USA: +1(669)289-8683 
Sign in
For the week’s topic of an introduction to the study of abnormal child psychology, analyze the primary arguments presented in either one of additional article posted on Canvas OR a relevant empirical, peer-reviewed article of your choosing.
Discuss how the author’s perspective contributes to the broader academic conversation on this subject. Reflect on the strengths and limitations of the author’s arguments, providing specific examples from the text. Include your critical evaluation of the evidence presented and how it supports or contradicts other sources you have encountered or your current knowledge of the study of abnormal child psychology. Ensure you properly cite (APA formatting, 7th edition) the additional article from Canvas in your discussion.
The past achievements and future promises of
developmental psychopathology: the coming of
age of a discipline
Dante Cicchetti1 and Sheree L. Toth2
1Institute of Child Development and Department of Psychiatry, University of Minnesota, USA;
2Mt. Hope Family Center, University of Rochester, USA
Over the past decades, developmental psychopathology has coalesced into a discipline that has made
significant contributions toward the understanding of risk, psychopathology, and resilience in
individuals across the life course. The overarching goal of the discipline has been to elucidate the
interplay among biological, psychological, and social-contextual aspects of normal and abnormal
development. In addition to directing efforts toward bridging fields of study and aiding in elucidating
important truths about the processes underlying adaptation and maladaptation, investigators in
developmental psychopathology have been equally devoted to developing and evaluating methods for
preventing and ameliorating maladaptive and psychopathological outcomes. Increasingly, efforts are
being made to conduct investigations at multiple levels of analysis and to translate basic research
knowledge into real-world contexts. In this article, the contributions, challenges, and future directions
of the field are highlighted. Keywords: Developmental psychopathology, interdisciplinary, multiple
levels of analysis, translational research.
Special Issues of scientific journals often signify
noteworthy junctures in the development and mat-
uration of a discipline. The publication of this Spe-
cial Issue commemorating the 50th anniversary
volume of the Journal of Child Psychology and Psy-
chiatry provides us with an occasion to reflect upon
the scientific discoveries, advances, and challenges
that have occurred and that have brought us to our
current state of knowledge in the field of develop-
mental psychopathology. As we contemplate these
historical events in the context of the future that
awaits us, we are provided with a unique and envi-
able opportunity for reflection, creativity, and pro-
gnostication regarding the issues that are likely to
exert a major impact upon determining the future
foci of the field of developmental psychopathology.
Although precise definitional divergence exists,
developmental psychopathology can be conceptual-
ized as an evolving interdisciplinary scientific field
that seeks to elucidate the interplay among the bio-
logical, psychological, and social-contextual aspects
of normal and abnormal development across the life
course. Because psychopathology unfolds over time
in a developing organism, it is critical to adopt a
developmental perspective in order to understand
the processes underlying individual pathways to
adaptive and maladaptive outcomes (Sroufe, 1989,
2007). A ‘developmental analysis’ presupposes
change and novelty, highlights the critical role of
timing in the organization of behavior, underscores
multiple determinants, and cautions against
expecting invariant relations between causes and
outcomes. Moreover, a developmental analysis is as
applicable to the study of the gene or cell as it is to
the investigation of the individual, family, or society
(Cicchetti & Pogge-Hesse, 1982).
Despite its relatively recent crystallization as a
coherent framework for examining and conceptual-
izing the links between the study of psychopathology
and development, developmental psychopathology
owes its ascendance and coalescence as a scientific
discipline to many historically based endeavors
within a variety of areas, including embryology, epi-
demiology, genetics, neuroscience, philosophy, psy-
chiatry, psychoanalysis, clinical, developmental,
experimental, and physiological psychology, and
sociology (Cicchetti, 1990). Before developmental
psychopathology could emerge as an integrative
discipline with its own integrity, the efforts of those
working in the aforementioned related fields had
been separate and distinct (Cicchetti, 1984). In part,
the lack of integration across disciplines stemmed
from long-standing tensions between the philo-
sophical traditions underlying academic training
and clinical practice and between basic and applied
research.
Principles inherent to a developmental
psychopathology perspective
An ongoing goal of developmental psychopathology
has been to become a science that not only bridges
fields of study and aids in the discovery of important
new truths about the processes underlying adapta-
tion and maladaptation across the life course, but
also to provide the best means of preventing andConflict of interest statement: No conflicts declared.
Journal of Child Psychology and Psychiatry 50:1-2 (2009), pp 16–25 doi:10.1111/j.1469-7610.2008.01979.x
� 2008 The Authors
Journal compilation � 2008 Association for Child and Adolescent Mental Health.
Published by Blackwell Publishing, 9600 Garsington Road, Oxford OX4 2DQ, UK and 350 Main Street, Malden, MA 02148, USA
ameliorating maladaptive and pathological outcomes
(Cicchetti, 1990; Sroufe & Rutter, 1984). Moreover,
the field of developmental psychopathology has
continuously sought to reduce the dualisms that
exist between empirical research and the clinical
study and treatment of childhood and adult high-
risk conditions and mental disorders, between the
behavioral and biological sciences, and between
basic and applied research (Cicchetti, 1990; Masten,
2006; Toth & Cicchetti, 1999).
The essence and uniqueness of a developmental
psychopathology perspective lies in its focus on both
normal and abnormal, adaptive and maladaptive,
developmental processes. A basic theme in the
writings of the early systematizers in the field is that
because all psychopathology can be conceived as a
distortion, disturbance, or degeneration of normal
functioning, it follows that, if one wishes to com-
prehend psychopathology more fully, then one must
understand the normal functioning with which psy-
chopathology is compared (Cicchetti, 1984, 1990,
1993; Rutter, 1986; Sroufe, 1990). Not only is
knowledge of normal biological, psychological, and
social processes exceedingly useful for assessing,
diagnosing, understanding, preventing, and treating
psychopathology, but also the deviations from and
distortions of normal development that characterize
pathological processes indicate in exciting ways how
normal development may be better investigated and
understood.
These naturally occurring conditions, including
populations of children reared in institutions,
children who have experienced abuse and neglect,
persons with brain damage, and individuals with
mental disorders, have provided an entrée into the
study of system organization, disorganization, and
reorganization that is otherwise not possible due to
the ethical constraints associated with conducting
experimental research with human participants
(Cicchetti, 2003; Rutter, 2007). Because there are
limits to experimental manipulations that can be
invoked with humans, and because the investigation
of a system in its smoothly operating normal or
healthy state does not afford the opportunity to
comprehend the interrelations among its component
subsystems, utilization of samples of individuals
who are experiencing difficulties frequently is the
only way to examine developmental processes in
their full complexity.
If we decide to bypass or ignore the study of these
atypical phenomena, then the eventual result is
likely to be the construction of theories that are
contradicted by the revelation of critical facts dis-
covered through research on maladaptation and
psychopathology (cf. Lenneberg, 1967). However,
when extrapolating from atypical populations with
the goal of informing developmental theory, it is
essential that a range of high-risk conditions and
mental disorders be investigated. The examination of
a single pathological or risk process may eventuate
in spurious conclusions if generalizations are made
solely on that condition or disorder. However, if a
specific biological or behavioral pattern is viewed in
the light of an entire spectrum of disordered modi-
fications, then it may be possible to attain significant
insight into the processes of development not gen-
erally achieved through sole reliance on studies of
relatively nondisordered populations.
Investigators in the field of developmental psycho-
pathology also are invested in comprehending indi-
vidual pathways to competent adaptation despite
exposure to significant adversity or prolonged trauma
(i.e., resilience – see Luthar, Cicchetti, & Becker,
2000; Masten, 2001). Moreover, developmental
psychopathologists emphasize the importance of
understanding the functioning of individuals who,
after having diverged onto deviant developmental
pathways, resume positive functioning and achieve
adequate adaptation (Cicchetti & Rogosch, 1997;
Masten, 2006; Zigler & Glick, 1986).
The field of developmental psychopathology tran-
scends traditional disciplinary boundaries and pro-
vides fertile ground for moving beyond descriptive
facts to a process-level understanding of adaptive
and maladaptive, normal and abnormal, trajectories
of individual development. Research conducted
within a developmental psychopathology framework
may challenge assumptions about what constitutes
health or pathology and may redefine the manner in
which the mental health community operationalizes,
assesses, classifies, communicates about, and treats
the adjustment problems and functional impair-
ments of infants, children, adolescents, and adults
(Cicchetti & Toth, 1998). Thus, one of developmental
psychopathology’s potential contributions lies in the
heuristic power it holds for translating facts into
knowledge, understanding, and practical application
(Cicchetti & Toth, 2000, 2006). Accordingly, such a
developmental perspective may aid in the prevention
and reduction of the individual and societal burden
of mental disorder, alleviate the onus of suffering
that mental illness engenders in individuals, their
families, and the communities in which they reside,
and contribute toward eliminating the stigma com-
monly associated with the presence of mental dis-
order (Hinshaw, 2007; Hinshaw & Cicchetti, 2000).
What have we learned thus far? Some
illustrations
During the four-plus decades since the emergence of
the field, substantial progress has taken place.
Indeed, remarkable advances have occurred in
understanding the complexity of causality, the
interaction of risk and protective factors, the prob-
abilistic rather than the causal status of risk and
protective factors, the heterogeneity of mental
disorder, and the importance of developmental
processes and mechanisms in elucidating pathways
The past achievements and future promises of developmental psychopathology 17
� 2008 The Authors
Journal compilation � 2008 Association for Child and Adolescent Mental Health.
14697610, 2009, 1-2, D
ow
nloaded from
https://acam
h.onlinelibrary.w
iley.com
/doi/10.1111/j.1469-7610.2008.01979.x by U
niversity O
f H
ouston L
ibrary, W
iley O
nline L
ibrary on [14/01/2024]. See the T
erm
s and C
onditions (https://onlinelibrary.w
iley.com
/term
s-and-conditions) on W
iley O
nline L
ibrary for rules of use; O
A
articles are governed by the applicable C
reative C
om
m
ons L
icense
to adaptation and maladaptation (Kraemer et al.,
1997; Rutter & Sroufe, 2000; Sroufe, 1997).
Although they had been in use in biology for nearly
three decades before they emerged in the vocabulary
of psychopathologists, concepts of developmental
pathways, multifinality and equifinality, now are
prominent in the field (Cicchetti, 1990; Cicchetti &
Rogosch, 1996; Sroufe, 1989).
It is known that a variety of developmental pro-
gressions may eventuate in a given disorder (i.e.,
equifinality), rather than expecting a singular prim-
ary pathway to the disorder. For example, Sroufe
(1989) discovered that there were multiple, alternat-
ive causal pathways to attention deficit hyperactiv-
ity disorder (ADHD), one predominantly biological,
the other largely attributable to insensitive caregiv-
ing. Likewise, Cicchetti and Rogosch (1997) demon-
strated that there were different developmental
pathways for resilient maltreated and resilient
nonmaltreated children. Ego overcontrol, or a more
reserved, guarded approach, appeared to be better
suited for maltreated children in adapting to their
particular environments. Restraining from emotional
reactivity in volatile family circumstances was
thought to serve a protective function for maltreated
children, but may be problematic for nonmaltreated
children.
Additionally, the same risk and protective factors
may lead to, or be associated with, different out-
comes (i.e., multifinality). For example, the develop-
ment of an insecure attachment relationship with
one’s primary caregiver in childhood may eventuate
in any number of outcomes for children, depending
on the context of their environments and their indi-
vidual competencies and coping strategies (Green-
berg, Speltz, & DeKlyen, 1993). One such outcome
may be conduct disorder, in a child who has the
genetic and neurobiological diathesis, who has an
insecure representational model of the self, and who
faces extremes of additional stress in the form of a
violent home and/or community environment in
conjunction with minimal support or nurturance
from caregivers (Richters & Cicchetti, 1993). Like-
wise, not all sexually abused children develop psy-
chopathology, let alone the same type of mental
disorder (Kendall-Tackett, Williams, & Finkelhor,
1993).
The knowledge that there are multiple pathways to
similar manifest outcomes and that there are differ-
ent outcomes of the same pathway ultimately may
contribute to the implementation of important
refinements in the extant diagnostic classification of
mental disorders (Richters & Cicchetti, 1993; Sroufe,
1997). Moreover, the incorporation of pathways
concepts also strongly calls attention to the impor-
tance of conducting process-oriented studies and of
reframing the questions asked in research on the
antecedents and consequences of mental disorder.
Specifically, rather than searching for the indicators
or predictors of later maladaptation or disorder, the
central focus of developmental psychopathology has
shifted to investigating and describing the interactive
processes that lead to the emergence and course of
disturbed behavior. Question such as ‘what are the
various factors that initiate and maintain individuals
on pathways probabilistically associated with a
particular disorder and a family of related out-
comes?’ and ‘what differentiates those individuals
progressing to disorder ‘‘X’’ from those progressing to
disorder ‘‘Y’’ and those who do not develop mal-
adaptively or do not develop a mental disorder?’ have
increasingly come to the fore. Although some
researchers emphasize one set of initiating and
maintaining conditions, whereas other researchers
accentuate divergent factors, the answer to ques-
tions such as those posed above require the utiliza-
tion of developmental studies. As scientists
increasingly conceptualize and design their invest-
igations with the pathways concepts of equifinality
and multifinality as a foundation, we will move pro-
gressively closer to attaining the unique goals of
developmental psychopathology, first explicated by
Sroufe and Rutter (1984): to explain the development
of individual patterns of adaptation and maladap-
tation.
Our knowledge of developmental biology, the area
of neuroscience that focuses on factors regulating
the development of neurons, neuronal circuitry, and
complex neuronal systems, including the brain, also
has burgeoned. A rapid growth in sophisticated
techniques that allow for anatomical and physiolo-
gical imaging of the brain to occur has taken place
(Thomas & Cicchetti, 2008). These new neuro-
imaging methods have been used to enhance our
understanding of normal and abnormal neurobio-
logical development and of the processes linking
neurodevelopmental factors and later disordered
outcomes (Cicchetti & Cannon, 1999).
There also has been increasing recognition of the
dynamic interplay of influences over developmental
time. One of the most dramatic examples of this has
been the research on experience-dependent brain
development (Greenough, Black, & Wallace, 1987). It
is now widely recognized that neurobiological devel-
opment and experience are mutually influencing
(Cicchetti & Tucker, 1994; Eisenberg, 1995). Rather
than adhering to a unidimensional belief in the
deterministic role that unfolding biology exerts on
behavior, it is now widely believed that brain func-
tion and its subsequent influence on behavior pos-
sesses self-organizing functions that can, in fact, be
altered by experiences incurred during sensitive
periods of development that occur across the life
course (Cicchetti & Tucker, 1994; Nelson & Bloom,
1997).
Experience-dependent synapse formation involves
the brain’s adaptation to information that is unique
to the individual (Black, Jones, Nelson, & Green-
ough, 1998) Experience-dependent synaptogen-
esis is localized to the brain regions involved in
18 Dante Cicchetti and Sheree L. Toth
� 2008 The Authors
Journal compilation � 2008 Association for Child and Adolescent Mental Health.
