attachment. London: Ho- Gunnar, M. R., & Vazquez, D. M. (2006). Stress, neurobiology and develop-
garth Press. mental psychopathology. In D. Cicchetti & D. Cohen (Eds.), Develop-
Brewin, C. R., Andrews, B., & Rose, S. (2003). Diagnostic overlap between mental psychopathology (Vol. 2, pp. 533–577). Hoboken, NJ: Wiley.
acute stress disorder and PTSD in victims of violent crime. American Hankin, B. L., Abramson, L. Y., Moffitt, T. E., Silva, P. A., McGee, R., &
Journal of Psychiatry, 160, 783–785. Angell, K. E. (1998). Development of depression from preadolescence
Bruce, J., Tarullo, A. R., & Gunnar, M. R. (2010). Disinhibited social behav- to young adulthood: Emerging gender differences in a 10-year longitu-
ior among internationally adopted children. Development and Psychopa- dinal study. Journal of Abnormal Psychology, 107, 128.
thology, 21, 157–171. Harrington, R., Fudge, H., Rutter, M., Pickles, A., & Hill, J. (1990). Adult
Butler, R. J. (2008). Wetting and soiling. In M. Rutter, D. Bishop, D. Pine, S. outcomes of childhood and adolescent depression: I. Psychiatric status.
Scott, J. Stevenson, E. Taylor, et al. (Eds.), Rutter’s child and adolescent Archives of General Psychiatry, 47, 465–473.
psychiatry (5th ed., pp. 916–929). Oxford: Blackwell. Hazell, P., O’Connell, D., Heathcote, D., Robertson, J., & Henry, D. (1995).
Cannon, M., Caspi, A., Moffitt, T. E., Harrington, H. L., Taylor, A., Murray, Efficacy of tricyclic drugs in treating child and adolescent depression: A
R. M., et al. (2002). Evidence for early-childhood, pan-developmental meta-analysis. British Medical Journal, 310, 897–901.
impairment specific to schizophreniform disorder: Results from a longi- Hermelin, B., & O’Connor, N. (1970). Psychological experiments with autis-
tudinal birth cohort. Archives of General Psychiatry, 59, 449–456. tic children. New York: Pergamon Press.
Casadio, P., Fernandes, C., Murray, R. M., & Di Forti, M. (2011). Cannabis Hounie, A. G., do Rosario-Campos, M. C., Diniz, J., Shavitt, R. G., Ferrao,
use in young people: The risk for schizophrenia. Neuroscience & Biobe- Y., Lopes, A. C., et al. (2006). Obsessive–compulsive disorder in Tour-
havioral Reviews, 35, 1779–1787. ette syndrome (Vol. 99). New York: Raven Press.
Cicchetti, D., & Toth, S. L. (2009). The past achievements and future prom- Hyde, L. W., Bogden, R., & Hariri, A. R. (2011). Understanding risk for psy-
ises of developmental psychopathology: The coming of age of a disci- chopathology through imaging gene–environment interactions. Trends in
pline. Journal of Child Psychology and Psychiatry, 50, 16–25. Cognitive Sciences, 15, 417–427.
Costello, E. J., Compton, S. N., Keeler, G., & Angold, A. (2003). Relation- Jaffee, S. R., Caspi, A., Moffitt, T. E., Polo-Tomas, M., Price, T. S., & Taylor,
ships between poverty and psychopathology. Journal of the American A. (2004). The limits of child effects: Evidence for genetically mediated
Medical Association, 290, 2023–2029. child effects on corporal punishment but not on physical maltreatment.
Dahl, R. E., & Harvey, A. G. (2008). Sleep disorders. In M. Rutter, D. Developmental Psychology, 40, 1047–1058.
Bishop, D. Pine, S. Scott, J. Stevenson, E. Taylor, et al. (Eds.), Rutter’s Johnstone, E. C., Ebmeier, K. P., Miller, P., Owens, D. G. C., & Lawrie, S. M.
child and adolescent psychiatry (5th ed., pp. 894–905). Oxford: Black- (2005). Predicting schizophrenia: Findings from the Edinburgh high-risk
well. study. British Journal of Psychiatry, 186, 18–25.
