Week 4 - Prenatal and postnatal exposures - BB(3)
Page 1: Introduction
Focus on prenatal and postnatal environmental exposures.
Presented by Dr. Alyson Dodd.
Page 2: Recap Last Week
Discussed aspects of genes:
Genetic predisposition
Heritability, genetic variants, and polygenic risk scores.
Pleiotropy:
Overlap in disorders.
Similarities in adult and child psychopathology:
Earliest manifestations and prediction of multiple disorders by PRS.
Emphasis on small effects in complex multifactorial disorders.
Page 3: Lecture Structure
Key Topics to be covered:
Importance of early development.
Examples of environmental risk factors:
Maternal infection
Alcohol exposure
Maternal distress
Concept of cumulative risk.
Page 4: Learning Outcomes
Understand how environmental challenges affect early development (prenatal & infancy).
Critically evaluate the relationship between prenatal/postnatal exposures and psychopathology.
Page 5: Missing Heritability
Discrepancies between twin and genome-wide association studies (GWA):
Potential reasons include:
Overestimation of genetic contributions.
Smaller, less noticeable effects not detected.
Rarer genetic variants might be overlooked.
Importance of environmental factors, particularly in infancy and childhood (Joseph, 2012).
Page 6: Early Environmental Factors
Prenatal influences (before birth):
Womb as the initial environment.
Importance of the infancy stage and its critical developmental impact.
Page 7: Critical Nature of Early Development
Plasticity in development most active during early stages.
Key developmental processes include:
Proliferation, pruning, myelination.
Cortical specialization:
Role of expectable stimuli and experiences in critical/sensitive periods (Nelson & Garbard-Durnam, 2021).
Page 8: Developmental Insults
Definition of developmental 'insults' or hazards:
Violations of expected environments (absence or presence).
Enhanced impacts during critical periods:
Molecular brakes help maintain structure and function.
Applies to both typical and atypical development (Nelson & Garbard-Durnam, 2021).
Page 9: Vulnerability of Developing Brain
Blood-brain barrier: not fully formed in the developing brain.
Vulnerability of growing cells.
Limited ability to break down toxins (Lanphear, 2015; Nelson & Garbard-Durnam, 2021).
Page 10: Impact of Toxins
Different toxins affect various developmental processes.
Windows of vulnerability exist, but not fully understood.
Complex and prolonged exposures can yield more severe negative effects (Lanphear, 2015; Nelson & Garbard-Durnam, 2021).
Page 11: Prenatal Infection and Psychopathology
Focus on pathogens, including viruses.
Increased interest in COVID-19 related outcomes.
Mechanisms linking prenatal infections to offspring psychopathology include:
Epidemiologic data from pandemics.
Biomarkers from maternal serum.
Hospital records and self-reports, all of which have limitations (Cheslack-Postava & Brown, 2022; Suleri et al., 2023).
Page 12: Mechanisms of Infection Exposure
Direct effects if infections cross the placenta, damaging the developing brain.
Indirect effects include:
Perinatal transmission and maternal immune activation.
Inflammatory cascades disrupting brain development.
Concept of a two-hit model that primes the immune system (based on animal models; Suleri et al., 2023).
Page 13: Infection Exposure and Psychopathology
Insights from a longitudinal population-based cohort study covering various infections during pregnancy.
Controlled for factors such as polygenic risk and early environmental influences.
Findings indicate that greater exposure correlates with increased psychopathology (total, internalizing, externalizing) across all trimesters (Suleri et al., 2023).
Page 14: Neurodevelopmental Disorders
Retrospective cohort studies in US hospitals show that maternal COVID-19 exposure links to higher rates of neurodevelopmental disorders in offspring.
Notable areas affected include:
Motor function, speech, and language during the first 12 months (Edlow et al., 2022).
Page 15: Schizophrenia Risk
Review of studies identifying increased risks for offspring exposed to:
Influenza, Toxoplasma gondii, and bacterial infections.
Less evidence found for herpes virus impacts.
Risk factors may interact with protective factors (Cheslack-Postava & Brown, 2022).
Page 16: Alcohol Exposure and Psychopathology
Alcohol is a teratogen that can cross the placenta.
Linked to Fetal Alcohol Spectrum Disorder (FASD) and subsequent developmental milestones.
Statistics indicate that 9.8% of alcohol use in pregnancy in the UK, with a 41.3% prevalence of alcohol exposure in general populations (Popova et al., 2017; Subramoney et al., 2018).
Page 17: Fetal Alcohol Spectrum Disorder (FASD)
Key characteristics include:
Distinctive facial dysmorphia.
Various health problems, intellectual disabilities, and delays in language, motor skills, and cognitive functions.
Associated behaviors include attention issues, hyperactivity, and aggression.
Page 18: Alcohol and Developmental Outcomes
Multiple detrimental outcomes from prenatal alcohol exposure identified through studies:
Dose-response relationship.
Developmental cascades observed, with postnatal environment potentially masking or exacerbating effects (Subramoney et al., 2018).
Page 19: Alcohol's Broader Impacts
Studies suggest even lower levels of alcohol exposure (not leading to FAS) are linked to increased risks of:
General problems, anxiety, depression, and conduct disorders.
Less evidence connecting prenatal alcohol exposure to internalizing or emotional problems (Easey et al., 2019).
Page 20: Early Exposure to Parent Distress
Interaction of genetic and environmental risk factors in development.
Pregnancy exposure leads to:
Biological pathways regarding the HPA axis regulation and prenatal stress hormones.
Childhood exposure involves environmental factors such as parenting.
Not designating intergenerational transmission as deterministic (Aktar et al., 2019; Bailey et al., 2021).
Page 21: Maternal Distress and Psychopathology
Longitudinal studies show strong links between maternal depression/stress during pregnancy and increased risk of psychopathology in adolescence.
Patterns of exposure leading to either stability at low levels or increased psychopathology.
Page 22: Prenatal Stress and Schizophrenia Disruption
Evidence indicates prenatal maternal stress heightens schizophrenia spectrum disorder risks.
Additional factors during pregnancy and potential postnatal insults contribute to risk cascades (Lipner et al., 2019).
Page 23: Cumulative Effects on General Psychopathology
Adverse cumulative prenatal exposures lead to dimensional psychopathology symptom development.
No clear association with childhood psychopathology linked to:
Birth method, preterm birth, substance use, or post-pregnancy substance use (Roffman et al., 2021).
Page 24: Cumulative Effects Insight
Contrasts with findings where cumulative effects of prenatal exposures (like unplanned pregnancy and substance use) are associated with dimensional psychopathology in childhood.
Note that none alone significantly increased risk (Roffman et al., 2021).
Page 25: Additional Considerations
Areas not covered in depth:
Medications (e.g., valproate)
Birth complications
Parental age, birth weight, timing of birth, diet, and potential accidents/injuries.
Page 26: Summary
Emphasizes the importance of both prenatal and postnatal environments in relation to psychopathology risk factors.
Highlights known (e.g., FASD) and potential correlates, recognizing the complexity of cumulative risk as it intersects with genetic factors.
Page 27: Exam Question
Prompt: Critically discuss how environmental factors during prenatal and postnatal periods may influence the risk of developing psychopathology.
Page 28: Core Reading
Essential and recommended readings covering various studies and findings related to environmental influences on psychopathology.
Notable citations include works by Roffman et al. (2021), Suleri et al. (2024), and others.
Page 29: Additional References
List of references augmenting core reading, including pivotal studies relating to perinatal mental health and environmental impacts on psychopathology.