14697610, 2009, 1-2, D
ow
nloaded from
https://acam
h.onlinelibrary.w
iley.com
/doi/10.1111/j.1469-7610.2008.01979.x by U
niversity O
f H
ouston L
ibrary, W
iley O
nline L
ibrary on [14/01/2024]. See the T
erm
s and C
onditions (https://onlinelibrary.w
iley.com
/term
s-and-conditions) on W
iley O
nline L
ibrary for rules of use; O
A
articles are governed by the applicable C
reative C
om
m
ons L
icense
processing information arising from the event
experienced by the individual. For example, children
endowed with normal brains may encounter a
number of experiences (e.g., extreme poverty, early
and chronic child abuse and neglect, etc.) that can
exert deleterious impacts upon neurobiological
development. Pathological experience may become
part of a vicious cycle, as the pathology induced in
brain structure may distort the child’s experience,
with subsequent alterations in cognition or social
interactions causing additional pathological experi-
ence and added brain pathology (Black et al., 1998;
Cicchetti & Tucker, 1994).
We increasingly recognize that the mechanisms of
neural plasticity are integral to the very anatomical
structure of cortical tissue, and that they cause the
formation of the brain to involve an extended mal-
leable process that presents developmental psy-
chopathologists with new avenues for understanding
the vulnerability of the brain as a basis for the
emergence of mental disorder. Perturbations that
take place in the developing brain can trigger a cas-
cade of growth and function changes that lead the
neural system down a path that deviates from that
usually taken in normal neurobiological develop-
ment, leading to the development of aberrant neural
circuitry that contributes to these early develop-
mental abnormalities eventuating in relatively
enduring forms of psychopathology (Cicchetti,
2002).
Furthermore, advances in molecular biology and
molecular genetics, including the completion of the
DNA sequencing of the human genome and the
publication of the map of human haplotypes that
provides valuable information about individual
genetic variation, have helped to engender renewed
interest in the contribution that investigations on
gene–environment (G · E) interaction can make to
unraveling the complex pathways to normality,
psychopathology, and resilience (Cicchetti & Curtis,
2006; Moffitt, Caspi, & Rutter, 2006). The empirical
contributions of a molecular genetic approach make
the search for the intermediate developmental
mechanisms in the (Gene fi Brain) · E intercon-
nection more accessible than ever before (Gottesman
& Hanson, 2005). Moreover, progress in molecular
genetics and on G · E research on psychopathology
raises hopes of developing interventions to prevent
and remediate mental disorder and to promote
resilience (Cicchetti & Curtis, 2006; Moffitt et al.,
2006).
Finally, developmental psychopathology has
played a significant role in contributing to the devel-
opment of clinical initiatives directed toward the
prevention and treatment of mental disorders. By
elucidating developmental mechanisms that are
linked with the initiation or avoidance of maladapta-
tion and psychopathology, theoretically-informed
interventions have been developed and evaluated
(Izard et al., 2002; Toth, Rogosch, Manly, & Cicchetti,
2006). For example, Fisher, Gunnar, Dozier, Bruce,
and Pears (2006) report the results of two randomized
controlled preventive trials involving infants,
toddlers, and preschoolers in foster care. These
interventions were able to exert positive effects on
many areas of functioning that have been shown to be
negatively affected by early stress – including hypo-
thalamic-pituitary-adrenal (HPA) axis activity,
behavior, and attachment to caregivers (see also
Cicchetti & Gunnar, 2008). Importantly, develop-
mentally-informed prevention and intervention
strategies also have contributed to refinements in
developmental theory (Cicchetti & Hinshaw, 2002).
Future perspectives
In a relatively brief period of time, the field of devel-
opmental psychopathology has demonstrated that it
can play a significant role in increasing our under-
standing of risk and psychopathology and in bridg-
ing the schism that has for too long separated the
worlds of basic research and clinical practice. In
order to sustain this momentum and to foster new
advances, a number of challenges that lie ahead
must be addressed. Perhaps most significantly,
there must be continued striving toward and pro-
gress made to attain enhanced fidelity among the
elegance and complexity of the theoretical models
extant in the field, the definitional parameters
inherent to a developmental psychopathology per-
spective, and the design, measurement, and data
analytic strategies employed in our investigations of
risk, disorder, and adaptation across the life course.
Multiple levels of analysis
In order to continue to foster the advances that have
occurred in understanding developmental processes
in both normal development and psychopathology,
it is essential that a multiple-levels-of-analysis
approach and an interdisciplinary perspective be
increasingly incorporated into the field. Because one
of the major goals of developmental psychopathology
is to comprehend individual patterns of adaptation
and to understand the ‘whole organism’ (Sroufe &
Rutter, 1984; Zigler & Glick, 1986), calls for inter-
disciplinary research and a multiple-levels-of anal-
ysis approach have been gaining momentum in
scientific laboratories across the country (Cicchetti &
Dawson, 2002; Cicchetti & Posner, 2005; Pellmar &
Eisenberg, 2000).
Although some problems are best addressed with
the methods and concepts of a single discipline,
other issues require interdisciplinary integration in
order to fully comprehend the complexities that are
present. This is particularly true when grappling
with psychopathology. Thus, investigators and
investigative teams must direct their collective
energies toward an examination of multiple levels of
The past achievements and future promises of developmental psychopathology 19
� 2008 The Authors
Journal compilation � 2008 Association for Child and Adolescent Mental Health.
14697610, 2009, 1-2, D
ow
nloaded from
https://acam
h.onlinelibrary.w
iley.com
/doi/10.1111/j.1469-7610.2008.01979.x by U
niversity O
f H
ouston L
ibrary, W
iley O
nline L
ibrary on [14/01/2024]. See the T
erm
s and C
onditions (https://onlinelibrary.w
iley.com
/term
s-and-conditions) on W
iley O
nline L
ibrary for rules of use; O
A
articles are governed by the applicable C
reative C
om
m
ons L
icense
analysis within the same individual. The sophis-
ticated and comprehensive portrayals of adaptation
and maladaptation that ensue will serve not only to
advance scientific understanding, but also to inform
efforts to prevent and ameliorate psychopathology.
Most of what is known about the correlates,
causes, pathways, and sequelae of mental disorders
has been gleaned from investigations that focused on
relatively narrow domains of variables. Although
growing attention has been directed toward discov-
ering the processes through which individuals at
high risk for psychopathology do not develop mal-
adaptively, until quite recently the empirical study of
resilience has focused exclusively on detecting the
psychosocial determinants of the phenomenon
(Charney, 2004; Curtis & Cicchetti, 2003; but see
Cicchetti & Curtis, 2007). To understand psycho-
pathology and resilience in their full complexity, all
levels of analysis must be examined and integrated.
Each level both informs and constrains all other
levels of analysis. Moreover, the influence of levels on
one another is almost always bidirectional. There-
fore, no component, subsystem or level of organiza-
tion possesses causal privilege in the developmental
system (Thelen & Smith, 1998). Because levels of
organization and processes are reciprocally interact-
ive, it is difficult, if not impossible, to impute ultim-
ate causation to one level over another. It is the
mutual relationship between at least two compon-
ents of the developmental system that influences
developmental organization or disorganization
(Gottlieb, 1992).
Since different levels of analysis constrain other
levels, as developmental psychopatholgists learn
more about multiple levels of analysis, researchers
conducting their work at each level will need to de-
velop theories that are consistent across all levels of
inquiry. When disciplines function in isolation, they
run the risk of creating theories that ultimately will
be incorrect because vital information from other
disciplines has either been ignored or is unknown.
As is true in systems neuroscience, it is essential
that an integrative framework that incorporates all
levels of analysis about complex systems in the
development of psychopathology or in the promotion
of resilience be utilized. Rather than adhering to a
single domain or unitary disciplinary focus, striving
for a multi-domain, multi-level synthesis may impel
researchers to broaden their visions and thereby
lead to the formulation of integrative developmental
theories that can elucidate both normal and abnor-
mal forms of ontogenesis across developing systems.
One of the major challenges confronting scientific
progress involves establishing communication sys-
tems among disciplines. For example, despite tre-
mendous technological advances in neuroimaging
and molecular genetics, great knowledge gaps
remain between scientists who possess competence
with the technologies and methods of brain imaging
and genetics and those who are focused on
addressing the complex issues inherent in the
investigation of development and psychopathology.
Consequently, the field has not yet made optimal use
of the advances in technology that have taken place.
In contrast with the viewpoint that mental
illnesses should be conceived as ‘brain disorders’ or
‘brain diseases,’ a multiple-levels-of analysis
approach suggests that mental disorders can better
be conceptualized in a more dynamic fashion that
reflects the probabilistic, bidirectional, and trans-
actional nature of genetic, neurobiological, social,
psychological, and pre- and postnatal environmental
influences over the life course. Whereas the brain is
clearly involved in all forms of mental disorder, many
other levels contribute and transact with the brain in
dynamic fashion to bring about experience-depen-
dent brain development. Although many types of
mental disorder may be characterized by strong
psychobiological predispositions, the ‘brain disorder’
concept may connote primacy or exclusivity for the
biology and fail to adequately capture the transac-
tional processes that are operative between biology
and the broader psychological and social environ-
ments. An alternative to the ‘brain disorder’ view-
point would be to conceptualize mental illnesses as
involving dysfunction among multiple and transact-
ing developmental processes.
Beyond the calls for research programs incorpo-
rating multiple levels of analysis seen in recent
overviews of the field, such research must actually
be supported by funding agencies, some of
whom continue to view multiple-levels-of-analysis
approaches to research questions as too broad and
risky to merit financial support. In addition, journal
editors need to encourage such research by
increasing their willingness to publish papers that
investigate a phenomenon across multiple levels of
analysis, some of which might fall somewhat outside
the purview of the particular journal. Furthermore,
research in developmental psychopathology that is
driven by broadly based theory incorporating mul-
tiple levels of analysis must increasingly be encour-
aged by faculty in the context of graduate training.
In order to ensure that future generations of
scholars in developmental psychopathology are
exposed to a broad, dynamic, systems-based,
multiple-levels-of-analysis perspective, undergradu-
ate and graduate programs in clinical and develop-
mental psychology need to encourage students to
take courses in a broad spectrum of areas. These
might include courses on basic molecular biology,
neuroendocrinology, neuroscience, and develop-
mental processes, as well as courses that incor-
porate information on brain-imaging technology,
molecular genetic methods, neuroendocrine and
immunological assay techniques, and other tools
involved in assessing neurobiological and genetic
processes. Likewise, students in basic science areas,
such as neuroscience or genetics, should be
encouraged to gain exposure to the fundamentals of
20 Dante Cicchetti and Sheree L. Toth
� 2008 The Authors
Journal compilation � 2008 Association for Child and Adolescent Mental Health.
14697610, 2009, 1-2, D
ow
nloaded from
https://acam
h.onlinelibrary.w
iley.com
/doi/10.1111/j.1469-7610.2008.01979.x by U
niversity O
f H
ouston L
ibrary, W
iley O
nline L
ibrary on [14/01/2024]. See the T
erm
s and C
onditions (https://onlinelibrary.w
iley.com
/term
s-and-conditions) on W
iley O
nline L
ibrary for rules of use; O
A
articles are governed by the applicable C
reative C
om
m
ons L
icense
basic normative and atypical developmental pro-
cesses. Further, specific interdisciplinary programs,
for both students and faculty, spanning interest
areas from clinical intervention to basic neurosci-
ence and genetics, would help to foster commun-
ication and collaborative research endeavors between
these scientific fields and developmental psycho-
pathology.
The importance of prevention and intervention
science to developmental psychopathology
Although progress has occurred in recent decades,
theory and empirical research on basic develop-
mental processes should increasingly be used to
inform prevention and intervention efforts to a
greater extent than is the norm (Toth & Cicchetti,
1999). Conversely, the scientific evaluation of ran-
domized clinical prevention and intervention trials
can provide unprecedented and essential insights
into affirming, challenging, and augmenting existing
developmental theories. For example, if the devel-
opmental course is altered as a result of the imple-
mentation of preventive interventions and the risk
for negative outcomes is reduced, then prevention
research will be able to contribute to specifying the
processes that are involved in the emergence of
maladaptive developmental outcomes and psycho-
pathology (Ialongo et al., 2006). As true experiments
in modifying the developmental course, prevention
trials can provide insight into the etiology and
pathogenesis of disordered outcomes.
It is now time to conduct intervention evaluations
that routinely incorporate both behavioral and bio-
logical measures into their design (Cicchetti &
Gunnar, 2008). Such multi-level intervention
evaluations would enable scientists not only to
assess theoretically predicted behavioral changes,
but also to ascertain whether abnormal biological
structures, functions, and organizations are modifi-
able or are refractory to intervention. There is grow-
ing support in the animal literature that efficacious
intervention modifies not only maladaptive behavior,
but also the cellular and physiological correlates of
behavior. Successful preventive interventions with
humans may alter behavior and physiology through
producing alterations in gene expression that create
a new structural organization in the brain (Kandel,
1999).
Presently, we do not know if the neurobiological
difficulties displayed by some persons with mental
disorders or individuals who have experienced sig-
nificant life adversity are irreversible or whether
there are particular sensitive periods when it is more
likely that neural plasticity will occur. Moreover, it is
not known whether some neural systems may be
more plastic than other neural systems or whether
particular neural systems may be more refractory to
change or have a more time-limited window when
neural plasticity can occur. The conduct of multi-
level interventions at various points in the develop-
mental lifespan has the potential to provide answers
to these provocative questions.
Furthermore, the incorporation of a neurobiolo-
gical framework into interventions seeking to improve
maladaptation, promote resilient functioning, or to
repair positive adaptations gone awry, may contrib-
ute to the ability to design individualized interven-
tions that are based on knowledge gleaned from
multiple levels of biological and psychological levels of
analysis. It is conceivable that efficacious, resilience-
promoting interventions may be conceptualized as
experience-dependent plasticity.
Cultural considerations and developmental
psychopathology
Over the course of the twentieth century, concep-
tualizations of culture and its role in both normal
and atypical human development have changed
significantly (Garcia Coll, Akerman, & Cicchetti,
2000). Specifically, with respect to understanding
the experience of psychopathology among minority
populations, an important paradigm shift has
occurred regarding ‘difference’ versus ‘deficit’
approaches (Garcia Coll et al., 1996). Whereas
historically differences between adaptation in
majority and minority groups were viewed as
reflecting deficits in the minority populations, it is
increasingly clear that differences also can function
as strengths for members of minority groups. More
recent models posit that varied cultures, lifestyles,
and developmental outcomes that differ from
standards derived from the White middle-class
mainstream are legitimate adaptations to contex-
tual demands or are valuable in their own right
(Garcia Coll et al., 2000). Although during its
infancy developmental psychopathology was con-
sidered to be at risk of becoming a monocultural
science, as the discipline has matured more inte-
grative approaches to understanding risk, resil-
ience, and psychopathology among minority groups
have emerged. In fact, research conceived within a
developmental psychopathology tradition has
increasingly elucidated varied pathways to adapta-
tion in different racial and ethnic groups. The
increased understanding that has emerged as a
function of broader and more accurate perspectives
on development within specific racial and ethnic
groups possesses significant implications for
understanding and treating individuals with men-
tal illness. Unfortunately, the stigmatization asso-
ciated with mental illness among some racial and
ethnic groups and continued disparities in
accessing high quality and empirically-supported
interventions highlights the importance of investi-
gations conceived within a developmental psycho-
pathology framework continuing to incorporate
cultural contexts into study designs and treatment
evaluations.
