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14 Chapter 2 Models of Child Development, Psychopathology, and Treatment
The Case of Max
Max is eight years old. He can often be found squirming
at his second-grade desk, looking out the window,
rearranging his pencils, knocking papers on the floor,
or talking to the kids sitting nearby. From his teacher’s
perspective, Max’s situation is becoming more and more
problematic, and she has referred him for evaluation.
Max’s parents recall that his pediatrician described him
as “perfectly normal,” although they say that he has always
been busy and somewhat intense. Max lives with his father
and mother, both of whom graduated from high school,
and his siblings. The family lives in one half of a duplex
home; Max’s maternal grandparents, who emigrated from
Honduras, live in the other half.
In kindergarten, Max was described as active and energetic,
but his teacher had no significant concerns. In first grade, his
difficulties increased over the course of the year, with most
problems involving incomplete classwork and bothering other
children. Max’s school problems have continued in second
grade, where his teacher describes him as generally disorganized
and as falling behind in reading and math.
Max’s parents provided other information that suggested
that his struggles were not everyday problems that would
resolve themselves. Beginning in first grade, they noticed
that Max was having some problems at home, including
irritability and impulsivity. His parents remembered
that these negative emotions and behaviors were more
pronounced after the school day. Also, Max began to argue
and fight more frequently with his 10-year-old brother,
and especially with his four-year-old sister. His parents
report that Max still enjoys playing with friends in the
neighborhood but is becoming increasingly resistant,
discouraged, and pessimistic about school. The more
stressful family problems coincided with Max’s father being
laid off from his job as a master electrician. Max’s father has
spent increasing amounts of time at home, with escalating
conflicts between him and Max’s mother (who does not
work outside the home) about childcare and discipline.
The Case of Aisha
Aisha is 14 years old. She spends a lot of her free time
alone in her room, feeling unhappy and not doing
much of anything. She rarely gets together with other
kids, who have mostly stopped asking her to join
them. Aisha’s mother is worried about her sadness and
withdrawal and has called her family physician for a
referral.
Aisha’s mother has been a single parent since Aisha’s
birth and is employed as a customer service representative
for a health care company. Aisha’s father has a long
history of hospitalizations for both major depression and
alcohol abuse. Following several extremely unpleasant
exchanges with Aisha’s mother when he came to visit
Aisha as an infant and toddler, Aisha’s father has had no
contact with her.
Aisha’s mother describes Aisha’s infancy and childhood
as normal. Throughout elementary school, Aisha was
generally quiet and cooperative and received average
grades. Although not especially social, she always had a
few good friends and was active in sports and with her
church youth group. Looking back, Aisha’s mother
remembers that Aisha seemed to worry more than most
other children, but not to the point where it interfered
with her schoolwork or social activities. Her transition
to middle school was challenging. Aisha’s mother reports
that Aisha seemed somewhat overwhelmed by the size of
the school and had difficulty adjusting to changing classes
and increased homework. Aisha had less contact with her
elementary school friends and has had trouble making
new friendships.
Although Aisha does not talk much about her situation,
her increasing withdrawal, apathy, and occasional
irritability are apparent. She no longer participates in
sports, has dropped out of her church youth group, and
spends most of her time at home alone. She is increasingly
behind in her schoolwork, and her grades have dropped
significantly.
The Role of Theory in Developmental Psychopathology
Models of development, psychopathology, and treatment
allow us to organize our clinical observations of children
and our research findings into coherent, informative
accounts. In this chapter, the cases of Max and Aisha will
illustrate key concepts related to typical developmental
processes, the emergence of disorder, and intervention goals
and strategies. For introductory purposes, the sections on
Max and Aisha present somewhat simplified examples. In
the next chapter and throughout the rest of this book, the
models will become increasingly complex and integrated.
Before the practices and principles of developmental
psychopathology are described in Chapter 3, we summarize
the major models that have contributed valuable ideas to our
contemporary understanding. Although these models are
presented separately and are often conceptualized as complete
and comprehensive in and of themselves, they are not mutually
exclusive. It is more useful to think of these models as providing
different and complementary perspectives on the complicated
phenomena of development, psychopathology, and treatment.
Dimensional and Categorical Models
To provide additional background for the upcoming summaries,
it is useful to consider how various definitions of disorder
correspond with dimensional versus categorical models of
psychopathology. Dimensional models of psychopathology
emphasize the ways in which typical feelings, thoughts, and
behaviors gradually become more serious problems, which then
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Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it.
