What is this article about?

There are a lot of therapies with the goal to treat mental disorders. However, there is not much known about how these treatments work, so there is not much known about the processes. This is bad, because understanding which factors facilitate and inhibit therapeutic change can guide researchers in improving treatments, relapse, and recurrence. The complex system approach is used to study change across different physical and natural systems, ranging from cells and neurons to political and economic systems. There have been attempts to use the complex systems science in psychology and psychiatry, but this is a slow process. One reason for this is the randomized controlled trial (RCT) design. RCT is important for evaluating treatment efficacy, but these treatments are often focused at one component of functioning, such as cognitions, emotions, behavior, or physiology, instead of at the multi-component pattern, as in the complex systems approach. Another barrier to the uptake of the complex systems approach is that different subdisciplines in psychology and psychotherapy use different jargon and concepts. This makes it difficult to detect common themes and principles. In this article, the authors advance the complex systems approach by presenting some basic principles in a way that is true to complexity science, and which is accessible to researchers and clinicians. The goal is to provide an integrative framework which helps to translate concepts into a common language and to provide a structure for conceptualizing and studying different treatments and clinical problems.

What are the general principles in complex adaptive systems?

Pattern formation and attractors

A dynamic system is defined as a set of interconnected elements (connected to each other) which evolve over time and self-organize into higher-order functional units, called attractor states. Self-organization is defined as the process by which lower-order processes interact and higher-order patterns emerge and influence lower-order processes in a top-down way. These attractor states predict behavior. When the states are changing, the attractor states ‘attract’ the behavior back to this. Attractor states that are well-established have strong interconnected elements, with reinforcing and inhibiting feedback loops. These feedback loops can decrease or increase the probability of activation over time and contexts. These attractor states do not change easily: there need to be significant disturbance before the patterns are broken. However, less developed attractors are more easily changed.

System change: tipping points and nonlinear transitions

Complex systems can adapt to defend against challenges. There can be deterministic (purposeful, causal) and stochastic (naturally occurring random events, fluctuations, noise) forces which can affect the complex systems. The chance of transitioning from one attractor to another depends on the strength of that attractor, the type of perturbation, the parameters that control system organization, and the strength of alternate attractors. Change can be gradual, but when the parameters reach a ‘tipping point’, the dominant state can shift suddenly. This type of change is often abrupt, with periods of turbulence, in which attractors destabilize and create the potential for phase or order transitions. During these transitions, systems can reorganize into new patterns of functioning, and this may lead one’s health to change from healthy to diseased. It can be important to know when these transitions will occur. For example, early warning signs of symptom exacerbation or transition to disease can inform medici about treatment decisions and can even be a matter of life and death. Therefore, scientists have identified early warning signs that occur often. Two of these early warning signs are critical fluctuations, and critical slowing. Transitions can involve movement from healthy to maladaptive states, but also movement in an opposite direction. For example, critical slowing precedes recovery with interventions.

Patterns are weak, until they are strengthened and stabilized through repeated activation across contexts and by feedback loops. There can also be a period of vacillation or ‘flickering’ between attractors. When a new attractor strengthens, it can compete with a pre-existing attractor to prevent a return to that attractor. For example, when someone is trying to create a healthy habit, their previous (unhealthy) habits are strong. One needs to repeatedly engage in this new healthy habit, until this habit is sufficiently strong, and consolidated and maintained in memory. Processes in complex systems can also operate on different timescales: some move slowly, and others move quickly.

Application to psychotherapy: network destabilization and transition model

The authors developed ‘the network destabilization and transition model’ (NDT) as a framework that includes concepts and principles from complexity sciences (dynamical systems theory, synergetics, and network science) and uses this for psychotherapy research. This model was initially meant to be used in the treatment of depression, but it can be used for psychotherapy in general. The goal of the authors is to stimulate new research and to provide a framework for understanding and organizing findings from different research.

The goal of psychotherapy is to promote new learning, so to move a person from entrenched patterns of psychopathology to more flexible and functional patterns of functioning. Some researchers describe psychopathology as an attractor state with interacting elements between cognitions, emotions, behavior, and physiology. The goal of therapy is to change these patterns and processes. Tschacher and Haken also suggest to consider contextual factors, the therapeutic relationship, and environmental and random factor (stochastic), which can all influence the change process.

There are different routes in which therapeutic change can happen. It can be that more than two patterns are relevant to psychopathology. And, it is not clear whether pathological and healthy states are different networks, or rather parts of a single, large network.

Change in psychotherapy can thus happen in different forms. First, there can be minor adjustments made to maladaptive patterns. For example, harm reduction strategies reduce some negative consequences of pathological patterns. However, they do not lead to complete abolishment of attractor states. For example, think of providing clean needles to drug addicts. Other therapies are distress tolerance, mindfulness, and positive emotion activation approaches. These can change the threshold of activation and automaticity of both pathological and more functional patterns. For example, behavioral, interpersonal, cognitive reappraisal, emotion regulation, or parenting skills can all be used to: reduce feedback loops that block new information and interfere with new learning, deactivate or unhook from the pathological patterns of the attractor, and/or compensate for, or override, new patterns. Also, these strategies can be used to decrease exposure to stochastic factors, or to reduce the influence of these factors. Thus, all of these strategies work within the pathological attractor, but they do not change the attractor directly!

Another type of change refers to ‘switching’ from a pathological to a healthy attractor. To achieve this, there should be an alternative available. For example, the therapist can provide a supportive environment and therapeutic alliance, so to increase the patient’s readiness, resources, and skills to develop healthy behaviors. For example, Beck’s recovery-oriented cognitive therapy for schizophrenia. In this intervention, patients learn to switch from a ‘patient mode’ to an ‘adaptive mode’. Thus, they need to switch from a disorder-focused mode to a mode in which they create positive beliefs, aspirations, strengths, and values. Then, this adaptive mode is constantly activated and exercised to increase its accessibility and strength. Also, the positive emotion activation approaches can help to build more healthy attractors. Further, another type of change involves destabilizing the pathological attractor and developing a new, healthier attractor. This can be achieved by exposure therapy, insight-oriented therapy, and emotion-focused and cognitive restructuring techniques.

What are some important considerations?

The complex systems approach as described is important for psychotherapy research. It emphasizes the need for longitudinal data, the study of discontinuous and nonlinear change, and a focus on patterns of functioning rather than single components.

Data collection considerations

When conducting research with time-series, it is important to select the appropriate time interval, namely the time interval (sampling rate) that is most sensitive for detecting changes in the variables of interest. For example, some variables change slowly, while others change more quickly.

Breadth and duration of assessment

When researchers use microanalytic assessments, such as assessments on a timescale of minutes, the sampling rate is high, but the disadvantage is that the number of variables and the duration of assessments is low. Ideally, researchers should measure pathological patterns and symptoms over the course of therapy, between sessions, and after therapy to capture therapeutic change. Researchers could also gather passive data (activity level, exercise, sleep, social media usage).

Level of analysis

Complex systems is an individual-level approach, and psychotherapy is in contrast often a nomothetic level of group averages. However, it is important to use individual-level data, because findings from one level might not directly generalize to another level. This individual-level data allows studying the dynamics of a given person., which can help in treatments. However, it is important for science to detect patterns and principles that generalize across all people. These problems can be bridged, by identifying common indices of early warning signals across systems and sciences. Ellison and colleagues used ecological momentary assessments methods and Group Iterative Multiple Model Estimation (GIMME) and show how these levels can be combined.

What are further important considerations?

Different trajectories of change

When using the complex systems approach, trajectories of symptom change are important. In psychotherapy, a general assumption is that change is gradual and linear. However, time course data has shown that this is not always the case, and that the process can follow a nonlinear course. Changes in therapy can follow a quadratic pattern (U-shape), a cubic pattern, a saw-toothed pattern, and other nonlinear patterns. Think of relapse in addiction treatment.

Early warning signals

Increased variability and turbulence in psychotherapy is seen as potential for change according to the complex systems approach. There have not been many studies that have looked at early warning signals in psychotherapy. There are different ways to measure early warning signals. For example, using Grid-Ware, recurrence quantification analysis, or dynamic complexity. Calculating dynamic complexity can be done through R.  An important avenue for future research is to examine which early warning signals predict transition across clinical problems and treatments, and which represent therapeutic change.

Patterns and feedback loops

Thus, as noted, attractors exist of interconnected elements. Thus, patterns are the focus of study, and not a single component. Again, recurrence quantification analysis and related tools (Grid-Ware), the Synergetic Navigation System can be used to study multi-component patterns for individuals. One can also use network analysis tools, which quantify the structure, density, connectivity, and threshold of activation of patterns, and how they change over time. This network analysis depicts and measures patterns of psychopathology for a certain sample, and also personalized for a specific individual. This may guide treatment decisions and selection. However, a limitation of network analysis is that it assumes ‘stationarity’, which means that each variable, over time, demonstrates similar means, variances, and relationships with other variables and with itself.

Interplay of pathological and new patterns of learning

The complex systems approach thus suggests that new attractors can develop, and can build in strength so that they can compete with or inhibit old attractors. Modern cognitive development and learning theories also suggest that psychotherapy promotes new learning, through establishment of new patterns. However, there has not been much research conducted into how this old-new attractor competition takes place.

What can be concluded?

Thus, the NDT model for therapeutic change is a conceptual framework. The goal is to identify and translate concepts from subdisciplines of complexity science to psychotherapy research. In turn, these concepts and methods can help to increase the effectiveness of therapeutic treatments. Also, having a common organizational structure may benefit science in general.

Executive function (EF) processes help us respond to the environment and regulate our thoughts and behaviours towards our goals. Meta-analytic evidence shows that EF deficits are pervasive across psychopathologies and EF tasks, proposing that they may be transdiagnostic risk factors for psychopathology. Four key limitations in the majority of prior research hinder progress in testing this hypothesis.

1. Most studies use standard neuropsychological test approaches that confound different aspects of EF, leading to seemingly undifferentiated nature of impairments across disorders.
2. Vast majority of research has investigated individual disorders without taking the pattern across disorders into account – ignoring comorbidity between disorders.
3. Most research has focused on adults, missing the key adolescent/emerging adult phase for EF development and psychopathology risk.
4. Few studies have examined how (mediation) and for whom (moderation) EF and psychopathology are related.

This study aims to address these limitations by linkages between latent dimensions of EF and latent psychopathology dimensions in a sample of adolescents and emerging adults.

Unity/Diversity Model of EF

EF is best characterized as separable but related cognitive processes, with unique and shared differences, genetic influences, and neural substrates. The unity/diversity model focuses on three aspects of EF.

1. Shifting, defined as switching between task sets or response rules (e.g. classification by shape or colour).
2. Inhibition, defined as suppressing or resisting automatic responses in order to make less automatic but task-relevant responses (e.g. Stroop task).
3. Updating, defined as monitoring for and adding task relevant information in working memory, and deleting irrelevant information.

These abilities correlate, suggesting there’s a common EF ability involved in all three aspects. Common EF is posited to be the ability to monitor for and maintain goal and context information and use that information to bias ongoing processing.

Each ability can be decomposed into what’s common across all three EF’s (unity) and what is unique to that particular ability (diversity). Two large, independent youth and adult samples support a model with common EF factor and updating – and shifting- specific factors’ common EF accounts for individual differences in inhibition. The different components of EF identified in this model differentially predict individual differences in clinically relevant behaviours, with recent evidence finding that the common EF is the primary predictor, relating to behavioural disinhibition, attentional problems, and transdiagnostic psychopathology. Meta-analytic evidence shows generally similar effect sizes across core EF domains, consistent with the theory that individuals with multiple forms of psychopathologies have impairments in the unitary component of EF.

Bifactor Models of Psychopathology and Links to EF

Psychopathology has also been shown to consist of both common and specific factors. As opposed to historical conceptualizations of disorders as categorical conditions they’re now conceptualized as continuous symptom dimensions.

There’s a long history of modeling internalizing and externalizing dimensions of psychopathology liability, recently expanded to include a common factor (p factor). P factor model has been replicated in multiple samples. Critical question to ask of such models is whether they’re related to theoretical and practically important risk factors and outcomes and can help advance clinical science (are they useful?). Significant evidence has validated p factor in relation to a wide variety of psychopathology risks and outcomes in developmental continuity.

These models thus hold promise for clarifying the many patterns between risk factors and categorically defined disorders. Recent conceptual models have proposed that executive dysfunction is a risk factor for common psychopathology. Several studies have found the p factor to be associated with poorer performance on EF tasks, including working memory and a single EF composite in children, working memory, flexibility, response inhibition, and updating tasks in adolescents, and working memory and shifting tasks in adults. P factor has also been linked to structure and function of prefrontal areas involved in EF in youth.

To note, these studies used manifest EF variables or single, unitary EF factors, and so didn’t directly test the hypothesis that common psychopathology liability is linked to poorer common EF. Only one study so far has tested links between the bifactor model of psychopathology and the unity/diversity model of EF. This study found that the common EF factor assessed at age 17 was predicted by p factor assessed across childhood and adolescence only for male participants and based on teacher, not parent, ratings. When modeled separately, internalizing related to poorer common EF across genders and raters, and externalizing related to better shifting-specific EF. So associations between the p factor and poor EF are consistently found across studies, but results have somewhat varied.

Mechanisms Linking EF and Psychopathology

There’s a lack of research investigating why EF is associated with psychopathology dimensions. Hankin et al (2016) posited that stress could mediate risk between EF and expression of common and internalizing psychopathology. Dependent stressors are negative life events partly influenced by a person’s behaviour (e.g. failing an exam). The stress generation model maintains that individual difference vulnerabilities related to psychopathology impair functioning and increase risk for dependent stressful life events. Poor EF has been proposed as a factor that can contribute to stress generation. Poor EF may contribute to functional impairments resulting in dependent stressors (e.g. failing an exam because of failure to plan). It was found that the link between EF task performance and internalizing symptoms increase with age due to increased association between EF and dependent stressors. Possibly because adult caretakers compensate for younger adolescents’ poor EF (e.g. reminders to complete homework), preventing poor EF from being translated into behaviours that lead to stressful life events.

Dependent stressful life events strongly predict rumination, a pattern of repetitive thought in response to an emotional state. Rumination is proposed to act as a transdiagnostic risk factor by amplifying current mood states and impairing problem solving. Predicts that rumination is associated with the p factor, but hasn’t been directly tested.

Mediation by stress generation and rumination could potentially explain why EF impairments are broadly associated with psychopathology. Study found that dependent stressful life events predicted internalizing symptoms both directly and via increased rumination – both factors transdiagnostic risks, stress predicts p factor.

Current Study

Recent research using latent dimensional models of psychopathology have begun to disentangle sources of the broad EF impairments observed across disorders. Research suggests that associations may be mainly driven by shared psychopathology liability (p factor). Most research on EF relating to p factor models hasn’t employed models that can differentiate between EF components. Lastly, mediating mechanisms of poor EF conferring risk for psychopathology remain speculative.

The current study tests associations between the unity/diversity model of EF and the latent dimensions of psychopathology liability in a community sample of youth during key adolescent to emergent adult period of enhanced psychopathology risk and continuing EF development.

This study is cross-sectional, but allows preliminary tests of potential mediating mechanisms which future longitudinal studies can investigate. Study aims to clarify potential risk pathways between EF impairments and forms of psychopathology liability, and accelerate progress in understanding how these impairments may contribute to co-occurrence across psychopathologies. This study extends previous research demonstrating that poor EF predicted anxiety and depression symptoms via stress generation and rumination, and that these effects were stronger in older youth.

They hypothesized that seemingly broad deficits on EF tasks associated with forms of psychopathology are best explained by poorer common EF associated with common psychopathology liability. Because of mixed and limited prior research, there’s no a priori hypotheses regarding externalizing or internalizing- specific liability factors and conduct exploratory analyses. If, as they predicted, the common EF was associated with the p factor, they hypothesized that this association would be partially mediated by the indirect path through dependent stressful life events and rumination, and that the EF-stress path would be stronger for older youth.