The past achievements and future promises of developmental psychopathology 21
� 2008 The Authors
Journal compilation � 2008 Association for Child and Adolescent Mental Health.
14697610, 2009, 1-2, D
ow
nloaded from
https://acam
h.onlinelibrary.w
iley.com
/doi/10.1111/j.1469-7610.2008.01979.x by U
niversity O
f H
ouston L
ibrary, W
iley O
nline L
ibrary on [14/01/2024]. See the T
erm
s and C
onditions (https://onlinelibrary.w
iley.com
/term
s-and-conditions) on W
iley O
nline L
ibrary for rules of use; O
A
articles are governed by the applicable C
reative C
om
m
ons L
icense
Translational research
The growth of basic research knowledge in develop-
mental psychopathology has significantly exceeded
its application to clinical disorders. To improve the
health and well-being of individuals, scientific dis-
coveries must be translated into practical applica-
tions (Gunnar & Cicchetti, in press). Translational
research involves a subset of interdisciplinary
research that integrates information from clinical
settings and basic research laboratories. In a report
of the National Advisory Mental Health Council
(2000, p. v) entitled Translating Behavioral Science
into Action, the workgroup concluded that ‘too few
researchers are attempting to bridge across basic,
clinical, and services research, and not enough are
working with colleagues in related allied disciplines
to move research advances out of the laboratory and
into clinical care, service delivery, and policy mak-
ing.’ In this report, ‘translational research is defined
as research designed to address how basic behav-
ioral processes inform the diagnosis, prevention,
treatment, and delivery of services for mental illness
and, conversely, how knowledge of mental illness
increases our understanding of basic behavioral
processes’ (p. iii). This formulation of translational
research is in direct accord with principles of devel-
opmental psychopathology – namely, the reciprocal
interplay between basic and applied research and
between normal and atypical development.
Translational research is needed to impart more
scientific knowledge of genetic, neurobiological,
cognitive, social-cognitive and emotional processes
to the understanding and treatment of mental dis-
orders. Rather than an all or none approach, the
conduct of translational research necessarily must
involve a process that includes various steps taken
along the way. There must be a recognition and
agreement that basic research should be conceived
within a conceptual framework that understands the
goal of informing future application.
Given the substantial monetary investment in
supporting both basic research with relevance to the
understanding and treatment of mental illness and
in randomized prevention and treatment trials, it is
of paramount importance that the knowledge gained
from such endeavors be exported into real-world
contexts. Researchers must be advocates, not only
for the scientific dissemination of knowledge, but
also for reaching policymakers and clinicians who
may lack the understanding or resources needed to
provide interventions that have been found to be
efficacious. It would be naı̈ve to suggest that
impediments to implementing evidence-supported
treatments in nonresearch settings do not exist.
However, although efforts to traverse the path from
the university laboratory to the clinical world may
cause apprehension, avoidance, and resistance,
such a journey must not be avoided. Rather, as a
field we need to embrace the diversity among us,
equally welcoming potentially elucidating contribu-
tions from basic researchers and frontline profes-
sionals. Such collaborative endeavors and active
efforts to improve the conduct and utilization of
research and the scientific base of practice will
benefit researchers, practitioners, policymakers, and
most importantly, vulnerable children and families.
Conclusion
Despite the significant advances that have occurred
in the field of developmental psychopathology,
important work lies ahead. Undoubtedly these
future developments will build upon the venerable
contributions of the past; however, as work in the
field becomes increasingly interdisciplinary and
technologically sophisticated, it is essential that
even more emphasis be directed toward the process
of development (Harter, 2006; Sroufe, 2007). Devel-
opment is always the result of interdependence,
co-actions, or co-determination among multiple
levels of influence (Gottlieb, 1992; Sroufe, 2007). It is
not only genes and environments, but also the
cumulative developmental history of the individual
that influence how future development will unfold
(Sroufe, 2007).
Much of the momentum generated by the devel-
opmental psychopathology framework has emanated
from receptivity to and respect for preexisting
knowledge in combination with a willingness to
question established beliefs, thereby continuing to
promote disciplinary growth. Moreover, develop-
mental psychopathologists have incorporated con-
cepts and methods derived from other disciplinary
endeavors that are too often isolated from each
other, thereby generating advances in knowledge
that might have been missed in the absence of cross-
disciplinary dialogue. The continuation and elabo-
ration of the mutually enriching interchanges that
have occurred within and across disciplines inter-
ested in normal and abnormal development will
enhance not only the science of developmental
psychopathology, but also increase the benefits to be
derived for society as a whole.
Acknowledgements
Our work on this paper was supported by grants
from the National Institute of Drug Abuse
(DA017741-01), the National Institute of Mental
Health (MH 067792-1), and the Spunk Fund, Inc.
Correspondence to
Dante Cicchetti, Institute of Child Development,
University of Minnesota, 51 East River Road, Min-
neapolis, MN 55455-0345, USA; Email: cicchett@
umn.edu
22 Dante Cicchetti and Sheree L. Toth
� 2008 The Authors
Journal compilation � 2008 Association for Child and Adolescent Mental Health.
14697610, 2009, 1-2, D
ow
nloaded from
https://acam
h.onlinelibrary.w
iley.com
/doi/10.1111/j.1469-7610.2008.01979.x by U
niversity O
f H
ouston L
ibrary, W
iley O
nline L
ibrary on [14/01/2024]. See the T
erm
s and C
onditions (https://onlinelibrary.w
iley.com
/term
s-and-conditions) on W
iley O
nline L
ibrary for rules of use; O
A
articles are governed by the applicable C
reative C
om
m
ons L
icense
References
Black, J.E., Jones, T.A., Nelson, C.A., & Greenough,
W.T. (1998). Neuronal plasticity and the developing
brain. In N.E. Alessi, J.F. Coyle, S.I. Harrison, & S.
Eth (Eds.), Handbook of child and adolescent psychi-
atry (pp. 31–53). New York: Wiley.
Charney, D.S. (2004). Psychobiological mechanisms of
resilience and vulnerability: Implications for success-
ful adaptation to extreme stress. American Journal of
Psychiatry, 161, 195–216.
Cicchetti, D. (1984). The emergence of developmental
psychopathology. Child Development, 55, 1–7.
Cicchetti, D. (1990). A historical perspective on the
discipline of developmental psychopathology. In
J. Rolf, A. Masten, D. Cicchetti, K. Nuechterlein, &
S. Weintraub (Eds.), Risk and protective factors in the
development of psychopathology (pp. 2–28). New
York: Cambridge University Press.
Cicchetti, D. (1993). Developmental psychopathology:
Reactions, reflections, projections. Developmental
Review, 13, 471–502.
Cicchetti, D. (2002). How a child builds a brain:
Insights from normality and psychopathology. In
W. Hartup & R. Weinberg (Eds.), Minnesota symposia
on child psychology: Child psychology in retrospect
and prospect (vol. 32, pp. 23–71). Mahwah, NJ:
Lawrence Erlbaum Associates.
Cicchetti, D. (Ed.). (2003). Experiments of nature: Con-
tributions to developmental theory [Special Issue].
Development and Psychopathology, 15, 833–1106.
Cicchetti, D., & Cannon, T.D. (1999). Neurodevelop-
mental processes in the ontogenesis and epigenesis of
psychopathology. Development and Psychopathology,
11, 375–393.
Cicchetti, D., & Curtis, W.J. (2006). The developing
brain and neural plasticity: Implications for normal-
ity, psychopathology, and resilience. In D. Cicchetti
& D. Cohen (Eds.), Developmental psychopathology
(2nd edn), Vol. 2: Developmental neuroscience (pp. 1–
64). New York: Wiley.
Cicchetti, D., & Curtis, W.J. (Eds.). (2007). A multi-level
approach to resilience [Special Issue]. Development
and Psychopathology, 19, 627–955.
Cicchetti, D., & Dawson, G. (Eds.). (2002). Multiple
levels of analysis [Special Issue]. Development and
Psychopathology, 14, 417–666.
Cicchetti, D., & Gunnar, M.R. (Eds.). (2008). Integrating
biological processes into the design and evaluation of
preventive interventions [Special Issue]. Development
and Psychopathology, 20(3), 737–1022.
Cicchetti, D., & Hinshaw, S.P. (Eds.). (2002). Prevention
and intervention science: Contributions to develop-
mental theory [Special Issue]. Development and Psy-
chopathology, 14, 667–981.
Cicchetti, D., & Pogge-Hesse, P. (1982). Possible con-
tributions of the study of organically retarded persons
to developmental theory. In E. Zigler & D. Balla
(Eds.), Mental retardation: The developmental-differ-
ence controversy (pp. 277–318). Hillsdale, NJ: Law-
rence Erlbaum Associates.
Cicchetti, D., & Posner, M.I. (Eds.). (2005). Integrating
cognitive and affective neuroscience and developmen-
tal psychopathology [Special Issue]. Development and
Psychopathology, 17, 569–891.
Cicchetti, D., & Rogosch, F.A. (1996). Equifinality and
multifinality in developmental psychopathology.
Development and Psychopathology, 8, 597–600.
Cicchetti, D., & Rogosch, F.A. (1997). The role of self-
organization in the promotion of resilience in mal-
treated children. Development and Psychopathology,
9, 799–817.
Cicchetti, D., & Toth, S.L. (1998). Perspectives on
research and practice in developmental psychopatho-
logy. InW. Damon (Ed.),Handbook of child psychology
(5th edn, Vol. 4, pp. 479–583). New York: Wiley.
Cicchetti, D., & Toth, S.L. (Eds.). (2000). Social policy
implications of research in developmental psycho-
pathology [Special Issue]. Development and Psycho-
pathology, 12, 551–885.
Cicchetti, D., & Toth, S.L. (Eds.). (2006). Translational
research in developmental psychopathology. [Special
Issue]. Development and Psychopathology, 18, 619–
933.
Cicchetti, D., & Tucker, D. (1994). Development and
self-regulatory structures of the mind. Development
and Psychopathology, 6, 533–549.
Curtis, W.J., & Cicchetti, D. (2003). Moving research on
resilience into the 21st century: Theoretical and
methodological considerations in examining the bio-
logical contributors to resilience. Development and
Psychopathology, 15, 773–810.
Eisenberg, L. (1995). The social construction of the
human brain. American Journal of Psychiatry, 152,
1563–1575.
Fisher, P.A., Gunnar, M.R., Dozier, M., Bruce, J., &
Pears, K.C. (2006). Effects of therapeutic interven-
tions for foster children on behavioral problems,
Key points
• Developmental psychopathology examines processes underlying the interrelation between adaptive and
maladaptive development over the life course.
• A multiple levels of analysis approach and an interdisciplinary perspective must be incorporated into the
field.
• Theory and empirical research on basic biological and psychological developmental processes must
increasingly be used to inform prevention and intervention initiatives.
• Investigations conceived within a developmental psychopathology framework must continue to incorpor-
ate cultural contexts into study designs and treatment initiatives.
• Scientific discoveries emanating from developmental psychopathology must be translated into practical
applications.
The past achievements and future promises of developmental psychopathology 23
� 2008 The Authors
Journal compilation � 2008 Association for Child and Adolescent Mental Health.
14697610, 2009, 1-2, D
ow
nloaded from
https://acam
h.onlinelibrary.w
iley.com
/doi/10.1111/j.1469-7610.2008.01979.x by U
niversity O
f H
ouston L
ibrary, W
iley O
nline L
ibrary on [14/01/2024]. See the T
erm
s and C
onditions (https://onlinelibrary.w
iley.com
/term
s-and-conditions) on W
iley O
nline L
ibrary for rules of use; O
A
articles are governed by the applicable C
reative C
om
m
ons L
icense
caregiver attachment, and stress regulatory neural
systems. Annals of the New York Academy of Sci-
ences, 1094, 215–225.
Garcia-Coll, C., Akerman, A., & Cicchetti, D. (2000).
Cultural influences on developmental processes and
outcomes: Implications for the study of development
and psychopathology. Development and Psycho-
pathology, 12, 333–356.
Garcia Coll, D., Lamberty, G., Jenkins, R., McAdoo,
H.P., Crnic, K., Waski, B.H., & Garica, H.V. (1996).
An integrative model for the study of developmental
competencies in minority children. Child Develop-
ment, 67, 1891–1914.
Gottesman, I.I., & Hanson, D.R. (2005). Human
development: Biological and genetic processes.
Annual Review of Psychology, 56, 263–286.
Gottlieb, G. (1992). Individual development and evolu-
tion: The genesis of novel behavior. New York: Oxford
University Press.
Greenberg, M.T., Speltz, M.L., & DeKlyen, M. (1993).
The role of attachment in the early development of
disruptive behavior problems. Development and Psy-
chopathology, 19, 191–213.
Greenough, W., Black, J., & Wallace, C. (1987).
Experience and brain development. Child Develop-
ment, 58, 539–559.
Gunnar, M.R., & Cicchetti, D. (Eds.). (in press). Meeting
the challenge of translational research in child psy-
chology: Minnesota symposium on child psychology
(vol. 35). New York: Wiley.
Harter, S. (2006). Self-processes and developmental
psychopathology. In D. Cicchetti & D. Cohen (Eds.),
Develsopmental psychopathology (2nd edn, vol. 1, pp.
370–418). New York: Wiley.
Hinshaw, S.P. (2007). The mark of shame: Stigma of
mental illness and an agenda for change. New York:
Oxford University Press.
Hinshaw, S.P., & Cicchetti, D. (2000). Stigma and
mental disorder: Conceptions of illness, public
attitudes, personal disclosure, and social policy.
Development and Psychopathology, 12, 555–
598.
Ialongo, N., Rogosch, F.A., Cicchetti, D., Toth, S.L.,
Buckley, J., Petras, H., et al. (2006). A developmental
psychopathology approach to the prevention of men-
tal health disorders. In D. Cicchetti & D. Cohen
(Eds.), Developmental psychopathology (2nd edn),
Vol.1: Theory and Method (pp. 968–1018). New York:
Wiley.
Izard, C.E., Fine, S., Mostow, A., Trentacosta, C., &
Campbell, J. (2002). Emotion processes in normal
and abnormal development and preventive interven-
tion. Development and Psychopathology, 14, 761–
787.
Kandel, E.R. (1999). Biology and the future of psycho-
analysis: A new intellectual framework for psychiatry
revisited. American Journal of Psychiatry, 156, 505–
524.
Kendall-Tackett, K.A., Williams, L.M., & Finkelhor, D.
(1993). Impact of sexual abuse on children: A review
and synthesis of recent empirical studies. Psycholo-
gical Bulletin, 113, 164–180.
Kraemer, H.C., Kazdin, A.E., Offord, D.R., Kessler, R.C.,
Jensen, P.S., & Kupfer, D.J. (1997). Coming to terms
with the terms of risk. Archives of General Psychiatry,
54, 337–343.
