Teratogens and Their Potential Impact on Mental Health: A Multifactorial Perspective
Abstract
Teratogens—agents that disrupt normal embryonic or fetal development—are increasingly recognized as critical contributors to neurodevelopmental and mental health disorders. While the classical focus has been on maternal exposures during pregnancy, recent advances highlight the importance of both maternal and paternal preconception exposures, mediated through genetic and epigenetic mechanisms, in shaping offspring brain development and subsequent mental health outcomes. This paper provides a comprehensive review of the mechanisms by which teratogens affect reproductive cells and prenatal brain development, leading to brain malformations and a spectrum of mental health disorders. It synthesizes evidence linking specific teratogens (e.g., alcohol, drugs, environmental toxins) to neurodevelopmental outcomes, details the brain abnormalities associated with major psychiatric conditions, and examines the interplay of biological, environmental, and psychosocial factors—including parental neglect, malnutrition, and abuse—in the multifactorial origins of mental illness. Epidemiological data, clinical implications, and public health considerations are discussed, with an emphasis on early intervention and policy. A summary table presents key mental health disorders and their associated brain abnormalities. The report concludes by identifying research gaps and advocating for an integrated, biopsychosocial approach to prevention and intervention. All direct quotations and key concepts from the GROK source are cited accordingly.
Introduction: Definitions and Scope
The etiology of mental health disorders is complex, involving a dynamic interplay between genetic, biological, environmental, and psychosocial factors. Teratogens are defined as substances or agents that cause congenital abnormalities or increase the risk of birth defects when exposure occurs during critical periods of development. Traditionally, research has focused on maternal exposures during pregnancy, such as alcohol, drugs, infections, and environmental toxins. However, emerging evidence underscores the significance of paternal preconception exposures—including lifestyle factors and environmental chemicals—that can induce heritable epigenetic changes in sperm, thereby influencing offspring neurodevelopment and disease susceptibility.
The scope of teratogenic impact extends beyond gross structural malformations to include subtle alterations in brain architecture, connectivity, and function, which may manifest as neurodevelopmental and psychiatric disorders later in life. Mental health conditions such as schizophrenia, autism spectrum disorder (ASD), attention-deficit/hyperactivity disorder (ADHD), depression, and anxiety have been linked to both genetic vulnerabilities and environmental insults during sensitive developmental windows.
This paper aims to synthesize current knowledge on the mechanisms by which teratogens—acting through both maternal and paternal lines—affect reproductive cells and prenatal brain development, leading to brain malformations and mental health disorders. It further explores the role of environmental and psychosocial factors, such as parental neglect, malnutrition, and abuse, in the multifactorial origins of mental illness. The analysis is grounded in the biopsychosocial model, emphasizing the necessity of integrating biological, psychological, and social perspectives for a comprehensive understanding of mental health.
Mechanisms: Teratogens Affecting Reproductive Cells
Maternal and Paternal Contributions
Historically, teratology has emphasized maternal exposures during pregnancy as the primary source of risk for congenital anomalies. However, paternal exposures prior to conception are now recognized as significant contributors to offspring health. Environmental agents—including chemicals, drugs, alcohol, and nutritional deficiencies—can induce epigenetic modifications in sperm, such as DNA methylation, histone modifications, and changes in non-coding RNAs, which are heritable and can alter gene expression in the developing embryo.
For example, studies have demonstrated that paternal folic acid deficiency can lead to skeletal defects in offspring via altered epigenetic programming of sperm histones. Similarly, preconception paternal alcohol exposure has been linked to craniofacial malformations and neurodevelopmental deficits in animal models, with evidence of corresponding epigenetic changes in sperm. Exposure to environmental toxicants such as heavy metals, pesticides, and industrial chemicals has also been associated with increased risk of congenital malformations and neurodevelopmental disorders in offspring.
Epigenetic Inheritance and the Concept of "Epiteratogens"
The term epiteratogen has been proposed to describe agents that, through epigenetic mechanisms, induce congenital malformations when acting outside of pregnancy, including during the formation of gametes. This paradigm shift recognizes that both maternal and paternal exposures—occurring even before conception—can have lasting effects on offspring health by altering the epigenetic landscape of reproductive cells.
Epigenetic mechanisms implicated in teratogenic effects include:
- DNA methylation: Heritable changes in gene expression without alteration of the DNA sequence.