Method

Participants

292 participants aged 13-22. Selected to maximize racial and economic diversity.

Procedure

Youth participated in hour lab visits, with breaks. Participants gave written informed consent (18-22) or parental consent (13-17). Youth completed three EF tasks assessing updating, shifting, and inhibition. Participants asked to complete self-report questionnaires online before their visit. All studies approved by IRB.

Measures

EF Tasks

EF tasks from Friedman et al. (2016) except for stop signal task. The Friedman et al. tasks have been found to have good internal and test-retest reliability, and convergent validity including significant factor loadings on common EF and, for updating and shifting tasks, the updating- and shifting-specific factors. Stop signal task validated in reference to mathematical models and neural indices of response inhibition.

Updating: for all updating tasks, the performance measure is the proportion of correct responses across all trials. Tasks: Keep track, Letter memory, Spatial 2-back twelve

Shifting: for all tasks, participants first practiced a block of each sub-task separately, followed by mixed-task blocks. Performance measure for shifting tasks is the switch cost: difference in mean response time between correct tasks switch trials and task repeat trials in mixed blocks. Participants instructed to respond as quickly as possible without making mistakes, indicated by an error beep. Tasks: Number-Letter, Colour-shape, Category switch

Inhibition: Tasks: Antisaccade, Stop signal, Stroop

Questionnaires

• Children’s Depression Inventory – CDI
• Penn State Worry Questionnaire for Children – PSWQC
• Manifest Anxiety Scale for Children – MASC
• Child Behaviour Checklist Youth SelfReport – YSR
• Multisite Multimodal Treatment Study of Children with ADHD – MTA
• Strengths and Difficulties Questionnaire – SDQ
• Adolescent Life Events Questionnaire Revised – ALEQR
• Children’s Response Styles Questionnaire – CRSQ

Discussion

This study aimed to understand possible risk pathways between poorer EF and internalizing and common psychopathology (p factor) liability. For older youth, poorer common EF, was associated with higher internalizing liability in a one-factor internalizing model, and higher common psychopathology (p factor) in the bifactor model. Poorer common EF was also associated with more dependent stressful life events in older youth, which in turn associated with higher rumination for all youth. For all youth, rumination and dependent stressful life events were associated with higher internalizing liability in one-factor internalizing model, and with higher levels of the p factor and internalizing-specific factor in bifactor model. Overall results suggest that the many-to-many relations between different forms of psychopathology and measures of different aspects of EF may be more parsimoniously explained by a link between common EF and both common psychopathology liability (p factor) and internalizing-specific liability in older youth – suggesting that stress and rumination may serve as mediators of these relations.

Specificity to EF Dimensions

Links with psychopathology liability were specific to the common EF factor, rather than updating- or shifting-specific EF. Consistent with a previous study testing associations between the p factor and the unity/diversity model and with most previous studies with more specific symptom dimensions as well as broad impairments. But one study found that depression symptoms were associated with lower common EF cross-sectionally, but prospectively predicted lower updating-specific EF, suggesting that associations may differ in some cases.

Why may common EF factor be linked to psychopathology liability? It’s thought to capture the ability to actively maintain and manage goals and use them to control ongoing processing, a demand shared by all EF tasks. On the other hand, updating- and shifting-specific demands are likely to occur only intermittently in daily life. So poor common EF may be likely to impair functioning, including in ways that increase stress. This relation is likely transactional, with stress leading to EF impairments.

Age Moderation

Common EF in this study significantly interacted with age, such that poorer common EF only associated with dependent stressful life events in older youth. This may be due to the role adults play in compensating for younger adolescents’ poor EF, buffering against stress generation.

Though age moderation is predicted based on past findings, other studies found associations between EF and the p factor in younger individuals. However, they also used different methods of assessing psychopathology which could account for the differences between those studies and the current one.

Stress and Rumination Effects

Primary focus of this study was to better understand EF-psychopathology liability links, but also provided new insights into how stressful life events and rumination relate to the bifactor model of psychopathology liability.

1. Dependent stressful life events were associated with all three psychopathology liability dimensions. Association with p factor is consistent with the model of stress as a transdiagnostic risk factor, but associations with internalizing- and externalizing-specific factors also suggest that stress further confers specific risk for internalizing and externalizing dimensions. Dependent stressful life events are a strong risk factor for depression and anxiety, so may be more strongly associated with the internalizing-specific factor than other types of stress.
2. Rumination hasn’t been previously examined in relation to the bifactor model. This study found rumination to be strongly associated with the p factor. It was also associated with higher internalizing-specific liability, but much weaker association – supports the view that rumination is a broad transdiagnostic risk factor rather than specific to depression or internalizing psychopathology. However, this additional association suggests it may confer risk for anxiety and depression via both common and specific mechanisms.
3. Youth who engage in higher rumination had lower externalizing-specific liability, after variance shared with internalizing was accounted for.

Limitations and Future Directions

There were several limitations in this study:

• Study was crosssectional, precluding conclusions about the temporal ordering of variables in the models.
• Tested a hypothesized process model based on previous research and theory, identifying possible mediating mechanisms as a promising start for future longitudinal studies.
• More longitudinal research is needed with EF and psychopathology assessed at multiple time points to see if EF is a risk or consequence of common psychopathology, or both (transactional relations).
• This study focused on psychopathology and EF in adolescence and emerging adulthood in a nonselected community sample. Future research is needed to determine if the model generalizes to other age groups, and to high-risk or clinical populations. More research is needed to test whether EF-stress generation links are specific to the late adolescence/emerging adulthood developmental period.

Translational Implications

More research is needed in order to translate these findings to practice. But better understanding the mechanisms by which EF may serve as a transdiagnostic risk factor for psychopathology has the potential to inform new targets for intervention. There’s a lot of interest in EF training as a potential prevention/treatment strategy, but until now there’s little evidence that training transfer to real-world functioning. Interventions aimed at disrupting the link between poor EF and stress generation could be a promising approach, rather than attempting to train EF.  This study found that the link between EF and dependent stressful life events was specific to common EF, suggesting that training in compensatory strategies for goal-management could potentially mitigate effects of poor common EF to reduce stress and potentially reduce psychopathology risk.

Conclusions

Broad patterns of poorer performance on EF tasks associated with forms of psychopathology symptoms may be best explained by associations between common EF and common psychopathology liability, though there are also internalizing-specific associations. Poorer common EF associated with internalizing and the pf factor via dependent stressful life vents and rumination in older youth. This developmental period of increased demands for independence may be a critical window for risk associated with poor EF. Interventions aimed at disrupting the link between poor goal-management and stress have potential for reducing dimensional psychopathology, particularly in emerging adults.

Background: we modeled both psychopathology and executive function (EF) as bi-factor models to study if EF impairments are transdiagnostic or relate to individual syndromes, and if such associations are with general or specific EF impairments.

Introduction

Problem domains of psychopathology are highly correlated, both concurrently and over time. Its proposed that the structure of psychopathology is best captured by a bi-factor model of general psychopathology on one side and specific problem domains on the other. Specific problem domains include internalizing (INT), externalizing (EXT), as well as ADHD and autism spectrum disorder (ASD) problem domains. The bi-factor model separates what is common across different psychopathology domains from what is unique for each domain.

EF is crucial for our daily functioning in guiding goal-directed behaviour. It includes a broad range of cognitive processes, e.g. suppressing automatic responses, switching between tasks, maintaining/updating information etc. Different theoretical models of EF share the idea that the structure of EF includes general and specific parts. EF’s have something in common, but are separable from one another.

EF impairments are widely accepted as a common characteristic of various psychiatric disorders. The focus has long been on finding distinct cognitive profiles for these disorders, which has produced inconsistent findings. Research hasn’t converged on which EFs are impaired in each disorder. Has been found that EF dysfunctions are generally widespread, severe, and pronounced in disorders that are severe and chronic e.g. schizophrenia. Conversely, no findings have been reported in younger populations with mild to moderately severe disorders like depression or anxiety. Caspi et al. (2013) has shown that poorer performance on EF tasks was associated with the general psychopathology factor (p factor) but not with specific INT and EXT factors.  Furthermore, EF seems more impaired when multiple conditions are present. together, findings suggest that EF impairments are more strongly associated with severity and chronicity of psychiatric problems than with distinct diagnoses – could explain discrepancies in research where focus has been on distinct disorders.

One could ask whether impairments in general or specific EF are related to psychopathology. Studies have previously only examined either EF performance on lumped or on separate neuropsychological tasks.  Studies using separate tasks have shown uniform impairments across tasks relating to psychopathology – may indicate that EF is not process specific when associated with psychopathology. This is also suggested by other studies that have lumped scores on EF tasks. Although these findings suggest an association at the general EF level, aggregation through sum or factor scores still captures the scores on individual tasks. Given this overlap, no firm conclusions can be made. In contrast, a bi-factor model splits the variance into general and specific parts. So bi-factor models allow for a clear-cut interpretation of the extent to which associations between psychopathology and EF can be summarized as generic or more separable.

To summarize, it’s generally agreed on that multiple EF impairments are involved in a range of disorders. But extensive research hasn’t agreed on distinct EF profiles for distinct disorders. This study investigates whether EF problems relate to severity/chronicity of psychopathology rather than type. It’s addressed whether general or specific EF impairments associate with psychopathology. This will be done by modeling psychopathology as measured over multiple occasions during the course of adolescence in a bi-factor model. Also, EF will be modeled as measured at two occasions during adolescence in a bi-factor model. Through this bi-factor approach, the study aims to understand the relationship between psychopathology and EF. Hypothesis: association is generic. EF impairments only associated with general psychopathology.

Method

Sample

2230 adolescents from the Tracking Adolescents’ Individual Lives Survey.

Measures

• Child Behaviour Checklist: parent rated questionnaire.
• Child Social Behaviour Questionnaire: captures six symptom dimensions typically seen in children with ASD.
• Executive functioning: using 1) Baseline Speed Task, 2) Feature Identification Task, 3) Sustained Attentional Dots Task, 4) Memory Search Letters Task, 5) Shifting Attentional Set Task

Discussion

Study modeled both psychopathology and EF as bi-factor models to examine whether EF impairments are transdiagnostic or relate to individual syndromes – and if these associations are with general or specific EF impairments. With the double bi-factor approach, the best model showed that impairments in multiple specific EFs are associated with general psychopathology. Especially true for ADHD and ASD problems. Furthermore, INT problems have a distinct association with cognitive flexibility. We can draw stronger conclusions with regard to findings from the ‘psychopathology side’ than the ‘EF side’ of the double bi-factor model. So we conclude that inconsistent findings in literature may be due to substantial transdiagnostic EF impairments. Also once these transdiagnostic impairments are captured, ADHD, ASD, and INT problems still have their specific EF profile. Thirdly, whether general or specific EF relates to the p-factor needs to be studied more.

Caspi et al. research was extended by including ADHD and ASD problems. IN line with their findings, this study showed associations with the p factor. The p factor captures all the shared variance between different problem domains and is often considered to reflect severity and chronicity of psychopathology.

INT and EXT problems alone don’t show much impairment in EF beyond severity and chronicity captured by the p factor. Caspi et al. found no associations between cognitive flexibility and INT problem domain like this study, but this could be due to cognitive flexibility being measured with different tasks. Results suggest that cognitive inflexibility may be a core cognitive deficit of INT problems. Makes sense when thinking about the connection between cognitive flexibility and rumination – key component of INT disorders. People with impaired cognitive flexibility less able to ‘reset’ their minds after daily hassles and therefore fixate on their thoughts evoking feelings of worry.

The ASD and ADHD problem domains show associations with specific EFs above and beyond associations with severity and chronicity of psychopathology. Both show impairments in visuospatial working memory, sustained attention, feedback responsiveness, and cognitive flexibility – impairments in psychomotor speed and working memory maintenance were specific to ADHD. Although the adolescent sample represents absent-to-very mild severity in ASD, study demonstrates that EF impairments are present. moreover, although ASD often is considered a more severe neurodevelopmental disorder than ADHD, this study found that EF impairments are somewhat more widespread/stronger in ADHD.

One of the biggest strengths of this study is the use of neuropsychological data in an epidemiological context – making for fairly unique data. Moreover, the study included ADHD and AS, lifespan conditions not be ignored as specific problem domains when trying to understand the structure of psychopathology. Finally, EF was modeled with a bi-factor model. By partialling out shared variance between EF tasks, measurement error and state-specific variance were minimized. Specific EFs may in part still measure non-EF-related variance as the study was unable to use multiple tasks for each specific cognitive process. Nonetheless, the task impurity problem was tackled to some extent.

This study had several limitations:

1. Consider the dropout rate of the sample – may not be fully representative of the general population.
2. Had a limited set of EF measures that assess fairly specific EF dimensions, rather than more complex processes or higher order EFs which are more closely related to behaviour.
3. Use of EF measures differs greatly between studies. Emphasizes need for future studies to determine if these conclusions hold in samples using different tasks.
4. Though there isn’t literal overlap in items and constructs, the items do tend not to be fully specific for the construct they measure – limiting the specificity of the psychopathology domains.
5. Use of parent-reported questionnaires may have different properties for INT and EXT issues.

By studying diverse psychopathology domains simultaneously, this study showed that EF problems cross diagnostic boundaries and play a domain-specific role in ADHD, ASD, and INT symptomatology. It’s concluded that the association between psychopathology and EF can’t simply be considered either generic or specific and examining both components of EF and psychopathology allows for clearer conclusions on distinct EF profiles for distinct disorders.

There’s considerable evidence that access to within-situation safety behaviours can interfere with the beneficial effects of exposure therapy for anxiety. Similar outcome has been observed in panic disorder. The best explanation is the cognitive account which says that patients attribute the absence of the feared outcome to their safety behaviour and fail to update their threat beliefs. Exposure in the absence of safety behaviour is thought to disconfirm excessive threat beliefs and lead to long-term fear reduction.

A closely related phenomenon that’s been demonstrated in the conditioning laboratory is protection from extinction. In this procedure, a Pavlovian conditioned stimulus (CS) is established as a predictor of an unconditioned stimulus (US), and is then subjected to extinction by presenting the CS without the US. “Protection” refers to finding that extinction is impeded by the presentation of an inhibitory CS during the extinction phase. The best explanation for this effect is that the inhibitory stimulus cancels the expectancy of the US generated by the target excitatory stimulus, so that there’s no discrepancy between what’s expecting and what happens, no extinction.

The phenomenon of protection from extinction provides a potential lab model for investigating the role of safety information during exposure therapy. A study found that a conditioned inhibitor interfered with extinction of a target excitatory stimulus. But the primary sources of inhibition or safety in therapy are thought to be safety behaviours produced by patients themselves, as opposed to an external source.

This study uses a procedure recently developed to study instrumental avoidance learning. It builds on the Pavlovian fear conditioning procedure where different coloured shapes serve as CSs for shock or no shock. Sometimes participants have access to response buttons. Access is signaled by illumination of the buttons, but participants have to press the right button to avoid shock. Skin conductance and shock expectancy are recorded.

Method

Participants

65 undergraduate students, who volunteered.

Apparatus

Participants tested individually in a darkened room. CS’ were coloured squares and the US was an electric shock produced by a constant current generator.

Skin conductance was measured through electrodes attached to the second and third fingers of the participant’s non-preferred hand.

Procedure

Participants were told the experiment consisted of a number of trials with rest periods in between and that on each trial, a coloured square appeared for 5 seconds followed by a 10 second waiting period, followed by either a 0.5 second shock or no shock. They were told there was a relationship between the colour of the squares and the occurrence of the shock that they should try and work out. Participants were told that response buttons may light up, and that pressing a lit button may cancel a pending shock.  Participants were asked to use the expectancy pointer during the waiting period after the square disappeared to indicate their expectancy of whether a shock would occur or not.

Following this, the Pavlovian acquisition phase was designed to establish the CS-US contingencies prior to introducing opportunity for an avoidance response. Two CSs, A and C, were paired with electric shock (A+, B+), and a third CS presented without a shock (B-). No response buttons were illuminated during this phase.  In the Avoidance acquisition phase, participants were given the opportunity to make a button-press response during presentations of stimulus A. To simplify learning, only the correct response button was illuminated. If they pressed the button, the shock was cancelled.