Lenneberg, E. (1967). Biological foundations of lan-
guage. New York: Wiley.
Luthar, S.S., Cicchetti, D., & Becker, B. (2000). The
construct of resilience: A critical evaluation and guide-
lines for futurework.Child Development, 71, 543–562.
Masten, A.S. (2001). Ordinary magic: Resilience pro-
cesses in development. American Psychologist, 56,
227–238.
Masten, A.S. (2006). Developmental psychopathology:
Pathways to the future. International Journal of
Behavioral Development, 31, 47–54.
Moffitt, T.E., Caspi, A., & Rutter, M. (2006). Measured
gene–environment interactions in psychopathology:
Concepts, research strategies, and implications for
research, intervention, and public understanding of
genetics perspectives on psychological science. Per-
spectives on Psychological Science, 1, 5–27.
National Advisory Mental Health Council. (2000).
Translating behavioral science into action: Report of
the National Advisory Mental Health Counsel’s behav-
ioral science workgroup (00-4699). Bethesda, MD:
National Institutes of Mental Health.
Nelson, C.A., & Bloom, F.E. (1997). Child development
and neuroscience. Child Development, 68, 970–987.
Pellmar, T.C., & Eisenberg, L. (Eds.). (2000). Bridging
disciplines in the brain, behavioral, and clinical sci-
ences. Washington, DC: National Academy Press.
Richters, J.E., & Cicchetti, D. (1993). Mark Twain
meets DSM-III-R: Conduct disorder, development,
and the concept of harmful dysfunction. Development
and Psychopathology, 5, 5–29.
Rutter, M. (1986). Child psychiatry: The interface
between clinical and developmental research. Psy-
chological Medicine, 16, 151–160.
Rutter, M. (2007). Proceeding from observed correlation
to causal inference: The use of natural experiments.
Perspectives on Psychological Science, 2, 377–395.
Rutter, M., & Sroufe, L.A. (2000). Developmental psy-
chopathology: Concepts and challenges. Development
and Psychopathology, 12, 265–296.
Sroufe, L.A. (1989). Pathways to adaptation and mal-
adaptation: Psychopathology as developmental devi-
ation. In D. Cicchetti (Ed.), Rochester symposium on
developmental psychopathology: The emergence of a
discipline (vol. 1, pp. 13–40). Hillsdale, NJ: Lawrence
Erlbaum Associates.
Sroufe, L.A. (1990). Considering normal and abnormal
together: The essence of developmental psycho-
pathology. Development and Psychopathology, 2,
335–347.
Sroufe, L.A. (1997). Psychopathology as an outcome of
development. Development and Psychopathology, 9,
251–268.
Sroufe, L.A. (2007). The place of development in devel-
opmental psychopathology. In A.S. Masten (Ed.),
Multilevel dynamics in developmental psychopatho-
logy: The Minnesota Symposia on Child Psychology
(vol. 34, pp. 285–299). Mahwah, NJ: Lawrence Erl-
baum Associates.
Sroufe, L.A., & Rutter, M. (1984). The domain of
developmental psychopathology. Child Development,
55, 17–29.
24 Dante Cicchetti and Sheree L. Toth
� 2008 The Authors
Journal compilation � 2008 Association for Child and Adolescent Mental Health.
14697610, 2009, 1-2, D
ow
nloaded from
https://acam
h.onlinelibrary.w
iley.com
/doi/10.1111/j.1469-7610.2008.01979.x by U
niversity O
f H
ouston L
ibrary, W
iley O
nline L
ibrary on [14/01/2024]. See the T
erm
s and C
onditions (https://onlinelibrary.w
iley.com
/term
s-and-conditions) on W
iley O
nline L
ibrary for rules of use; O
A
articles are governed by the applicable C
reative C
om
m
ons L
icense
Thelen, E., & Smith, L.B. (1998). Dynamic systems
theories. In W. Damon & R. Lerner (Eds.), Handbook
of child psychology: Vol. 1. Theoretical models of
human development (pp. 563–634). New York: John
Wiley & Sons, Inc.
Thomas, K., & Cicchetti, D. (Eds.). (2008). Imaging
brain systems in normality and psychopathology
[Special Issue]. Development and Psychopathology,
20(4), 1023–1365.
Toth, S.L., & Cicchetti, D. (1999). Developmental psy-
chopathology and child psychotherapy. In S. Russ &
T. Ollendick (Eds.), Handbook of psychotherapies
with children and families (pp. 15–44). New York:
Plenum Press.
Toth, S.L., Rogosch, F.A., Manly, J.T., & Cicchetti, D.
(2006). The efficacy of toddler–parent psychotherapy
to reorganize attachment in the young offspring of
mothers with major depressive disorder. Journal
of Consulting and Clinical Psychology, 74, 1006–
1016.
Zigler, E., & Glick, M. (1986). A developmental approach
to adult psychopathology. New York: Wiley.
Manuscript accepted 21 April 2008
The past achievements and future promises of developmental psychopathology 25
� 2008 The Authors
Journal compilation � 2008 Association for Child and Adolescent Mental Health.
14697610, 2009, 1-2, D
ow
nloaded from
https://acam
h.onlinelibrary.w
iley.com
/doi/10.1111/j.1469-7610.2008.01979.x by U
niversity O
f H
ouston L
ibrary, W
iley O
nline L
ibrary on [14/01/2024]. See the T
erm
s and C
onditions (https://onlinelibrary.w
iley.com
/term
s-and-conditions) on W
iley O
nline L
ibrary for rules of use; O
A
articles are governed by the applicable C
reative C
om
m
ons L
icense
Comprehensive Psychiatry 87 (2018) 143–152
Contents lists available at ScienceDirect
Comprehensive Psychiatry
j ourna l homepage: www
.
e lsev ie r .com/ locate /comppsych
Psychiatry and developmental psychopathology: Unifying themes and
future directions
Theodore P. Beauchaine a,⁎, John N. Constantino b, Elizabeth P. Hayden c
a Department of Psychology, Nisonger Center for Excellence in Developmental Disabilities, The Ohio State University, United States of America
b Departments of Psychiatry and Pediatrics, Washington University School of Medicine, United States of America
c Department of Psychology, Brain and Mind Institute, Western University, Canada
Preparation of the editorial was supported by Gran
Institutes of Health, and by the National Institutes of Hea
(SoBC) Common Fund. Declarations of interest: none.
⁎ Corresponding author at: Department of Psychology,
Neil Avenue, Columbus, OH 43210, United States of Amer
E-mail address: beauchaine.1@osu.edu (T.P. Beauchain
https://doi.org/10.1016/j.comppsych.2018.10.014
0010-440X/© 2019 The Authors. Published by Elsevier Inc
a b s t r a c t
a r t i c l e i n f o
Article history:
Received 18 August 2018
Accepted 30 October 2018
In the past 35 years, developmental psychopathology has grown into a flourishing discipline that shares a scien-
tific agenda with contemporary psychiatry. In this editorial, which introduces the special issue, we describe the
history of developmental psychopathology, including core principles that bridge allied disciplines. These include
(1) emphasis on interdisciplinary research, (2) elucidation ofmulticausal pathways to seemingly single disorders
(phenocopies), (3) description of divergent multifinal outcomes from common etiological start points
(pathoplasticity), and (4) research conducted acrossmultiple levels of analysis spanning genes to environments.
Next, we discuss neurodevelopmental models of psychopathology, and provide selected examples. We empha-
size differential neuromaturation of subcortical and cortical neural networks and connectivity, and how both
acute and protracted environmental insults can compromise neural structure and function. Todate, developmen-
tal psychopathology has placed greater emphasis than psychiatry on neuromaturationalmodels ofmental illness.
However, this gap is closing rapidly as advances in technology render etiopathophysiologies of psychopathology
more interrogable.We end with suggestions for future interdisciplinary research, including the need to evaluate
measurement invariance across development, and to constructmore valid assessmentmethodswhere indicated.
© 2019 The Authors. Published by Elsevier Inc.
Keywords:
Psychiatry
Developmental psychopathology
Multifinality
Equifinality
Neurodevelopment
Interdisciplinary
1. Introduction
In 1974, Thomas Achenbach published his foundational text, which
defined and named the emerging field of developmental psychopathol-
ogy [1]. At the time, the new disciplinewas so nascent that the first sen-
tence of Chapter 1 reads, “This is a book about a field that hardly exists
yet” (p. 3). In the 35 years since, developmental psychopathology has
burgeoned into a discipline with its own first-tier scientific journal [2],
frequent special issues in journals from related disciplines [3–5], widely
cited interdisciplinary texts and edited volumes [6,7], important scien-
tific and theoretical advances [8,9], and dedicated graduate programs.
Few disciplines enjoy such rapid proliferation and success. Although it
is beyond the scope of this editorial to recount the full history of devel-
opmental psychopathology (others have done so in greater detail than
limited space permits [10,11]), some historical context is necessary for
t DE025980 from the National
lth Science of Behavior Change
The Ohio State University, 1835
ica.
e).
.
any discussion of how the field aligns with and complements modern
child, adolescent, and adult psychiatry.
2. The emergence of a new discipline
For those who were trained in the current interdisciplinary era, it
may be difficult to appreciate structural forces that fostered the emer-
gence of developmental psychopathology. In 1974—the same year
Achenbach published his foundational text—Robert Spitzer was
appointed to the DSM taskforce to update the DSM-II. Psychiatry was
grappling with diagnostic validity concerns, and a major shift in philos-
ophywas underway [12,13]. This shift, instantiated in publication of the
Feigner Criteria [14,15], gravitated psychiatry away from rationally de-
rived diagnosis toward an etiopathophysiological approach that was
more consistent with modern medicine. At the time, child and adoles-
cent disorders in the DSM-II were few in number, adevelopmental,
and derived inductively rather than from empirical relations among
and across syndromes [12,16]. Although this state of affairs has im-
proved markedly since, at the time psychiatry was constrained by a di-
agnostic system that had yet to undergo significant revisions.
In contrast to the adevelopmental, inductive approach of theDSM-II,
from its inception developmental psychopathology was empirically
driven, deductive, and transactional [17]. Several years prior to
http://crossmark.crossref.org/dialog/?doi=10.1016/j.comppsych.2018.10.014&domain=pdf
https://doi.org/10.1016/j.comppsych.2018.10.014
https://doi.org/10.1016/j.comppsych.2018.10.014
http://www.sciencedirect.com/science/journal/0010440X
www.elsevier.com/locate/comppsych
144 T.P. Beauchaine et al. / Comprehensive Psychiatry 87 (2018) 143–152
publication of the DSM-III in 1980 [18], Achenbach and colleagues pub-
lished a series of papers in which they described a factor-analytic ap-
proach to assessing psychopathology in children and adolescents
[19,20]. This effort culminated in development of the Child Behavior
Checklist [21], which remains among themost widely used instruments
for assessing child and adolescent psychopathology [22]. Although the
CBCL is a complement to rather than a substitute for structured diagnos-
tic interviews, its age-based, sex-based, and population-based norms
provided ameans of evaluating emergence andmaintenance of psycho-
pathology across intervals spanning toddlerhood to late adolescence, at
a time when very little developmental research existed [23]. An enor-
mous volume of research conducted since shows that population distri-
butions of characterizing traits underlying major child, adolescent, and
adult psychiatric disorders—as ascertained by the CBCL and related
measures—are unequivocally continuous in nature. Boundaries be-
tween normal function and clinical impairment are therefore not carved
in nature and instead are set rationally, consistent with the notion that
most or all psychiatric disease states reflect severe manifestations of
quantitative traits. Furthermore, longitudinal research conducted since
the CBCL was developed shows that (1) almost all psychiatric disorders
have roots in childhood behavioral function, and (2) environmental en-
richment often mollifies vulnerability, whereas environmental adver-
sity often magnifies vulnerability. These observations have direct
implications for prevention and reducing disease burden.
3. Developmental psychopathology and psychiatry: selected tenets
and unifying themes
The need to consider development in the ontogenesis of mental dis-
orders is of course a defining feature of developmental psychopathology
[10,11]. However, early on, other principles also set the field apart from
related disciplines. Several of these principles, although elegant theoret-
ically, were difficult to verify or apply without soon-to-evolve advances
in computing power, statistical modeling, psychiatric genetics, and
neuroimaging. In addition, most samples in both developmental and
psychiatric research were too small to map complexities and heteroge-
neities of human behavior—an issue now addressed by collaborative re-
search consortia and publicly shared databases. As envisioned by Dante
Cicchetti over 30 years ago [24], these advances in technology and
methodology have melded disciplines with common scientific interests
but different philosophical traditions into today’s interdisciplinary ap-
proach. Indeed, one can browse the table of contents of virtually any de-
velopmental psychopathology or psychiatry journal and find common
research questions addressing genetic, epigenetic, neural, neurohor-
monal, and environmental contributors to mental illness. Many of
these papers are written by authors who cross disciplinary boundaries.
In sections to follow we review selected tenets of developmental
psychopathology, some of which were novel when proposed, but are
now infused in contemporary interdisciplinary thinking. Our intent is
to outline how these principles contribute to current understanding of
mental illness, and how theymight be applied to improve future under-
standing of psychopathology—regardless of discipline.We focus on four
interrelated principles, all of which acknowledge and embrace etiologi-
cal complexity, an important theme in modern child, adolescent, and
adult psychiatry [25,26]. These principles include calls for (1)multidisci-
plinary translational research [27,28], (2) specification of multicausal
pathways to seemingly singlediagnostic syndromes [26,29], (3)descrip-
tion of divergentmultifinal outcomes from common etiological starting
points [29,30], and (4) research conducted acrossmultiple levels of anal-
ysis spanning genes to environments [31,32]. After discussing these
principles, we turn our attention to the importance of disrupted
neuromaturational processes in developing psychopathology. We pro-
pose that the relative value placed on neurodevelopment still differen-
tiates developmental psychopathology from contemporary psychiatry,
but this gap is narrowing quickly [33,34]. Although our descriptions
are necessarily brief and illustrated by way of selected examples, ex-
tended discussions can be found in sources cited herein.
3.1. Multidisciplinary, interdisciplinary, and transdisciplinary science
In the history of psychopathology research, multi-, inter-, and trans-
disciplinary approaches are fairly recent developments that are some-
times attributed to emergence of the Research Domain Criteria (RDoC)
[28,35]. With its explicit matrix of behavioral and emotional constructs
specified across units of analysis spanning genes to self-reports, RDoC
represents an unambiguous paradigm shift away from historical em-
phases on pathognomonic signs, universal causes, and single levels of
analysis in efforts to explain mental illness [31]. As noted elsewhere,
however, RDoC thinking extends at least as far back as the mid-20th
Century [36], with proponents in psychiatry, psychology, and related
disciplines [37–39]. Yet it was not until Thomas Insel, Bruce Cuthbert,
and others at the National Institute of Mental Health initiated RDoC
that multidisciplinary and interdisciplinary science were formally rec-
ognized as essential tomapping pathophysiologies of major mental dis-
orders [40].