Physiological Models 15
Serotonin pathways
Dopamine
may intensify and become clinically diagnosable disorders.
With dimensional models, there are no sharp distinctions
between adjustment and maladjustment. Dimensional models
also are referred to as continuous or quantitative. Categorical
models of psychopathology, in contrast, emphasize discrete
and qualitative differences in individual patterns of emotion,
cognition, and behavior. With categorical models, there are clear
distinctions between what is normal and what is not. Categorical
models are sometimes referred to as discontinuous or qualitative.
Important differences between dimensional and categorical
models are illustrated by referring to Max and Aisha. For
instance, do the difficulties experienced by Max and Aisha
reflect extremes of typical difficulties (dimensional examples),
or are they problems of a different sort altogether (categorical
examples)? What do parents, teachers, and clinicians gain from
the dimensional perspective, which emphasizes the connections
between kids who are struggling and kids who are not? And
what is gained from the categorical perspective, which instead
emphasizes the patterns of the problematic emotions, thoughts,
and behaviors that give rise to significant maladjustment?
Physiological Models
Historical and Current
Conceptualizations
Physiological models propose that there is a physiological—
a genetic, structural, biological, and/or chemical—basis
for all psychological processes and events. Early physiological
models focused on genes, brain structure and function, and
how prior development inf luenced, directed, a nd constrained
later development. Contemporary conceptualizations are
even more complex, taking into account behavior genetics
and epigenetics, gene-by-environment-by-time effects, the
organization and reorganization of brain networking across
development, and brain-body-behavior processes.
Brain Structure and Function
Animal and human studies provide information and insight
into the multiple components and processes that contribute
to healthy and well-functioning brains. With respect to brain
development, we need to consider how children’s brains adapt
to their environments over time in ways that are like all other
children as well as in ways that are uniquely their own (Johnson
et al., 2015). We must appreciate both how specific brain regions
are associated with types of activity (e.g., emotion, language,
motivation) and how interactions and connectivity (via neural
networks and neurotransmitter systems) among brain regions
contributes to overall brain function (refer to Figure 2.1).
Advances in neuroscience have led to detailed descriptions
and remarkable images of development, organization,
and reorganization. Neuroscientists provide evidence of
prolonged and hierarchical brain development with earlier
developing regions (such as the amygdala) influencing
the neurobiology of later-developing regions (such as the
prefrontal cortex) (Tottenham, 2020). These advances
Figure 2.1 An illustration of structures and pathways: The brain circuits underlying motivation
Anterior
cingulate
pathways
Prefrontal
cortex
Nucleus
accumbens
Amygdala
cortex
VTA
Raphe nuclei
Substania
nigra
Hippocampus
Source: Harvard Center on the Developing Child, The Brain Circuits Underlying Motivation: An Interactive graphic. https://developingchild.harvard.edu/resources
/the-brain-circuits-underlying-motivation-an-interactive-graphic/
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16 Chapter 2 Models of Child Development, Psychopathology, and Treatment
BirthConception
include the study of gray matter (processes and functions)
and white matter (connectivity within and between regions).
Gray matter and white matter development is observed in
detail, with some regions displaying simpler growth patterns
and others showing more complex ones (Nelson, 2011;
Vertes & Bullmore, 2015; refer to Figure 2.2).
Atypical brain structure such as reduced gray matter
volume is frequently observed in youths with disorders.
This reduced volume is associated with general distress and
dysfunction rather than with a specific disorder (Snyder
et al., 2017). Atypical white matter microstructures and
lower rates of myelination are also notable in children
and adolescents with disorders. Both of these patterns are
associated with many disorders rather than a single disorder
(Neumann et al., 2020; Vanes et al., 2020).
Research focused on the human connectome—the
diagram of the brain’s neural connections—makes use of
innovative tools and techniques to map the anatomical and
functional features of brain networks (Fox, 2018; Vertes &
Bul lmore , 2015; htt p://ww w.huma nc onnec tomeproje ct.org / ).
In contrast to explanations of microscopic connectivity
Figure 2.2 Sequence of events in brain maturation
(e.g., between neurons), explanations of the connectome
focus on macroscopic connectivity (e.g., between brain
regions). Similar to anatomic structures, wiring patterns
are not fully in place at birth, with some connectivity tracts
maturing early (such as those underlying visual, auditory
and sensorimotor processing) and other tracts maturing
later (such as those underlying complex cognitive and
emotional activity). There are also changes related to the
balance between separation and specialization of function
and overall integrated functioning.