- Histone modifications: Post-translational changes affecting chromatin structure and gene accessibility.
- Non-coding RNAs: Regulatory RNAs that modulate gene expression during development.
These mechanisms enable the transmission of environmental "memories" across generations, influencing susceptibility to neurodevelopmental and psychiatric disorders.
Genetic Susceptibility and Gene-Environment Interactions
Not all individuals exposed to teratogens develop congenital anomalies or mental health disorders, highlighting the importance of genetic susceptibility. Variants in genes involved in drug metabolism, folate pathways, and neurotransmitter systems can modulate individual risk. For instance, polymorphisms in the MTHFR gene (involved in folate metabolism) have been associated with increased risk of neural tube defects and neurodevelopmental disorders following exposure to certain antiepileptic drugs.
Gene-environment interactions are central to the multifactorial etiology of mental illness, with epigenetic modifications serving as a molecular interface between genetic predisposition and environmental exposures.
Mechanisms: Prenatal Brain Development Vulnerability
Critical and Sensitive Periods
The developing brain is characterized by prolonged periods of vulnerability to environmental insults, extending from early gestation through adolescence. Critical periods refer to windows during which specific brain structures or functions are particularly susceptible to disruption, with exposure to teratogens during these times resulting in permanent alterations.
- First trimester: Formation of the neural tube and neurogenesis; teratogenic exposure can cause severe structural malformations such as neural tube defects.
- Second trimester: Neuronal migration and early synaptogenesis; disruption can impair brain organization and circuitry.
- Third trimester: Rapid brain growth, myelination, and synaptogenesis; exposure typically results in functional deficits rather than gross malformations.
The timing, dose, and duration of teratogenic exposure are critical determinants of outcome, with earlier exposures generally producing more severe and widespread effects.
Molecular and Cellular Mechanisms
Teratogens disrupt brain development through multiple mechanisms:
- Interference with neurotransmitter systems: Many psychoactive substances mimic or block neurotransmitters, altering neurogenesis, cell migration, and synaptic formation. For example, cocaine and methamphetamine disrupt dopamine signaling, while opioids and cannabis affect their respective receptor systems.
- Induction of oxidative stress: Environmental toxins and lifestyle factors can increase reactive oxygen species (ROS), damaging DNA, proteins, and lipids in developing neural cells.
- Epigenetic dysregulation: Teratogens can alter DNA methylation and histone modifications, leading to aberrant gene expression during critical periods of brain development.
- Impaired placental function: Some agents reduce blood flow or nutrient delivery to the fetus, indirectly affecting brain growth and maturation.
These disruptions can result in abnormal neurogenesis, increased apoptosis, altered synaptic connectivity, and impaired myelination, collectively contributing to the risk of neurodevelopmental and psychiatric disorders.
Specific Teratogens and Neurodevelopmental Outcomes
Alcohol
Alcohol is one of the most well-established human teratogens, with prenatal exposure leading to a spectrum of outcomes collectively termed Fetal Alcohol Spectrum Disorders (FASD). FASD encompasses physical, cognitive, behavioral, and emotional deficits, including:
- Structural brain abnormalities: Reduced intracranial volume, smaller corpus callosum, caudate, hippocampus, cerebellum, and thalamus.
- Cognitive and behavioral impairments: Intellectual disability, attention deficits, memory problems, executive dysfunction, and increased risk of ADHD and ASD.
- Comorbid neurodevelopmental disorders: High rates of ADHD, autism spectrum disorder, oppositional defiant disorder, and disruptive behavior disorders.
Longitudinal imaging studies confirm that these brain volume deficits persist into adulthood, with stepwise associations between the severity of dysmorphia and the extent of brain changes.
Drugs of Abuse
Opioids, cocaine, methamphetamine, nicotine, and cannabis are associated with a range of neurodevelopmental outcomes:
- Opioids: Neonatal Opioid Withdrawal Syndrome (NOWS), lower birth weight, smaller head circumference, and long-term deficits in motor control and communication.
- Stimulants (cocaine, methamphetamine): Disruption of dopamine and serotonin signaling, leading to emotional dysregulation, executive function deficits, and increased risk of ADHD.
- Nicotine: Reduced birth weight, attention deficits, and increased risk of behavioral problems.
- Cannabis: Interference with the endocannabinoid system, associated with attention problems and cognitive deficits in early childhood.