Notably, multidisciplinarity has always been a central tenet of the
developmental psychopathology perspective [41]. A primary objective
of editor Dante Cicchetti in establishing the journal Development and
Psychopathology in 1989 was to encourage authors from a wide range
of disciplines and theoretical viewpoints to contribute, with the explicit
goal of synergizing scientific advances across child, adolescent, and
adult psychiatry; child, adolescent, and adult clinical psychology, neuro-
science, developmental psychology, and both behavioral and molecular
genetics. In the past 30 years, Development and Psychopathology has
published over 60 special issues in which experts from diverse fields
and perspectives were invited to contribute. Cicchetti also edited all
three editions of thehighly influential interdisciplinary volumeDevelop-
mental Psychopathology [6,42,43], which also attracted authors with di-
verse training and shaped the emergingmultidisciplinary field. By 2006,
these efforts yielded a science that, compared with other disciplines,
was “more developmental, contextual, multilevel, dynamic, multidisci-
plinary, and collaborative” (p. 50) [44]. Developmental psychopathol-
ogy also placed high value on translational animal research, from
which epigenetic mechanisms of neural plasticity, neurohormone regu-
lation, and other vulnerabilities to mental illness were initially discov-
ered [45,46].
More recently, cross-disciplinary collaboration has progressed at a
remarkable pace, extending well beyondwhat was envisioned a gener-
ation ago. Distinctions between unidisciplinary,multidisciplinary, inter-
disciplinary, and transdisciplinary science are depicted in Fig. 1 [35].
Over the past several decades—and particularly since the turn of the
last century—disciplinary boundaries have become increasingly diffuse
as psychiatry leverages scientific discoveries across related fields. As
just three examples, (1) modern neuroimaging cannot be conducted
without advanced scanning sequences and new imagingmodalities de-
vised by physicists, (2) modern psychiatric genetics cannot be con-
ducted without experts in both molecular genetics and Bayesian
statistics, and (3) neurogenetics, which specifies neural functions that
mediate relations between multifactorial genetic burden and behavior,
cannot be conducted without expertise in all these domains [47].
Given such developments and other important technological advances,
the value of transdisciplinary research is likely evident to readers, sowe
turn our attention to other principles.
3.2. Multicausal pathways to common behavioral syndromes
In a 1996 editorial for a special issue of Development and Psychopa-
thology, Cicchetti and Fred Rogosch noted how equifinality—a term
used in developmental psychopathology research to describe multiple
causal pathways to apparently single behavioral syndromes—has al-
ways been a hallmark of the discipline [48]. In that special issue,
Fig. 1. Progression from unidisciplinary to multidisciplinary to interdisciplinary to transdisciplinary science. At each step, disciplines become more integrated and interdependent.
Psychiatry and developmental psychopathology have entered a transdisciplinary era [35,41].
145T.P. Beauchaine et al. / Comprehensive Psychiatry 87 (2018) 143–152
equifinal pathways to antisocial behavior, depression, disruptive behav-
ior disorders, schizophrenia, and other mental health outcomes were
considered. As a concept, equifinality originated in biology to describe
how open living systems can and often do reach similar developmental
endpoints through diverse and complex causal processes—including
stochastic effects—across functional levels of analysis [49,50]. Inmodern
psychiatric genetics, multifinal outcomes are often referred to as
phenocopies. At the time, however, equifinality was not an influential
concept in mainstream psychiatry. Instead, searches for distinct causes
of mental disorders and associated pathognomonic signs predominated
given how useful the approach had been in modern medicine
[31,36,37].
Although there was always recognition in psychiatry of heterogene-
ity within diagnostic classes, equifinality and associated developmental
processes were typically not invoked as causal explanations. One likely
reason is that without yet-to-emerge technological advances discussed
above, specific mechanisms of equifinality could not be observed di-
rectly. In child and adolescent psychiatry, this state of affairs began to
change in the early 1990s, when both theDSM-IV field trials and a land-
mark paper by TerrieMoffitt suggested two developmental pathways to
conduct disorder [51–53]. Moffitt proposed that those who initiate de-
linquency in early childhood suffer from heritable neuropsychological
vulnerabilities that persist across the lifespan, whereas those who initi-
ate delinquency in adolescence suffer from no such impairment.
146 T.P. Beauchaine et al. / Comprehensive Psychiatry 87 (2018) 143–152
Neuropsychological testing largely upholds this distinction, demon-
strating at least two equifinal pathways to conduct disorder [54]. The
resulting DSM-IV subtyping of life-course persistent vs. adolescent-onset
conduct disorder embeds equifinality in the modern psychiatric no-
menclature. These subtypes are carried forward to the DSM-5 [55].
At present, nowhere is the principle of equifinality more evident
than in psychiatric genetics. In merely 15 years since the human ge-
nome was sequenced [56], molecular geneticists have migrated away
from conducting candidate gene studies with dozens to hundreds of
participants toward large-scale genome-wide association studies
(GWAS) that include tens of thousands of people [57]. As power of
GWAS increases and methods such as genomewide complex trait anal-
ysis (GCTA) and approximate Bayesian polygenic analysis (ABPA) be-
come mainstream, it is increasingly clear that hundreds and even
thousands of genes affect complex behavioral traits, and that few if
any particular genes are necessary or sufficient for psychiatric impair-
ment [26,31]. Furthermore, epigenome-wide association studies
(eGWAS) are providing insights into environmentally mediated gene
regulation [58], and central roles for both de novomutations and herita-
ble copy number variants (CNVs) in the pathogeneses of psychiatric dis-
orders have become clear [59]. Thus, in little more than a decade,
oligogenic and polygenic theories have been largely abandoned in
favor of complex, multifactorial models that include heritable, epige-
netic, and stochastic effects [31,60]. Although the importance of
genomewide significant single nucleotide polymorphisms (SNPs) in
pathophysiologies of psychopathology should not be understated,
they individually account for limited proportions of liability [61,62].
Importantly, even though psychiatric disorders may be more com-
plex genetically than many other medical conditions, any such distinc-
tion is a matter of degree. Fig. 2 depicts ABPA relations between
numbers of syndrome-relevant GWAS SNPs and proportions of pheno-
typic variation explained for several complex diseases [62]. Over 8300
SNPs—almost all of very small effect size (i.e., well below genomewide
significant)—are required to explain 50% of population-based pheno-
typic variation in schizophrenia liability. By comparison, 1000 or more
SNPs are required to explain similar levels of phenotypic variation in
Fig. 2. Relations between numbers of syndrome-relevant GWAS single nucleotide
polymorphisms (SNPs) and proportions of phenotypic variation explained for
schizophrenia (SCZ), celiac disease, myocardial infarction (MI), rheumatoid arthritis
(RA), and type II diabetes (T2D). Shaded regions represent posterior probability
densities, derived from approximate Bayesian polygenic analysis (ABPA). Collectively,
8332 SNPs explain 50% of population based phenotypic variation in schizophrenia
liability. Reproduced with permission from “Genome-wide association analysis identifies
13 new risk loci for schizophrenia”, by S. Ripke et al. [62], Nature Genetics, 45: 1150–9.
myocardial infarction and type II diabetes [63]. Thus, genetic vulnerabil-
ities to schizophrenia and other psychiatric and medical disorders may
be orders-of-magnitude more multicausal than envisioned only a de-
cade ago [26]. Furthermore, polygenic risk score analyses indicate con-
siderable overlap in genetic vulnerability to major psychiatric
disorders [64,65]. Although validity of ABPA and related methods is
still being evaluated, complex multifactorial genetic vulnerability is in-
disputable. It is important to note, however, that etiological complexity
is not confined to molecular genetics. In remaining sections we discuss
additional levels of analysis thatmediate and interactwith genetic influ-
ences to eventuate in psychopathology [66].
3.3. Multifinal outcomes from common etiological start points
As a construct, multifinality can be defined in at least two ways. A
common yet perhaps overly general definition refers to different long-
term functional outcomes (e.g., well-adjusted, psychopathological)
given similar rearing contexts (e.g., maltreatment, poverty). By this def-
inition, a wide range of moderating and contextual variables, including
genetic burden, temperament, and trauma exposure might explain di-
verse outcomes. In this article, we use a more restrictive definition of
multifinality—different long-term functional outcomes given equiva-
lent, pre-existing vulnerabilities (e.g., genetic, neural). Of particular in-
terest are mechanisms through which the same neurobiological
vulnerabilities eventuate psychopathology only for those who are ex-
posed to impinging environments (i.e., Gene × Environment interac-
tion) [32,66]. This form of multifinality overlaps with the concept of
pathoplasticity in psychiatry. Notably, although multifinality is a
founding principle of developmental psychopathology [1,29], psychia-
try has been more cautious toward adopting the construct, perhaps be-
cause pathoplastic outcomes can only be inferred when common
etiological start points are assumed—a highly implausible supposition
in most psychiatric research given the complexity of genetic and other
vulnerabilities to psychopathology.
Appropriate caution notwithstanding, four important developments
bolster arguments formultifinality. First, elegant animalmodels, includ-
ing those articulated by Michael Meaney and colleagues and extended
by others, reveal stress-induced, epigenetically-mediated changes in
neural structure and function in brain regions implicated in motivation,
mood regulation, and social affiliation [45,46]. Many of these changes
confer long-lasting behavioral adaptations, including impairments that
persist into rodent homologues of adolescence and adulthood [67].
Such findings provide unambiguous evidence of pathoplasticity given
genetically identical rodent strains and tight experimental control
over environments.
Second, in a landmark study with humans, Mario Fraga and col-
leagues reported diverging DNA methylation patterns across the
lifespan for monozygotic twin pairs [68]. Whereas twin toddlers
showed almost no epigenetic differences, middle-age twins showed
highly distinguishable epigenome profiles of 5-methylcytosine and his-
tone acetylation. These findings complemented extensive animal re-
search by demonstrating environmentally moderated gene expression
in humans, and initiated the current explosion of studies on the epige-
nome and psychopathology. In fact, psychiatry has witnessed profound
advances in and proliferation of psychiatric epigenetics in only 13 years
since the Fraga et al. paper.
Third, molecular genetic studies of rare neuropsychiatric conditions
have long established the phenomenon of pleiotropy, whereby a rare
variant known to exert deleterious causal influences does so to varying
degrees of severity across individual carriers. Such variation may
emerge from interacting environmental influences (see below) and/or
interactionswith variable elements of family genetic background, as ob-
served in 22q11.2 and 16p11.2 deletion syndromes [69,70]. The concept
of pleiotropy also applies to heritable behavioral expressions ofmultiple
dimensions of psychopathology, including liability to internalizing dis-
orders, externalizing disorders, and psychotic disorders [71,72].
147T.P. Beauchaine et al. / Comprehensive Psychiatry 87 (2018) 143–152
Fourth, behavioral genetics research indicates strongnon-shared en-
vironmental effects on mental health outcomes. Large twin studies
show that common molecular genetic risk is often shaped by non-
shared environmental influences into alternative expressions of psy-
chopathology (e.g., major depression, generalized anxiety) [71]. These
studies are critically important because they include monozygotic
twins reared together vs. reared apart, and therefore demonstrate im-
pinging effects of unique environmental experience for thosewith iden-
tical DNA sequences and identical epigenetic profiles at birth. Notably,
magnitudes of effects of shared (common) environmental influences
are relatively low for most though not all psychiatric syndromes in
childhood, suggesting that (1) social and rearing influences within typ-
ical ranges of variation in the population (to the extent that such varia-
tion is represented in a given study andwhen considered independently
of other domains of causation) are not as influential on psychopathology
as genetic and non-shared environmental factors; (2) their effects may
nevertheless be pronounced when interacting with genetic or non-
shared environmental factors (rather than being analyzed as isolated
main effects; see below); and (3) may exhibit non-linear associations
with psychopathology [73]. Thus, whereas common environmental influ-
ences across typical ranges of variation exert modest effects, severe dis-
ruptions of environment—as in deprivation and maltreatment—exert
profound deleterious effects, even when controlling for genetic variation.
Children with genetic liability who incur severe environmental risk are
therefore more vulnerable to psychopathology than children without ge-
netic lability who incur the same environmental risk [74].
Finally, in the 1990s Sandra Scarr proposed a reconciliation of ge-
netic and environmental hypotheses regarding individual variation in
behavior by advancing the notion that in given environmental contexts,
genetic variation guides reconstruction of experience to optimize what
children assimilate from that experience to meet their individual devel-
opmental needs [75]. Recently, an example of this phenomenonwas ob-
served serendipitously in research on early autism endophenotypes:
Variation in normal infants’ visual engagement of dynamic social scenes
ascertained by eye tracking exhibits wide variation in the population, is
under stringent genetic control (on a time scale of tens of milliseconds),
and comprises an enduring trait-like feature in which eye gaze patterns
specify highly-individualized approaches to assimilating information
from the social environment [76].
Taken together, evidence from animal, behavioral genetic, epigenetic,
and molecular genetic research converge on a conclusion of multifinal
Gene × Environment causation of psychopathology [32,61,66]. This pro-
vides an ideal segue into our next section.
3.4. Multiple levels of analysis spanning genes to environments
Given the clear migration toward interdisciplinary and transdisci-
plinary research noted above and depicted in Fig. 1, it may seem unnec-
essary to promote science that transcends levels of analysis spanning
genes to environments. Historically, however, developmental psycho-
pathologists, psychiatrists, and other behavioral scientists have tended
to focus on 1 or 2 variables (e.g., symptoms, candidate genes)—and by
extension 1 or 2 levels of analysis—in their research. This approach is ex-
emplified in both main effects and two-way interaction models of psy-
chopathology, the latter of which originated in mid-20th Century
diathesis-stress theories of schizophrenia [77]. Although groundbreak-
ing at the time, these theories assumed either monogenic or oligogenic
inheritance of liability to a discretely distributed disorder [78]. Such
models are straightforward and therefore easy to test and interpret,
but they cannot capture the etiological complexity of psychopathology
discussed herein [25,26,31]. In fact, they can obscure associations be-
tween predictors and outcomes when diagnostic cut points are speci-
fied incorrectly or arbitrarily [79]. Nevertheless, main effects and
simple interaction models predominated across disciplines until re-
cently [24] and are still well represented in published research.
There are several likely reasons for lingering influence of research that
assesses main effects and simple interactions. These include intuitive ap-
peal of causal models that are easy to communicate, test, and interpret
[80]; limited statistical power to test higher-order interactions in small
samples [81]; expertise required to implement methods that parse vari-
ance across nested levels of analysis [82]; highly specialized training in
single disciplines [83]; difficulties measuring environments with preci-
sion in large scale genetics studies [84]; pressure to disaggregate interre-
lated findings intomultiple publications [85]; and the human tendency to
overvalue one’s preferred methods and research questions and under-
value research from outside one’s area of expertise [86].