Understanding t he roles and act ivities of the neurotransmitter
systems is essential to understanding central nervous system
function and dysfunction. Neurotransmitters such as
dopamine, serotonin, glutamate, and acetylcholine are chemical
messengers that have excitatory, inhibitory, or modulating
effects on neurons embedded in elaborate neural networks.
Other signaling molecules such as neurotrophins (e.g., brainderived neurotrophic factor, BDNF) also influence growth,
differentiation, and maintenance of neural systems. Many of
the most common medications that are used to treat disorders
target neurotransmitters and related neural signaling functions.
The intensity of color in each bar reflects the intensity of developmental change observed across time.
Neurogenesis
Consolidation
Synaptogenesis
Competitive elimination (synapses)
Anatomy
Neuroimaging
Axon growth
Myelination
DTI
fMRI
Competitive elimination (axons)
MRI
Then Grey matter volume
Then Cortical thickness
Increasing white matter volume
Anatomical connections
in place at birth
Functional connections progressively form
rst locally, then over longer distances
EEG
Maturation of white
matter tracts
Increasingly small-world connectivity
16 32 4 months 25 10 15 20 25+
Weeks
Source: Vertes & Bullmore (2015). Growth connectomics: The organization and reorganization of brain networks during normal and abnormal development.
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Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it.
Years
Physiological Models 17
The brain’s ability to
Amount of effort
Brain Growth and Development
in Environmental Context
Compared to other mammals, the human brain develops
over a very lengthy timeline. Keeping an evolutionary
framework in mind, this slow development “allows for
the species-expected collaboration between child and parent
in the co-construction of the human brain” (Tottenham,
2020, p. 350). In addition, protracted brain development
supports the adaptation of children embedded in specific
environments with “repeated, slow, and thus enhanced
learning opportunities” (Tottenham, 2020, p. 351).
In one example of brain–environment interaction, Bell
and Fox (1996) documented patterns of physiological and
electroencephalograph (EEG) activity in groups of eightmonth-olds with various crawling histories. Comparisons of
non-crawling infants, beginning crawlers, and experienced
crawlers provide evidence that brain development specific
to crawling involves an initial overproduction of cortical
connections that are then “pruned” with additional
crawling experience. This pattern of overproduction and
pruning illustrates how the brain’s development responds to
environmental feedback, resulting in increasingly efficient
and environment-specific processing. Another example of
experience-dependent brain development involves changes
in brain structure and function related to music training.
Researchers found that children who received music lessons
between 6 and 8 years of age (compared to children who
participated in sports) exhibited different rates of cortical
maturation and different connection patterns among brain
regions (Habibi et al., 2018).
Sensitive (or critical) periods in brain development are
spans of time when environments have especially powerful
and enduring impacts. These sensitive periods may be
domain- or component-dependent (e.g., in the auditory
system or related to specific components of language). Many
researchers, for example, have described specific periods
in which the development of limbic system circuitry (i.e.,
amygdala-medial prefrontal cortex connections) in either
nurturing or adverse caregiving environments leads to later
differences in emotion regulation (e.g., Doom & Gunnar,
2013; Tottenham, 2020). While brain development is
mostly similar for typically developing children, differences
among typically developing children have also been observed
(Nelson, 2011). That is, we often expect that differences in
brain structure, function, and development will be observed
between typically and atypically developing children, but we
also must understand that there is diversity (e.g., variability)
within groups of typically developing children.
Neural plasticity illustrates several physiological
processes related to brain development, organization, and
reorganization. Numerous examples of neural plasticity,
involving changes in anatomy and neurochemistry, have
been described for brain systems (e.g., visual, motor,
language, and learning and memory systems as well as
neurotransmitter systems). In cases where the developing
brain is affected by early adversity, plasticity allows
for better outcomes following positive and enriched
environmental experiences. And, while we once believed
that brain development was relatively complete by age three
and that any damage was permanent and irreversible, we
now understand that plasticity is associated with important
growth after the age of three and with the lifelong potential
for new, improved, and recovered function.