D’Onofrio, B. M., Rathouz, P. J., & Lahey, B. B. (2011). The importance of Johnstone, E. C., Frith, C. D., Crow, T. J., Husband, J., & Kreel, L. (1976).
understanding gene–environment correlations in the development of anti- Cerebral ventricular size and cognitive impairment in chronic schizophre-
social behavior. In K. S. Kendler, S. R. Jaffee, & D. Romer (Eds.), The dy- nia. Lancet, 308, 924–926.
namic genome and mental health: The role of genes and environments in Jones, P. B., & Fung, W. L. A. (2005). Ethnicity and mental health: The ex-
youth development (pp. 340–364). New York: Oxford University Press. ample of schizophrenia in the African-Caribbean population in Europe.
D’Onofrio, B. M., Van Hulle, C. A., Goodnight, J. A., Rathouz, P. J., & La- In M. Rutter & M. Tienda (Eds.), Ethnicity and causal mechanisms
hey, B. B. (2011). Is maternal smoking during pregnancy a causal envi- (pp. 227–261). New York: Cambridge University Press.
ronmental risk factor for adolescent antisocial behavior? Testing etiologi- Karg, K., Burmeister, M., Shedden, K., & Sen, S. (2011). The serotonin
cal theories and assumptions. Psychological Medicine, 1, 1–11. transporter promoter variant (5-HTTLPR), stress, and depression meta-
Einfeld, S., & Emerson, E. (2008). Intellectual disability. In M. Rutter, D. analysis revisited: Evidence of genetic moderation. Archives of General
Bishop, D. Pine, S. Scott, J. Stevenson, E. Taylor, et al. (Eds.), Rutter’s Psychiatry, 68, 444–454.
child and adolescent psychiatry (5th ed., pp. 820–840). Oxford: Black- Kendler, K. S., & Baker, J. H. (2007). Genetic influences on measures of the
well. environment: A systematic review. Psychological Medicine, 37, 615–
Ellis, B. J., Boyce, W. T., Belsky, J., Bakermans-Kranenburg, M. J., & van 626.
IJzendoorn, M. H. (2011). Differential susceptibility to the environment: Kendler, K. S., & Prescott, C. A. (2006). Genes, environment, and psychopa-
An evolutionary–neurodevelopmental theory. Development and Psycho- thology: Understanding the causes of psychiatric and substance use dis-
pathology, 23, 7–28. orders. New York: Guilford Press.
Fearon, P., Kirkbride, J. B., Morgan, C., Dazzan, P., Morgan, K., Lloyd, T., Kim-Cohen, J., Caspi, A., Moffitt, T. E., Harrington, H. L., Milne, B. J., &
et al. (2006). Incidence of schizophrenia and other psychoses in ethnic Poulton, R. (2003). Prior juvenile diagnoses in adults with mental disor-
minority groups: Results from the MRC AESOP Study. Psychological der: Developmental follow-back of a prospective-longitudinal cohort. Ar-
Medicine, 36, 1541–1550. chives of General Psychiatry, 60, 709–717.
Fedorowicz, V. J., & Fombonne, E. (2005). Metabolic side effects of atypical Kouros, C. D., & Garber, J. (2010). Dynamic associations between maternal
antipsychotics in children: A literature review. Journal of Psychopharma- depressive symptoms and adolescents’ depressive and externalizing
cology 19, 533–550. symptoms. Journal of Abnormal Child Psychology, 38, 1069–1081.
Garber, J., Ciesla, J. A., McCauley, E., Diamond, G., & Schloredt, K. A. Larsson, H., Dilshad, R., Lichtenstein, P., & Barker, E. D. (2011). Develop-
(2011). Remission of depression in parents: Links to healthy functioning mental trajectories of DSM-IV symptoms of attention-deficit/hyperactiv-
in their children. Child Development, 82, 226–243. ity disorder: Genetic effects, family risk and associated psychopathology.
Garber, J., & Cole, D. A. (2010). Intergenerational transmission of depres- Journal of Child Psychology and Psychiatry, 52, 954–963.
sion: A launch and grow model of change across adolescence. Develop- Laurens, K. R., Hobbs, M. J., Sunderland, M., Green, M. J., & Mould, G. L.
ment and Psychopathology, 22, 819–830. (2011). Psychotic-like experiences in a community sample of 8000 chil-
1212 M. Rutter

dren aged 9 to 11 years: An item response theory analysis. Psychological and specific language impairment. Journal of Child Psychology and Psy-
Medicine, 1, 1–10. chiatry, 50, 843–852.
Leckman, J. F., & Bloch, M. H. (2008). Tic disorders. In M. Rutter, D. Plomin, R., & Bergeman, C. S. (1991). The nature of nurture: Genetic influ-
Bishop, D. Pine, S. Scott, J. Stevenson, E. Taylor, et al. (Eds.), Rutter’s ence on “environmental” measures. Behavioral and Brain Sciences, 14,
child and adolescent psychiatry (5th ed.). Oxford: Blackwell. 373–386.