In the Extinction phase, stimulus C was presented six times without shock. Protection group was given the chance to make the button-press response for this stimulus. The button was not illuminated for the control group. In the final (Test) phase, the impact of the extinction trials was examined by presenting C alone, without response opportunities.

Discussion

The experiment provided clear evidence for protection from extinction of a Pavlovian fear CS by an instrumental avoidance response. Control group showed normal extinction of stimulus C, whereas the Protection group, who made the avoidance response during the Extinction phase, showed little extinction. Adds to the evidence for protection from extinction in humans and extends it from external stimuli to an internal response.

Participants weren’t given a choice of responses, so the illumination of the correct response button was strongly correlated with the absence of the shock US. Was the critical factor in the protection effect light? No, the light was only correlated with the absence of the US as a result of performance of the instrumental button-press response.  

In general, the same pattern was observed in this experiment on both expectancy ratings and skin conductance. One point of divergence between the measures – when the avoidance response was made available in the Avoidance acquisition phase, it led to a modest reduction in shock expectancy ratings to stimulus A. Presumably due to prior instructions given that suggested pressing a response button may cancel shock. Opposite effect was observed on the skin conductance measure – making the avoidance response available led to an increase in skin conductance on the first A*(+) trial. This could be due to arousal associated with performing the avoidance response.

We interpret the protection from extinction effect as analogous to the role of within-situation safety behaviours in preserving threat beliefs and anxiety in patients undergoing exposure therapy. Shock expectancy ratings = threat beliefs, skin conductance = anxiety/fear. The results are consistent with the cognitive account proposed by Salkovskis et al. (1999). By this account, the Protection group attributed absence of the expected electric shock on C*= trials to the avoidance response. So when the response wasn’t available in the Test phase, they retained their high shock expectancy to C and showed strong anxiety. The Control group didn’t have an alternative explanation for the absence of the expected electric sock on C- trials, and were forced to revise their expectancy shock downwards – lowered their ratings and skin conductance responses in the Test phase.

It seems strange to account for conditioned responding in terms of a cognitive mechanisms as it’s been seen as a low-level, reflexive process. But recent evidence suggests that it may depend on high-level cognitive processes. This perspective is compatible with cognitive threat appraisal theories of anxiety. Expectancy of harmful outcomes may give a common explanatory mechanism cross fears derived from learning, observation, and instruction. Results imply that habituation of an innate fear response and extinction of an acquired fear response may both be based on a reduction in expectancy of threat.

Lastly, clinically, the present results support the strategy of minimizing safety behaviours during exposure therapy and giving participants clear cognitive rationale for doing so. The avoidance procedure provides a potential lab model to investigate the cognitive and other mechanisms underlying protection of beliefs against disconfirming evidence. This could be used to study potential positive benefits of safety manipulations, as well as interactions with other variables of therapeutic relevance like pharmacological agents.

Social Phobia/Anxiety Disorder is an interpersonal disorder, a condition where anxiety disrupts a person’s relationship with others. This paper aims to determine what’s known about the interpersonal aspects of social anxiety and understand how it effects the development of relationships.

Interpersonal theory incorporates developmental experiences, social cognition, motivation, and social behaviour in a cohesive model and can therefore provide a structural framework for this review – using different research areas.

Social anxiety is conceptualized and measured differently across domains. The various concepts are related but not interchangeable. E.g. developmental researchers study temperaments of behavioural inhibition and social timidity, whereas personality/social psychologists study shyness and social anxiety (as situation-induced states) and personality disorder.

1. Interpersonal Perspective

Interpersonal models of psychopathology share the assumption that good social relationships are tied to a person’s psychological well-being and that poor social relationships contribute to psychopathology. Central feature of this perspective – self-perpetuating interpersonal cycle. We expect people to treat us the same way now that they have previously, and tend to repeat the behavioural strategies learned to handle earlier events. Furthermore, people expecting others to respond positively to them engage in behaviours eliciting favourable responses, vice versa those anticipating negative responses adopt self-protective strategies likely eliciting negative responses.

Interpersonal models also maintain that dysfunctional interpersonal patterns result from ongoing interaction between the individual and the social environment. Our relationships shape our habitual social behaviour as well as our sense of self and others.

2. Social Anxiety Disorder and Social Relationships

People with social phobia generally have fewer social relationships than others (fewer friends, dating and sexual relationships, less likely to marry). But we don’t know much about how they function in the relationships they do develop. E.g. study on marital relationships in social phobic patients found patients to report greater life satisfaction than those without partners but also more marital distress.

A study using structured interviews to assess university students’ relationships with friends, acquaintances etc. found social anxiety to be associated with various dysfunctional strategies in those relationships – expected strategies of nonassertiveness and avoidance of emotional expression/conflict. Socially anxious individuals reported over-reliance on others – result of dependence on the few relationships they have. Over-reliance (and nonassertiveness) was found to mediate the relationship between social anxiety and chronic interpersonal stress. Together these findings indicate that even when socially anxious people develop relationships, they view them as less intimate, functional, and satisfying than those without social anxiety.

3. Self-Perpetuating Interpersonal Cycles

Writers from different perspectives have observed that socially anxious people behave in ways that lead to negative social outcomes. Suggests that people with social phobia may establish negative interpersonal cycles between themselves and others in which they adopt behavioural strategies evoking negative reactions.

3.1. Behavioural Patterns

Behaviours commonly associated with social anxiety are low social skill, nonassertiveness, and visible anxiousness. Differences between socially anxious and nonanxious people on specific anxiety-related micro behaviours (poor eye contact, trembling, low self-disclosure etc.) have also been found. Research suggests socially anxious individuals to appear less skillful and anxious than others, providing suggestions as to behaviours that contribute to this impression.

Variability in behavioural patterns have been found in socially anxious populations – findings point to individual differences in how socially anxious people experience their interpersonal issues.

Other researchers report evidence of critical or angry behaviour in socially anxious samples. One study found that shy people reported feeling critical and non-affectionate towards their friends/others. Another found that social phobic patients reported more state/trait anger, and a tendency to express anger when criticized or treated unfairly, or even without provocation. Studies in the context of domestic violence found that 35% of wife batterers scored above the clinical cutoff on avoidant personality disorder. Avoidant personality traits predicted not only assault, but also spousal murder.

3.2. Others’ reactions

The interpersonal perspective posits that people with psychological problems often elicit negative responses form others. Shy individuals generally rate negatively on interpersonal dimensions (warmth, likeability etc.) by objective interviewers and close friends. Research indicates shy people to be seen as less intelligent by peers though there’s no actual association between social anxiety and intelligence. Conversely, long-term acquaintances rate shy people more positively than recent ones, suggesting other may become more positive about them with longer exposure.

Several studies found others less likely to want future interactions with socially anxious students after an initial discussion. It’s concluded that the social behaviour of anxious students led their partners to disengage from relationship development. Anxiety-related behaviour was one main factor precipitating disengagement, as well as failing to reciprocate others’ self-disclosures.

Authors concluded that socially anxious students were rated negatively by their friends, and they irritated/alienated strangers quickly.

3.3. Summary

Research suggests socially phobic people to show distinctive and less functional social behaviour than others. There’s an increase in empirical support for interpersonal variability in the behaviour of socially anxious people. They seem to evoke less positive reactions from others, even in brief encounters and studies suggest that the absence of prosocial behaviour is as important to others’ reactions as visible signs of anxiety.

These findings could have clinical implications. Socially anxious people worry about displaying anxiety-related symptoms, when the use of prosocial behaviours could be more important in developing relationships. Important for future research is determining if behavioural patterns and social responses found in social phobic individuals are specific to social phobia or shared with other psychological disorders – could arise form comorbid conditions rather than just social phobia, e.g. depression.

4. Social Skill Deficit or Self-Protective Strategy

If people with social anxiety behave in ways that disrupt relationship development, the next question is why. Traditional explanation for this is that they have social skill deficit’s, and failed to learn effective social behaviour – anxiety is partially a reaction to those deficits and negative responses. However, it seems to depend on the social context whether they will display avoidant/maladaptive social behaviour. Speculation that dysfunctional behaviour results from cognitive and emotional processes activated through social cues – leading to self-protective behaviour.

4.1. Summary

There’s some flexibility in the strategies used by socially anxious people to deal with social events. Self-protective behaviours elicited by social cues is inconsistent with the concept of a social skill deficit – which implies a chronic behavioural deficiency. More researched is needed to determine if there are limits on behavioural flexibility in social phobic people.

5. Cognitive Processing of Social Information

Cognitive theorists propose that social cues activate negative beliefs and assumptions about the self and others, leading to selective processing of threat information and biased interpretation of events – heightens anxiety and leads to the use of self-protective behavioural strategies.

Three topics of interpersonal relevance in cognitive model research:

1. Critical aspect of negative social schema is relational information
2. Whether people with social phobia show selective processing of negative interpersonal cues
3. Whether people with social phobia show negative biases in their interpretation of other people

5.1. Social Schema and the Self

Researchers in social cognition posit that social anxiety arises from the activation of a relational schema – knowledge structures based on experience with significant others. It’s argued relational information forms a key part of our sense of self. Some suggest that social anxiety arises when someone becomes aware of a discrepancy between knowledge about the actual- and ought-self (the self one believes others things one ought to be). Baldwin (1992) suspected that socially anxious people develop negative schema about the self in relation to others, which are readily activated by social cues. Schema result in negative expectations for social events -> anxiety.

Research has demonstrated priming procedures to increase awareness of discrepancies between the actual and ought-self. Authors concluded that activating relational information is critical to the onset of social anxiety.

Baldwin went further to examine how activation of information about others affects someone’s subjective experience of the self. He concluded that information about others is intertwined in memory with information about self, and activating one type of information affects the other.

5.2. Selective Attention to Social Cues

Cognitive models suggest socially anxious people to selectively process threat-related information. Threat information can be internal or external.

In support of selective processing, a study found that socially phobic people showed selective attention to negative social cues in a public speaking task. Other studies found them to display memory omissions for partner-related information in social interactions.

5.3. Interpretation of Social Cues

According to cognitive writers, selective processing of threat cues leads to biased interpretation of social events. Interpretation biases have been studied in three contexts: 1) judgments of self, 2) judgments of others’ reactions to self, 3) interpretations of other people’s behaviour/characteristics apart from their reactions to oneself.

Not as clear if social phobic people display biases in their interpretations of other people’s behaviour and characteristics. Studies on social interpretation yield inconsistent results.

Two lab studies of patients with social phobia weren’t able to find negative biases in patients’ interpretations of others’ characteristics in getting acquainted discussions. A recent study suggested that negative interpretation bias may be confined to people with particular social developmental histories.

5.4. Summary

The literature supports the idea that activation of relational information may play a key role in triggering social anxiety. One possibility is that relational information activation exerts its effect by altering the person’s subjective sense of self.

Right now, findings provide greater support for the existence of negative interpretation biases in judgments of self and others-in-relation-to-self than for biases in interpretations of other people’s general characteristics.

Interpersonal writers propose that habitual interpersonal patterns are the result of a social development process that begins in childhood interactions and with significant others and continues through peer relationships in adolescence.

6. Social Pathogenesis

Research gives persuasive evidence that there are heritable, biological processes that increase vulnerability to social anxiety. Particularly, the presence of behavioural inhibition (BI) early in life is shown to predict social timidity in childhood and adolescence. Kagan concluded that BI is “influenced in a major way by environmental conditions existing during the early years of life.

Developmental researchers have identified a number of early social learning experiences that are associated with behavioural inhibition, shyness, and social anxiety. For example, parental encouragement of open communication and social involvement is associated with less shyness at 12- and 24- months, and reductions in social inhibition were observed in temperamentally active infants whose mothers weren’t too responsive to fretting and crying. Conversely, patients with late-onset shyness are more likely to report parental abuse than those with early-onset shyness, who were most likely to have shy parents. Social anxiety can be produced by adverse social experiences even in children who aren’t initially inhibited.

Two themes: 1) behaviour between children and parents is interactive with each party influencing the other, 2) there’s variability in the interpersonal environments associated with social phobia.

7. Self-Perpetuating Cycles

Association between Bi and dysfunctional child-rearing styles begs the question of whether parental behaviours are causal factors in the development of social fears or responses to the child’s temperament.

Several researchers address bi-directional models of parent-child relationships. Other research has demonstrated that the physiological correlates of behavioural inhibition were moderated by the security of the attachment bond between mother and child.

Research over the last decade increasingly supports a bi-directional relationship where inhibited/anxious children and their parents display a cyclical interaction pattern, perpetuating social anxiety.

8. Variability in Social Learning Experiences

Research points to at least three dimensions that characterize early social experiences in these individuals: 1) parental over-protection and control, 2) parental hostility and abuse, and 3) lack of family socializing. Over protective, intrusive parental behaviour has received greatest research attention.

Developmental studies revealed that mothers of anxious-withdrawn children responded to their children’s shy behaviour with attempts to direct and control how the child behaved. Anxious children also displayed the highest degree of noncompliance, a pattern that may perpetuate dysfunctional transactions between mothers and their children.

But some patients with social phobia also report histories of physical and sexual abuse. An analysis found that sexual assault by a relative and exposure to verbal aggressiveness between parents had unique effects on social phobia onset in women. Childhood physical and sexual abuse seems to pose a risk for later development of social phobia.

Social phobic patients also report more emotional abuse and neglect in their childhoods. Observational studies confirm self-report findings, mothers of extremely anxious-withdrawn children tended to use non-responsiveness, statements of devaluation, or criticism and punishment in response to their child’s behaviour in a lab task.

Some patients report having limited exposure to social interactions during their development with parents encouraging this. Restricted social exposure may exacerbate social fears by constraining the development of social skills or limiting opportunities to learn that social situations can be harmless.

Interestingly, the three social development dimensions mentioned before were found to be largely independent. Principle of equifinality – there can be multiple pathways through which psychological disorders develop.

Most studies don’t address whether negative peer interactions are the cause or outcome of social anxiety, or both. It’s been concluded that shyness interferes with friendship formation, but doesn’t evoke rejection, whereas rejection can exacerbate the cognitive aspects of shyness. Supports an interactive model of social anxiety and peer relationships.

8.1. Summary

Social developmental factors and social anxiety have been addressed in numerous ways. Each method of assessment is limited in its own way, but taken as a whole the research supports the idea that the pathogenesis of social anxiety resides in an interaction of innate temperament with a family environment that either fails to help fails to help children overcome their innate timidity or exacerbates their fears through overprotection, control, abuse, isolation, or modeling.

9. Interpersonal Processes in Treatment

First question is whether interpersonal heterogeneity found in developmental histories and social behaviour of social phobic people affects treatment response. There’s little research on this, but studies indicate that some interpersonal patterns associate with poor treatment outcome. Example: studies on avoidant personality reported people with ‘warm’ problems (fear of offending/disagreeing with others) reflects a desire to maintain contact with others – more likely to benefit from CBT teaching relationship development skills. Those with ‘cold’ problems (emotional detachment/hostility) – less likely to benefit from treatment.

Second question is whether social anxiety and dysfunctional interpersonal behaviour characterizing social phobia impairs patients’ ability to collaborate with therapists and benefit from treatment. Different conclusions reported. One explanation for inconsistent findings could be that individual and group therapy place different demands on patients. It’s also possible that interpersonal relationships with therapists are crucial to motivating those individuals.

One study showed that difficulties establishing therapeutic alliance may be confined to some individuals. E.g. self-reported childhood parental abuse was associated with weak therapeutic alliance and more negative patient-therapist interactions. It’s unclear if negative treatment response was a direct function of weak working alliance or due to some pre-existing characteristic of patients that affect their relationships with therapists as well as producing difficult interpersonal problems.

Three models of patient-therapist relationship:

1) Dynamic interpersonal therapy: patient-therapist interactions are viewed as an opportunity for patients to experience how biases in their expectations and interpretations of others’ behaviour lead them to engage in maladaptive behaviours in therapy sessions.