As important as plasticity is across development, a
balance between plasticity and stability is critical. Indeed,
“one of the outcomes of normal development is to stabilize
the neural networks initially sculpted by experience. Rather
than being passively lost, the brain’s intrinsic potential
for plasticity is actively dampened” (Takesian & Hensch,
2013, p. 3). It makes sense that plasticity is constrained
across development. Increases in perceptual and cognitive
efficiency, for example, depend on the strengthening
of specific neural pathways over time (and associated
weakening and pruning of other pathways). Ongoing
research explores the mechanisms underlying both plasticity
(i.e., molecular triggers) and stabilization (i.e., molecular
brakes) and how either might be influenced or modified to
treat neurodevelopmental or neurodegenerative disorders.
Figure 2.3 illustrates the relationship across development
between plasticity (i.e., the brain’s ability to adapt or change)
and the amount of effort required for such change.
There has been a decades-long emphasis on brain growth
and organization during the first three years of life with
overwhelming evidence of the importance of early nurturing
and experience. We now know, in addition, that meaningful
brain development continues to occur throughout later
childhood, adolescence, and adulthood (refer again to
Figure 2.2). The National Institutes of Health’s (NIH)
Adolescent Brain Cognitive Development (ABCD) Study
is the largest long-term study of brain development and
youth outcomes in the US (abcdstudy.org). Researchers are
Figure 2.3 Brain plasticity and effortful
change over time
change in response
to experiences
246810 20 30 40 50 60 70
th
Source: Harvard Center on the Developing Child. Brain Architecture.
such change requires
Age
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18 Chapter 2 Models of Child Development, Psychopathology, and Treatment
Environmental
Environmental
collecting multiple types of data, including repeat magnetic
resonance images (MRIs), from over 10,000 healthy children
and adolescents, examining the impact of varied experiences
on the brain, adaptation, and maladaptation. One example
of ABCD Study research provides evidence that school
environments are associated with cognitive networks and
connectivity among brain regions in 9- and 10-year-old
children (Rakesh et al., 2022). This study, along with
numerous others, provides important information about
typical and atypical brain structure and function across the
lifespan.
Brain-Body-Behavior Processes
Children’s brains do not develop and function separately
from other physiological systems. All physiological
systems—including brain, cardiovascular, immune,
metabolic, and neuroendocrine systems—interact
with one another, adapting to the environments in
which the child develops (National Scientific Council
on the Developing Child, 2020; refer to Figure 2.4).
We know that early experiences of stress and trauma
negatively impact many developing biological systems
(including the stress-response system and the immune
system). We also know that there are myriad biological
contributions (as well as psychological and sociocultural)
contributions to sex differences in types of disorders
(Merikangas & Almasy, 2020; refer to Figure 2.5).
And we know that pubertal timing and hormones
influence the development of adolescent disorders (Hamlat
et al., 2019). These types of brain-body-behavior research
findings will be further described in upcoming chapters.
Genes and Environments
Genetics play a critical role in physiological models. We
need to think about the many ways that the genetic makeup
of an individual, or genotype, influences the observable
characteristics of an individual, or phenotype. Our
understanding of genetics (i.e., genes and heredity) is ever
expanding and involves work in both behavior genetics
and molecular genetics. Research techniques used to
investigate the influence of genes include twin, family,
and adoption studies as well as genetic sequencing, genetic
screening, and genome-wide association studies. Table 2.1
provides definitions of key terminology.
Explanations for both typical development (and
all variations of well-adjusted children) and atypical
development (and all variations of children who display
distress and dysfunction) depend on understanding genes,
genetic variants, and the processes by which multiple
genetic and nongenetic effects lead to physiological and
psychological outcomes. Behavior genetics, the study
of the joint effects of genes and environments, provides
a framework for understanding many sources of genetic
Figure 2.4 Biological systems interact with each other and the environment
Stressors
Neuroendocrine System
Maintain hormonal balance
Immune System
infection & heal injury
Source: Harvard Center on the Developing Child, http://developingchild.harvard.edu/science/key-concepts/brain-architecture/
Defend against
Brain & Autonomic
Nervous System
Manage & respond
Stress
Response
Fight or ight
Stressors
Heart &
Cardiovascular System
Pump blood, distribute
oxygen & glucose
Gut & Metabolic
System
Turn food into energy
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Male to Female Ratio
Female > Male Male > Female
Disorder
Figure 2.5 Male to female sex ratio of disorders
Male to female sex ratio of disorders sorted from most to least prevalent among females.
Eating Disorders: Anorexia
Eating Disorders: Bulimia
Post–traumatic Stress Disorder
Anxiety Disorders
Major Depressive Disorder
Bipolar Disorder
Schizophrenia
Attention Deficit Hyperactivity Disorder (Adult)
Substance Use (U.S.)