These considerations notwithstanding, more basic models of mental
illness are clearly givingway to complex characterizations that subsume
established findings into rapidly evolving discoveries across levels of
analysis [26]. In our own work, for example, we have advanced a
neurodevelopmental model of externalizing behavior in which genetic
burden, epigenetic regulation of neural function, neurohormonal influ-
ences, and impinging exogenous risk exposures (e.g., in utero stress ex-
posure, hypoxic events) combine/interact in complex ways to disrupt
both resting striatal activity and striatal reactivity while anticipating ap-
petitive stimuli [87,88]. Such neural response patterns characterize a
wide range of impulse control disorders, including ADHD, conduct dis-
order, intentional self-injury, and both active and remitted addiction
[89–91]. A multiple levels of analysis depiction of this model appears
in Fig. 3. Although space constraints preclude full elaboration, several
points are worth noting.
First, the temporal sequence of externalizing progression depicted at
the bottom of Fig. 3 has been described for over 50 years by scientists
across disciplines including sociology [92], psychology [52], psychiatry
[93], and criminology [94]. Notably, however, only a subset of children
who exhibit ADHD early in life progress to more severe externalizing
behavior across development. Thus, although ADHD is a serious mental
health concern that confers lifelong impairment in educational, occupa-
tional, and other functional outcomes [95], it need not eventuate in
antisociality. Traditionally, psychiatry has interpreted multifinal out-
comes of ADHD as evidence for discrete disorders, but an alternative
view is one of common liability, with differences in symptom expres-
sion emerging at various levels of disease progression, in interaction
with exogenous risk and protective factors [96,97]. Thus, similar to
medical conditions such as type II diabetes, (1) early vulnerabilities
present very differently than end-state structural and functional out-
comes, (2) disease progression is potentiated by environmental risk,
and (3) disease progression may be halted in protective environments.
Such an interpretation is supported by findings of common behavioral
genetic, molecular genetic, and neural vulnerabilities across externaliz-
ing disorders [96,98], with broadening neural dysfunction later in onto-
genesis, as discussed below [99].
Specific environmental riskmediators of externalizing progression are
well characterized. Impulsive children, including those with ADHD, are
more vulnerable to externalizing progression when they are exposed to
authoritarian parenting and maltreatment [100], when they are reared
in low SES neighborhoods with high rates of violence and criminality
[101], and when substances of abuse are readily available [102], among
other risk factors. Such findings underscore the need to avoid biological
reductionism in modeling and treating psychopathology [80]. Indeed,
psychopharmacologic treatment of ADHD symptoms in childhood often
does not spare affected individuals from downstream adverse outcomes
of these protracted biological vulnerability × environmental risk interac-
tions [103], even though sustained treatment in adulthood reduces crim-
inal activity [104]. Taken together, these findings and others suggest that
as with physical diseases, biological vulnerabilities and environmental
risk factors interact complexly across time to yield observed psychopath-
ological endpoints [10,26,87,105].
Fig. 3 also emphasizes a fundamental role of emotion in externaliz-
ing behavior. Neither genetic influences nor neural functions exert di-
rect effects on behavior. Rather, they confer behavioral biases through
Fig. 3. Etiological complexity ofwell characterized externalizing progression formany affectedmales. Low tonic striatal activity and blunted striatal reactivity while anticipating incentives
arise from accrual of and complex interactions among genetic influences (heritable SNPs and CNVs, de novo mutations, epigenetic effects), impinging exogenous risk exposures (TBI,
hypoxia), and neurohormone regulation. Any single research study can address very few of these influences. For simplicity of presentation, other neural systems that modulate striatal
function are omitted [31]. Striatal dysfunction imbues an irritable, anhedonic mood state, which in turn elicits a temperamental/behavioral bias toward reward seeking to upregulate
aversive mood. Genetic, neural, and temperamental vulnerabilities are expressed syndromally as ADHD, which predisposes to externalizing progression specifically in high risk
environments [87].
148 T.P. Beauchaine et al. / Comprehensive Psychiatry 87 (2018) 143–152
their indirect effects on temperamental, emotional, and psychological
states. Many forms of psychopathology—including externalizing disor-
ders—are characterized by emotional and psychological responses that
are either too intense or too enduring to be adaptive [106]. Contempo-
rarymodels of externalizing behavior specify a central role of anhedonia
and irritability—affective byproducts of striatal under-responding—in
motivating impulsive, reward-seeking, and substance-abusing behav-
iors [87,107,108].
4. Neurodevelopment and psychopathology
Thus far in this editorial we have considered themes that unify, dove-
tail, and bridge the research agendas of psychiatry and developmental
psychopathology. All of these themes are well represented in contempo-
rary interdisciplinary research. By comparison, neurodevelopmental the-
ory—which is central to the developmental psychopathology perspective
—fits less neatly into this mold. Despite longstanding exceptions in the
psychiatry literature [109], particularly in research on autism and schizo-
phrenia [26,110,111], broad application of neurodevelopmental theory in
psychiatric research is a more recent development [32–34]. This may be
an instance of psychiatry waiting for advanced technology—in this case
neuroimaging and genetics—to verify otherwise difficult-to-test
neuromaturational models [112].
Literature on the neurodevelopment of psychopathology is complex
and therefore cannot be reviewed herein. Instead,we focus on three im-
portant considerations, including (1) differential neuromaturation of
subcortical vs. cortical structures, (2) increasing contributions of
cortically-mediated executive function, self-regulation, and emotion
regulation deficits to psychopathology across adolescence and young
adulthood, and (3) effects of endogenous insults including substance
use and correlates of poverty on cortical development.
Neuroscientists have known formanyyears that neuromaturation of
frontal brain regions including the orbitofrontal cortex, the anterior cin-
gulate cortex, and the dorsolateral, ventrolateral, and ventromedial pre-
frontal cortices (PFCs) lags behind neuromaturation of deep, subcortical
brain regions [113,114]. PFC neuromaturation is of course critical for ex-
ecutive function, including self-regulation of behavior and affect [115].
Among other mechanisms, such regulation occurs through top-down-
149T.P. Beauchaine et al. / Comprehensive Psychiatry 87 (2018) 143–152
inhibition of subcortically-generated impulses and emotions [116,117].
Notably, typically developing children and adolescents show stronger
subcortical responses but weaker and more diffuse PFC responses to
emotion-eliciting events than adults [118]. According to contemporary
neurodevelopmental theory, age-related increases in self-regulation
occur in part through improved connectivity and improved top-down
inhibition of subcortical structures by functional subdivisions of the
PFC [33,106,112]. Although specific neural networks differ, both
neuromaturation of the PFC and efficiency of subcortical-cortical con-
nectivity become increasingly compromised across development in in-
ternalizing and externalizing disorders [119]. Given space constraints,
we focus here on externalizing disorders, building on our discussion
from previous sections.
Volumetric prefrontal neuromaturation among children and adoles-
cents with ADHD lags about two years behind that of typically develop-
ing controls [120], and adolescent males who develop severe conduct
disorder fail to exhibit normative gray matter pruning in the
orbitofrontal cortex and anterior cingulate cortex (ACC) from ages 10
to 14 years [121]. Furthermore, volumetric deficiencies in the ACC are
accompanied by disrupted connectivity with subcortical structures im-
plicated in reward processing [122,123]. Although a more thorough
summary of this literature is not possible here, several recent reviews
suggest that conduct disorder is associated with structural and func-
tional deficiencies that both subsume and extend beyond those ob-
served in ADHD [87,117].
Taken together, such findings suggest that externalizing progression
may be in part attributable to persistent underdevelopment of prefron-
tal regions implicated in self-regulation and executive function
[120,121,124]. Thus, as depicted in Fig. 4, multifactorially derived
striatal (subcortical) vulnerabilities that predispose to impulsivity and
ADHD are amplified across development if coupled with deficient PFC
Fig. 4. A neurodevelopmental model of externalizing progression for many affected males
vulnerability (top panel, left). Progression to more severe externalizing conduct occurs in con
regulation deficits (top panel, right). Environmental risk factors potentiate this progression
dysfunction to overall impairment across development.
neuromaturation. According to this perspective, disrupted PFC develop-
ment potentiates vulnerability to externalizing progression by
compromising volitional control over subcortically generated affect
and impulses [87,105].
From a developmental psychopathology perspective, a crucial point
concerns effects of environment on neural structure and function across
development. Research conducted in the past decade shows strong ef-
fects of adversity in childhood and adolescence on neurodevelopment
—not only in prefrontal regions implicated in executive function and
self-regulation, but also in subcortical structures implicated in impulsiv-
ity. For example, children reared in poverty show reduced volumes in a
wide range of cortical and subcortical brain regions comparedwith their
peers, effects that are larger the poorer children’s families are [125,126].
Furthermore, family stress and adversity measured in childhood are as-
sociated in dose-response fashion with reduced functional neural
responding to incentives in adulthood in both cortical subcortical re-
gions [127].
Compelling neurodevelopmental research on substance use and ad-
diction is also emerging. Consistent with animal models articulated
many years ago, longitudinal work now demonstrates that (1) low
striatal responding to incentives predicts vulnerability tomarijuana, co-
caine, and methamphetamine abuse and addiction three years later
[128]; and (2) heavy drinking in adolescence induces faster graymatter
loss and slower white matter growth than expected compared with
both moderate drinking and abstinence [129]. In turn, early adolescent
alcohol and drug use compromise neural connectivity and development
of executive function into adulthood,with likely implications for further
progression of externalizing behavior [130,131]. Taken together, these
findings suggest that frontal brain regions that subserve executive func-
tions, self-regulation, and emotion regulation are exquisitely sensitive
to environmental insults, with almost certain implications for
. Early in life, impulsivity (ADHD) derives largely from subcortically-mediated neural
junction with deficient in cortical neuromaturation, which gives rise to self- and emotion
(see text). The bottom panel shows relative contributions of subcortical and cortical
150 T.P. Beauchaine et al. / Comprehensive Psychiatry 87 (2018) 143–152
worsening externalizing behavior across development for already vul-
nerable individuals who are reared in contexts of cumulative risk. Al-
though we restrict discussion here to externalizing outcomes, similar
neurodevelopmental perspectives have been articulated for depression,
anxiety, and obsessive-compulsive disorder [117,119].
5. Summary and conclusions
Tremendous strides have been made in specifying etiologies of psy-
chopathology using developmentally informed approaches, some of
which were articulated initially in developmental psychopathology
but now cut across disciplines. This is especially noteworthy given the
relative youth of developmental psychopathology. In this closing sec-
tion, we offer some broad recommendations that might help guide fu-
ture work, with recognition that subdisciplines have field-specific
concerns.
Advances in our scientific understanding of mental illness will al-
most certainly require developmentalmacrotheories that integrate find-
ings across disciplines and levels of analysis [26,32,87]. In some cases,
such theories may be necessary to advance prevention and treatment
efforts. For example, only with an integrated understanding of (1) pre-
disposing temperamental and emotional vulnerabilities to delinquency,
(2) the well-characterized developmental pathway of externalizing
psychopathology depicted in Fig. 3, and (3) relevant environmental
risk mediators, were implementers of the NIMH Fast Track project
able to reduce—as assessed via random assignment—substance use, vio-
lent crime convictions, drug convictions, and high-risk sexual behaviors
among young adults who were enrolled in a targeted prevention pro-
gram in elementary and middle school [132]. The theory of externaliz-
ing behavior described above represents but one among several
examples of developmental macrotheories [26,133].
Thesemacrotheories cannot be developed at single levels of analysis.
In fact, no single level of analysis accounts for all or evenmost of the var-
iance in any functional outcome. Additionally, given the complexity of
psychopathology and the extensive expertise and resources required
to conduct research across levels of analysis, few individual research
laboratories can address even a fraction of relevant influences. Thus,
progression of interdisciplinary and transdisciplinary science is a wel-
come and necessary development [35]. In fact, lingering arguments
over which level of analysis (e.g., genetic, neural, environmental) de-
serves primacy in causal models of most mental disorders are anachro-
nistic given complex, interactive determinants of human behavior
[25,26,32,105].
Having said that, the transdisciplinary science that is so essential to
modern psychiatry and developmental psychopathology will almost
certainly benefit from more careful attention to issues of multimodal
measurement across development. For example, studies of effects of
stress on psychopathology can and likely should measure predictors
and outcomes across levels of analysis including genetic vulnerability,
immune responding and gene expression, neural responding, auto-
nomic responding, subjective accounts of stress responding, and objec-
tive interview measures of life events to minimize recall bias. In fact,
multimodal assessment was emphasized recently by the National Advi-
soryMentalHealth CouncilWorkgroup on Tasks andMeasures for RDoC
[134], who called for more standardized, precise, and developmentally
sensitive assessment methods.
Developmentally sensitive, multimodal assessment yields rich
datasets and opportunities to map the etiology of psychopathology, yet
deliberate planning is required to ensure adequate diagnostic and mea-
surement precision [135]. As noted by the Council Workgroup [134], lab-
oratory measurement paradigms sometimes become standard without
being subjected to adequate validation. At other times, well-validated
paradigms are avoided in favor of novel tasks of unknown validity
[136]. To complicatematters further, tasks, questionnaires, and diagnostic
assessmentmeasures that are valid at one agemaynot be valid at another
age, yet measurement invariance across development is rarely tested
[137]. In such cases, claims about group differences in behavior change
across time are difficult if not impossible to interpret [138].
All of these issues limit the extent to which existing datasets can be
compared and combined, yet interdisciplinary science requires effective
collaboration, shared data, and common data collectionmethods. As de-
scribed in the Council Workgroup report and elsewhere [134,139,140],
although strides have been made toward construction and validation
of common assessment methods, additional work is needed using de-
velopmentally informed designs. Furthermore, at least some measures
that are considered standard in thefield require further validation [141].
In closing, transdisciplinary research, including the growing partner-
ship between psychiatry and developmental psychopathology, is a wel-
come development that has already enriched our understanding of
emerging mental illness. We anticipate continued growth in years to
come as new technologies increase our ability to specify
etiopathophysiologies and elucidate the daunting complexity of psychi-
atric disorders across all relevant levels of analysis. As problems with
measurement invariance and precision are addressed, we look forward
to continued discoveries that improve our capacity to prevent and treat
psychiatric disorders.
Acknowledgements
We thankDante Cicchetti for his helpful comments on an earlier ver-
sion of this article.
References
[1] Achenbach TM. Developmental psychopathology. New York: Ronald Press; 1974.
[2] Cicchetti D., ed. Development and psychopathology. New York: Cambridge Univer-
sity Press. https://www.cambridge.org/core/journals/development-and-
psychopathology
[3] Beauchaine TP, Goodman SH, editors. Ontogenic process models of psychopathol-
ogy [special section], 124. J Abnorn Psychology; 2015.
[4] Tackett JL, Sharp C, editors. A developmental psychopathology perspective on per-
sonality disorder [special issue], 28. J Pers Disord; 2014.
[5] Sonuga-Barke E, editor. Annual research review: reimagining the environment in
developmental psychopathology: from molecules to effective treatments [special
issue], 59. J Child Psychl Psyc; 2018.
[6] Cicchetti D, editor. Developmental psychopathology. 3rd ed. Hoboken, NJ: Wiley;
2016.
[7] Beauchaine TP, Hinshaw SP, editors. Child and adolescent psychopathology. 3rd ed.
Hoboken, NJ: Wiley; 2017. p. 33–67.