2) Second view is that it is an essential or at least facilitative factor in treatment. Treatment techniques are more likely to be effective if delivered by a supportive, empathic therapist.

3) Third view is that it is a marker of treatment progress. Therapist or patient dissatisfaction with the working alliance signals that treatment isn’t effectively addressing a key element of the patient’s problem.

10. General Discussion

Social anxiety is associated with fewer and more negative social relationships at all stages of life. To close, this review draws attention to the fact that in addition to suffering from anxiety-related symptoms, people with social phobia have a history of interpersonal experiences that shape their beliefs about themselves and others, their interpersonal strategies, and their response to treatment. Their beliefs and strategies trap them in an interpersonal cycle that prevents them from accomplishing those goals. The ultimate goal of treatment should be enabling social phobic people to establish closer and more satisfying interpersonal relationships.

Introduction

Two important characteristics of antidepressants: 1) they aren’t as effective as an ideal antidepressant would be, and 2) there’s a delay in their maximal effect. A proposed biological mechanism for the delay in onset is that different classes of antidepressants cause slow changes in pre- or postsynaptic mechanisms that increase serotonin function – responsible for mood improvement. Another proposed mechanism is based on a cognitive neuropsychological model suggesting that antidepressants “change the relative balance of positive to negative emotional processing,” resulting in later changes in mood. This paper suggests another mechanism involving serotonin-induced changes in social behaviour that will improve mood.

Serotonin and Social Behaviour in Animals and Humans

Aggression is a more dramatic aspect of social behaviour. A meta-analysis concluded that serotonin “has an overall inhibitory effect on aggression” in various animals. Findings suggest that serotonin may alter social behaviour along the continuum of agnostic to affiliative. Research suggests this may also be true in humans.

Acute tryptophan depletion increases aggressive responses and decreases affiliative behaviour according to lab tests. Conversely, tryptophan supplements may decrease aggression and increase positive social behaviour. Tryptophan given to schizophrenic patients decreased the number of incidents on the ward requiring intervention. Another study gave aggressive patients tryptophan, leading to a decreased need for injections of antipsychotics and sedatives to control agitated/violent behaviour. The first study found tryptophan to decrease quarrelsome behaviour but not affect agreeable behaviours (possible ceiling effect). This was tested in the latter study, where participants were psychiatrically healthy but in the upper levels of the population distribution for irritability. In these individuals, tryptophan decreased quarrelsome behaviours and increased agreeable ones. This change occurred without an effect of tryptophan on their appraisal of the agreeableness of their interaction partners – suggesting a direct effect on behaviour instead of an indirect effect mediated by changes in participants’’ cognitive appraisal of others. This is consistent with the fact that altered serotonin function can influence social behaviour in organisms with primitive nervous systems.

Effect of Antidepressants on Social Behaviour in Healthy Humans

Seretti and colleagues reviewed 30+ studies where the effects of antidepressants were compared with placebo in healthy participants. They concluded that generally there were no effects on mood. The effects that did occur were more consistent when the antidepressants were given (sub)chronically rather than acutely, and effects included alterations in social behaviour.

Knutson and colleagues found SSRI paroxetine to decrease subjective irritability and increase affiliative behaviour on a dyadic lab puzzle task in healthy volunteers. Tse and Bond conducted 5 studies where the effects of antidepressants were compared to placebo given to healthy participants, results as followed:

1. Citalopram increased self-directedness but not cooperativeness.
2. Citalopram had no effect on ratings by roommates, but increased cooperative behaviour in a laboratory game.
3. Reboxetine, but not citalopram, caused participants to show more cooperative communication with a confederate behaving nonsociably and to give more cooperative communications in a mixed-motive game.
4. No effect of reboxetine on behaviour along agreeable-quarrelsome dimension, but roommates considered participants more cooperative and agreeable when receiving reboxetine.
5. Reboxetine had no significant effect on irritability, cooperation, or any other measure.

Variability in results is due to various factors (differences in study design, outcome measures, sample sizes). But several studies found changes consistent with improvements in behaviour along the agreeable-quarrelsome dimension – providing modest support for the idea that antidepressants may decrease agonistic and increase affiliative social behaviours in humans. Reboxetine is suggested to increase serotonin function – serotonin may be a mediator of the effects of antidepressants.

Effect of Antidepressants on Social Behaviour in Patients

Irritability occurs in roughly half of depressed patients, and usually resolves with successful treatment. Reviews suggest that about 1/3 of depressed patients experience anger attacks. One study compared effects of sertraline, imipramine, and placebo on anger attacks in patients with atypical depression and dysthymia. Anger attacks ceased in 50% of patients in active treatment groups compared to 37% in placebo group.

Studies have compared effects of antidepressants and placebo on agonistic behaviour in patients with diagnoses other than depression. One found that fluoxetine decreased anger in patients with borderline personality disorder (BPD), and another found it to decrease irritability and aggression in patients with various personality disorders. However, another study found no effect of SSRI fluvoxamine on aggression in women with BPD. A study treating aggressive schizophrenic inpatients with found that it decreased the frequency of aggressive incidents.

Overall results from various studies support the idea that patients with elevated irritability may respond quicker to treatment with SSRIs than patients with only depressed mood. Results provide evidence that SSRIs can decrease aggression, anger, and irritability.

Social Interactions During Depression and Depressed Mood

Hames and colleagues reviewed interpersonal processes thought to be involved in initiating and maintaining depression. Depressed patients tend to have social skills deficits, seek reassurance excessively while also seeking negative feedback and exhibit both interpersonal inhibition and dependency. Many studies looked at how depressed mood influences social behaviour in interaction partners – no direct evidence that the response of others toward those with depressed moods was mediated directly by irritability/anger associated with depression. But it’s a plausible explanation given that quarrelsome/aggressive behaviours tend to be reciprocated by others.

Complementarity in Social Interactions and its Implications for Mood Regulation

People respond to the behaviours of others in a way governed partly by the specific behaviour of the other. It’s proposed that a person’s interpersonal actions evoke a complementary response leading to a repetition of the person’s original actions and that a certain level of intensity tends to evoke a response of similar intensity. Many studies support the idea that quarrelsomeness tends to evoke quarrelsomeness and agreeableness evokes agreeableness, though the exact response can be modulated by the context. Taken together, research suggests that in most people, more agreeable behaviours toward others will tend to be reciprocated and result in a more positive mood. Vice versa for quarrelsome behaviours – resulting in a negative mood.

Complementarity of behaviours, together with changes in mood/appraisal of others, could contribute to an iterative cycle in everyday life.

Possible Role of Changes in Social Behaviour Along the Agreeable-Quarrelsome Dimension in the Effects of Antidepressants on Mood

Research suggests:

1. Most antidepressants enhance serotonin function
2. Serotonin influences behaviour along the agreeable-quarrelsome dimension
3. Depressed patients tend to be irritable and sometimes have anger attacks
4. People tend to respond to quarrelsome behaviour with quarrelsome behaviour – same for agreeable behaviour.
5. More quarrelsome interactions tend to be associated with negative mood, and agreeable behaviour with positive mood.

Hypothesis based on the effects of antidepressants and serotonin on mood -> changes in social behaviour are a way in which antidepressants can improve mood. The change in mood after each interaction will be small, but after many interactions the effect should be much greater. Consistent with the idea of slow onset of action of antidepressants.

Increases in positive affect associated with more positive social interactions and decreases in negative affect associated with fewer negative interactions may play a role in improvement of mood in depressed patients. But increases in positive affect may be more important than decreases in negative affect. Research show positive and negative affect to be separate dimensions rather than opposites on one continuum. Enhancement of positive social behaviour may be more primary in the action of antidepressants than the inhibition of negative social behaviour.

Role of More Prosocial Behaviour and Other Mechanisms in Mediating the Response to Antidepressants

Slow onset of antidepressants is possibly due to initial inhibit firing of serotonergic neurons, though adaptive changes occurring result in important increases in serotonin function. Research on tryptophan suggests small increases in serotonin release to be enough to promote more positive social interactions. But improvement in mood mediated by changes in social behaviour may be important in initial effects of antidepressants, and may be augmented by direct effects on mood associated with larger increases in serotonin functioning happening later.

Cognitive neuropsychological model of antidepressant action suggests that from initiation of treatment, antidepressants create implicit positive biases in attention, appraisal, and memory and that delay in effects on mood are because of the time it takes for these emotional processing biases to influence mood.

The cognitive neuropsychological and social interaction models suggest that antidepressant alter responses to stimuli. In the cognitive model, change is to a more positive appraisal of neutral and emotional stimuli. In the social model, the stimuli are people whom a depressed patient encounters daily – change is a shift away from quarrelsome and toward agreeable behaviour. The important difference is in how the altered response to a stimulus improves mood. In the cognitive model changes occur in the mind (positive appraisals of stimuli) and in the social model the change is in behaviour.

The models are different but not mutually exclusive. Antidepressants may be moving to more agreeable behaviour while simultaneously reinforcing this change through more positive cognitive appraisal of situations. This initiates a cycle of more positive social behaviour resulting in a clinically significant improvement tin mood. 

Conclusion

Evidence is stronger for increased serotonin function and antidepressants decreasing aggressive behaviour than for increasing agreeable behaviour. There’s inconsistency in results on the effects of antidepressants on behaviour – could be attributed to use of measures. Also a lot of the evidence for agreeable social behaviour is mainly based on studies on healthy rather than depressed people. Lastly, if more positive social interactions are a clinically significant factor in the action of antidepressants, then patients who have more social interactions early in treatment may be expected to respond better to it.

Introduction 

There are differences between all individuals in the way they respond to acute/chronic stress. Many individuals who experience traumatic events exhibit only minimal effects on their biological, psychological, and emotional functioning. However, some individuals consistently respond to even the slightest changes in their physical or social environment with profound emotional, psychological, and physiological distress that often reappears without any obvious subsequent provocation.

What factors underlie these differences in responses to stress? Are they due to individual genes, their environment, or an interaction of both? This review tries to answer those questions based on rhesus monkeys and discusses some implications of those findings.

20% of monkeys these findings are based on, that grew up in a naturalistic setting, consistently react to novel, mildly stressful social situations with unusual fearful and anxious-like behaviour, accompanied by prolonged hypothalamic-pituitary-adrenal (HPA) axis activation. 

5-10% of the monkeys growing up in the same conditions are likely to exhibit impulsive and/or inappropriate aggressive patterns of behavioural response under similar circumstances. Monkeys in the latter subgroup also show chronic deficits in serotonin metabolism. 

Development of Individual Differences in Stress Reactivity

Monkeys that grow up in a naturalistic setting spend most of their first month in intimate physical contact with their mother, establishing a strong and enduring bond between mother and infant. From the second month the infant starts to explore their immediate environment, using their mother as a secure base. Later, they spend increasing amounts of time away from their mothers and begin to establish relationships with other (same-aged) members of their social group. Through the rest of their childhood they spend any hours in active social play with these peers. Nearly every social behaviour important in adulthood is developed, practiced, and perfectured during peer play, most notably behaviours leading to successful sexual reproduction and the socialization of aggression (appears at 4-6 months of age).

Excessively aggressive and/or fearful monkeys show significant deviations from their species-normative pattern of social development. Fearful infants leave their mothers to explore their environment at a later age and exhibit low rates of exploratory behaviour later on. They seem reluctant to interact with monkeys other than their mother, resulting in less peer play. When physically separated from their mothers they will exhibit excessive behavioural distress, accompanied by higher and prolonged levels of cortisol which are predictive of differential responses to other situations later in life. 

Overly aggressive infants, especially males, typically display their aggressive tendencies initially in the context of social play with peers. They readily respond to play invitations and tend to initiate rough-and-tumble play bouts, often escalating into episodes of actual physical aggression with their play partners. Other monkeys in their social groups start avoiding most interactions with these aggressive youngsters, resulting in increased social isolation. Studies reveal a significant negative relationship between the incidence of aggression in the context of play and 5-HIAA concentrations; the most aggressive males tend to have the lowest CSP 5-HIAA levels. 

Heritability analyses have shown that individual differences in behavioural and adrenocortical response to separation have a significant genetic component, as well as that differences in CSF 5-HIAA are remarkably stable over the lifespan which are also highly heritable. 

Effects of differential social Rearing Environment

In the same rhesus monkey colony, other monkeys have been reared from birth on in the absence of any adults, but in continuous presence of same aged peers, after an initial month in the researchers’ neonatal nursery. After 6 months of peer-only (PO) rearing, infants are introduced in large social groups containing same-aged PO-reared and mother-and-same-aged(MP)-reared monkeys. Both PO- and MP-reared monkeys remained in the same group until puberty.

PO-reared monkeys quickly develop strong attachment-like bonds with each other within days after release from neonatal nursery. However, these ‘hyperattachments’ tend to be nonfunctional, largely because a peer isn’t as good as mother in providing a secure base for exploration or soothing an infant when it becomes frightened/upset. As a result, PO-reared infants tend to explore and play less compared to MP-reared infants in their first 6 months. PO-reared monkey groups also show more extreme behavioural and adrenocortical responses to social separation at 6 months of age. They display similar behavioural and serotonergic characteristics that differentiate overly aggressive MP-reared monkeys from others in their cohort. Potential reason for this is that they may experience play deprivation though they’re in continuous presence of potential playmates, as they grow older they become more aggressive, more than most of their MP-reared group members. 

Early social experiences like maternal deprivation can have significant and long-lasting effects on behavioural and biological development over and above any contributions to individual differences attributable to heritable factors. 

GxE Interactions

Rhesus monkeys have the same 5-HTT gene and functional polymorphism as humans. As a result of genotyping the monkeys from the colony, researchers have been able to search for possible GxE interactions involving differential early experience and allelic variation in the 5-HTT gene. Monkeys carrying the short allele of this gene show delayed early neurobiological development, impaired serotonin functioning, and excessive aggression, HPA reactivity and alcohol consumption as they grow up, only if they have been PO-reared, MP-reared carrying the same short allele exhibit species normative patterns. MP-reared monkeys with the same short allele consume less alcohol than their MP-reared counterparts carrying the long allele, raising the assumption that having the short allele represent a significant risk factor for PO-reared, while the opposite for MP-reared monkeys is true. Though it seems apparent that significant GxE interactions occur in monkeys and humans, the demonstration of such interactions has been largely statistical and hence subject to multiple interpretations. When talking about a good gene protecting an individual from a bad environment, MP-rearing buffers individuals carrying less efficient allele from developing the aberrant patterns shown by PO monkeys with the same allele - a good environment can protect people from carrying a bad gene from detrimental developmental outcomes.

These two competing interpretations of the same data sets are not necessarily mutually exclusive. Following the author of the article, different developmental processes representing both interpretation can take place in the same individual during the same periods of development. New research demonstrates that different maternal licking/grooming of rat pups during their second postnatal week can alter gene expression with consequences that are life-long and can be transmitted to the next generation of offspring. Given the findings, the possibility that specific early social experiences can similarly alter gene expression in primates no longer seems far-fetched. If true, this could have implications for the prevention of adverse outcomes in individuals carrying the less efficient allele of these and other ‘candidate’ genes.

Summary

Rhesus monkeys exhibit individual differences in their reactions to environmental stress like humans. Some are excessively fearful in response to changes in their environment throughout development; others are overly impulsive/aggressive. Its possibly to identify genetic and environmental factors that contribute to these different response patterns, but recent evidence suggests that GxE interactions may be at least as important in shaping individual development in this species, possibly through mechanisms by which specific aspects of the environment influence expression of certain genes at certain times of development. Lastly, because GxE interactions require genetic variation at the species level to take place, the fact that rhesus monkeys - and humans - apparently possess greater allelic variability in certain genes than other primate species may contribute to their remarkable resilience and adaptive success relative to other primates.

Introduction 

The early-life social environment can induce stable changes that influence neurodevelopment and mental health, meaning that they have a persistent impact on gene expression and behavior through epigenetic mechanisms. The hypothalamus-pituitary-adrenal (HPA) axis is sensitive to changes in the early-life environment that associate with DNA methylation of neuro-specific exon 17 of the glucocorticoid receptor (GR). 