Substance Use (Opioid) (U.S.)
Alcohol Dependence (U.S.)
Physiological Models 19
Attention Deficit Hyperactivity Disorder (Child)
Autism Spectrum Disorder
0 1 2 3 4
Source: Merikangas & Almasy (2020). Using the tools of genetic epidemiology to understand sex differences in neuropsychiatric disorders.
inf luence and allows resea rchers to estimate the heritability
of many psychological characteristics. One of the most
important shifts in thinking about genetics involves
moving beyond early views on nature versus nurture to
current complex descriptions of gene-by-environment-
by-time (G 3 E 3 T) effects and gene-by-environmentby-time interactions (refer to Table 2.2). Examples of
G × E × T findings include those describing the impact
of stress and trauma on the activity of the hypothalamuspituitary-adrenal (HPA) system (Doom & Gunnar, 2013)
and those describing the increasing impact of genes on
performance of that symphony). Epigenetics, like synaptic
pruning, is a way to think about how children’s particular
environments “get under their skin.” If we understand
synaptic pruning as identifying a mechanism by which
the brain “listens” to the environment, then we can also
understand that epigenetics identifies a mechanism by
which genes “listen” to the environment. In both cases,
meaningful experiences such as trauma, especially in early
life and during adolescence, and the social context in which
they occur, have the capability to become biologically
embedded with lifelong impacts on developmental health.
intelligence and personality as children age (e.g., Koenis
et al., 2018; Mottus et al., 2019). Other examples of G ×
E × T processes are those focused on the pace or timing
of development (such as accelerated aging or atypical
timelines of development) (Roubinov et al., 2021).
Finally, we need to consider cutting-edge research
in epigenetics, the study of how environmental factors
influence gene expressivity (O’Donnell & Meaney, 2020).
Epigenetics is focused on the activity of the gene rather
than the presence of the gene (refer to Box 2.1). To illustrate
this distinction, leading researcher Moshe Szyf (2013)
analogizes the genome, deoxyribonucleic acid (DNA), as
the script of a movie (or the score of a symphony), with
epigenetics as the movie as it is actually filmed (or the
Physiological Models and Disorder
Physiological models of typical de velopment clearly inf luence
our understanding of maladaptation. For some disorders,
psychopathology unfolds according to a “maturational
blueprint,” with disorder innately and inevitably related to
damage or dysfunction (Sameroff, 2000). Certain severe
forms of intellectual developmental disorder are examples
of this type of psychopathology. For most disorders of
childhood and adolescence, however, this straightforward
model of physiological cause and psychopathological
effect can be set aside. Genetically informed models of
psychopathology must account for the high heritability
of various disorders as well as findings related to genetic
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20 Chapter 2 Models of Child Development, Psychopathology, and Treatment
Table 2.1 Some Basic Definitions Related to Genetics
Additive genetic variance: Individual differences caused by the cumulative effect of independent genes.
Allele: One of two or more alternative forms of a gene.
Behavior genetics: The study of the combined effects of genetics and the environment; with respect to
developmental psychopathology, the focus is on the relationship of genetic variation and psychological traits,
symptoms, and disorders.
Copy number variations (CNVs): Copy number variations (or copy number variants) refer to multiple copies of a
particular gene in an individual’s genome. Genetic variation results from insertions, deletions, and duplications
across these variants.
Deoxyribonucleic acid (DNA): Double-stranded molecule that encodes genetic information.
DNA methylation: An epigenetic process by which gene expression is influenced by adding a methyl group to a
chromosome region.
Epigenetics: The processes and mechanisms that influence gene expression.
Epigenome: Epigenetic events throughout the genome.
Gene: The basic unit of inheritance.
Gene expression: Transcription of DNA into messenger RNA (mRNA).
Genome: The complete set of genes including all the DNA sequences of an organism. The human genome
contains about 3 billion DNA base pairs.
Genomics: A field of study focused on genes and gene functions.
Genomewide association studies (GWAS): A research method that involves rapidly scanning markers across the
genome of many people to find genetic variations associated with a particular phenotype (such as a disease or
disorder).
Genotype: The genetic constitution of an individual.
Heritability: The proportion of phenotypic differences among individuals that can be attributed to genetic
differences in a particular population.
Molecular genetics: Investigation of the effects of specific genes at the DNA level.
Nonadditive genetic variance: Individual differences due to the effects of alternate forms of genes.