Polysubstance exposure can result in additive or synergistic adverse effects on neurodevelopment, with evidence of reduced IQ and elevated behavioral problems in exposed children.
Medications
Certain prescription medications are recognized teratogens, including antiepileptic drugs (e.g., valproate, phenytoin), isotretinoin, warfarin, and some immunosuppressants. These agents can cause both structural malformations and neurodevelopmental impairments, such as intellectual disability, language delays, and increased risk of ASD and ADHD.
Environmental Toxins
Heavy metals (lead, mercury, arsenic, cadmium), pesticides, and endocrine-disrupting chemicals (e.g., bisphenol A, phthalates) are linked to neurodevelopmental disorders:
- Lead: Associated with reduced IQ, attention deficits, and increased risk of behavioral problems.
- Mercury: Prenatal exposure (e.g., Minamata disease) causes microcephaly, cerebral palsy, and intellectual disability.
- Pesticides and EDCs: Disrupt hormonal regulation and induce oxidative stress, affecting brain development and increasing risk of ASD and ADHD.
Infections
Maternal infections during pregnancy, such as rubella, cytomegalovirus, and toxoplasmosis, can cause microcephaly, intellectual disability, and sensory deficits, with increased risk of neurodevelopmental and psychiatric disorders.
Malnutrition
Maternal malnutrition, particularly deficiencies in micronutrients like folate and iodine, impairs neurogenesis and myelination, increasing the risk of neural tube defects, intellectual disability, and cognitive deficits.
Brain Abnormalities Linked to Mental Health Disorders
Overview
Neuroimaging and neuropathological studies have identified a range of structural and functional brain abnormalities associated with major psychiatric and neurodevelopmental disorders. While these findings are often non-specific and show considerable heterogeneity, certain patterns have emerged.
Table: Mental Health Disorders and Associated Brain Abnormalities
| Mental Health Disorder |
Associated Brain Abnormalities / Notes |
| Depression (Major Depressive Disorder) |
Reduced hippocampal volume; prefrontal cortex changes; altered amygdala activity; subtle white matter changes |
| Anxiety Disorders |
Hyperactivity in the amygdala and prefrontal cortex; altered connectivity in limbic circuits |
| Schizophrenia |
Enlarged ventricles; reduced gray matter in frontal and temporal lobes; abnormal dopamine activity; cortical thinning |
| Autism Spectrum Disorder |
Abnormal brain morphology; increased or decreased brain volume; altered connectivity; synaptic dysfunction |
| ADHD |
Prefrontal cortex abnormalities; dopamine imbalance; delayed cortical maturation |
| Obsessive-Compulsive Disorder |
Hyperactivity in orbitofrontal cortex, anterior cingulate cortex, and caudate nucleus |
| PTSD |
Reduced hippocampal volume; hyperactive amygdala; impaired prefrontal regulation |
| Borderline Personality Disorder |
Limbic system dysregulation; instability in mood and behavior |
| Intellectual Disability |
Structural and functional brain differences; reduced brain volume |
| Substance Use Disorders |
Dopamine system dysregulation; reduced activity in orbitofrontal cortex and cingulate gyrus |
| Reactive Attachment Disorder |
Limbic system dysfunction; impaired social relationships |
| Catatonic Schizophrenia |
Motor control region abnormalities; motor immobility or excessive movement |
| Down Syndrome |
Intellectual disability; brain development abnormalities |
| Fragile X Syndrome |
Impaired synaptic plasticity; mutations in FMR1 gene |
| Rett Syndrome |
Reduced MeCP2 expression; impaired synaptic plasticity |
Sources: GROK Source
Elaboration and Analysis
Depression is associated with reduced gray matter volume in the prefrontal cortex, hippocampus, and anterior cingulate cortex, as well as altered connectivity in fronto-limbic networks. Functional studies reveal reduced activation in reward circuits and atypical neurotransmitter levels (serotonin, norepinephrine, dopamine, GABA).
Anxiety disorders involve hyperactivity of the amygdala, hippocampus, and hypothalamus, with disrupted regulation by the prefrontal cortex. Neurotransmitter imbalances (serotonin, norepinephrine, GABA) are implicated, and structural imaging shows variable changes in limbic and cortical regions.
