Genetics
Describe the difference between heritability and gene-environment interaction. How do these influence our understanding of individual differences in psychopathology?
Heritability: statistic that describes the proportion of variability, or degree to which variation in a trait is influenced by genetic differences among individuals, usually expressed as a percentage
Gene environment interaction: developing a disorder depends on an individual's genetic makeup, but expression of that disorder depends on environment. Genes and environment do not operate additively, impact of one is conditional on presence or level of the other, * explains why some people exposed to stressors develop psychopathology and others do not
* moving beyond nature versus nurture; heritability quantifies the overall genetic contribution to differences in a trait, while GxE describes how genes and environment interact to produce those differences
genetic predisposition does not guarantee a disorder, but it does increase the likelihood of developing it
What is the tripartite model and how can you use it to help differentiate between anxiety and depression?
Tripartite Model (Clark & Watson, 1991):
Negative Affect (NA):
General distress and negative emotions (e.g., sadness, fear, irritability)
Common to both anxiety and depression
Positive Affect (PA):
Ability to feel joy, enthusiasm, and energy
Low in depression (e.g., anhedonia)
Normal in anxiety
Physiological Hyperarousal (PH):
Physical symptoms like racing heart, shortness of breath, tension
High in anxiety
Low or absent in depression
How to Use the Tripartite Model to Differentiate:
Both anxiety and depression = High Negative Affect
Depression = Low Positive Affect
Anxiety = High Physiological Hyperarousal
What is the diathesis stress model?
Psychological framework that explains how mental disorders develop from the interaction between a vulnerability (diathesis) and environmental stressors
Diathesis: a predisposition or vulnerability to a disorder, can be biological (e.g., genetics), psychological (e.g., cognitive), or environmental (e.g., early trauma)
Stress: life events that trigger the disorder
Interaction: A disorder may not manifest unless the stress activates the underlying diathesis, some individuals may have a high vulnerability but never show symptoms without a major stressor
Utilizing Ellis and DelGuidice 2019- briefly define the Adaptive Calibration Model and provide some of the potential evidence for its existence
Theory that explains how children's stress response systems (particularly the HPA axis) adapt to environmental conditions. It suggests that variation in stress responsivity is not inherently pathological but instead can be adaptive depending on the context.
Evidence:
Research shows different patterns of cortisol reactivity in children exposed to varying levels of adversity e.g., blunted cortisol in chronically stressed or maltreated children (consistent with the unemotional profile)
Early life stress and behavior: children in unsafe or unpredictable environments often show vigilant or hyper responsive behaviors- e.g., increased sensitivity to threat cues - these behaviors are adaptive in some contexts but may look pathological in others
Studies across diverse populations show that stress response variation aligns with environmental demands (e.g., rural vs. urban settings, resource-scarce vs. resource-abundant)
Discuss how sleep problems contribute to emotional dysregulation in children. What are 2 evidence-based interventions for pediatric sleep problems?
Sleep problems significantly contribute to emotional dysregulation in children by impairing brain's ability to manage stress, control impulses, and regulate mood.
Inadequate or poor sleep quality sleep disrupts activity in key areas of brain such as PFC and amygdala, leading to increased irritability, mood swings, difficulty managing frustration, and heightened reactivity
Sleep, particularly REM sleep, is linked to processing and regulating emotions. During REM, the brain replays emotional experiences, helping to “detox” strong emotional responses.
Children with chronic sleep issues often show more symptoms of anxiety, depression, and behavioral disorders, and may struggle with peer relationships and academic functioning due to poor emotional control
Interventions: Bedtime fading (Piazza and Fisher, 1991), CBT-I (CBT for insomnia) focuses on identifying or modifying unhelpful thoughts or behaviors related to sleep, including sleep hygiene education/relaxation training
Discuss the implications of polygenic inheritance for diagnosis and intervention in developmental psychopathology
Shift from a gene for disorder model to recognizing that multiple genes influence the development of a disorder (not just one anxiety gene)
Implications for diagnosis: shift from categorical to dimensional thinking, conditions exist on a continuum with normal variation
polygenic inheritance supports assessment psychopathology along dimensions of severity and frequency
Diagnostic cutoffs are arbitrary because of human variation (goal of diagnosis is then on identifying when naturally occurring tendencies become harmful)
No genetic tests for most disorders
Places importance on understanding family history
Implications for intervention: focus on management, not elimination; shifts from eliminating the problem to managing behavioral tendencies
Personalized and multimodal approaches
Explain how PTSD may be misdiagnosed as ADHD or depression- what are the implications for treatment?