Nonshared environment: Environmental influences that contribute to differences between family
members.
Phenotype: An observed characteristic or behavior of an individual that results from the combined effects of
genotype and environment.
Polygenic trait: A trait influenced by many genes.
Shared environment: Environmental factors responsible for resemblance between family members.
Single nucleotide polymorphism (SNP): Refers to variation at a single position in a DNA sequence.
Whole-genome sequencing: Determining the complete sequence of DNA base pairs for a genome.
overlap. That is, rather than a correspondence between
particular genetic variants and one disorder, there appears
to be a more limited set of risk alleles that impair general
processes (e.g., cognitive or emotion functions) across many
disorders. For some disorders, however, specific genetic
liability becomes more apparent over time. A longitudinal
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research design is needed to provide these important data
(Riglin et al., 2020).
Risk alleles include common variants, shared by
individuals with and without disorders; rare variants, both
inherited and de novo (newly appearing); and many different
combinations of variants. Polygenic models emphasize the
Physiological Models 21
Table 2.2 Gene-by-Environment-by-Time (G 3 E 3 T) Effects and Interactions
Gene-by-environment effects (or correlations) involve differential exposure to environments or experiences.
There are three types of gene-by-environment effects:
1. Passive correlations, in which children are exposed to different environments provided by their genetically
related parents. Examples: Extraverted children raised by extraverted parents are exposed to more social
opportunities; highly intelligent children raised by highly intelligent parents are exposed to more educational
opportunities.
2. Active correlations, in which children select or create their own environments as a function of their genetic
background. Examples: Extraverted children seek out other children on the playground; highly intelligent
children choose to read or tinker with electronics during unstructured times.
3. Evocative correlations, in which children experience different reactions or responses to their genetically
influenced emotions or behaviors. Examples: Extraverted children who display rambunctious behavior may
be disciplined more frequently than introverted children; highly anxious children may be shielded from even
mildly stressful situations by parents and teachers, while less anxious children may be encouraged to deal
with difficult situations.
Gene-by-environment interactions involve differential sensitivity or susceptibility to environments or
experiences. Subsets of children respond to particular environments in different ways. Examples: Some
children whose genetic backgrounds make them vulnerable to poor outcomes in the presence of maltreatment
may be the same children who display excellent outcomes in the presence of high-quality caregiving.
Gene-by-environment-by-time effects and interactions. In addition to the dynamic interplay of genes and
environments, it is increasingly clear that time, in the form of sensitive periods, serves as a third interacting
factor driving developmental outcomes. This more complete model (G 3 E 3 T) is especially important in
helping to elucidate the effects of adversity occurring early in development. Linking genetic susceptibility,
sensitive (or critical) periods, and environmental context improves our understanding of both risk and resilience
across development.
well-established findings that many genes have small effects
and attempt to account for the multiple types of genetic
variations and processes that influence the development of
both mild and severe forms of disorders. Even with these
compelling data, we need to be cautious about overstating
our hypotheses and findings. The phrase “X is a gene for
Y” is widely used, but it is inappropriate for psychology and
psychiatry.
According to the physiological diathesis–stress model,
atypical brain structure, function, or development does not
by itself lead to disorder. Rather, diatheses (or predispositions)
such as neurological damage at birth or genetic risk for
disorder, in combination with additional stress (either
physiological or environmental), lead to the emergence of a
disorder. Diathesis–stress models call attention to the lack
of a one-to-one correspondence between the genotype and
phenotype for most forms of psychopathology, and they
are an example of gene-by-environment-by-time effects or
interactions.
Two examples illustrate the diathesis–stress model. In the
first case, a child with phenylketonuria (PKU) is born with
a particular metabolic dysfunction, an inactive liver enzyme
(a physiological diathesis of genetic origin). The presence
of phenylalanine (a physiological stressor) in the child’s
diet and the subsequent metabolic abnormalities result in
severe intellectual dysfunction. Treatment of this condition
involves a diet low in phenylalanine beginning shortly after
birth; this intervention is associated with more typical
intellectual development. In the second case, a child’s health
and well-being may be adversely affected by maternal drug
abuse during pregnancy (again, a physiological diathesis, but
this one of nongenetic origin). After birth, poor parenting
(a psychosocial stressor) of these at-risk children may lead to
a disorder. High-quality parenting, in contrast, may buffer
or protect the child from especially negative outcomes.