Schizophrenia is characterized by reduced gray matter, enlarged ventricles, and abnormalities in the frontal and temporal lobes, anterior cingulate cortex, thalamus, and hippocampus. Dopamine dysregulation is central, but glutamate and GABA abnormalities are also observed. These changes may begin before clinical onset and progress over time.
Autism spectrum disorder shows increased or decreased brain volume, atypical connectivity, and altered activation in social and language processing regions. Subcortical structures (basal ganglia, amygdala) may be involved, and synaptic dysfunction is a key feature.
ADHD involves delayed cortical maturation, particularly in the prefrontal cortex, and dopamine system abnormalities. Imaging studies reveal reduced volume and altered connectivity in attention and executive function networks.
Other disorders such as obsessive-compulsive disorder, PTSD, borderline personality disorder, and intellectual disability exhibit distinct but overlapping patterns of brain abnormalities, often involving limbic and prefrontal circuits.
Parental Environmental and Psychosocial Factors
Parental Neglect, Abuse, and Maltreatment
Early life experiences are critical determinants of mental health. Adverse childhood experiences (ACEs)—including abuse, neglect, and household dysfunction—significantly increase the risk of depression, anxiety, PTSD, borderline personality disorder, and other conditions in adulthood.
- Neglect: Disrupts neural circuits in the prefrontal cortex and amygdala, leading to deficits in attention, working memory, impulse control, and cognitive flexibility. Chronic stress from neglect induces HPA axis dysregulation and epigenetic changes, further compromising neural plasticity.
- Abuse: Physical, sexual, or emotional abuse is strongly linked to mood and anxiety disorders, PTSD, and personality disorders. Maltreatment alters brain structure and function, particularly in the hippocampus, corpus callosum, cerebellum, and prefrontal cortex.
Socioeconomic disadvantage, social isolation, and dysfunctional family dynamics exacerbate vulnerability to mental illness, while strong social support acts as a protective factor.
Malnutrition
Malnutrition during pregnancy and early childhood impairs neurogenesis, myelination, and synaptic development, resulting in cognitive deficits, lower IQ, and increased risk of neurodevelopmental and psychiatric disorders. Both undernutrition and overnutrition (obesity) can affect executive function, attention, and emotional regulation.
Chronic Stress
Chronic stress disrupts the HPA axis, leading to prolonged elevation of cortisol, which damages brain structures such as the hippocampus and impairs cognitive and emotional regulation.
Intergenerational and Transgenerational Effects
Parental exposures and experiences—including stress, malnutrition, and substance use—can induce epigenetic changes that are transmitted to offspring, influencing neurodevelopment and mental health risk across generations.
Interplay of Biological and Environmental Factors (Multifactorial Model)
The Biopsychosocial Model
The biopsychosocial model posits that mental health is determined by the interaction of biological (genetics, brain chemistry), psychological (thoughts, emotions, behaviors), and social (relationships, socioeconomic status, culture) factors. This integrated framework is essential for understanding the multifactorial origins of mental illness.
- Biological factors: Genetic predisposition, epigenetic modifications, neurotransmitter imbalances, brain structure and function.
- Psychological factors: Cognitive patterns, emotional regulation, coping skills.
- Social factors: Family environment, social support, cultural context, socioeconomic status.
Gene-Environment Interactions
Mental disorders rarely result from a single cause. Instead, gene-environment interactions shape vulnerability and resilience. For example, individuals with a genetic predisposition to schizophrenia may only develop the disorder in the presence of environmental stressors or teratogenic exposures.
Epigenetic mechanisms mediate these interactions, translating environmental signals into heritable changes in gene expression that affect brain development and function.
The Exposome Concept
The exposome encompasses the totality of environmental exposures from conception onward, including chemical, nutritional, psychosocial, and lifestyle factors. This holistic approach recognizes the cumulative and interactive effects of multiple risk factors on neurodevelopment and mental health.
Epidemiology and Risk Estimates
Prevalence of Teratogenic Exposures
- Birth defects: Occur in 3–6% of infants globally, with teratogenic exposures accounting for 4–10% of cases.
- Prenatal exposure to teratogenic medications: Affects approximately 1 in 16 pregnancies (6.1% of live births in recent US studies).
- Fetal Alcohol Spectrum Disorders: Estimated prevalence of 617 per 1000 live births for some degree of FASD in certain populations.
- Neurodevelopmental disorders: Affect around 15% of children and adolescents worldwide.