DNA methylation is a process by which methyl groups are added to the DNA molecule. Methylation can change the activity of a DNA segment without changing the sequence. When located in a gene promoter, DNA methylation typically acts to repress gene transcription.

In rats, the offspring of mothers with an increased frequency of pup licking/grooming (LG) show increased GR expression, greater negative feedback regulation over hypothalamic corticotropin releasing factor (CRF), and more modest responses to stress compared with offspring of low LG mothers. Variations in maternal LG are linked to an epigenetic modification of a neuron-specific exon 17 GR promoter such that increased maternal LG associates with decreased methylation of the exon 17 promoter and increased hippocampal GR expression. 

In humans, evidence for a long-term effect of early-life adversity (ELA) on the epigenetic state of the human genome was observed while investigating the methylation state of the GR gene in the hippocampus of individuals who committed suicide and had a history of child abuse. ELA in humans reprograms the DNA methylation patterns of the GR gene exon 1F (GR1F) expression in the hippocampus of suicide completers with a history of child abuse compared to non-abused suicide completers and healthy control subjects. Another study has found that children born in mothers with depression, irrespective of SSRI use, exhibited higher GR1F methylation levels. 

The article summarizes 40 articles that either used humans or mammals like mice or rats to find evidence for their hypotheses.

Early life adversity 

Experimental groups and GR region Studied

In animal models, ELA was characterized by either the use of maternal care or maternal separation models. All of the animal studies examined exon 17 when studying the GR region. 

In human studies, ELA was defined as exposure to traumatic events in childhood, including emotional, physical, or sexual abuse, neglect, early parental death, and other traumatic events. The majority of human studies examined exon 1F, one examined exon 1D, while 2 also included exon 1B and 1C and 3 studies examined exon 1H, when studying the GR region.

Effect on Methylation

The ELA group contains results from 10 studies for each animal and human studies. 

7/10 animal studies reported a significant increase in methylation in the exon 17 promoter due to ELA, while 3 studies reported no such change. 9/10 human studies reported increased promoter methylation with ELA.  

Parental Stress

Experimental groups and GR region Studied

One animal study used a variety of non-pain-inducing, non-habituating, stressors over a course of 7 days to stress mouse dams. The study examined exon 17 when studying the GR region. 

Human studies examined the methylation status of children of women who had experienced anxiety and mood disorders (2 studies), pregnancy-related anxiety (1 study), violence (1 study), or war stress (2 studies) during pregnancy. Another study examined the effects of parental stress on GR gene methylation in adolescence, and an additional study examined the methylation pattern of individuals whose parents had experienced war but not during pregnancy. 7/8 studies examined exon 1F, while one study examined exons 1B and 1D, when studying the GR region. 

Effect on Methylation

All 8 studies investigating exon 1F, respectively 17 for animals, reported an increased methylation of exon 1F/17 in offspring of parentally stressed individuals. Of these, 2 studies also reported decreased methylation at specific CpG sites and in particular conditions, such as that the stressor during pregnancy only existed during the first or second trimester of the pregnancy. The one study that was investigating exon 1B and 1D reported a decrease in methylation of exon 1B and an increase in methylation of exon 1D in children of women experiencing fear of delivery in all trimesters or fear of the integrity of the baby in the first trimester. 

Psychological stress/ Psychopathology 

Experimental groups and GR region Studied

3 animal studies used acute or chronic stress models to assess the impact of social stressors on GR gene methylation. All of which examined exon 17 region.

8 human studies examined the effects of psychopathologies on human GR gene methylation. Specifically, one study involved response to stress, a second BPD, a third bulimia nervosa, another two PTSD and an additional two depression. Of which 6/8 examined exon 1F and in addition 3 studies examined exon 1B, and 2 studies examined 1J and 1E. 

Effect on Methylation 

In the animal models, 2/3 studies reported increased exon 17 methylation in stressed animals. 

In human studies, results were more varied. One study reported increased methylation of exon 1 F, while 3 studies reported no change and 2 reported decreased methylation. Among the other exon variants examined, there was no consensus on the effect of psychological stress/psychopathology on methylation status. 

Conclusion

This article reviewed a set of 40 studies that research GR gene methylation in relation to various psychological stressors, including parental stress, ELA in social environments in animals, ELA in humans, and psychological stress or psychopathology in adults, by, in most of the studies, investigating the GR exon variant 1F or 17 for animals. 

The majority of the studies concerning ELA and in utero adversity reported increased methylation at the respective exon. In particular negative early-life social environment were associated with greater exon 1F methylation in the large majority of the studies. These findings show a compelling consensus across studies and methodologies (eg. Tissue samples from different locations were used in different studies, such as brain or blood tissue) Furthermore, childhood maltreatment associates with increased exon 1F methylation and the promoter methylation status was closely correlated with both the frequency and severity of maltreatment. One study reported that increased methylation of the exon 1F NR3C1 gene promoter in leukocytes is associated with the disruption of normal parent-offspring interaction or maltreatment, and linked an attenuated cortisol response. Another study supported this claim and noted that parental loss was also associated with increased methylation on the same gene promoter. 

Recent evidence suggests that epigenetic plasticity is sustained in the brain throughout adulthood, potentially as a mechanism to cope with the evolving demands of the environment, yet, there are clear moments during development when plasticity is heightened and these may be more strongly associated with the establishment of life-long epigenetic modifications. 

Studies with adults revealed that childhood maltreatment is associated with an increased HPA response to stress. Subsequent statistical analyses revealed that childhood abuse was the strongest predictor of adrenocorticotropic hormone (ACTH) responsiveness, followed by the frequency of abusive events, adulthood traumas, and depression. An interaction term of childhood and adulthood trauma proved to be the best predictor for ACTH responses, suggesting that a history of childhood abuse is related to increased stress reactivity, which is further enhanced when additional trauma occurs in adulthood. 

Cerebrospinal fluid CRF concentrations were correlated with the severity and duration of physical and sexual abuse, and high CRF may arise due to GR downregulation and impaired negative feedback inhibition. Some subjects having experienced childhood abuse exhibit a decreased cortisol production, which may reflect an adaptation to chronically stressful situations, whereas elevated cortisol production may prime individuals to react to unpredictable stressors, and these situations may both constitute ELA. Currently, it is difficult to draw conclusions  on the overall impact of GR methylation variations on basal and reactive cortisol levels, as the majority of studies investigating GR promoter methylation did not measure cortisol levels. 

These findings suggest that childhood adversity stably influences HPA responses to stress, which is consistent with the idea that childhood maltreatment sensitizes neural and endocrine responses to stress, thus establishing a vulnerability for mood disorders. 

Recent studies suggest that epigenetic programming of HPA function occurs at multiple levels of the HPA axis in addition to effect on hippocampal GR expression. 

Environmental conditions that increase the frequency of LG in the rat are associated with decreased paraventricular CRF expression. Augmented maternal care in return, reduced the number of excitatory synapses onto CRF neurons. Decreased CRF, through disruption of maternal care in mice, showed enhanced glutamatergic transmission to hypothalamic CRF neurons in offspring. Moreover, prolonged periods of maternal separation alter the methylation state of the promoter for the Avp gene, increasing hypothalamic arginine vasopressin synthesis and HPA responses to stress. These findings reveal that the quality of postnatal maternal care in rodents epigenetically programs gene expression at multiple levels of the HPA axis to regulate both basal and stress induced activity. 

A remarkable feature of all the findings is the coordinated epigenetic effects on multiple genes, in multiple tissues, that collectively serve to increase HPA responsivity in stress responses in early social adversity. 

Introduction

Alcoholism is a progressive neurocognitive disorder, where premorbid vulnerability factors interact with neuroadaptations resulting from excessive drinking. Lack of cognitive control over impulses can be a risk factor for and a consequence of addition, with increased evidence indicating that the latter maybe strong when excessive substance use starts in adolescence. Recent research emphasizes the importance of the malleable adolescent brain in the early development of addiction (note: clinical patients typically adult, with large age-range). Some of the later stages of addiction usually occur later in life. But some of the neurocognitive abnormalities in addiction may reverse after prolonged abstinence or targeted training.

Biomedical research emphasizes that addiction should be seen as a chronic brain disease, but this shouldn’t lead to the conclusion that nothing can be done about it. In addition to traditional treatments, a novel set of training-paradigms have been developed, known as Cognitive Bias Modification (CBM). These have generated positive first results in the treatment of problem drinking in a community sample, and alcoholism in patients. These interventions aim to directly change the automatic/implicit cognitive motivational processes involved in addiction, of which patients may not always be aware and are difficult to control/change by more traditional means. This study focuses on re-training one of these implicit processes: automatically triggered action tendency to approach alcohol.

A first clinical study on the effects of CBM tested effects of four sessions of A-AAT (alcohol approach-avoidance task) training in alcohol-dependent patients in an inpatient setting. Results showed patients’ alcohol-approach bias to change to alcohol-avoidance bias – generalizing to untrained pictures in the same task. Patients in the training group showed 13% less relapse in one year after treatment compared to the control group.

Little is known about predictors of successful training. Various studies found implicit cognitive processes to be a better predictor of alcohol use in people with relatively weak executive control (EC) capacities. Recent study found that EC moderates the relation between alcohol-approach tendencies and drinking behaviour in high-risk adolescents and may also moderate training effects (stronger effects in those with weak EC). One can conclude that approach-bias re-training may work well for patients with weak EC and so we should use a classic Stroop colour-word interference task as a potential moderator. Deviant brain activation during a Stroop task has been associated with risk for addiction in adolescents with family history of alcoholism, and children with ADHD when they’re off medication.

This study has two main objectives: 1) to test if the effect of adding computerized approach-bias re-training to cognitive behavioural treatment increases abstinence in alcoholic inpatients, and whether the effect on treatment outcome would be mediated by the amount of change in approach-bias. 2) to investigate whether success of training can be predicted by patients’ level of EC and/or background variables.

Methods

Participants

Alcohol-dependent patients administered to a three-months inpatient treatment. We included every patient with a primary alcohol dependency diagnoses. Exclusion criteria were neuro-cognitive problems, strong withdrawal symptoms, history of schizophrenia, and visual or hand-motoric handicaps. None of the patients received anti-craving medications. The final analytical sample consisted of 475 patients.

Assessment and outcome measures

Patients were diagnosed at intake using the computerized version of the CIDI (Composite International Diagnostic Interview) and a diagnostic interview. Both the CIDI and interview ere the basis for the final expert ratings on diagnoses made by clinical psychologists.

Experimental Task

Alcohol-AAT (Approach-Avoidance Task)

The alcohol AAT measures the automatic approach tendency toward alcohol. Participants asked to react to the format of pictures using a joystick, ignoring the pictures’ contents. Two categories of pictures – 20 alcoholic beverages, and 20 soft drinks. Pushing a picture away would decrease its size, and pulling a picture closer would increase its size.

Alcohol- AAT (Approach-Avoidance Task)-Training Version

For CBM, A-AAT was used. Training effect was achieved by presenting alcohol pictures in the push-away format and soft-drink pictures in the pull-closer format.

Colour Stroop (EC)

Variety of the Colour Stroop task was used. To assess strength of inhibitory EC in alcohol-dependent patients. Participants had to decide whether the colour name and colour of the ink were same or different.

Questionnaires

Beck Depression Inventory (BD): Used to measure the severity of depressive symptoms.

Rosenberg Self-Esteem Scale (RSES): Addresses feelings of global self-worth.

Symptom Checklist 90-R (SCL90-R): Measures the physical and psychological impairment of a person within the past seven days. Indicates general level of distress.

Alcohol Abstinence Self Efficacy Scale (AASE): Assesses a patients’ confidence to stay abstinent in 20 different situations as well as their temptation to drink in these situations.

Alcohol Use Disorders Identification Test (AUDIT): A screening instrument for problematic alcohol consumption, constructed by the WHO.

Conditions and Experimental Manipulations

Participants randomly assigned to one of the two groups (training vs no training). Experimental group received 12 sessions to respond with an avoidance movement to alcohol pictures and approach movement to non-alcohol drinks. Achieved by presenting alcohol pictures in landscape format and soft drinks in portrait. During training, participants had to correct errors. Each training sessions started with a short A-AAT assessment to measure training effects of the previous session. Control group received no training at all instead of a sham-training, because no significant difference between no-training and sham-training was found in a previous study.

Procedure, study design, data analysis

First week of therapy, patients took part in a ‘neuropsychological checkup’ including the A-AAT. The previously mentioned questionnaires were also filled out, within the diagnostic phase. After pretest, patients randomly assigned to training conditions. As well as experimental manipulation, patients received treatment as usual, consisting of abstinence-oriented inpatient CBT-based treatment. One year after discharge, patients received a follow-up questionnaire about alcohol consumption since treatment.

The main outcome variable was treatment outcome one-year follow-up. Successful outcomes were 1) no relapse at all or 2) a single lapse shorter than 3 days ended by the patient without further negative consequences. ‘No success’ was defined as relapse or death, ‘no information’, or refusal.

To predict who will profit from the training, the predictive value of the implicit measure (A-AAT) and the questionnaires, as well as demographic facts, and the measure of EC were of interest.

Discussion

Main findings were that the effects of a computerized alcohol-avoidance training were replicated on the process trained and on long-term clinical outcomes. Second, this long-term effect was mediated by the change in alcohol-approach tendencies from pre- to post-test. Third, regarding moderators, the strength of alcohol-approach tendencies at pretest, but not hypothesized weakness of EC predicted the amount of change in approach-tendencies – age significantly predicted who would profit most from training.

Clinical effects of CBM in short-term and long-term were replicated. Strengthens the suggestion to add CBM to regular treatment, to supplement treatment of addictive disorders. Short-term effects were mainly due to the experimental group developing strong alcohol-avoidance bias, whereas no change in bias for soft drinks occurred. For the control group there was no change in either drink. Long-term alcohol-dependent patients are likely to feel approach (negative reinforcement effect of alcohol) and avoidance (awareness of negative long-term effects of drinking) impulses. But despite this awareness, salient situational cues may still trigger approach-tendencies in a patient in a risky situation after leaving the clinic. CBM could reduce ambivalence by strengthening avoidance impulses, weakening tendencies, and/or control over these tendencies.

Regarding long-term effects, fewer relapses occurred in the training group, and the training condition remained a significant predictor of treatment outcome. Could be argued that training only increased patients’ willingness to answer follow-up questionnaires, maybe because they liked the training/had positive memories of their stay at the clinic (social desirability). But an increased return rates in the sham-training condition was not found. It seems likely that the lack of significance is due to response bias indicating that patients are more likely to answer if they’re still abstinent.

Regarding moderation, amount of change in alcohol-approach bias was moderated by the A-AAT prescore. It makes intuitive sense that re-training of a cognitive bias has the strongest effect in participants who start the training with a strong cognitive bias. But present findings also indicate that matching on the individual level will be difficult. Hypothesis that weak EC would predict stronger effect of alcohol-avoidance training wasn’t confirmed. Was found that age moderated the treatment effect, and higher age is correlated with weaker EC.

From a broader developmental perspective, the present findings are interesting. They reject the notion that CBM can only have an influence on young malleable brains. More positive effects were found for older alcoholic patients. These findings are promising from a treatment perspective. Many individuals experiencing problems with alcohol spontaneously ‘mature out’ of these problems, also in adult community samples many individuals succeed in spontaneous recovery without formal treatment. People who enter formal treatment tend to be older and have comorbid other psychiatric problems. CBM may train control over the impulse to drink again in a concentrated way, and the alcohol-stimuli may help trigger this ability in risky situations after treatment discharge. One could also investigate training of general EC abilities. Goal-management and mindfulness training have provided initial promising results in addiction, also interventions with a cognitive training element.

Finally, though these results are promising, there are some limitations.