The diathesis–stress model was an early and highly
influential approach to understanding how specific risks
for psychopathology interacted with various stressors to
trigger the onset of various disorders. The basic premise of
this diathesis–stress model—that genetic profile and other
biological factors interact with environmental influences
to produce individual differences—has been updated
and extended. Rooted in developmental and evolutionary
theory, differential susceptibility (also called differential
sensitivity or biological sensitivity to context) asserts that
although it is true that some children are differentially
vulnerable to stressful environments (i.e., these children
do worse than others in similarly adverse circumstances),
it is also true that these same children differentially
thrive with developmentally appropriate and encouraging
environments (i.e., these children do better than others in
similarly nurturing circumstances). At its heart, differential
susceptibility maintains that some children are, at a
genetic and biological level, very sensitive to both positive
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22 Chapter 2 Models of Child Development, Psychopathology, and Treatment
Box 2.1 Emerging Science
Behavior Genetics, Epigenetics, and Developmental Psychopathology
Remarkable advances in scientific knowledge and technology
have enabled investigators from many disciplines to ask, and
begin to answer, questions about the biopsychosocial nature
of human experience. Behavior genetics is the study of the
relationships between genetic variation and psychological
processes and characteristics, including personality and
psychopathology. Variant forms of specific genes are
known as alleles (or polymorphisms), and researchers study
whether these variations are associated with physiological or
psychological characteristics as well as with increased risk for
disorders. Combining data from decades of twin, family, and
adoption studies with new data from the Human Genome
Project (a collaborative effort by the U.S. Department of
Energy and the National Institutes of Health (NIH) that
sequenced the approximately 20,000 genes in human DNA,
(U.S. Department of Energy Genomic Science, genomics.
energy.gov), researchers have agreed upon a number of
important findings. These findings include the following
(Plomin et al., 2016):
● All psychological traits show significant and substantial
genetic influence.
● No traits are 100% heritable.
● Genetic impact is caused by many genes with small effects.
● Environments matter.
In addition to ongoing work in behavior genetics,
complementary research on epigenetics holds enormous
promise for helping to explain the ways in which the
environment “gets under the skin” and facilitates or hinders
genetic expression (refer to the NIH Roadmap Epigenome
Project; www.roadmapepigenomics.org). Epigenetics helps
to “explain how environment and genome operate in concert to
define individual variation from the level of cellular function to
complex traits” and refers to the processes and mechanisms
that direct the activity of cell DNA—gene expression, or how the
gene functions—but does not change the DNA itself—the
presence of the gene (O’Donnell & Meaney, 2020, p. 328).
Epigenetics is a kind of individual-environment plasticity.
“This plasticity refers not to variation in nucleotide sequence,
which remains largely invariant over the life span, but to the
biochemical environment within which genetic information is
transduced into cellular signals. This biochemical niche is the
epigenome and can be considered as the software that directs
the activity of the DNA sequence hardware” (O’Donnell &
Meaney, 2020, pp. 328–329). The combination of human
genetic variability and epigenetic processes means that
individuals are able to adapt to a wide range of environmental
challenges and opportunities.
Epigenetics research, focused on the DNA molecules that
contain genetic information stored as codes, may examine
individual (or candidate) genes, small sets of genes, or much
larger gene sets (using genome-wide or epigenome-wide assays).
“Gene expression is the process by which genes . . . make the
specific proteins that determine the structure and function of
the indiv idua l gene. Gene expression is initiated by tra nscription
factors. . . . Epigenetic mechanisms regulate this transcriptional
machinery, and in so doing, control gene expression” (Lester
et al., 2016, p. 30). Epigenetic regulation of transcription
processes takes place over time (G
× E × T) and involves
interactions among various epigenetic mechanisms (i.e.,
biochemical modifications) (O’Donnell & Meaney, 2020).
The most frequently studied epigenetic mechanism is DNA
methylation. “Levels of methylation are associated with how
well DNA is transcribed. . . . As methylation levels increase,
there is less transcription until the level of DNA methylation
reaches the point at which the gene is switched off. . . . In the
absence of DNA methylation, gene transcription is allowed to
occur. Although DNA methylation is often described as an
“on-off” switch, it is, in fact, more like a “dimmer” switch that
gradually decreases gene expression as methylation increases.
In other words, if all the cells associated with a particular gene
are unmethylated, the population of cells can produce the
amount of protein consistent with a fully active gene.
