Social Environment and Mental Illness

• This review explores the relationship between the social environment and neurobiology in the emergence of mental illness in young individuals

Introduction

• The social environment and experiences of adversity profoundly impact cognitive, social, and emotional function in young people
• Childhood adversity stands out as a strong indicator for the emergence of mental illness during the first two decades of life
• Alterations in brain development are thought to contribute to mental illness onset
• Better prevention and intervention strategies can reduce the burden of child and adolescent mental illness
• Research explores the dynamics between the social environment and neurobiology shape emergence of mental illness
• Brain plasticity, which is high during childhood and adolescence, enables the brain to reorganize neural pathways based on environmental input
• Critical mechanisms of plasticity: overproduction/elimination of synapses during childhood/adolescence
• Also, overproduction of neurons in early development, apoptosis, and alterations in central nervous system receptors can impact plasticity
• Pertinent to mental illness development is recognizing that social environmental exposures during increased brain plasticity periods may alter neurodevelopment
• Altered neurodevelopment can change susceptibility to mental health problems using experience-expectant or experience-dependent processes
• Experience-expectant processes: changes due to presence/absence of environmental stimuli the neural system expects early in life.
• Expected inputs during sensitive periods can increase impact on brain organization
• Experience-dependent plasticity: the brain can reorganize and adapt based on individual experiences/environmental stimuli
• Experience-dependent plasticity occurs through the lifespan but diminishes when brain matures
• Adverse experiences contribute to experience-dependent plasticity

Models of Neurodevelopmental Mechanisms Linking the Social Environment with Psychopathology (i.e., Mediation Models)

• Theories explain neurodevelopmental mechanisms linking adverse social environmental experiences with mental health
• Adverse experiences directly impact the developing brain, which increases the risk of developing psychopathology
• The Stress Acceleration Hypothesis (SAH) builds on evolutionary theories to posit faster biological development is an adaptive strategy for earlier reproduction in adversity
• SAH proposes adverse experiences, especially related to caregiving, lead to faster neurodevelopmental processes for reaching "adult-like" functioning earlier
• Specifically, the accelerated development of emotion-processing, emotion regulation, and memory brain regions
• Adaptive to transition from parent-regulation to self-regulation sooner when parental care is missing or inconsistent
• Precocious development of circuitry may cause impairment in emotion regulation abilities and creates long-term mental health consequences
• Originally posited for caregiver-related adversity, the SAH model was extended to early adverse experiences with chronic stress
• Chronic stress accelerates brain development through the SAH process, repeated use of stress-regulation circuitry, increasing glucocorticoid levels, and activating inflammatory processes
• Adversity, specifically low socioeconomic status, is likely associated with a slower brain development pattern across childhood and adolescence
• Prediction that adversity and low socioeconomic status are associated to slower brain development came from longitudinal evidence
• Slow rate-of-change and persistently lower cortical thickness, area, and volume throughout childhood and adolescence may mediate links with poor mental health
• Specific mechanisms suggested include impaired synaptic pruning and slower neural circuit refinement
• Latent vulnerability theory suggests that early maltreatment creates an underlying latent vulnerability that increases future mental health risk
• This latent vulnerability involves alterations to neural systems modulating threat processing, reward-processing, executive control, and emotion regulation
• Alterations aren't specified to accelerate or delay neural development