Leckman, J. F., Denys, D., Simpson, H. B., Mataix-Cols, D., Hollander, E., Potenza, M. N. (2006). Should addictive disorders include non-substance-re-
Saxena, S., et al. (2010). Obsessive–compulsive disorder: A review of the lated conditions? Addiction, 101, 142–151.
diagnostic criteria and possible subtypes and dimensional specifiers for Poulton, R., Caspi, A., Moffitt, T. E., Cannon, M., Murray, R., & Harrington,
DSM-V. Depression and Anxiety, 27, 507–527. H. L. (2000). Children’s self-reported psychotic symptoms and adult
LeCouteur, A., Bailey, A., Goode, S., Pickles, A., Gottesman, I., Robertson, schizophreniform disorder: A 15-year longitudinal study. Archives of
S., et al. (1996). A broader phenotype of autism: The clinical spectrum in General Psychiatry, 57, 1053–1058.
twins. Journal of Child Psychology and Psychiatry, 37, 785–801. Premack, D., & Woodruff, G. (1978). Does the chimpanzee have a theory of
Luyster, R. J., Wagner, J. B., Vogel-Farley, V., Tager-Flusberg, H., & Nel- mind? Behavioral and Brain Sciences, 1, 515–526.
son, C. A. (2011). Neural correlates of familiar and unfamiliar face pro- Rapoport, J. L., Buchsbaum, M. S., Weingartner, H., Zahn, T. P., Ludlow, C.,
cessing in infants at risk for autism spectrum disorders. Brain Topogra- & Mikkelsen, E. J. (1980). Dextroamphetamine: Its cognitive and behav-
phy, 24, 220–228. ioral effects in normal and hyperactive boys and normal men. Archives of
Lynskey, M. T., Vink, J. M., & Boomsma, D. I. (2006). Early onset cannabis General Psychiatry, 37, 933–943.
use and progression to other drug use in a sample of Dutch twins. Behav- Rapoport, J. L., & Gogtay, N. (2011). Childhood onset schizophrenia: Sup-
ior Genetics, 36, 195–200. port for a progressive neurodevelopmental disorder. International Jour-
Main, M., & Solomon, J. (1986). Discovery of an insecure–disoriented at- nal of Developmental Neuroscience, 29, 251–258.
tachment pattern. In T. B. Brazelton & M. W. Yogman (Eds.), Affective Rapoport, J. L., & Shaw, P. (2008). Obsessive–compulsive disorder. In M.
development in infancy (pp. 95–124). Norwood, NJ: Ablex. Rutter, D. Bishop, D. Pine, S. Scott, J. Stevenson, E. Taylor, et al.
Mataix-Cols, D., Frost, R. O., Pertusa, A., Clark, L. A., Saxena, S., Leckman, (Eds.), Rutter’s child and adolescent psychiatry (5th ed., pp. 719–736).
J. F., et al. (2010). Hoarding disorder: A new diagnosis for DSM-V? De- Oxford: Blackwell.
pression and Anxiety, 27, 556–572. Rice, F., Harold, G. T., Boivin, J., Hay, D. F., Van Den Bree, M., & Thapar,
McGue, M., Iacono, W.G., Legrand, L. N., & Elkins, I. (2001). Origins and A. (2009). Disentangling prenatal and inherited influences in humans
consequences of age at first drink: II. Familial risk and heritability. Alco- with an experimental design. Proceedings of the National Academy of
holism: Clinical and Experimental Research, 25(8), 1166–1173. Sciences, 106, 2464–2467.
Meaney, M. J. (2010). Epigenetics and the biological definition of Gene  Robins, L. N. (1966). Deviant children grown up: A sociological and psy-
Environment interactions. Child Development, 81, 41–79. chiatric study of sociopathic personality. Baltimore, MD: Williams &
Meyer-Lindenberg, A., & Weinberger, D. R. (2006). Intermediate pheno- Wilkins.
types and genetic mechanisms of psychiatric disorders. Nature Reviews Robins, L. N. (1978). Sturdy childhood predictors of adult antisocial behav-
Neuroscience, 7, 818–827. iour: Replications from longitudinal studies. Psychological Medicine, 8,
Moffitt, T. E. (1993). Adolescence-limited and life-course-persistent antiso- 611–622.
cial behavior: A developmental taxonomy. Psychological Review, 100, Robins, L. N. (1993). Vietnam veterans’ rapid recovery from heroin addic-
674–701. tion: A fluke or normal expectation? Addiction, 88, 1041–1054.