Conversely, if the gene is fully methylated, it will produce very
little or none of the protein. . . . The amount of methylation
related to behavior varies by gene. Some behaviors may be
affected by only slight changes in DNA methylation, while
others may require a larger percent change” (Lester et al., 2016,
pp. 30–31). Other epigenetic mechanisms include histone
modifications and RNA signaling.
Epigenetic signals may serve as disease or disorder
biomarkers. Epigenetic biomarkers are the focus of risk research
on post-traumatic stress disorders and maternal depression and
may provide important information about individuals’ response
to treatments (O’Donnell & Meaney, 2020). Epigenetic models
and research findings are increasingly influential in
understanding the development and maintenance of disorders
such as autism spectrum disorder, stress and trauma-related
disorders, ADHD, and anxiety and depressive disorders and
are discussed in upcoming chapters.
and negative aspects of their environments (Boyce, 2016;
Pluess, 2015; Zhang et al., 2021). Figure 2.6 provides a
comparison of outcomes for diathesis-stress and differential
susceptibility models.
A frequently used metaphor helps illustrate the construct
of differential susceptibility. Many children do well in a
Copyright 2024 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s).
Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it.
variety of circumstances, ranging from nurturing, positive
environments to much more stressful and challenging
environments. These individuals are referred to as dandelion
children. Other children, known as orchid children, seem
to be especially reactive and compromised in challenging
settings. At the same time, however, growing up in an
Physiological Models 23
Diathesis Stress
Outcome
e
High vulnerability Low vulnerability
Differential Susceptibility
Outcome
e
High susceptibility Low susceptibility
Figure 2.6 A comparison of diathesis-stress and differential susceptibility models
Positive
Negative
Adverse
Environment
Source: Zhang and Belsky (2022). Three phases of Gene × Environment interaction research: Theoretical assumptions underlying gene selection.
Not Advers
enriched environment may be especially valuable for the
orchid child, who flourishes under such conditions (Boyce,
2012). It is important to note, however, that the metaphor
of orchid and dandelion children does not accurately reflect
all the information we have about differential susceptibility.
Children are not divisible into two groups (very reactive and
non-reactive) (Zhang et al., 2021). Differential susceptibility
appears to be normally distributed with children ranging
from highly susceptible → moderately susceptible → much
less susceptible to environmental contexts. Further, children
appear to be variably susceptible to specific contexts.
Children who are highly susceptible to parent and family
environments, for example, may be less susceptible to peer
Positive
Negative
Adverse
Environment
difficulties, consistent with a diagnosis of attention-deficit
hyperactivity disorder (ADHD), are not typical of other
similar-age children.
Because the disorder is physiologically based with ongoing
physiological dysfunction, the first choice for intervention
is a physiological treatment. The clinical literature suggests
that stimulant drugs such as Ritalin, Adderall, or Concerta
are effective for children with ADHD, so a trial of stimulant
medication would be prescribed. In addition, although
pharmacological treatment is the primary intervention,
behavior strategies would be routinely included in both the
school and home settings. Psychoeducational information
and support would also be provided to Max and his family.
or neighborhood environments (Zhang et al., 2021).
Thinking about Aisha
Physiological Models and Treatment
Within the physiological framework, prevention and
intervention efforts focus on the physiological processes that
increase risks associated with child and adolescent disorders
and the role of medications and other biologically-based
treatments in improving adaptation and adjustment. With
these kinds of prevention and intervention efforts, careful
attention must be paid to the ongoing development of the
brain and related physiological systems.
Thinking about Max
From a physiological perspective, clinicians are likely to
conceptualize Max’s difficulties as primarily due to atypical
brain function. Because of underarousal of key parts of his
brain (and other neurological processes), Max lacks sufficient
focus and sustained engagement with the environment,
resulting in inattentive and impulsive behavior. These
Again, from a physiological perspective, we note with special
interest Aisha’s family history, which includes her father’s
episodes of clinical depression, and consider the possibility
of a genetic vulnerability to depression. Aisha’s various
problems, then, might be usefully conceptualized as the
psychological expression of atypical biological and chemical
processes. Aisha’s symptoms may be a result of low levels of
the neurotransmitter serotonin or dysregulation of multiple
neurotransmitter systems.
The first step in her treatment plan will likely include
a trial of antidepressant medication, although special
consideration must be given to the use of such medication
with youth. Treatment recommendations may also include
psychoeducational information and support as well as
suggestions that Aisha participate in structured social
activities as a way of helping her be more active and successful
in friendships.
Supportiv
Copyright 2024 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s).
Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it.