Hypervigilance may look like hyperactivity
Concentration problems with both, impulsivity in response to trauma; hyperactivity is more situational or episodic in PTSD, may be hard to differentiate between this versus continuous problem (especially if trauma has not been disclosed)
Misdiagnosed as depression: overlap in symptoms, social withdrawal, sleep distrubances, low mood, irritability (clinicians may overlook trauma history and focus on affective symptoms)
Implications for treatment: leads to inappropriate treatment (stimulants or antidepressants without addressing trauma), may worsen symptoms if trauma is ignored or potentially re-traumatize, delays healing and increases risk of chronic mental health issues
How to avoid misdiagnosis: always consider trauma as a potential factor (individuals may not readily bring it up)
Use trauma informed assessment/interviews
Consider symptom context and function
Collaborate with caregivers and school providers to gather more information
How would the ACM and ALM differ in explaining behavioral outcomes of children living in poverty?
ALM: Poverty exposes children to chronic stress, which over time accumulates - allostatic load, or biological wear and tear that impairs emotional, cognitive, and physical health/functioning
Name and describe two transdiagnostic factors, associated diagnoses, and mechanisms of each
Executive dysfunction: impairment in higher order cognitive processes such as working memory, cognitive flexibility, planning, inhibition
Associated diagnoses: ADHD (impulsivity, poor attention, difficulty with organization); Depression (difficulty initiating tasks, impaired decision making); ASD (trouble with flexibility and planning); Anxiety (shifting/flexibility)
Mechanisms: genetic, teratogens, environmental/chronic stress
Irritability: a low frustration tolerance, frequent anger, proneness for temper outbursts
Associated diagnoses: Depression, anxiety disorders, DMDD, ODD, ADHD
Why is inter-rater agreement often low among parents, teachers, and clinicians? How should clinicians manage this discrepancy?
Low agreement due to different perspectives, contexts, and normative frames of reference
Perspectives: stress of parent or teacher can change degree to which they recognize behavior as problematic; Emotional involvement of parents can sometimes lead to exaggeration of problems
Contexts: parents observe child in variety of spaces, teachers observe child in structured setting, clinicians observe for a brief period in novel/unfamiliar environment
Normative reference: parents can misunderstand normal behavior, teachers have better frame of reference due to seeing many children
Inter-rater agreement tends to be higher for externalizing behavior vs. internalizing
How can clinicians manage discrepancy? Triangulate information, weigh sources of info based on clinical judgement (consider each informant's context, potential biases, normative reference), focus on impairment across settings, identify inconsistencies and explore potential reasons (ask follow up questions), educate informants on typical childhood development, consider transdiagnostic factors that might look different across contexts
Define GE-I, GE-C
Passive GE-C, Evocative GE-C, Active GE-C; provide examples for each
Gene Environment Interaction: genetic predispositions moderate how an individual responds to environmental influences (E.g., a child with genetic vulnerability for depression may develop depressive symptoms if exposed to significant life stressors, whereas a child without genetic risk might not be as impacted by same environment)
Gene Environment Correlation: Genetic factors influence the environments individuals are exposed to or select, genes and environments are not independent
Passive: Parents provide both genes + environment (E.g., genetic predisposition for reading ability + house filled with books and frequent reading supports reading ability)
Evocative: An individual's genetically influenced traits elicit specific responses from others (E.g., temperamentally irritable child may receive more negative feedback from others, which in turn influences social development)
Active: Individuals actively seek out environments that align with their genetic tendencies (E.g., a genetically extroverted child may choose to join drama club, enhancing social skills + reinforcing extroverted behaviors)
List component parts of an anxiety/phobic response with several indicators of each component
Choose an anxiety-trauma, OCD, related disorder and describe the anxiety/phobic response characteristic of the disorder using the components
Cognitive component: involves thoughts, beliefs, mental appraisals related to perceived threat (e.g., catastrophizing)
Physiological Component: Bodily responses triggered by the automatic nervous system (e.g., increased heart rate, shortness of breath)
Behavioral Component: Observable actions taken in response to or in anticipation of anxiety (e.g., avoidance, escape)
Emotional/Affective Component: Subjective emotional experience associated with fear or anxiety (e.g., feelings of fear, dread, panic)
Example: Panic Disorder
Cognitive: experiences catastrophic misinterpretations of bodily sensations (e.g., I am having a heart attack)
Physiological: onset of intense physical symptoms associated with panic (e.g., racing heart, shortness of breath)
Behavioral: avoidance of situations which in the past have induced panic
Emotional: intense fear or dread during panic attacks or intense worry between episodes (e.g., ongoing anxiety about when the next attack will happen)
Allostatic Load- cumulative wear and tear on the body due to chronic repeated exposure to stress
When facing stress, body's stress response systems (e.g., HPA axis + sympathetic nervous system) activate to help us cope (i.e., allostasis- body's ability to return to stability/adapting through change)
This process is beneficial in the short term, because it releases stress hormones (cortisol and adrenaline) necessary for fight or flight
If stressors are chronic, repeated or if stress response fails to shut off (even after the stressor is gone), leads to allostatic load, or long-term physiological cost of ongoing or poorly managed physiological arousal
What are transdiagnostic factors? Name 3 and how they contribute to multiple psychiatric conditions.