Moffitt, T. E., Caspi, A., Harrington, H., & Milne, B. J. (2002). Males on Robins, L. N., Davis, D. H., & Goodwin, D. W. (1974). Drug use by US army
the life-course-persistent and adolescence-limited antisocial pathways: enlisted men in Vietnam: A follow-up on their return home. American
Follow-up at age 26 years. Development and Psychopathology, 14, Journal of Epidemiology, 99, 235–249.
179–207. Roisman, G. I., Monahan, K. C., Campbell, S. B., Steinberg, L., & Cauffman,
Morgan, C., Fisher, H., Hutchinson, G., Kirkbride, J., Craig, T. K., Morgan, E. (2010). Is adolescence-onset antisocial behavior developmentally nor-
K., et al. (2009). Ethnicity, social disadvantage and psychotic-like experi- mative? Development and Psychopathology, 22, 295–311.
ences in a healthy population based sample. Acta Psychiatrica Scandina- Rutter, M. (1989). Pathways from childhood to adult life. Journal of Child
vica, 119, 226–235. Psychology and Psychiatry, 30, 23–51.
Morris, M. C., Ciesla, J. A., & Garber, J. (2010). A prospective study of stress Rutter, M. (1993). An overview of developmental neuropsychiatry. Educa-
autonomy versus stress sensitization in adolescents at varied risk for de- tional and Child Psychology, 10, 4–11.
pression. Journal of Abnormal Psychology, 119, 341–354. Rutter, M. (2000). Genetic studies of autism: From the 1970s into the millen-
Murray, R. M., & Lewis, S. W. (1987). Is schizophrenia a neurodevelopmen- nium. Journal of Abnormal Child Psychology, 28, 3–14.
tal disorder? British Medical Journal, 295, 681–682. Rutter, M. (2003). Categories, dimensions, and the mental health of children and
Obel, C., Olsen, J., Henriksen, T. B., Rodriguez, A., Järvelin, M. R., Moila- adolescents. Annals of the New York Academy of Sciences, 1008, 11–21.
nen, I., et al. (2011). Is maternal smoking during pregnancy a risk factor Rutter, M. (2007). Proceeding from observed correlation to causal inference:
for hyperkinetic disorder? Findings from a sibling design. International The use of natural experiments. Perspectives on Psychological Science,
Journal of Epidemiology, 40, 338–345. 2, 377–395.
Odgers, C. L., Caspi, A., Broadbent, J. M., Dickson, N., Hancox, R. J., Har- Rutter, M. (2008). Developing concepts in developmental psychopathology.
rington, H. L., et al. (2007). Prediction of differential adult health burden In J. J. Hudziak (Ed.), Developmental psychopathology and wellness:
by conduct problem subtypes in males. Archives of General Psychiatry, Genetic and environmental influences (pp. 3–22). Arlington, VA: Amer-
64, 476–484. ican Psychiatric Publishing.
Odgers, C. L., Moffitt, T. E., Broadbent, J. M., Dickson, N., Hancox, R. J., Rutter, M. (2010). Child and adolescent psychiatry: Past scientific achieve-
Harrington, H., et al. (2008). Female and male antisocial trajectories: ments and challenges for the future. European Journal of Child Adoles-
From childhood origins to adult outcomes. Development and Psychopa- cent Psychiatry, 19, 689–703.
thology, 20, 673–716. Rutter, M. (2011). Research review: Child psychiatric diagnosis and classifi-
Pertusa, A., Frost, R. O., & Mataix-Cols, D. (2010). When hoarding is a cation: Concepts, findings, challenges and potential. Journal of Child
symptom of OCD: A case series and implications for DSM-V. Behaviour Psychology and Psychiatry, 52, 647–660.
Research and Therapy, 48, 1012–1020. Rutter, M. (2012a). Gene–environment interdependence. European Journal
Petry, N. M. (2007). Gambling and substance use disorders: Current status of Developmental Psychology, 9, 391–412.
and future directions. American Journal on Addictions, 16, 1–9. Rutter, M. (2012b). “Natural experiments” as a means of testing causal infer-
Phillips, K. A., Stein, D. J., Rauch, S. L., Hollander, E., Fallon, B. A., Barsky, ences. In C. Berzuini, P. Dawid, & L. Bernardinelli (Eds.), Causality:
A., et al. (2010). Should an obsessive–compulsive spectrum grouping of Statistical perspectives and applications (pp. 253–272). Chichester:
disorders be included in DSM-V? Depression and Anxiety, 27, 528–555. Wiley Ltd.