[8] Sroufe LA, Rutter M. The domain of developmental psychopathology. Child Dev
1984;55:17–29.
[9] Rutter M, Sroufe LA. Developmental psychopathology: concepts and challenges.
Dev Psychopathol 2000;12:265–96.
[10] Cicchetti D. A historical perspective on the discipline of developmental psychopa-
thology. In: Rolf J, Masten A, Cicchetti D, Nuechterlein K, Weintraub S, editors.
Risk and protective factors in the development of psychopathology. New York,
NY: Cambridge University Press; 1990. p. 2–28.
[11] Hinshaw SP. Developmental psychopathology as a scientific discipline: a 21st cen-
tury perspective. In: Beauchaine TP, Hinshaw SP, editors. Child and adolescent psy-
chopathology. 3rd ed. Hoboken, NJ: Wiley; 2017. p. 3–32.
[12] Beauchaine TP, Klein DN. Classifying psychopathology: the DSM, empirically-based
taxonomies, and the research domain criteria. In: Beauchaine TP, Hinshaw SP, ed-
itors. Child and adolescent psychopathology. 3rd ed. Hoboken, NJ: Wiley; 2017.
p. 33–67.
[13] Demazeux S. Psychiatric epidemiology, or the story of a divided discipline. Int J
Epidemiol 2014;43:i53–66.
[14] Feighner JP, Robins E, Guze SB, Woodruff RA, Winokur G, Munoz R. Diagnostic
criteria for use in psychiatric research. Arch Gen Psychiat 1972;26:57–63.
[15] Robins E, Guze SB. Establishment of diagnostic validity in psychiatric illness: its ap-
plication to schizophrenia. Am J Psychiatry 1970;126:983–7.
[16] American Psychiatric Association. Diagnostic and statistical manual of mental dis-
orders. 2nd ed. Washington, DC: Author; 1968.
[17] Cicchetti D. Developmental psychopathology: reactions, reflections, projections.
Dev Rev 1993;13:471–502.
[18] American Psychiatric Association. Diagnostic and statistical manual of mental dis-
orders. 3rd ed. Washington, DC: Author; 1980.
[19] Achenbach TM. The classification of children’s psychiatric symptoms: a factor-
analytic study. Psychol Monogr 1966;80:1–37.
[20] Achenbach TM, Edelbrock CS. The classification of child psychopathology: a review
and analysis of empirical efforts. Psych Bull 1978;85:1275–301.
[21] Achenbach TM, Edelbrock CS. Manual for the child behavior checklist and revised
child behavior profile. Burlington, VT: University of Vermont Department of Psy-
chiatry; 1983.
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0005
https://www.cambridge.org/core/journals/development-and-psychopathology
https://www.cambridge.org/core/journals/development-and-psychopathology
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0010
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0010
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0015
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0015
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0020
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0020
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0020
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0025
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0025
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0030
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0030
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0035
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0035
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0040
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0040
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0045
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0045
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0045
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0045
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0050
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0050
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0050
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0055
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0055
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0055
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0055
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0060
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0060
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0065
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0065
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0070
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0070
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0075
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0075
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0080
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0080
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0085
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0085
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0090
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0090
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0095
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0095
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0100
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0100
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0100
151T.P. Beauchaine et al. / Comprehensive Psychiatry 87 (2018) 143–152
[22] Achenbach TM. The Achenbach system of empirically based assessment (ASEBA):
development, findings, theory, and applications. Burlington, VT: University of Ver-
mont Research Center for Children, Youth, and Families; 2009.
[23] Edelbrock C, Achenbach TM. A typology of child behavior profile patterns: distribu-
tion and correlates for disturbed children aged 6–16. J Abnorm Child Psychol 1980;
8:441–70.
[24] Cicchetti D. The emergence of developmental psychopathology. Child Dev 1984;
55:1–7.
[25] Cohen BM. Embracing complexity in psychiatric diagnosis, treatment, and research.
JAMA Psychiat 2016;73:1211–2.
[26] Constantino JN. Deconstructing autism: from unitary syndrome to contributory de-
velopmental endophenotypes. Int Rev Psychiatr 2018;30:18–24.
[27] Gunnar R, Cicchetti D. Meeting the challenge of translational research in child de-
velopment: opportunities and roadblocks. In: Cicchetti D, Gunnar M, editors. Min-
nesota symposia on child psychology: meeting the challenge of translational
research in child psychology. Hoboken, NJ: Wiley; 2009. p. 1–27.
[28] Cuthbert BN, Insel TR. Toward the future of psychiatric diagnosis: the seven pillars
of RDoC. BMC Med 2013;11:126.
[29] Cicchetti D, Toth SL. The past achievements and future promises of developmental
psychopathology: The coming of age of a discipline. J Child Psychol Psychiatr 2009;
50:16–25.
[30] Beauchaine TP, Klein DN, Crowell SE, Derbidge C, Gatzke-Kopp L. Multifinality in
the development of personality disorders: a biology × sex × environment interac-
tion model of antisocial and borderline traits. Dev Psychopathol 2009;21:735–70.
[31] Beauchaine TP, Constantino JN. Redefining the endophenotype concept to accom-
modate transdiagnostic vulnerabilities and etiological complexity. Biomark Med
2017;11:769–80.
[32] Uher R, Zwicker A. Etiology in psychiatry: embracing the reality of poly-gene-
environmental causation of mental illness. World Psychiatry 2017;16:121–9.
[33] Casey BJ, Oliveri ME, Insel T. A neurodevelopmental perspective on the Research
Domain Criteria (RDoC) framework. Biol Psychiatry 2014;76:350–3.
[34] Bessette KL, Burkhouse KL, Langenecker SA. An interactive developmental neuro-
science perspective on adolescent resilience to familial depression. JAMA Psychiat
2018;75:503–4.
[35] Eyre HA, Lavretsky H, Forbes M, Raji C, Small G, McGorry P, et al. Convergence sci-
ence arrives: how does it relate to psychiatry? Acad Psychiatry 2017;41:91–9.
[36] Beauchaine TP, Thayer JF. Heart rate variability as a transdiagnostic biomarker of
psychopathology. Int J Psychophysiol 2015;98:338–50.
[37] van Praag HM. No functional psychopharmacology without functional psychopa-
thology. Acta Psychiatr Scand 2010;122:438–9.
[38] Beauchaine TP. Vagal tone, development, and Gray’s motivational theory: toward
an integratedmodel of autonomic nervous system functioning in psychopathology.
Dev Psychopathol 2001;13:183–214.
[39] Fowles DC. Psychophysiology and psychopathology: a motivational approach. Psy-
chophysiology 1988;25:373–91.
[40] Insel T, Cuthbert B, GarveyM, Heinssen R, KozakM, Pine DS, et al. Research Domain
Criteria (RDoC): toward a new classification framework for research onmental dis-
orders. Am J Psychiatry 2010;167:748–51.
[41] Cicchetti D. A multiple-levels-of-analysis perspective on research in development
and psychopathology. In: Beauchaine TP, Hinshaw SP, editors. Child and adolescent
psychopathology. Hoboken, NJ: Wiley; 2008. p. 27–57.
[42] Cicchetti D, Cohen DJ, editors. Developmental psychopathology. Hoboken, NJ:
Wiley; 1995.
[43] Cicchetti D, Cohen DJ, editors. Developmental psychopathology. 2nd ed. Hoboken,
NJ: Wiley; 2006.
[44] Masten AS. Developmental psychopathology: pathways to the future. Int J Behav
Dev 2006;30:47–54.
[45] Weaver ICG, Cervoni N, Champagne FA, D’Alessio AC, Sharma S, Seckl JR, et al. Epi-
genetic programming by maternal behavior. Nat Neurosci 2004;7:847–54.
[46] Beauchaine TP, Neuhaus E, Zalewski M, Crowell SE, Potapova N. Effects of allostatic
load on neural systems subserving motivation, mood regulation, and social affilia-
tion. Dev Psychopathol 2011;23:975–99.
[47] Bogdan R, Salmeron BJ, Carey CE, Agrawal A, Calhoun VD, Garavan H, et al. Imaging
genetics and genomics in psychiatry: a critical review of progress and potential.
Biol Psychiatry 2017;82:165–75.
[48] Cicchetti D, Rogosch FA. Equifinality and multifinality in developmental psychopa-
thology. Dev Psychopathol 1996;8:597–600.
[49] Mayr E. The evolution of living systems. P Natl A Sci 1964;51:934–41.
[50] Cicchetti D, editor. Regulatory processes [special issue]Dev Psychopathol; 1996. p. 8.
[51] American Psychiatric Association. Diagnostic and statistical manual of mental dis-
orders. 4th ed. Washington, DC: Author; 1994.
[52] Moffitt TE. Adolescence-limited and life-course-persistent antisocial behavior: a
developmental taxonomy. Psychol Rev 1993;100:674–701.
[53] Lahey BB, Loeber RF, Quay HC, Applegate B, Shaffer D, Waldman I, et al. Validity of
DSM-IV subtypes of conduct disorder based on age of onset. J Am Acad Child Psy-
chiatry 1998;37:435–42.
[54] Raine A, Moffitt TE, Caspi A, Loeber R, Stouthamer-Loeber M, Lynam D.
Neurocognitive impairments in boys on the life-course persistent antisocial path.
J Abnorm Psychol 2005;114:38–49.
[55] American Psychiatric Association. Diagnostic and statistical manual of mental dis-
orders. 5th ed. Arlington, VA: Author; 2013.
[56] National Genome Research Institute. The human genome project completion: fre-
quently asked questions. https://www.genome.gov/11006943/human-genome-
project-completion-frequently-asked-questions/, Accessed date: 10 July 2018.
[57] Collins AL, Sullivan PF. Genome-wide association studies in psychiatry: what have
we learned? Br J Psychiatry 2013;202:1–4.
[58] Egervari G, Kozlenkov A, Dracheva S, Hurd YL. Molecular windows into the human
brain for psychiatric disorders. Mol Psychiatr 2018 [epublished ahead of print].
[59] Girirajan S, Campbell CD, Eichler EE. Human copy number variation and complex
genetic disease. Annu Rev Genet 2011;45:203–26.
[60] Iacono WG. Endophenotypes in psychiatric disease: prospects and challenges. Ge-
nome Med 2018;10:11.
[61] Plomin R.Missing heritability, polygenic scores, and gene-environment correlation.
J Child Psychol Psychiatry 2013;54:1147–9.
[62] Ripke S, O’Dushlaine C, Chambert K, Moran JL, Kähler AK, Akterin S, et al. Genome-
wide association analysis identifies 13 new risk loci for schizophrenia. Nat Genet
2013;45:1150–9.
[63] Stahl EA, Raychaudhuri S, Remmers EF, Xie G, Eyre S, Thomson BP, et al. Genome-
wide association study meta-analysis identifies seven new rheumatoid arthritis
risk loci. Nat Genet 2010;42:508–14.
[64] Cross-Disorder Group of the Psychiatric Genomics Consortium. Lancet 2013;381:
1371–9.
[65] Brainstorm Consortium. Analysis of shared heritability in common disorders of the
brain. Science 2018;360:8757.
[66] Rutter M, Moffitt TE, Caspi A. Gene-environment interplay and psychopathology:
multiple varieties but real effects. J Child Psychol Psychiatry 2006;47:226–61.
[67] Mead HK, Beauchaine TP, Shannon KE. Neurobiological adaptations to violence
across development. Dev Psychopathol 2010;22:1–22.
[68] Fraga MF, Ballestar E, Paz MF, Ropero S, Setien F, Ballestar ML, et al. Epigenetic dif-
ferences arise during the lifetime of monozygotic twins. P Natl A Sci 2005;102:
10604–9.
[69] Hoeffding LK, Trabjerg BB, Olsen L, Mazin W, Sparsø T, Vangkilde A, et al. Risk of
psychiatric disorders among individuals with the 22q11.2 deletion or duplication:
a Danish nationwide, register-based study. JAMA Psychiat 2017;74:282–90.
[70] Finucane B, Challman TD, Martin CL, Ledbetter DH. Shift happens: family back-
ground influences clinical variability in genetic neurodevelopmental disorders.
Genet Med 2016;18:302–4.
[71] Lahey BB, Van Hulle CA, Singh AL, Waldman ID, Rathouz PJ. Higher-order genetic
and environmental structure of prevalent forms of child and adolescent psychopa-
thology. Arch Gen Psychiatry 2011;68:181–9.
[72] Greenwood TA, Light GA, Swerdlow NR, Radant AD, Braff DL. Association analysis of
94 candidate genes and schizophrenia-related endophenotypes. PLoS One 2012;7:
e29630.
[73] Constantino JN. Prevention of child maltreatment: strategic targeting of a curvilin-
ear relationship between adversity and psychiatric impairment. World Psychiatry
2018;17:103–4.
[74] Cicchetti D. Resilience under conditions of extreme stress: a multilevel perspective.
World Psychiatry 2010;9:145–54.
[75] Scarr S. Developmental theories for the 1990s: development and individual differ-
ences. Child Dev 1992;63(1):19.
[76] Constantino JN, Kennon-McGill S, Weichselbaum C, Marrus N, Haider A, Glowinski
AL, et al. Infant viewing of social scenes is under genetic control and is atypical in
autism. Nature 2017;547:340–4.
[77] Gottesman II, Shields J. Schizophrenia in twins: 16 years’ consecutive admissions to
a psychiatric clinic. Brit J Psychiatry 1966;112:809–18.
[78] Meehl PE. Schizotaxia, schizotypy, schizophrenia. Am Psychol 1962;17:827–38.
[79] MacCallumRC, Zhang S, Preacher KJ, Rucker DD. On the practice of dichotomization
of quantitative variables. Psychol Methods 2002;7:19–40.
[80] Parnas J. TheRDoCprogram:psychiatrywithoutpsyche? World Psychiatry 2014;13(1).
[81] McClelland GH, Judd CM. Statistical difficulties of detecting interactions and mod-
erator effects. Psych Bull 1993;114:376–90.
[82] Bryk SW, Raudenbush AS. Hierarchical linear models. Thousand Oaks, CA: Sage;
1992.
[83] Larson EL, Landers TF, Begg MD. Building interdisciplinary research models: a di-
dactic course to prepare interdisciplinary scholars and faculty. Clin Transl Sci
2011;4:38–41.
[84] Manolio TA, Collins FS, Cox NJ, Goldstein DB, Hindorff LA, Hunter DJ. Finding the
missing heritability of complex diseases. Nature 2009;461:747–53.
[85] Rawat S, Meena S. Publish or perish: where are we heading? J Res Med Sci 2014;
19:87–9.
[86] Hobin JA, Deschamps AM, Bockman R, Cohen S, Dechow P, Eng C. Engaging basic
scientists in translational research: identifying opportunities, overcoming obsta-
cles. J Transl Med 2012;10:72.
[87] Beauchaine TP, Zisner A, Sauder CL. Trait impulsivity and the externalizing spec-
trum. Annu Rev Clin Psychol 2017;13:343–68.