Transdiagnostic factors are underlying processes or traits that contribute to the development or maintenance of multiple psychiatric disorders, rather than being specific to just one diagnosis. Helps to explain comorbidity and why individuals may shift between diagnoses over time
Emotional dysregulation (depression, anxiety, BPD)
Irritability: ADHD, ODD, DMDD, Depression, Anxiety, PTSD
inattention: anxiety, depression, ADHD, ASD
Discuss how cumulative exposure to stressors might alter gene expression and state the specific physiological process that modifies gene expression
Prolonged exposure to stress during the development can influence gene expression through the process of epigenetic modification, specifically DNA methlyation
Mechanism:
Stress activates the HPA axis, increasing cortisol and other stress hormones
Chronic HPA activation can lead to methylation of glucocorticoid receptor genes, reducing the body's ability to regulate stress effectively
This can alter brain development (especially in PFC and amygdala) and result in long term changes in behavior and emotional regulation.
Using the concept of "goodness of fit", explain how understanding a child's genetic tendencies can guide environmental interventions
Originates from Thomas and chess's work on temperament- optimal child development occurs when there is a compatibility between a child's inherent characteristics, and opportunities in their environment
How to create a better fit:
Identify inherent tendencies instead of just labeling a child anxious or ADHD (e.g., identifying underlying traits like low impulse control)
Remember normal variation, variation in behavioral tendencies is normal and we are not trying to eliminate "defective" part of a child
Tailor environmental demands and opportunities: adjust expectations (e.g., provide movement or fidget breaks), modify and build structure/routine, adapt parent and teaching styles (e.g., providing predictable routines and clear structure)
Facilitate active gene-environment correlation: help children choose adaptive environments
Prevent "poor fit" and promote resilience through early identification, mitigating risk factors, change the environment to be more supportive
Explain the concept of equifinality and multifinality and provide examples of each using disorders/symptoms from risk factor research
Example- any child with MDD could have developed it through many distinct pathways like strong genetic predisposition to depression, experience with chronic peer rejections, etc.
Multifinality- same condition or risk factor can lead to multiple different outcomes or disorders
Example- child experiencing severe maltreatment (i.e., ACEs- a significant risk factor) could lead to a wide array of outcomes
E.g., PTSD, BPD, CD, GAD, MDD
Allostatic load- its relevance for understanding the long-term effects of childhood adversity
Long term effects of accumulated allostatic load can lead to
Physical health problems (cardiovascular disease)
Brain functioning: deficits in PFC, nucleus accumbens
Increased vulnerability to MH disorders
Behavioral and cognitive deficits: impairment in attention/EF
Intergenerational transmission: parents who experienced high allostatic load may have impaired parenting capacities, which may inadvertently expose child to chaotic/stressful environment
Briefly describe the role of stress in the lives of P -12 students and how exposure to stressful life events and circumstances might influence the development of intervention plans to assist children with behavioral or academic support. Explain how cumulative risk from such factors as chronic poverty, abuse or neglect, poor mental health of a parent or caregiver, or other stressful components of contexts or environments might influence the effectiveness of any proposed intervention.