Phillips, K. A., Wilhelm, S., Koran, L. M., Didie, E. R., Fallon, B. A., Feus- Rutter, M. (2012c). Resilience as a dynamic concept. Development and Psy-
ner, J., et al. (2010). Body dysmorphic disorder: Some key issues for chopathology, 24, 335–344.
DSM-V. Depression and Anxiety, 27, 573–591. Rutter, M. (2012d). Achievements and challenges in the biology of environ-
Pickles, A., Simonoff, E., Conti-Ramsden, G., Falcaro, M., Simkin, Z., Char- mental effects. Proceedings of the National Academy of Sciences, 109,
man, T., et al. (2009). Loss of language in early development of autism 17149–17153.
DP: A paradigm shift or just a relabeling? 1213

Rutter, M. (in press-b). Nature–nurture integration. In M. Lewis & K. Ru- Susser, E., Neugebauer, R., Hoek, H. W., Brown, A. S., Lin, S., Labovitz, D.,
dolph (Eds.), Handbook of developmental psychopathology (3rd ed.). et al. (1996). Schizophrenia after prenatal famine: Further evidence. Ar-
New York: Springer Science. chives of General Psychiatry, 53, 25–31.
Rutter, M. (2013). Resilience: Clinical implications. Journal of Child Psy- Taub, E. (2000). Constraint-induced movement therapy and massed practice.
chology and Psychiatry, 54, 474–487. Stroke, 31, 986–988.
Rutter, M., Giller, H., & Hagell, A. (1998). Antisocial behavior by young Taub, E., Ramey, S. L., DeLuca, S., & Echols, K. (2004). Efficacy of con-
people. New York: Cambridge University Press. straint-induced movement therapy for children with cerebral palsy with
Rutter, M., Kreppner, J., & Sonuga-Barke, E. (2009). Emanuel Miller lec- asymmetric motor impairment. Pediatrics, 113, 305–312.
ture: Attachment insecurity, disinhibited attachment, and attachment dis- Thapar, A., Harrington, R., Ross, K., & McGuffin, P. (2000). Does the def-
orders: Where do research findings leave the concepts? Journal of Child inition of ADHD affect heritability? Journal of the American Academy of
Psychology and Psychiatry, 50, 529–543. Child & Adolescent Psychiatry, 39, 1528–1536.
Rutter, M., Kumsta, R., Schlotz, W., & Sonuga-Barke, E. (2012). Longitu- Thapar, A., & Rutter, M. (2009). Do prenatal risk factors cause psychiatric
dinal studies using a “natural experiment” design: The case of adoptees disorder? Be wary of causal claims. British Journal of Psychiatry, 195,
from Romanian institutions. Journal of the American Academy of Child 100–101.
& Adolescent Psychiatry. Advance online publication. Thompson, P. M., Bartzokis, G., Hayashi, K. M., Klunder, A. D., Lu, P. H.,
Rutter, M., & Rutter, M. (1993). Developing minds: Challenge and continu- Edwards, N., et al. (2009). Time-lapse mapping of cortical changes in
ity across the life span. London: Penguin Books. schizophrenia with different treatments. Cerebral Cortex, 19, 1107–1123.
Rutter, M., & Sonuga-Barke, E. J. (2010). Conclusions: Overview of findings Uher, R., & Rutter, M. (2012a). Basing psychiatric classification on scientific
from the ERA study, inferences, and research implications. Monographs foundation: Problems and prospects. International Review of Psychiatry,
of the Society for Research in Child Development, 75, 212–229. 24, 591–605.
Rutter, M., & Sroufe, L. A. (2000). Developmental psychopathology: Con- Uher, R., & Rutter, M. (2012b). Classification of feeding and eating disor-
cepts and challenges. Development and Psychopathology, 12, 265–296. ders: Review of evidence and proposals for ICD-11. World Psychiatry,
Rutter, M., & Uher, R. (2012). Classification issues and challenges in child 11, 80–92.
and adolescent psychopathology. International Review of Psychiatry, 24, van den Brand, R., Heutschi, J., Barraud, Q., DiGiovanna, J., Bartholdi, K.,
514–529. Huerlimann, M., et al. (2012). Restoring voluntary control of locomotion
Schäfer, I., & Fisher, H. L. (2011). Childhood trauma and psychosis—What after paralyzing spinal cord injury. Science, 336, 1182–1185.
is the evidence? Dialogues in Clinical Neuroscience, 13, 360–365. Vargha-Khadem, F., Issacs, E., Van Der Werf, S., Robb, S., & Wilson, J.