Risk Estimates
- Schizophrenia: Lifetime risk of 1% in the general population; increases to 10% with a first-degree relative, and up to 50% in monozygotic twins.
- ADHD and ASD: Strong genetic and environmental contributions, with heritability estimates of 0.7–0.8 for ADHD and 0.7–0.9 for ASD.
- Malnutrition and low birth weight: Associated with increased risk of cognitive deficits, intellectual disability, and psychiatric disorders.
Disparities
- Socioeconomic and racial disparities: Higher rates of preterm birth, low birth weight, and adverse mental health outcomes among marginalized populations, often due to increased exposure to environmental toxins, poor nutrition, and limited access to prenatal care.
Clinical Implications and Early Intervention
Screening and Early Identification
Early identification of at-risk infants—through universal screening for prenatal exposures and developmental surveillance—is critical for timely intervention. Pediatricians and primary care providers play a key role in screening for prenatal alcohol and substance exposure, as well as for signs of developmental delay or behavioral problems.
Early Intervention Programs
Early intervention can mitigate the long-term effects of prenatal teratogen exposure and adverse childhood experiences. Programs include:
- Developmental screening and evaluation: To determine eligibility for services under mandates such as the Individuals with Disabilities Education Act (IDEA).
- Therapeutic services: Occupational, speech, and behavioral therapy to address motor, communication, and emotional regulation deficits.
- Parent-child interaction therapy: To strengthen relationships and improve parenting skills.
- Family-centered care: Coordinated systems involving medical, behavioral health, and social services to address the multifaceted needs of children and families.
Prevention and Public Health Strategies
- Preconception and prenatal counseling: To reduce exposure to known teratogens and optimize maternal and paternal health.
- Nutritional supplementation: Folic acid and iodine to prevent neural tube defects and support brain development.
- Policy interventions: Regulation of environmental toxins, improved access to prenatal care, and targeted support for high-risk populations.
Ethical, Public Health, and Policy Considerations
Ethical Issues
- Germline interventions: Emerging epigenetic therapies targeting reproductive cells raise ethical questions about unintended consequences for future generations.
- Stigma and discrimination: Individuals and families affected by teratogenic exposures or mental health disorders may face stigma, necessitating sensitive, nonjudgmental care and public education.
- Equity: Addressing disparities in exposure, access to care, and outcomes is a public health imperative.
Policy Recommendations
- Environmental regulation: Policies to limit the use and release of harmful chemicals, improve workplace safety, and reduce environmental injustice.
- Access to care: Expansion of Medicaid and other programs to ensure prenatal care and early intervention services for all populations.
- Education and training: For healthcare providers on the identification and management of teratogenic exposures and neurodevelopmental disorders.
Literature Review: Key Studies and Reviews
A robust body of literature supports the multifactorial origins of mental illness, integrating findings from epidemiology, neuroimaging, genetics, and developmental neuroscience:
- Longitudinal imaging studies confirm persistent brain volume deficits in FASD and other teratogen-exposed populations, with stepwise associations between exposure severity and brain changes.
- Genetic studies reveal shared genetic architecture across multiple psychiatric disorders, with significant overlap in risk genes and biological pathways.
- Epigenetic research demonstrates that both maternal and paternal exposures can induce heritable changes affecting offspring neurodevelopment and mental health.
- Behavioral teratology links prenatal exposure to drugs and environmental agents with increased risk of externalizing disorders (e.g., ADHD, conduct disorder, substance use disorder) and internalizing disorders (e.g., depression, anxiety).
- Environmental health studies highlight the disproportionate burden of toxic exposures and adverse outcomes among marginalized populations, emphasizing the need for policy action.
Discussion: Synthesis and Theoretical Frameworks
Integrating Biological and Environmental Perspectives
The evidence reviewed supports a developmental origins of mental health and disorders (DOMHaD) framework, which posits that all major psychiatric disorders have their roots in early development, shaped by the interplay of genetic, epigenetic, and environmental factors. This perspective aligns with the biopsychosocial model, emphasizing the necessity of considering multiple levels of influence—from molecular to societal—in understanding and addressing mental illness.
Key themes include:
- Transgenerational transmission: Both maternal and paternal exposures can induce heritable epigenetic changes affecting offspring neurodevelopment and mental health.
- Critical and sensitive periods: The timing of exposure is crucial, with certain developmental windows conferring heightened vulnerability to environmental insults.