When stress is chronic or intense, it can significantly impair attention, memory, emotional regulation, and executive functioning
Students under stress may exhibit:
Academic struggles (e.g., poor concentration, reduced cognitive flexibility)
Behavioral issues (e.g., acting out, aggression, withdrawal)
Emotional dysregulation (e.g., anxiety, irritability, hopelessness)
Evans (2004) introduced concept of cumulative risk exposure, noting that the total number of stressors, not just the presence of any one, predicts poorer developmental outcomes.
Implications for Intervention:
Children exposed to multiple chronic stressors may show blunted stress responses, reduced adaptability, and more persistent behavioral challenges.
Interventions may be less effective unless they also address basic needs, provide environmental consistency, and build protective factors (e.g., adult support, stable routines).
Multisystem approaches may be needed (e.g., coordination between school, mental health services, and family support systems).
Define and Differentiate between risk and protective factors? Why is it problematic to use risk factors as diagnostic criteria?
Risk factor: any behavior, characteristic, or condition that increases the likelihood of developing a particular disease, disorder, or negative outcome. Does NOT imply causation, risk factor simply increases the probability of occurrence
Protective factors: any behavior, characteristic, or condition that decreases the likelihood of a negative outcome, or mitigates the impacts of risk factors
Why problematic to use as diagnostic criteria?
Lack of causation
Lack of specificity- risk factors are transdiagnostic, so they increase the risk of multiple disorders, not just one
Equifinality- same disorder can develop from many different pathways
Multifinality- same risk factor can lead to different disorders/outcomes
No direct clinical utility for diagnosis: helps us to conceptualize the case but cannot be used to diagnose; diagnosis requires observable behaviors
Risk of stigmatization or mislabeling; using environmental or demographic risk factors (e.g., poverty/family structure) can lead to inappropriate labeling
Describe some of the potential pathways in which poverty may impact mental health
(Evans, 2004) – Poverty's Impact Begins Pre-Pregnancy and In Utero:
Diminished Access: Poorer areas lack access to sexual education, reproductive care, and safe contraceptives.
Unsafe Behaviors & Poor Prenatal Care: Pregnant women in poverty may engage in drug/alcohol use (knowingly or unknowingly) and receive inadequate prenatal care (fewer appointments, poor nutrition/vitamins, unhealthy prenatal environments).
Direct Infant Risk: These factors increase the risk for: Infant substance abuse or fetal alcohol syndrome, Spina bifida (from low folic acid), and a range of neurodevelopmental outcomes (from maternal drug/alcohol use, low folic acid, higher maternal stress).
Lack of Environmental Richness in Childhood:
Unsafe Neighborhoods: Leads to limited safe outdoor play areas.
Fewer Educational Resources: Impoverished households have fewer books, which predicts lower scholastic achievement.
Parental Stress & Capacity: Parents in poverty are more likely to be: Disabled, In single-parent or multi-generational households, Working multiple jobs or long hours.
Childcare Challenges: Difficulty obtaining accessible, affordable, or quality childcare.
Parenting Practices: Parents may be less responsive and use more authoritarian parenting styles.
Child's Experiences: Children may have increased passive screen time (McArthur et al., 2022) and fewer opportunities for environmental exploration.
Developmental Deficits: These factors contribute to lack of development in: Problem-solving skills. Behavior and cognitive regulation skills. Enhanced vocabulary and language skills. (Any of which can be implicated in mental health disorders).
School-Related Risk Factors:
Unsafe School Environments: Low-income schools have a higher presence of weapons and physical assaults.
Teacher Quality & Management: More likely to have underqualified, newer teachers, leading to poorer classroom behavior management and less quality instruction time.
Limited Opportunities: Students have less access to extracurricular activities.
Poor Facilities & Support Staff: Schools tend to be older, with fewer support staff (speech-language pathologists, behavior interventionists, school psychologists).
Undiagnosed Disabilities: Can lead to under-recognized or under-diagnosed educational or behavioral disabilities.
Negative Outcomes: Unsafe, unwelcoming, and under-funded schools lead to higher risk of behavior, academic, or mental health problems.
Poverty and Maslow's Hierarchy of Needs:
Unmet Basic Needs: When physiological and safety needs are not met due to under-resourced environments Higher Needs Unattainable: More advanced needs (love & belonging, self-esteem, self-actualization) cannot be pursued or achieved Increased Mental Health Risk: When psychological/emotional needs are unmet, or met through immature/maladaptive behaviors, the risk for mental health problems increases.