1. Measure of EC used here was a variety of the Stroop Task, may have been easier than the original.
2. Brain activity during the task could also be measured.
3. Both the current study and the one by Wiers et al. (2011) were conducted in the same clinic and carried out by the same research group. To draw firm conclusions about the use of this CBM as a treatment it needs to be tested in a multi-center study with different treatment facilities.
4. Success of the CBM treatment may depend on the motivation of patients.
5. Important line of future research is to identify necessary conditions for the CBM to be effective.
6. A related domain of further applied interest concerns the possibility of a ‘take-home’ training. CBM is simple and computerized, so patients could continue their training outside the clinic at home – may increase the transfer of success achieved with training.
7. Another issue concerns mediation and moderation. Present finding that age moderated the effectiveness of the A-AAT retraining is valuable when it comes to matching trainings to patient. But age correlated with a number of other potential predictors so it’s important to disentangle these variables in future studies.

Conclusion

In conclusion, CBM seems to be a promising treatment add-on for treating addiction as well as other psychopathology. Older people seem to profit most from the training, but this variable is correlated with various other variables. Next research steps should be to clarify underlying mechanisms in CBM compared to other training-interventions, and address issues of implementation. Finally, it’s important for theoretical and clinical reasons to investigate the question of moderation: which training works best for whom?

Introduction

The treatment in which a drug addict is repeatedly exposed to stimuli associated with addicted behaviour is known as Cue Exposure with Response Prevention (CERP). The response that these cues evoke is generally considered to be conditioned drug responses. These can be psychophysiological (changes in heart rate), behavioural (drug-seeking behaviour), or subjective (craving). These responses increase the chance than an addict will take drugs.  The treatment leads to the gradual extinction of the conditioned drug response. Unfortunately, no research has yet found a substantial effect on relapse by extinguishing cue reactivity. Apparently the effect (extinction of cue reactivity) does not generalize beyond the treatment setting. This can be explained by the fact that conditioned responses can recover after extinction, and extinction is seeing as the ‘unlearning’ of something which is meant to be permanent.

This article describes a number of ways in which CERP can be improved so that it’s more effective in combating relapse. First it describes how contemporary learning theory defines extinction and how it explains the recovery of conditioned responding. Second, different methods to prevent the recovery of extinguished cue reactivity are discussed. Then suggestions for future research are addressed.

Theoretical Notes

Pavlov indicated that extinction is not forever. Extinguished responses can recover; he calls this spontaneous recovery. In addition, the renewal effect shows that extinction is not the same as learning form an association. The renewal effect means that a conditioned response after cancellation can be renewed if the conditioned stimulus is presented in an environmental context different form the context in which the extinction took place. The statement by Bouton (1994) reads as follows: conditioned stimulus has acquired an ambiguous meaning after extinction. After extinction, a stimulus predicts the presentation and absence of an unconditioned stimulus. So the conditioned stimulus has a stimulating meaning during conditioning and an inhibitory meaning during extinction. Spontaneous recovery of a response can occur because someone doesn’t understand the meaning of a conditioned response when it’s presented in a different environment than the one it was learned in.

The treatment of drug addicts is difficult because they use drugs in many different places and situations. So there are too many practical problems to offer a ‘standard’ CERP. Offering CERP in different environments would increase the chance of generalization. However, offering CERP in multiple environmental contexts could cause a delay of extinction. Moreover, it’s unclear how many different contexts are needed. The perfect CERP would be a treatment that considers and controls for the probability of renewal effects and spontaneous recovery, and takes into account the above problems.

A promising option is to add so-called retrieval cues in the CERP treatment. Retrieval cues are striking features of an extinction environment, whereby the inhibitory meaning of the conditioned response is recognized outside the environment. If a retrieval cue is presented outside the original environment, this reduces the chance of renewals. An example of a retrieval cue would be using a reminder card.

Conclusion

learning and motivation is a dynamic research area, and so, contemporary learning theory continues to be an important resource for the implementation and development of behavioural therapy. Based on principles derived from contemporary learning theory, CERP incorporating retrieval cues can be a promising adjustment of standard cue exposure treatment. It doesn’t require extending the length of treatment and may control for the previously mentioned limitations.

When cue reactivity is extinguished and recovery of conditioned drug responding can be prevented by cue exposure with retrieval cues, it’s predicted that relapse of addictive behaviour can be more successfully prevented.

Contemporary cognitive models of classical conditioning provide a framework for understanding people’s fears and phobias. According to these models, classical conditioning is the acquisition of associations between representations of stimuli or events. For an explanation of classical conditioning, see a number of previously summarized articles.

Recently a distinction has been established between two different forms of learning in classical conditioning: expectancy learning and merely referential learning. Expectancy learning arises when showing the CS activates the expectation of a real US event. Referential learning arises when showing the CS activates the representation of the US, without the expectation of the US also arising. So the CS ensures that someone thinks of the US, but doesn’t expect the US.

Evaluative conditioning (EC) is a type of referential learning: the observation that the presentation of neutral stimuli with (dis)liked stimuli changes the valence of the stimuli in a (negative) positive direction. Evaluative learning resembles expectancy-learning in that it is sensitive to US revaluation. So the shift in valence of the CS seems to be based on the association between Cs and US representations. Research into evaluative learning and expectancy learning differs in two areas:

1. The type of learning: evaluative conditioning studies often used rather unobtrusive stimuli like flavours, or pictures of human faces, paintings, statues etc. that were rated as positive or negative by the individual participant. Whereas expectancy-learning have utilized biologically significant stimuli like food or shock, that are unconditional stimuli in a strict sense: they elicit a similar and innate/unlearned positive or negative response in all subjects.
2. Response systems are different: evaluative investigations focus primarily on the verbal ratings of CS valence and expectancy investigations primarily on the nonverbal motor/autonomous responses such as the skin conductance response.

In addition to verbal assessments, it’s important to investigate nonverbal and physiological responses. A good way is the performance on affective priming tasks. Positive or negative stimuli are presented, which the participant must give a value as quick as possible to (positive or negative). Each stimulus is preceded by a prime stimulus, which is negative, positive, or neutral, and must be ignored. The valence of the prime stimulus appears to influence the speed at which the stimuli are assessed. This is based on the automatic processing of the prime stimulus.

Current research is looking into whether evidence can be found for both forms of learning within the same conditioning procedure. This conditioning procedure includes images of human faces as CS+ and CS- and an electrocutaneous stimulus as US. The valence was investigated through the affective priming procedure and verbal assessments. Expectancy learning has been examined by assessments of US-expectancy. Arousal and fear ratings were also assessed for exploratory reasons.

In addition, this study aims to analyze whether evaluative learning as demonstrated in aversive conditioning is comparable to evaluative learning with non-aversive US. In addition to the CS+ and the CS-, therefore, CS-positive and CS-negative were included, positive and negative adjectives, respectively. Finally, this study looks at the extent to which specific instructions for imagining can enhance learning. Previous research has shown that mental imagery can potentiate the effects of acquisition.

Method

32 students (11 men, 21 women) were examined.

Experiment consisted of three phases:

1. Stimulus selection: participants assessed 60 photos of faces. The intensity of the US was also measured in this phase by means of electrodes.
2. Acquisition: CS+, CS-, CS-positive, and CS-negative were shown to the participants. A corresponding sound was played during presentation of CS-positive and -negative.
3. Affective priming: the affective priming task was offered.

Results & Discussion

After the acquisition, the participants indicated that the "electrocutaneous US" was intense and unpleasant and that they were shocked. During the acquisition, the CS + had become a valid predictor of the US. Not only did the participants find the US annoying and they were aware of the contingency between CS + and US / CS- and not a US, expectation learning had also emerged. In addition, there have been shifts in the evaluation of the CS + and CS-. After acquisition, the participants gave the US with positive adjectives a positive rating and the negative US a negative rating. No expectation learning is involved in the conditioning of the CS positive and the CS negative. Moreover, no significant difference was found in the degree of evaluative learning between the two types of conditioning procedures.

To increase the level of learning, half of the participants were asked to imagine something about the relationship between the CS and the specific US. It turned out that the two groups did not differ in the degree to which they liked or disliked the different types of US. There was also no significant effect on the level of evaluative learning. The degree of arousal was influenced by the conditioning procedures: the CS + was found to be more arousing than the CS-. The CS + also generated more fear than the CS-. The CS negative generated more fear than the CS positive.

In conclusion, the experience of contingent presentation of a neutral face (CS +) and an aversive electrical stimulus (US) has changed the experience of the CS + in two ways:

• The CS + became a predictor for the US.
• The CS + itself became more negative.

Thus, evaluative learning and expectation learning can occur together. Moreover, the results of the affective priming procedure prove that affective priming can occur with aversive conditioned stimuli. An alternative to this affective priming procedure is the modulation of an acoustic shock reflex: a defensive reflex due to an unexpected sound. This varies with the valence that one gives to a picture. This modulation can be a good way to measure valence after acquisition, but it cannot measure the effects of extinction. A substantial fright reflex is only found with pictures that cause a lot of excitement, and they usually disappear after extinction.

In addition to the fact that expectation learning and evaluative learning can occur together, a conclusion can also be drawn from the results found. This is that the amount of evaluative learning resulting from an aversive conditioning procedure has no interaction with the type of conditioning preparation. Thus, evaluative learning can also be generalized to conditioning procedures with more biological US stimuli. This shows that clinical fears based on the experience of contingency between the neutral stimulus and negative stimulus cause not only that the CS becomes a predictor of a negative experience, but also that the CS is viewed more negatively. A combination of exposure and counter conditioning would be a good way to prevent relapse of patients.

A number of things can be interesting for follow-up research. Firstly, to investigate whether the conditioning effects found are also found in other types of stimuli. Secondly, to investigate whether the same evaluative shifts are found if the CS is subsequently masked during acquisition. Third, to investigate the precise nature of the conditioned response, which remains after extinction.

Introduction

An important consideration in the cognitive analysis of emotions is their evolutionary origins. Regarding anxiety, there’s a system that ensures that attention is paid to threatening environmental an interoceptive stimuli that are relative to the person’s motivational state. This allows a quick and effective response to threatening stimuli. In the case of fear, a bias can then arise in selective attention to threatening information.

A feature of recent cognitive theories is the emphasis on the role of attentional processes in etiology and the maintenance of anxiety. Something can be said about all of these theories, which is why it’s subsequently explained from a cognitive-motivational point of view what the specific mechanisms are that are responsible for an attentional bias in anxiety.

Cognitive Theories

According to recent cognitive theories, biases in information processing play an important role in the etiology and maintenance of emotional disorders, such as generalized anxiety disorder (GAD) and major depressive disorder (MDD). Beck developed a schema model where relevant schemas have become dysfunctional and Bower proposed a semantic network theory of emotions where each emotion represents a node in an associative network in memory.

Both theories say that anxiety and depression are associated with an emotion-related bias in all aspects of information processing. However, this is not entirely true, because anxiety is mainly associated with a bias in selective attention and depression with a bias in selective memory.

Williams (1988) then developed a revised cognitive theory about anxiety and depression. Some characteristics of this theory are:

• Different emotional disorders are associated with different patterns of cognitive bias.
• People who have a permanent tendency to show preattentive, automatic vigilance for threat are more susceptible to the development of anxiety disorders when under stress.
• Trait anxiety influences the direction of preattentive and attentional biases to threat stimuli. People with high trait anxiety orient their attention towards the threat and people with low trait anxiety direct their attention away from it. This is the interaction hypothesis.
• Cognitive behavioural therapy is effective because these biases are corrected.

Williams then says that two mechanisms are responsible for the pre-attentive and attentional bias towards threats. This is the Affective Decision Mechanism (ADM) and the Resource Allocation Mechanism (RAM). The ADM assesses the degree of threat of stimuli. The output of this mechanism depends on the stimulus, but also on the degree of anxiety that the person currently has (state anxiety). The output serves as input for the RAM, which determines the allocation of resources of the processes.

The effect of RAM depends on the degree of trait anxiety of the person. As the output of ADM increases, the difference between people with high and low trait anxiety (interaction hypothesis) becomes clear.

Later, the Williams model was adapted using connectionist terms (1997). However, the interaction hypothesis remains an important key point in the model. Various other theories are an addition to this model. The main focus is on the assumption that preattentive processes play a role in anxiety. These processes are important in the evaluation of stimuli and in giving direction to the focus of selective attention and the response that is given as a result. These processes are said to be vulnerable to the development of clinical anxiety.

However, a number of comments can be made about these cognitive theories:

• The interaction hypothesis says that people with low trait anxiety turn away from a threatening stimulus. However, this is not smart when it comes to really threatening stimuli and would mean that the threat detection system is not functional.
• Several studies have found a bias in preattentive processes in anxiety disorders, but not in depression. This is strange, because depressed people also have a higher level of anxiety
• The theories make little use of recent neurobiological systems that play a role in anxiety.

Below are two biological formulations of anxiety:

1. Gray says that a vulnerability to anxiety is associated with individual differences in Behavioral Inhibition System (BIS) activity. This system compares current with expected stimuli and takes action if they do not match or if there are aversive stimuli. BIS ensures inhibition of current behavior, which increases the arousal and for greater attention to the stimuli. Anxious people have an overactive BIS.
2. LeDoux is known for his belief that the amygdala plays a major role in emotions and that it is activated by a threatening stimulus. Attention processes play a lesser role in his model.

Cognitive-motivational point of view

According to this position, there are two motivation-related systems that, in combination with each other, play a key role in mediating fear. These are the Valence Evaluation System and the Goal Engagement System. They can each be placed on an axis in a two-dimensional network.

A motivational analysis of these factors says that a bias in pre-attentive processes and initial orientation with regard to emotional stimuli depends on the combined functioning of valence evaluation and goal engagement. According to the cognitive-motivational point of view, the Valence Evaluation System ensures the value of a threatening stimulus. This depends on the stimulus itself, but also on the context, the degree of anxiety at that moment (state anxiety), previous experiences, and the degree of arousal.

In addition, the Valence Evaluation System is more sensitive to people with high trait anxiety. Trait anxiety is then seen as an increased output of the Valence Evaluation System, which reflects a bias in the valuation of threats. The output from the Valence Evaluation System serves as input for the Goal Engagement System, which is responsible for mediating preattentive and attention responses. Nothing is done about it with little threat. In the event of a high threat, this is immediately aimed at and other processes are stopped.

According to this view, there is no linear relationship between the valuation of threatening stimuli and attentional bias. When there is no threat, no attention is paid to the stimulus. With a little threat, the attention goes away from the stimulus. With a medium to high threat, there is an increased degree of attention given to the stimulus that ultimately gets stuck at a certain (high) level.

Some advantages of this system are:

The cognitive-motivational view says that an attentional bias or pre-attentive bias does not play a causal role in the etiology of an anxiety disorder. Such a bias can also be found in people with low trait anxiety when the stimuli have a high threat.

The presence of such a bias for mildly threatening stimuli may be a sign of a sensitivity to anxiety, but this may not be a determining factor. The primary factor that determines this sensitivity, according to the cognitive motivational point of view, is a bias in the Valence Evaluation System. The attention processes may possibly be important in the maintenance of anxiety.

Research into attentional bias in anxiety

Studies that investigate a bias in selective attention to emotional stimuli use the (emotional) Stroop test, probe detection task and color perception task, the latter being a variant of the probe detection task, where a word pair is represented of which a word is neutral and the other emotionally. After that, two colored fields appear instead of the words at the same time, but fearful people think that the colored field that replaces the emotional word appears earlier. The Stroop task bases the conclusions on interference, but these are complex and sometimes difficult to interpret because of confounds and "strategic override". The latter emerges when phobics are tested in the vicinity of the feared stimuli. At that moment the interference effect disappears. The probe detection task is less sensitive to this.

The problem with all these tasks is that it only exposes part of the attentional bias, because the tasks depend on the time the stimulus is presented. All of these tests provided evidence for attentional bias, but were performed with stimuli that the test subject could consciously focus on.