[88] McDonough-Caplan HM, Beauchaine TP. Conduct disorder: a neurodevelopmental
perspective. In: Martel MM, editor. Developmental pathways to disruptive,
impulse-control, and conduct disorders. Cambridge, MA: Elsevier; 2018. p. 53–89.
[89] Plichta MM, Scheres A. Ventral-striatal responsiveness during reward anticipation
in ADHD and its relation to trait impulsivity in the healthy population: a meta-
analytic review of the fMRI literature. Neurosci Biobehav Rev 2014;38:125–34.
[90] Sauder CL, Derbidge CM, Beauchaine TP. Neural responses to monetary incentives
among self-injuring adolescent girls. Dev Psychopathol 2016;28:277–91.
[91] Luijten M, Schellekens AF, Kühn S, Machielse MWJ, Sescousse G. Disruption of re-
ward processing in addiction: an image-based meta-analysis of functional mag-
netic resonance imaging studies. JAMA Psychiat 2017;74:387–98.
[92] Robins LN. Deviant children grown up. Baltimore, MD: Williams & Wilkins; 1966.
[93] Loeber R, Burke JD, Lahey BB, Winters A, Zera M. Oppositional defiant and conduct
disorder: a review of the past 10 years, part I. J Am Acad Child Psychiatry 2000;39:
1468–84.
[94] Eme R. Beauchaine ontogenic process model of externalizing psychopathology: a
biosocial theory of crime and delinquency. J Crim Just 2015;43:443–9.
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0105
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0105
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0105
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf5115
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf5115
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf5115
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0110
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0110
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0115
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0115
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0120
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0120
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0125
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0125
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0125
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0125
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0130
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0130
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf5145
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf5145
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf5145
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0140
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0140
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0140
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0145
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0145
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0145
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0150
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0150
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0155
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0155
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0160
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0160
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0160
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0165
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0165
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0170
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0170
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0175
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0175
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0180
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0180
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0180
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0185
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0185
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0190
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0190
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0190
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0195
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0195
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0195
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0200
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0200
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0205
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0205
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0210
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0210
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0215
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0215
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0220
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0220
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0220
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0225
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0225
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0225
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0230
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0230
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0235
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0240
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0245
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0245
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0250
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0250
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0255
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0255
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0255
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0260
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0260
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0260
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0265
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0265
https://www.genome.gov/11006943/human-genome-project-completion-frequently-asked-questions/
https://www.genome.gov/11006943/human-genome-project-completion-frequently-asked-questions/
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0275
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0275
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0280
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0280
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0285
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0285
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0290
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0290
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0295
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0295
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0300
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0300
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0300
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0305
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0305
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0305
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0310
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0310
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0315
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0315
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0320
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0320
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0325
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0325
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0330
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0330
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0330
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0335
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0335
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0335
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0340
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0340
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0340
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0345
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0345
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0345
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0350
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0350
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0350
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0355
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0355
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0355
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0360
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0360
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0365
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0365
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0370
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0370
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0370
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0375
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0375
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0380
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0385
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0385
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0390
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0395
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0395
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0400
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0400
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0405
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0405
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0405
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0410
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0410
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0415
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0415
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0420
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0420
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0420
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0425
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0425
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0430
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0430
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0430
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0435
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0435
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0435
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0440
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0440
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0445
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0445
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0445
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0450
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0455
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0455
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0455
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0460
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0460
152 T.P. Beauchaine et al. / Comprehensive Psychiatry 87 (2018) 143–152
[95] Barkley RA, Fischer M, Smallish L, Fletcher K. Young adult outcome of hyperactive
children: adaptive functioning in major life activities. J Am Acad Child Psychiatry
2006;45:192–202.
[96] Beauchaine TP, Hinshaw SP. The Oxford handbook of externalizing spectrum disor-
ders. New York, NY: Oxford University Press; 2016.
[97] Beauchaine TP, Cicchetti D. A new generation of comorbidity research in the era of
neuroscience and the Research Domain Criteria. Dev Psychopathol 2016;28:891–4.
[98] Gizer IR, Otto JM, Ellingson JM. Molecular genetics of the externalizing spectrum.
In: Beauchaine TP, Hinshaw SP, editors. The Oxford handbook of externalizing
spectrum disorders. New York, NY: Oxford University Press; 2016. p. 149–69.
[99] Beauchaine TP. A developmental psychopathology perspective on the emergence
of antisocial and borderline personality pathologies across the lifespan. In: Lejuez
CW, Gratz KL, editors. Handbook of personality disorders. NY: Cambridge Univer-
sity Press, New York; 2018 [in press].
[100] Ahmad SI, Hinshaw SP. Attention-deficit/hyperactivity disorder, trait impulsivity,
and externalizing behavior in a longitudinal sample. J Abnorm Child Psychol
2017;45:1077–89.
[101] LynamDR, Caspi A, Moffitt TE, Wikström PH, Loeber R, Novak S. The interaction be-
tween impulsivity and neighborhood context in offending: the effects of impulsiv-
ity are stronger in poorer neighborhoods. J Abnorm Psychol 2000;109:563–74.
[102] Lee SS, Humphreys KL, Flory K, Liu R, Glass K. Prospective association of childhood
attention-deficit/hyperactivity disorder (ADHD) and substance use and abuse/de-
pendence: a meta-analytic review. Clin Psychol Rev 2011;31:328–41.
[103] Hinshaw SP, Arnold LE. ADHD, multimodal treatment, and longitudinal outcome:
evidence, paradox, and challenge. WIRES Cogn Sci 2015;6:39–52.
[104] Lichtenstein P, Halldner L, Zetterqvist J, Sjölander A, Serlachius E, Fazel S, et al. Med-
ication for ADHD and criminality. N Engl J Med 2012;367:2006–14.
[105] Beauchaine TP, McNulty T. Comorbidities and continuities as ontogenic processes:
toward a developmental spectrum model of externalizing behavior. Dev
Psychopathol 2013;25:1505–28.
[106] Beauchaine TP. Future directions in emotion dysregulation and youth psychopa-
thology. J Clin Child Adolesc 2015;44:875–96.
[107] Wakschlag LS, Perlman SB, Blair RJ, Leibenluft E, Briggs-Gowan MJ, Pine DS. The
neurodevelopmental basis of early childhood disruptive behavior: irritable and cal-
lous phenotypes as exemplars. Am J Psychiatry 2018;175:114–30.
[108] Zisner A, Beauchaine TP. Neural substrates of trait impulsivity, anhedonia, and irri-
tability: mechanisms of heterotypic comorbidity between externalizing disorders
and unipolar depression. Dev Psychopathol 2016;28:1179–210.
[109] Perry BD, Pollard R. Homeostasis, stress, trauma, and adaptation: a
neurodevelopmental view of childhood trauma. Child Adolesc Psychiatr Clin
1998;7:33–51.
[110] Munson J, Dawson G, Abbott R, Faja S, Webb SJ, Friedman SD, et al. Amygdalar vol-
ume and behavioral development in autism. Arch Gen Psychiatry 2006;63:686–93.
[111] Harrison PJ. Schizophrenia: a disorder of neurodevelopment? Curr Opin Neurobiol
1997;7:285–9.
[112] Casey BJ, Getz S, Galvan A. The adolescent brain. Dev Rev 2008;28:62–77.
[113] Gogtay N, Giedd JN, Lusk L, Hayashi KM, Greenstein D, Vaituzis AC, et al. Dynamic
mapping of human cortical development during childhood through early adult-
hood. P Natl A Sci 2004;101:8174–9.
[114] Brain Development Cooperative Group. Total and regional brain volumes in a
population-based normative sample from 4 to 18 years: the NIHMRI study of nor-
mal brain development. Cereb Cortex 2004;22:1–12.
[115] Heatherton TF. Neuroscience of self and self-regulation. Annu Rev Psychol 2011;62:
363–90.
[116] Zilverstand A, ParvazMA, Goldstein RZ. Neuroimaging cognitive reappraisal in clin-
ical populations to define neural targets for enhancing emotion regulation. A sys-
tematic review. Neuroimage 2017;151:105–16.
[117] Arnsten AFT, Rubia K. Neurobiological circuits regulating attention, cognitive con-
trol, motivation, and emotion: disruptions in neurodevelopmental psychiatric dis-
orders. J Am Acad Child Psychol 2012;51:356–67.
[118] Macdonald A, Goines K, Novacek D, Walker E. Prefrontal mechanisms of comorbidity
froma transdiagnostic and ontogenic perspective. Dev Psychopathol 2016;28:1147–75.
[119] Gold AL, Shechner T, Farber MJ, Spiro CN, Leibenluft E, Pine DS, et al. Amygdala-
cortical connectivity: associations with anxiety, development, and threat. Depress
Anxiety 2016;33:917–26.
[120] Shaw P, Malek M, Watson B, Sharp W, Evans A, Greenstein D. Development of cor-
tical surface area and gyrification in ADHD. Biol Psychiatry 2012;72:191–7.
[121] De Brito SA, Mechelli A, Wilke M, Laurens KR, Jones AP, Barker GJ, et al. Size mat-
ters: increased grey matter in boys with conduct problems and callous-
unemotional traits. Brain 2009;132:843–52.
[122] Sauder CL, Beauchaine TP, Gatzke-Kopp LM, Shannon KE, Aylward E. Neuroana-
tomical correlates of heterotypic comorbidity in externalizing male adolescents. J
Clin Child Adolesc 2012;41:346–52.
[123] Shannon KE, Sauder C, Beauchaine TP, Gatzke-Kopp L. Disrupted effective connec-
tivity between the medial frontal cortex and the caudate in adolescent boys with
externalizing behavior disorders. Crim Justice Behav 2009;36:1141–57.
[124] Cubillo A, Halari R, Smith A, Taylor E, Rubia K. A review of fronto-striatal and
fronto-cortical brain abnormalities in children and adults with ADHD and new ev-
idence for dysfunction in adults with ADHD during motivation and attention. Cor-
tex 2012;48:194–215.
[125] Hair NL, Hanson JL, Wolfe BL, Pollak SD. Association of child poverty, brain develop-
ment, and academic achievement. JAMA Pediatr 2015;169:822–9.
[126] Hanson JL, Hair N, Shen DG, Shi F, Gilmore JH,Wolfe BL, et al. Family poverty affects
the rate of human infant brain growth. PLoS One 2013;8:e80954.
[127] Birn RM, Roeber BJ, Pollak SD. Early childhood stress exposure, reward pathways,
and adult decision making. P Natl Acad Sci 2018;114:13549–54.
[128] Blair MA, Stewart JL, May AC, Reske M, Tapert S, Paulus MP. Blunted frontostriatal
BOLD signals predict stimulant and marijuana use. Biol Psychiat Cogn Neurosci
Neuroimaging 2018 [epublished ahead of print].
[129] Pfefferbaum A, Kwon D, Brumback T, Thompson WK, Cummins K, Tapert SF, et al.
Altered brain developmental trajectories in adolescents after initiating drinking.
Am J Psychiatry 2018;175:370–80.
[130] Nguyen-Louie TT, Simmons AN, Squeglia LM, Alejandra Infante M, Schacht JP,
Tapert SF. Earlier alcohol use onset prospectively predicts changes in functional
connectivity. Psychopharmacology (Berl) 2018;235:1041–54.
[131] Nguyen-Louie TT, Matt GE, Jacobus J, Li I, Cota C, Castro N, et al. Earlier alcohol use
onset predicts poorer neuropsychological functioning in young adults. Alcohol Clin
Exp Res 2017;41:2082–92.
[132] Conduct Problems Prevention Research Group. Impact of early intervention on psy-
chopathology, crime, and well-being at age 25. Am J Psychiatry 2015;172:59–70.
[133] Cicchetti D, Toth SL. The development of depression in children and adolescents.
Am Psychol 1998;53:221–41.
[134] National Advisory Mental Health Council Workgroup on Tasks and Measures for
Research Domain Criteria. Behavioral assessment methods for RDoC constructs. Be-
thesda, MD: National Institute of Mental Health; 2016.
[135] Lilienfeld SO, Treadway MT. Clashing diagnostic approaches: DSM-ICD versus
RDoC. Annu Rev Clin Psychol 2016;12:435–63.
[136] Kryski KR, Smith HJ, Sheikh HI, Singh SM, Hayden EP. Assessing stress reactivity
indexed via salivary cortisol in preschool-aged children. Psychoneuroendocrinology
2011;36:1127–36.
[137] Curran P, Willoughby M. Implications of latent trajectory models for the study of
developmental psychopathology. Dev Psychopathol 2003;15:581–612.
[138] Meitinger K, Davidov E, Schmidt P, BraunM.Measurement invariance: testing for it
and explaining why it is absent. Surv Res Methods 2017;11:4.
[139] Weintraub S, Bauer PJ, Zelazo PD, Wallner-Allen K, Dikmen SS, Heaton RK, et al. I.
NIH toolbox cognition battery (CB): introduction and pediatric data. Monogr Soc
Res Child 2013;78:1–15.
[140] Gershon RC, Wagster MV, Hendrie HC, Fox NA, Cook KF, Nowinski CJ. NIH
toolbox for assessment of neurological and behavioral function. Neurology 2013;
80:S2–6.
[141] Kotelnikova Y, Olino TM, Klein DN, Kryski KR, Hayden EP. Higher- and lower-order
factor analyses of the children’s behavior questionnaire in early and middle child-
hood. Psychol Assessment 2016;28:92–108.
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0465
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0465
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0465
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0470
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0470
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0475
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0475
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0480
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0480
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0480
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf5495
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf5495
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf5495
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf5495
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0490
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0490
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0490
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0495
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0495
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0495
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0500
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0500
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0500
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0505
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0505
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0510
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0510
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0515
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0515
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0515
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0520
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0520
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0525
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0525
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0525
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0530
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0530
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0530
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0535
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0535
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0535
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0540
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0540
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0545
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0545
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0550
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0555
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0555
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0555
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0560
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0560
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0560
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0565
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0565
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0570
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0570
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0570
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0575
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0575
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0575
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0580
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0580
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0585
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0585
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0585
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0590
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0590
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0595
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0595
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0595
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0600
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0600
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0600
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf5615
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf5615
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf5615
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0605
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0605
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0605
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0605
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0610
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0610
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0615
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0615
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0620
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0620
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0625
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0625
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0625
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0630
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0630
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0630
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0635
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0635
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0635
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0640
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0640
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0640
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0645
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0645
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0650
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0650
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0655
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0655
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0655
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0660
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0660
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0665
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0665
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0665
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0670
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0670
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0675
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0675
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0680
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0680
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0680
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0685
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0685
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0685
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0690
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0690
http://refhub.elsevier.com/S0010-440X(18)30177-9/rf0690
- Psychiatry and developmental psychopathology: Unifying themes and future directions
1. Introduction
2. The emergence of a new discipline
3. Developmental psychopathology and psychiatry: selected tenets and unifying themes
3.1. Multidisciplinary, interdisciplinary, and transdisciplinary science
3.2. Multicausal pathways to common behavioral syndromes
3.3. Multifinal outcomes from common etiological start points
3.4. Multiple levels of analysis spanning genes to environments
4. Neurodevelopment and psychopathology
5. Summary and conclusions
Acknowledgements
References