Poverty and the Adaptive Calibration Model (ACM):
Increased Stress & Faster Life Trajectory: Impoverished children and adolescents face higher environmental and personal stress, leading to a "faster life trajectory." Behavioral Manifestations: This faster trajectory contributes to: Greater impulsivity. Engagement in risky behaviors (e.g., substance use, risky sexual behavior), Increased mortality.
Epigenetic Changes: Environmental stress can cause epigenetic changes to the nervous system, leading to genetic modifications across generations, perpetuating the cycle of risk even with environmental changes.
What is emotion socialization and how is it relevant to BPD?
Emotion socialization- the process by which parents and other caregivers influence a child's understanding, experience, expression, and regulation of emotions. Happens through multiple mechanisms:
parental reactions to child's emotions
Parental emotion expression
parental discussion of emotions
general atmosphere of emotional expression
Biosocial development model of BPD (Marsha linehan)- BPD rises from transaction between a child's biological vulnerability( e.g., high emotional sensitivity) and an invalidating environment
Invalidating environment: Child's emotional expression are consistently dismissed, punished > child learns feelings are wrong or exaggerated, and their emotional responses are inappropriate
Describe how life history theory explains the development of "fast" v. "slow" strategies in children exposed to different environmental conditions
Explains that humans develop "fast" or "slow" strategies for allocating their limited resources (time, energy) towards growth, reproduction, and survival based on their perception of environmental conditions (specifically regarding harshness and predictability; Stearns, 1992)
Fast strategies: develop in unpredictable or harsh environments with scarce resources and survival to old age in uncertain environments
Natural selection favors traits that prioritize early reproduction, high risk taking, and short term survival Goal is to maximize chances of passing off genes quickly before individual succumbs to environmental threats
Behaviorally- riskier, more dangerous lifestyles because they want to grow up/live faster and might not have as long to live
Characterized by early puberty, more offspring with less parental investment, focus on immediate gains over future planning
*High levels of cortisol related to this strategy
Slow strategies: develop in predictable/safe + resource rich environments, where there is higher liklihood of long term survival and successful investment in offspring
Individuals can afford to invest more in growth in development, long term survival and stable relationships
Behaviorally: delay reproduction, investing fewer, high quality offspring through significant parental care, prioritizing future oriented behaviors like education and skill acquisition
How does equifinality complicate diagnosis and treatment planning in child psychopathology. Provide examples
Equifinality: all diagnostic categories have multiple causal pathways, no single path to getting any of the diagnoses
How it complicates diagnosis:
Challenges to identify "the cause" of the disorder, and symptom presentation for one child can look the same as another but underlying factors could be different
Difficulty with differential diagnosis; presentation could look the same, but underlying mechanism could be different (e.g., selective mutism vs hearing impairment)
Diagnostic heterogeneity- children with same diagnosis can have different presentations
Need for comprehensive assessment
comorbidity- child can meet criteria for multiple diagnoses, making it difficult to determine "primary"
Example: pathways leading to ADHD can include genetic predisposition, prenatal drug exposure, toxic stress, sleep deprivation, undiagnosed LD, anxiety
Intervention development:
challenges to one size fits all approach
Knowing a diagnosis does not tell you WHY a child has that diagnosis, the treatment should target underlying mechanism for a specific child
Focus on individualized treatment
Example: Child diagnosed with ADHD, if primary pathway is believed to be genetic/neurobio- ef training and stimulants
If pathway is thought to be influenced by chronic stress- interventions should focus on strengthening family relationships, lessening family stress etc
Describe the difference between the adaptive calibration model and the and allostatic load model
in terms of cost benefit trade offs
individual differences
cost benefit:
ACM: to be adaptive , a trait does not have to be cost free- only yield a positive overall contribution to fitness
ALM: adaptive refers to traits and behaviors that are socially desirable
Individual differences:
ACM: consider heightened stress responsivity in dangerous, unpredictable environment (e.g., vigilant) - hypothesized that the cost of repeated stress activation is offset by improved management of danger >leading to increased anxiety, but few instances of danger will be missed
ALM: globally optimal responsivity levels; same pattern of responsivity would be treated as dysfunctional bc stress response may be deployed even in absence of true danger