Studies that investigated whether there is also a bias for selective attention to threatening information that is offered unconscious (pre-attentive bias) have used dichotic listening tasks and visual masking paradigms. The latter are a better means to counteract consciousness and have been performed with the Stroop test and the dot probe task. To check whether the test subjects were really unaware of the stimuli, a consciousness check was performed in two ways: test subjects were asked whether they saw a word in the masked phase and whether the letters were displayed word or not. This showed that the thresholds of consciousness for different stimuli are different. Someone may be aware of a stimulus, but not of its content. With both test designs, it was ultimately demonstrated that there is also a pre-attentive bias in people with an anxiety disorder. This suggests that the bias is already at an early stage of processing information.

It has also been shown that the pre-attentive bias for threatening stimuli can be a cognitive vulnerability factor for emotional disorders. This means that people who have a permanent tendency to automatically selectively focus attention on threatening stimuli are more likely to develop an anxiety disorder when in stressful situations.

The influence of state and trait variables on preattentive and attentional bias

Evidence for the relative influence of trait and state variables on attentional bias contains three areas, namely correlations between bias and self-reported anxiety, the effect of short and long term stressors on preattentive and attentional bias, and the effect of reducing state anxiety through treatment. The last two are discussed.

The effect of stressors

The interaction hypothesis contains two components that are important for the mechanisms that underlie attentional bias. The first is that there is no difference between people with high and low trait anxiety when there is no stress. As the state anxiety increases, a difference becomes apparent and the people with high trait anxiety become sensitive to threatening stimuli. This sensitivity therefore appears to be a latent and not a manifest vulnerability factor for fear.

The second component deals with responses to the attention of people with low trait anxiety. These people tend to divert their attention from a threatening stimulus.

The first part of the hypothesis has been confirmed in various studies, although short-term stressors also elicited attentional bias in people with low trait anxiety, long-term stressors only elicited attentional bias in people with high trait anxiety. If evidence for the second component were also found, this means that the cognitive key factor underlying the vulnerability to anxiety is mediated by the mechanism that determines the direction of attention bias.

No significant evidence was found for the second part of the hypothesis, as a result of which the relative effects of state and trait anxiety on preattentive and attentional bias remain uncertain. It is true that no distinction is made between different options such as.

A threshold effect where the effects of state and trait variables are additive so that vulnerability to threatening words is primarily shown by people with high trait anxiety who are under stress.

A curvilinear relationship between the threatening value of the stimulus and the attention responses to the threat.

Different patterns of bias in people with high or low trait anxiety, which become apparent under increasing state anxiety. There is not enough evidence that with increasing threat people with a low trait anxiety turn away from the stimulus.

The effect of anti-anxiety treatment

It was argued that if the attentional bias for threat is a long-term cognitive vulnerability factor for anxiety, it is still present after treatment. However, studies show that this bias does disappear after therapy (in people with a generalized anxiety disorder). The question was whether a change had taken place in controlled strategies or in the automatic unconscious processes. The latter turned out to be the case.

Attention bias for illustrated stimuli

The studies described above have only been performed with the help of word stimuli and these have a limited scope in terms of threatening value. Illustrated stimuli such as emotional faces or scenes have a somewhat larger scope.

There are a number of tasks that can be used to examine an attentional bias for emotional faces, including the dot-probe detection task, popout tasks, and eye movement. Most of the studies revealed emotion-related effects, although there was a variability in the results with regard to the primary influence on attentional bias. Some claimed it was state anxiety, others trait anxiety or negative emotional valence in general. Differences have been found with regard to studies that have used word pairs. For example, with illustrated stimuli, there is no need for a certain stressor to provoke the bias for threatening faces. This is true with word stimuli. The hypothesis that an attentional bias for threatening stimuli is a characteristic for only people with a high trait anxiety therefore only applies if it concerns relatively weak threatening stimuli such as words.

The interaction hypothesis says that the more threatening the stimulus is, people with high trait anxiety focus their attention on the stimulus and people with low trait anxiety turn their attention away from it. The cognitive-motivational point of view says that an increasing threatening stimulus also causes a bias in people with low trait anxiety. If this did not happen, the Valence Evaluation System would not work.

Research with neutral and emotional scenes has indeed found that there is a general greater vulnerability to highly threatening scenes compared to mildly threatening ones. In addition, the low-fear group showed avoidance for mildly threatening scenes and this avoidance decreased as the stimulus became more threatening. People with high trait anxiety also exhibited greater vulnerability to threatening scenes than people with low trait anxiety. These results therefore speak against the interaction hypothesis and for the cognitive motivational view.

Time course of attentional bias

There is therefore sufficient evidence for a bias in pre-attentive attention and attention processes, but the research described so far focused primarily on initial orientation towards the threatening stimulus. The question now is what happens next. The hypothesis is that people with high trait anxiety or clinical anxiety first focus their attention on the stimulus and then try to avoid detailed processing taking place so as not to become overly anxious. This can ensure that the fear is maintained.

Preattentive and attentional bias in depression

The question is whether depression is associated with an attentional bias for negative stimulation similar to the bias in anxiety. Studies have shown that depressed people do not have a pre-attentive bias for negative information, so do not automatically focus on this. When the stimulus is offered longer and the information has come to the attention, they have a greater difficulty in separating themselves from it. Depressed people do show a bias with regard to later processes such as sustained attention. This is consistent with the predictions of the cognitive motivational point of view, which says that the manifestation of a bias for aversive stimuli in preattentive and orientation processes depends on two things: goal engagement and valence.

Introduction

Cognitive theories of vulnerability to depression state that cognitive factors are causes in the disorder. This article examines a cognitive theory for depression, namely the dual process model.

A General Dual Process Model

Most dual process models of cognition have three components. First, there is an associative processing component. Associative processing is responsible for fast and effortless information processing. Information previously associated with a particular stimulus becomes active again upon seeing the same stimulus. Past experiences facilitate the processing of current information. Smith and DeCoster (2000) state that associative processing is guided by the correspondence between the current stimulus and information obtained from a previous stimulus. Our impression of a stimulus is a combination of what we see at the moment and what our previous experiences tell us. Associative processing is stable and is being built up slowly. Learning new rules is automatic and does not depend on attention, but it requires many common experiences. This allows it to run faster.

Secondly, there is the reflective processing. Reflective processing is more conscious, but slower than associative processing. It is sequential rather than parallel. It can be influenced by a single experience. Learning new rules depends on attention.

Thirdly, there is the question of when to use associative and when to use reflective processing. Most dual process models agree that associative processing is automatically used. Reflective processing is discussed when expectations are not met. Associative processing is dominant until an unexpected stimulus is discussed, or when associative processing does not lead to the intended outcome. In those cases, they switch to reflective processing. Even when expectations do not come true, there are cases where reflective processing is not possible. Reflective processing takes effort and if cognitive means are limited, reflective processing can be disturbed.

The interaction between associative and reflective processing is important for the regulation of emotions. Forgas (2000) states that associative processing is used to maintain a certain emotional state by bringing in information that is congruent with the current emotion. Reflective processing is used to change emotion by bringing in information that is incongruent with current emotion.

A Dual Process Model for Cognitive Vulnerability to Depression

There is a negative bias with regard to one's self-image during associative processing. This has a cognitive vulnerability to depression. There is a lot of evidence that how a person feels about himself contributes a lot to vulnerability to depression. A self-schema is an organized representation of one's previous experiences. Beck (1979) stated that vulnerability to depression is increased when self-schemas are negative.

When someone has a negative associative processing, reflective processing can still happen to this negative bias. There are at least three cases where associative processing is not corrected. First, when biased associative processing violates expectations, but the cognitive means are not present to switch to reflective processing. In the absence of cognitive burden, people who are vulnerable to depression can use reflective processing to correct their negative associative processing. However, when the cognitive burden is increased through time pressure, a competitive task (such as remembering 6 numbers) or stress, one cannot fall back on reflective processing. The result is that the person's cognitive vulnerability becomes visible.

Secondly, when biased associative processing does not violate anyone's expectations and therefore there is no need for reflective processing. Biased associative processing does not trigger reflective processing in depressed people. Depressed people respond the same to functional and dysfunctional statements, while non-depressed people make more use of reflective processing when expectations are violated.

And third, when biased associative processing violates expectations, but that reflective processing cannot adequately adjust negative bias associative processing. An example is self-reflection. It is often thought that thinking about depression, wondering where the symptoms come from and what the consequences of the symptoms are helps to overcome depression. However, this is not the case. Thinking about depression actually increases depression.

Under each of these circumstances, associative processing is not adequately corrected and therefore a cognitive vulnerability to depression arises. If associative processing remains uncorrected, a negative spiral is created in which the vulnerability to depression becomes worse. The more negative one is in life, the less cognitive means are available to switch to reflective processing. This dual process model emphasizes a negative bias about one's self-image in associative processing and the inability to use reflective processing to correct such biases.

Development of Cognitive Vulnerability

Associative processing is influenced by the rules that have gradually been formed. However, some experiences may have more influence on forming an associative memory network than others. These experiences can be divided into early experiences, affective experiences and cultural biases.

The experiences that someone has early in his / her life have more influence on the formation of an associative memory network than experiences that someone experiences later in life. Depression can develop in people who have experienced experiences early in life that have a negative influence on their self-image.

Affective experiences also have an important role in forming associative processing. Evidence has been found for the hypothesis that associative processing is correlated with parts of the brain that regulate emotional experiences. This suggests that a negative affective experience can have a lot of influence on associative processing.

Finally, cultural beliefs influence the formation of associative processing. Cultural beliefs are often shared by an entire social community. People who belong to a minority group often have the same opinion as the rest of the community. Evidence has been found that African Americans and Whites both have implicit prejudices against African Americans. African-Americans have an associative bias against their own race because they have adopted the negative opinion of society.

Overcoming Cognitive Vulnerability

A dual process model provides some ways in which one can correct for their cognitive vulnerability. Firstly, expectations can be adjusted so that negative bias associative processing gives a trigger to switch to reflective processing. The correct cognitive means must then be present to switch to reflective processing. Another way is to adopt a reflective attitude and realize that the outcome of associative processing is only one perspective and does not necessarily have to be the truth. These strategies only affect the short term. An ideal strategy would be to influence associative processing in such a way that it no longer has a negative outcome. The repeated transition to reflective processing can change associative processing. This process is called consolidation. Consolidation occurs when a person has gained enough experience with a certain association that this new association is integrated into the associative system. However, this process can take weeks to years. This shows that repeated exposure to new associations is needed to consolidate the results from reflective processing to associative processing. A cognitive vulnerability can thus be reduced by repeatedly using reflective processing to correct the bias that results from associative processing.

Conclusion

This article examines a dual process model for the cognitive vulnerability to depression. This model emphasizes the interaction between two models of information processing, namely an associative and a reflective processing model. Associative processing is a fast, automatic form of information processing, while reflective processing is slower and requires more effort. It is assumed that negative associative processing, in particular about self-esteem, increases cognitive vulnerability to depression. However, this bias can be corrected by using reflective processing if the cognitive means allow this. Therefore, a cognitive vulnerability to depression is mainly seen when the cognitive means do not allow this correction.

Uncorrected negative associative processing leads to a depressed mood. As determined by Forgas and Ciarrochi (2002), reflective processing is important for the regulation of depressive moods. If there is no reflection, this depressive mood will only get worse.

Disruption of homeostasis

Intake of food and drugs have in common that they cause the disruption of homeostasis in our body. There are a number of regulatory systems that are linked to the change of a certain physiological parameter, such as body temperature and the level of glucose in the blood. These systems can then initiate neural responses when a change occurs. Eventually, they can anticipate the disruption of homeostasis and respond to it in advance.

When drugs and food enter our bodies, they act on countless biological processes and thus bring about change. Some of these effects are wanted, others not. Through classical conditioning, people are able to maintain the positive effects of taking drugs and food by minimizing their negative effects. This is a learning principle that is subject to all regulatory systems in our body.z

Biological consequences of food

It used to be thought that the reason people eat is that the level of fuel for energy in critical tissues in the brain is too low. These are the so-called "depletion-repletion" models and there is something to argue with. People do not only eat when they are hungry, so when they still have enough energy. In addition, the balancing processes of eating food take place too slowly. This does not mean that the body itself does not initiate processes if the glucose level is low. That is indeed the case. A low level of glucose causes a number of regulatory responses to take place that have the consequence that a glucose secretion takes place in the blood immediately from the body itself.

However, food and the level of glucose in the body are related to each other. Eating increases the level of glucose in the blood when carbohydrates come from the stomach. To deal with this, the body secretes insulin from the kidneys on which less glucose is released from the liver into the blood. This will restore the balance. It has been discovered that this release of insulin can be brought under stimulus control using classical conditioning.

This means that if a person is confronted with stimuli (CS) that imply that food intake will follow (UCS), the body will release insulin before food is taken (CR) to prevent excessive levels of glucose in the blood. The body gives a kind of anticipated counter-reaction.

In addition to the level of glucose, there are other parameters that are regulated as a result of eating. These are, for example, body temperature and metabolic level for which a counter-reaction is given before the food is taken.

It is important with these findings that people can be flexible with their food intake and that they do not have to do so at set times. Normally someone eats several small meals a day. However, if a person's lifestyle restricts them to taking two meals a day, they must be large to maintain body weight. If no equilibrium restoring processes were to take place in the body, for example, the glucose level would rise considerably. However, a person can only eat large meals if the meal can be predicted.

The influence of drugs on regulatory systems

Even when drugs are taken, there is an interaction with tissues and molecules in the body. The effects of exogenously administered drugs that bind to certain receptors are similar to the effects of endogenous hormones and neurotransmitters. The exception is that the effects of drugs come about in unusual ways or combinations. Drugs can change normal physiology in countless ways and most drugs work in different ways at the same time, creating the well-known drug effect. So just like food, drugs cause certain parameters in the body to change, thereby disrupting homeostasis.

In the case of drugs, these disruptions can also be corrected by learned anticipated responses. Here too the classical conditioning principle seems to be at work. The conditioned stimulus is the environmental cue. The unconditioned stimulus is the drug effect. After repeated offers from the CS-UCS, a conditioned response is elicited by the CS in the absence of the drug. Taking drugs, for example, can cause body temperature to fall (hypothermia) and this is the drug effect.

The unconditioned response (UR) is then the processes that cause the body temperature to rise again. After a few pairings of the CS with the drug effect, the CS alone provokes an increase in body temperature (CR). The net result of the drug intake is then zero and the person has become tolerant.

Research with ethanol has also shown that tolerance for hypothermia due to the ethanol stimulus situation is specific. So a cue is needed that predicts the drug effect that causes tolerance to occur. Taking the drugs on its own is not enough. The condition for tolerance is therefore that there is an association between a regulatory neural reflex (UR) with a certain CS.

In an experiment with rats, it has been shown that they can become tolerant to motor disco coordination based on classical conditioning. The experiment consists of three groups of rats who all learned how to walk on a treadmill (CS) without making mistakes.

The experimental group was then placed in a narrow cylinder which was then rotated so that the rats became dizzy (motor disc coordination = UCS). Every adjustment to the engine control system is then an UR. When the rats were placed on the treadmill, they made many mistakes, but after repeating this procedure, they became tolerant and made fewer errors (CR).

The control group was also placed in a cylinder, but it was not turned. The last group was put in the cylinder that was turned around, but never just before they had to walk on the treadmill.

When the experimental rats proved tolerant, all three groups were spun around in the cylinder. The experimental group then made significantly fewer errors on the treadmill. If instead of spinning the cylinder, ethanol is administered to all rats, the effect appears to be the same. Rats that were tolerant of the motor-coordinating effect of the rotating cylinder were also tolerant of the same effects but then provoked by ethanol. This phenomenon is called cross-tolerance. So it can be that someone is tolerant of a certain drug without ever having taken it.

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It has long been accepted that panic attacks often occur in certain types of anxiety disorders. Panic attacks later became a separate subject of investigation, and Donald Klein is partly responsible for this. He showed that people with anxiety disorder with panic attacks respond to imipramine and people with anxiety disorder without panic attacks do not: the so-called pharmacological dissociation. The DSM-III then accepted this distinction by including "panic disorder" and "agoraphobia with panic" in the diagnoses.