- Gene-environment interactions: Genetic susceptibility modulates individual risk, with epigenetic mechanisms serving as the interface between genes and environment.
- Cumulative risk: The exposome concept recognizes the additive and interactive effects of multiple exposures over the life course.
- Plasticity and resilience: While early insults can have lasting effects, interventions during sensitive periods can promote recovery and resilience.
Implications for Prevention and Intervention
A multifactorial approach to mental health necessitates:
- Comprehensive risk assessment: Incorporating genetic, epigenetic, environmental, and psychosocial factors.
- Early identification and intervention: Targeting at-risk individuals and families before the onset of clinical symptoms.
- Integrated care: Coordinating medical, behavioral, and social services to address the complex needs of affected populations.
- Policy action: Reducing environmental exposures, promoting equity, and supporting research and surveillance.
Conclusion and Research Gaps
The origins of mental illness are multifactorial, involving the intricate interplay of genetic, epigenetic, biological, environmental, and psychosocial factors. Teratogens—acting through both maternal and paternal lines—can disrupt reproductive cells and prenatal brain development, leading to brain malformations and a spectrum of mental health disorders. The timing, dose, and nature of exposure, as well as individual genetic susceptibility, are critical determinants of outcome.
Environmental and psychosocial factors, such as parental neglect, malnutrition, and abuse, further modulate risk, often through epigenetic mechanisms that can be transmitted across generations. The biopsychosocial model provides a comprehensive framework for understanding and addressing mental illness, emphasizing the need for integrated prevention, early intervention, and policy action.
Research gaps remain, including:
- Mechanistic understanding: Further elucidation of the molecular and cellular pathways linking teratogenic exposures to specific brain abnormalities and mental health outcomes.
- Longitudinal studies: More prospective, multi-generational studies to track the effects of preconception and prenatal exposures over the life course.
- Intervention research: Development and evaluation of targeted interventions, including epigenetic therapies and family-centered care models.
- Equity and access: Addressing disparities in exposure, care, and outcomes among marginalized populations.
In summary, advancing mental health requires a holistic, interdisciplinary approach that integrates biological, environmental, and social determinants, with a focus on prevention, early identification, and equitable access to care.
Table: Mental Health Disorders and Associated Brain Abnormalities
| Mental Health Disorder |
Associated Brain Abnormalities / Notes |
| Depression (Major Depressive Disorder) |
Reduced hippocampal volume; prefrontal cortex changes; altered amygdala activity; subtle white matter changes |
| Anxiety Disorders |
Hyperactivity in the amygdala and prefrontal cortex; altered connectivity in limbic circuits |
| Schizophrenia |
Enlarged ventricles; reduced gray matter in frontal and temporal lobes; abnormal dopamine activity; cortical thinning |
| Autism Spectrum Disorder |
Abnormal brain morphology; increased or decreased brain volume; altered connectivity; synaptic dysfunction |
| ADHD |
Prefrontal cortex abnormalities; dopamine imbalance; delayed cortical maturation |
| Obsessive-Compulsive Disorder |
Hyperactivity in orbitofrontal cortex, anterior cingulate cortex, and caudate nucleus |
| PTSD |
Reduced hippocampal volume; hyperactive amygdala; impaired prefrontal regulation |
| Borderline Personality Disorder |
Limbic system dysregulation; instability in mood and behavior |
| Intellectual Disability |
Structural and functional brain differences; reduced brain volume |
| Substance Use Disorders |
Dopamine system dysregulation; reduced activity in orbitofrontal cortex and cingulate gyrus |
| Reactive Attachment Disorder |
Limbic system dysfunction; impaired social relationships |
| Catatonic Schizophrenia |
Motor control region abnormalities; motor immobility or excessive movement |
| Down Syndrome |
Intellectual disability; brain development abnormalities |
| Fragile X Syndrome |
Impaired synaptic plasticity; mutations in FMR1 gene |
| Rett Syndrome |
Reduced MeCP2 expression; impaired synaptic plasticity |
Sources: GROK Source
Note: All direct quotations and key concepts from the GROK source are cited accordingly. This report integrates findings from a wide range of reputable sources, synthesizing current knowledge on the multifactorial origins of mental illness with a focus on teratogenic mechanisms, brain abnormalities, and the interplay of biological and environmental factors.
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