Siegenthaler, E., Munder, T., & Egger, M. (2012). Effect of preventive inter- (1992). Development of intelligence and memory in children with hemi-
ventions in mentally ill parents on the mental health of the offspring: Sys- plegic cerebral palsy. Brain, 115, 315–329.
tematic review and meta-analysis. Journal of the American Academy of Vorria, P., & Ntouma, M. (2012). Early experiences and later development:
Child & Adolescent Psychiatry, 51, 8–17. A follow-up study of adopted adolescents who spent their infancy in res-
Silberg, J. L., Maes, H., & Eaves, L. J. (2010). Genetic and environmental idential group care (Report to The Nuffield Foundation). London: Nuf-
influences on the transmission of parental depression to children’s de- field Foundation.
pression and conduct disturbance: An extended children of twins study. Walkup, J. T., Ferrão, Y., Leckman, J. F., Stein, D. J., & Singer, H. (2010).
Journal of Child Psychology and Psychiatry, 51, 734–744. Tic disorders: Some key issues for DSM-V. Depression and Anxiety, 27,
Silberg, J. L., Maes, H., & Eaves, L. J. (2012). Unraveling the effect of genes 600–610.
and environment in the transmission of parental antisocial behavior to Weinberg, W. A., Harper, C. R., & Brumback, R. A. (2008). Substance use
children’s conduct disturbance, depression and hyperactivity. Journal and abuse: Epidemiology, pharmacological considerations, identification
of Child Psychology and Psychiatry, 53, 668–677. and suggestions towards management. In M. Rutter, D. Bishop, D. Pine,
Sroufe, L. A., & Rutter, M. (1984). The domain of developmental psychopa- S. Scott, J. Stevenson, E. Taylor, et al. (Eds.), Rutter’s child and adoles-
thology. Child Development, 55, 17–29. cent psychiatry (5th ed., pp. 437–462). Oxford: Blackwell.
St. Clair, D., Xu, M., Wang, P., Yu, Y., Fang, Y., Zhang, F., et al. (2005). Weinberger, D. R. (1987). Implications of normal brain development for the
Rates of adult schizophrenia following prenatal exposure to the Chinese pathogenesis of schizophrenia. Archives of General Psychiatry, 44, 660–
famine of 1959–1961. Journal of the American Medical Association, 669.
294, 557–562. Wimmer, H., & Perner, J. (1983). Beliefs about beliefs: Representation and
Stattin, H., & Magnusson, D. (1990). Pubertal maturation in female develop- constraining function of wrong beliefs in young children’s understanding
ment (Vol. 2). Hillsdale, NJ: Erlbaum. of deception. Cognition, 13, 103–128.
Stein, D. J., Grant, J. E., Franklin, M. E., Keuthen, N., Lochner, C., Singer, H. World Health Organization. (1992). International classification of mental
S., et al. (2010). Trichotillomania (hair pulling disorder), skin picking and behavioural disorders (ICD-10). Geneva: Author.
disorder, and stereotypic movement disorder: Toward DSM-V. Depres- Zeanah, C. H., & Gleason, M. M. (2011). Reactive attachment disorder: A
sion and Anxiety, 27, 611–626. review for DSM-V. Washington, DC: American Psychiatric Association.
Stenbacka, M., Allebeck, P., & Romelsjoe, A. (1993). Initiation into drug Zohar, J., Fostick, L., Cohen, A., Bleich, A., Dolfin, D., Weissman, Z., et al.
abuse: The pathway from being offered drugs to trying cannabis and pro- (2009). Risk factors for the development of posttraumatic stress disorder
gression to intravenous drug abuse. Scandinavian Journal of Social Med- following combat trauma: A semiprospective study. Journal of Clinical
icine, 21, 31–39. Psychiatry, 70, 1629–1635.
Stigler, K. A., Potenza, M. N., Posey, D. J., & McDougle, C. J. (2004). Zubin, J. (1967). Classification of the behavior disorders. Annual Review of
Weight gain associated with atypical antipsychotic use in children and Psychology, 18, 373–406.
adolescents: Prevalence, clinical relevance, and management. Pediatric
Drugs, 6, 33–44.

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