Empirical Evidence for Mediation Models from Longitudinal Studies

• Others' reviews include both cross-sectional and longitudinal studies or don't focus on studies investigating mental health outcomes using statistical tests for mediation; since models predict developmental trajectories, cross-sectional data is inappropriate
• Cross-sectional examinations of brain structure/function/connectivity can provide useful information about the impact of environmental exposures on development
• Longitudinal research is needed to test deviations from typical developmental trajectories as proposed models
• Studies investigating the links between adverse social environments and brain development help to test models
• Interpretation of adaptive versus maladaptive nature of adverse environmental impacts on brain development was tested through mental health outcomes and statistical tests of mediation
• Studies of longitudinal neurobiological mediators of associations between adverse social environmental variables and mental health outcomes reviewed to determine impacts
• Links identified with mental health point to adaptive and maladaptive neurobiological changes after adversity that support the SAH, Tooley et al., and the latent vulnerability theory
• Both childhood abuse and neglect associated with increased within-salience network (SN) resting-state connectivity between ages 16 to 19
• The pattern of connectivity mediated associations with lower problematic substance use and higher depressive symptoms
• Maltreatment-associated increases in SN connectivity may be associated with reduced reward sensitivity which decreases the likelihood of adolescents engaging in risky but rewarding behaviors & increase the risk for depression
• Adversity-related alterations in resting-state connectivity development have been reported to be similarly associated with more positive mental health outcomes
• Lifetime negative life experiences linked to reductions in cortico-limbic resting-state functional connectivity over time (from age 9 to 13), which is associated with lower internalizing symptoms
• Normative patterns of connectivity development reflect accelerated maturation of neural circuitry for emotion processing/regulation, which improves wellbeing
• Aligns with the integrated model of dimensions of environmental experience and change of pace theory
• Increases in connectivity between cortical networks (default mode, frontoparietal, dorsal attention, salience networks) from age 16 to 19 mediated the relationship between childhood maltreatment and later depressive symptoms
• Findings potentially driven by neglect experiences
• Delayed functional connectivity development may reflect a mechanism that underlies cognitive impairments in depressed adolescents with deprivation history

Models of Neurodevelopmental Factors That Modify Associations Between Social Environmental Factors and Mental Health (i.e., Moderation Models)

• Person-by-environment interaction frameworks are used to understand individual risk or vulnerability to mental health problems
• People are variably influenced by environmental factors and one source of variability is person-centered factors, like brain structure and function
• Developmental theories purport that there is an "optimal" trajectory of human development that adversity can derail
• Evolutionary-developmental theories argue that there is no single optimal trajectory of development
• Instead, humans evolved to develop in adverse and supportive environments and there could be multiple adaptive developmental trajectories
• Optimal development is context-dependent, focusing on early social environments that are negative/adverse, marked by chronic stress, or positive/supportive/low stress
• The models where neurobiology is used to examine interactions b/w biology and environment in relation to psychopathology in kids/adolescents
• The broad class of developmental theories includes the dual-risk model, diathesis-stress theory, and cumulative stress theory
• Certain individuals possess inherent vulnerabilities to poor developmental outcomes, including psychopathology, that can be triggered by environmental stressors
• Cumulative stress theory suggests at-risk individuals are more likely to develop psychopathology if there's an accumulation of stressors exceeding a certain threshold across the lifespan
• the biological diathesis is not adaptive
• Evolutionary-developmental models argue that individuals vary in their susceptibility to environmental influence, for better/worse
• Highly susceptible individuals benefit more from supportive environments and suffer more in adverse circumstances, compared to those with low susceptibility
• Differential susceptibility theory doesn't discount dual-risk/diathesis-stress processes. The same biological factor could lead to different outcomes in different contexts
• Match/mismatch hypothesis, which posits those with high "programming sensitivity" are more likely to be at mental health risk if there's a mismatch between early programming environment and later adult environment

Integration of Models

• A relatively consistent patterns have surfaced
• Increased striatal reactivity to positive/rewarding stimuli appears to reflect a vulnerability or diathesis associated with high internalizing problems within in the context of a negative social environment
• Larger hippocampal volumes appeared to reflect a susceptibility marker related to those higher internalizing problems within in the context of a negative social environment

Limitations of the current literature and future directions

• The current theories and most of the literature centers around risk factors and deficits associated with brain development and mental health
• This oversimplifies the complexity of development, with other factors often overlooked
• Also, contributes to the stigmatization of mental illness
• Shifting focus towards towards resilience rather than risk could potentially address these limitations
• Regarding adaptive brain changes, there are open questions about whether these brain changes are inherent or driven by supportive environments

Type of enviroment and timing of environmental and brain measures

• Early and mid-adolescent periods has been suggested as particularly important for the expression of differential susceptibility
• Some have suggested that measures of neurobiology may be more likely to reflect susceptibility during adolescence relative to other periods
• More studies of early-mid childhood are needed to test mediation-based theories, particularly those focusing on the early rearing environment or early adversity
• The authors also mention the need that the timing of the exposure of the social environmental factor of interest is likely importnat in shaping neurodevelopment