A panic attack consists of a strong sense of fear or calamity that suddenly arises and is combined with many different physical characteristics. These can be: breathlessness, palpitations, chest pain, dizziness, tingling in feet and hands, feeling of suffocation, fainting, sweating, shaking and a feeling of unreality. The majority of people who suffer from panic attacks have a panic disorder or agoraphobia with panic. A panic disorder is only diagnosed if there have been at least three panic attacks in the last three weeks and these panic attacks do not only occur in certain anxious situations. Agoraphobia with panic is diagnosed when someone shows fear and avoidance of a certain type of situation and has a history of panic attacks.

Panic attacks can be triggered by various pharmacological and physiological agents such as caffeine, carbon dioxide and yohimbine. These drugs hardly cause panic attacks in people without a history of panic attacks, but do cause some sensations that are characteristic of a panic attack. This shows that certain biochemical changes have a panic-inducing effect and that people who are sensitive to these drugs therefore have a biochemical disorder. However, a psychological explanation has also been found for this phenomenon: the drugs do not have a direct panic-inducing effect, but only cause panic if the physical sensations are interpreted in a certain way. This is essential for the cognitive theory described in this article. It states that panic attacks are the result of catastrophic misinterpretations of certain bodily sensations. These are usually sensations such as dizziness and lack of breath (which normally occur with anxiety), but can also be other sensations. This misinterpretation means that the sensations are experienced as much worse than they are. The order of a panic attack is as follows. Various incentives can cause panic attacks. These can be external incentives, but are more often internal incentives. When these stimuli are perceived as a threat, fear arises, along with a number of physical sensations. If this sensation is seen as catastrophic, more fear arises. This creates more physical sensations, etc.

Some panic attacks are preceded by a period of heightened anxiety, some not and come "suddenly." In the first case there are two types of panic attacks. In the first type, the period of increased anxiety is caused by the expectation of an attack, for example in a busy place for someone with agoraphobia. In the second type, the period of increased anxiety is not caused by the expectation of an attack. In the case of panic attacks that appear to be sudden, the cause of an attack is usually the perception of a physical sensation caused by an emotion (anger, for example) or by a harmless event such as getting up, exercising, or drinking coffee. The sensation is then interpreted in a catastrophic way. Other sensations that can cause a panic attack include breath shortage due to movement or sensations that are normally not part of a panic attack. In addition, sensations that arise from the perception of mental processes can also contribute to the vicious circle of panic attacks (for example, the fear of going crazy if their minds get stuck). For some patients, the sensations and associated interpretations remain constant over time, for some, these change.

The literature supports the model on the following points:

• Essential components of panic anxiety. The thinking of patients with panic attacks is dominated by thoughts that cause a catastrophic interpretation of sensations, such as thoughts of death or illnesses.
• The order of events in a panic attack. Patients often mention a physical feeling as one of the first things they feel during a period of anxiety.
• The role of hyperventilation in panic attacks. The sensations associated with hyperventilation often resemble the sensations associated with a panic attack. In some patients, voluntary hyperventilation does indeed cause a "panic-like" feeling and hyperventilation occurs with panic attacks. Hyperventilation only leads to panic if the physical sensations are experienced as unpleasant and are interpreted in a catastrophic way.
• Panic can be caused by sodium lactate. Patients with panic attacks interpret the feeling caused by sodium lactate in a catastrophic way; 60-90% of patients get an attack when they are given sodium lactate.
• Effects of psychological treatment. The most used and successful treatments are behavioral and behavioral cognitive treatment. CO2 inhalation is an example of a treatment, because CO2 inhalation is very effective in inducing panic attacks. This allows the patients to "get used" to the feeling. Neither the behavioral cognitive treatment of Clark nor the behavioral treatment of Griez and van den Hout has been compared with other psychological treatments.

This makes it difficult to say anything about the cause of the effectiveness. In contrast to the treatment of panic disorders, there is a generally accepted treatment for agoraphobia with panic, namely in vivo exposure. The question is whether behavioral cognitive and behavioral treatments can add anything to this.

• The role of biological factors in panic. There are three ways in which biological factors influence the vicious circle of panic attacks. First, biological factors can influence the cause of an attack. Secondly, biological factors can influence the extent to which a threat brings about changes in physical sensations. Thirdly, biological factors can play a role in the extent to which sensations are interpreted in a catastrophic way.
• Effects of pharmacological treatment. Three drugs have been investigated, showing that propranolol is ineffective and diazepam is not effective in the long term. Imipramine appears to be effective, but is always offered in combination with gradual exposure to dreaded stimuli. It is therefore possible that imipramine has no direct effects.

Further evaluation of the model can follow if the following predictions are investigated:

• Patients with panic attacks interpret physical sensations more catastrophically than anxious patients and the control group.
• Pharmacological agents only cause a panic attack if the sensations are catastrophically interpreted and the effects of these agents can be blocked by manipulations.
• Treatments that do not change the tendency for catastrophic interpretation in patients are more likely to experience relapse than treatments that do.

Introduction

One generation ago there were few psychiatrists and psychologists who approached mental disorders with a developmental perspective. Nowadays this is different. The development perspective is very popular and is therefore frequently used.

Causes of schizophrenia in childhood

Originally, schizophrenia is conceptualized as a psychosis that generally begins in adolescence or early adulthood. Children who later developed schizophrenia, however, already had social, emotional and behavioral problems in their childhood. For example, poor attention in children is a predictor of later schizophrenia. Epidemiological and longitudinal studies of the entire population have also shown that there are predictors of schizophrenia in early childhood, despite the fact that schizophrenia itself does not become public until adolescence or early adulthood. These predictors include a delay in motor development, difficulties in understanding language and cognitive functioning. These associations with schizophrenia are independent of socio-economic, obstetric and educational effects. Research has also shown that schizophrenia in adults is often preceded by social-emotional behavioral problems. However, this also applies to many other psychopathological disorders and therefore it is not possible to identify specific predictors of schizophrenia.

There are three problems that seek a solution when it comes to predicting schizophrenia from childhood and adolescence traits. First of all, a distinction is often made between predictors (risk factors) and prodromal (early manifestations of a disorder) factors. In general, this classification is also correct, but there is also a large proportion of people who already exhibit prodromal factors, but who do not continue to develop the disorder afterwards. Secondly, the question is what causes it that these risk factors or early manifestations sometimes lead to the occurrence of a disorder sometimes and sometimes not. Three possible answers for this are that brain development in adolescence is crucial, that excessive use of cannabis contributes to the development of the disorder (only if you already have risk factors or early manifestations of schizophrenia), and that certain types of social removal, such as relocation and insulation, make a major contribution.

Neuro-developmental disorders

Neuro-developmental disorders have eight main characteristics. The first is that they reveal themselves through a backlog or a deviation in psychological traits that are influenced by the growth process. Furthermore, the course of the disorder does not contain any periods in which things go better. In general, the disorder becomes a little less severe, the more mature a person becomes, but the disappearance, the disorder almost never does. Furthermore, the disorders all contain a specific or general cognitive impairment. There is also a lot of overlap between the various disorders. The genetic influence on these disorders is very large, but environmental influences also play a role. Finally, it is striking that especially men have this category of disorders.

Autism and related disorders

Sometimes characteristics of autism are already visible in the first year of life of a child, but usually characteristics are not really visible for 18 months and a diagnosis can usually only be made from 2 years. The best predictor for autism is the IQ and the use of language at the age of 5 years. Yet IQ is not a very good predictor, because many children with an IQ above 70 could develop an autistic disorder.

Specific language disorder

The name suggests that this disorder only causes language problems, but this is not entirely true. But one in six people with this disorder has a permanent paid job and one in six has never had a paid job. The majority do not live independently, more than half have problems with friendships and just over a quarter have ever had a long-term relationship. Even though the language problems persist into adulthood, the biggest problem is actually social functioning and social relationships.

Research into this disorder has revealed a number of striking things. Children who have problems with language development at an early age can often catch up with this backlog, but the problems often come back when these children go to school and then the problems persist well into adulthood. It also appeared that there is a certain overlap between autism and a specific language disorder. Genetic factors play an important role, especially in a somewhat worse form of the disorder. Furthermore, this disorder should not be referred to as a language disorder, but rather as a more general social / cognitive disorder.

Dyslexia

Dyslexia can only be diagnosed after a child has reached an age at which the child should normally be able to read. Yet dyslexia is largely genetic and there are also a number of characteristics (cognitive and linguistic) visible in the years before a child goes to school.

ADHD

ADHD is strongly influenced by genetic factors, is mainly found in men, is associated with many other cognitive defects and is thought to originate in problems with cognitive processing. The problems lie mainly in poor control of behavior, problems with the executive functions of inhibition and working memory and an aversion to slowness.

ADHD often occurs together with ODD and CD, probably because they have common underlying genes. In addition, children with ADHD have a greater chance of developing psychopathological disorders later. The prognosis for ADHD is poor, especially when someone shows hyperactivity at school or at school and at home. ADHD certainly has effects in adulthood, but these often no longer meet the diagnostic criteria that are set for ADHD in children.

Depression

If depression occurs in adolescence, the chance of more depression in adulthood is high. It is often assumed that this chance is greater for women, but this is probably not the case. If depression occurs before puberty, there is no great chance of developing depression later. Therefore, it is thought that depression that occurs in childhood differs significantly from depression that occurs in adolescence or adulthood. This idea is supported by the fact that children and adults respond very differently to antidepressants.

Heredity plays a greater role in depression that develops in adolescence or adulthood than in depression that develops in childhood. Probably this is because depression in adolescence is mainly triggered by negative experiences and the extent to which someone gets caught up in it is genetically determined.

Negative experiences can cause depression in different ways. Children and adults who are depressed behave in such a way that they increase the chance that they will end up in situations where they will experience stress, which will make the depression worse. Cognitive biases are also likely to play a major role in vulnerability to depression. Children can have a bias for negative statements and memories from the age of five.

Comorbidity

Anxiety often starts in childhood and is a predictor of major depression in adulthood. Probably the same genes underlie this, but the expression of these genes is different in different stages of life. Particularly a separation disorder, a general anxiety disorder and a panic disorder are good predictors for a later major depression. There are also various indications that a major depression in adolescence is precisely a predictor of anxiety in adulthood and especially of a general anxiety disorder.

The question remains whether anxiety and depression are two different disorders, whether they have the same underlying problem or whether they are in a causal relationship with each other. The conclusion that, in general, anxiety disorders are a risk factor in the development of depression can be drawn. This relationship is probably mediated by hormonal influences in puberty and an increased chance of negative experiences and cognitions.

Antisocial behavior

Most adults who exhibit antisocial behavior have a long history of behavioral problems. Yet it is not the case that all children with behavioral problems start to show antisocial behavior later in their adulthood.

Heterogeneity

Antisocial youth can be divided into two groups, which differ in when the behavior arose, when risk factors were already present and in how long the behavior remains present. The poor prognosis is for people who have problems early in childhood, who are male, who have neuro-development problems and who have a negative environment. Antisocial behavior that only emerges in adolescence has a better prognosis, since abnormal behavior is a little part of this phase and the behavior generally disappears when these young people start to take their responsibilities.

Not all people who show behavioral problems at an early age also show antisocial behavior in adulthood. A small group is developing a positive adaptation style, but it is not entirely clear why this is. There is also a group that exhibits behavioral problems early on, but where the later problems are of a completely different kind. These people show symptoms of social isolation, poor development of friendships and a vulnerability to anxiety and depression in adulthood. This group often shows an aversion to social situations and neuropsychological problems in childhood. It seems logical that it is simply a question of personal characteristics or that early negative experiences and problems lead to avoidance behavior or, conversely, to openly antisocial behavior.

It is also questionable whether the prognosis for people who show antisocial behavior until adolescence is really so much better than for an earlier start of this behavior. After all, these people show much more criminal behavior and substance abuse later on, and problems with mental health also often occur.

Persistence and removal mechanisms

Genetic factors play a major role in the origin and continuation of antisocial behavior, but there is certainly interaction with the environment. Genetic factors can cause people to react negatively to the person who is someone and can determine in which situations someone comes.

If such a person comes into contact with stable, positive relationships, the early process of behavioral problems can be turned around positively. The extent to which someone benefits from all kinds of positive circumstances also depends on the person himself. Change moments can be associated with moments when someone's past is really separated from the future, such as new opportunities for relationships, social networks, new options for controlling behavior, structural activities and a new identity formation.

Risks of psychiatric disorder in adulthood

Antisocial behavior in childhood and adulthood is strongly associated with later psychiatric disorders. Behavioral problems at the age of 11-15 increase the risk of all psychiatric disorders, both internal and external, at the age of 26. Many factors probably play a role in this, such as encouraged substance abuse by friends, poor family ties and a need for money for drugs and alcohol. Behavioral problems often have different dysfunctions, both in behavioral and emotional areas.

Substance abuse

The vast majority of young people do experiment with alcohol and drugs, but in general this does not result in substance abuse in adulthood. This result depends, among other things, on other disorders that people may have and especially behavioral problems correlate strongly with later substance abuse. ADHD also increases the chance of later substance abuse, but it is possible that this chance is also mediated by behavioral problems associated with ADHD. The link between depression and substance abuse is more complicated. Depressed people may use alcohol and drugs as a kind of self-medication, but a direct effect of depression on substance dependence has not yet been found. However, the prediction from substance abuse to a later depression is very strong. Substance abuse in adulthood is associated with both hereditary and psychosocial problems.

Umbrella themes

Concepts that are often used when looking at the psychopathology phenomenon are heterotypic continuity and psychopathological progress. These concepts suggest that there is meaningful continuity with the different disorders, but that the manifestations of these may differ at different stages of life. Examples include reading problems in children who predict spelling problems in adulthood, neurodevelopmental problems in young children, psychosis-like symptoms in later childhood and psychoses and schizophrenia in adolescence and adulthood, and early anxiety symptoms as predictors of later depression. However, it is still not entirely clear why anxiety symptoms are a predictor of later depression (most common) or depression of later anxiety disorders. With schizophrenia, the development is even more complicated. Language and motor deficits are predictors of schizophrenia, but there is little continuity in this.

The same applies to psychotic symptoms. The predictors of schizophrenia are therefore much more common than schizophrenia itself.

It is not entirely clear how the process from a specific language disorder to a general social disadvantage fits into this picture. It is not logical to see social problems as completely independent of the language disorder, so there are probably social problems before and these probably start with a delay in the use and understanding of language. The term heterotypic continuity is therefore probably also applicable here. The change from early behavioral problems to later substance abuse and from ADHD to a later antisocial personality disorder can probably be better reflected with the concept of psychopathological progress.

Early onset of symptoms

It is often assumed that an early onset of symptoms is a direct cause of the severity of psychopathology. Real structural research into this has not yet been done, so it is not yet possible to say anything with certainty about this statement. In general, psychopathology that has a long history of symptoms is more serious than psychopathology that does not.

Mediators of continuity and discontinuity

Genetic factors most likely play a mediating role in psychopathology. It also plays a role that the chance of a relapse increases if someone has already had an experience with a disorder. In addition, some disorders increase the chance of someone entering a risky environment and negative experiences in childhood or adulthood increase the chance of depression. Furthermore, the way an individual responds to a disorder influences the chance of a later relapse and the way people think about the disorder influences the course of the disorder.

Predictions

First of all, the question is whether later psychopathology includes abnormalities that may be present at an early age. Then it must be examined whether it is at all possible to measure these deviations reliably and validly. False negatives and false positives are very common in research into the early symptoms of psychopathology, so attention needs to be paid to that. A balance must therefore be found for the risk of many versus the benefits for a number of people.

Theoretical perspectives

Development largely involves continuity and change and both concepts contain coherence, laws and organization. There is an unchanging interaction between genes and environment and development in the early years continues to influence later development. There are many individual differences in the course and causes of a disorder and there is an extensive continuity between normality and psychopathology.

Directions for further investigation

Attention must be paid to the alternatives that compete with each other as mediators for psychopathology, and this requires many measurements, research designs and data analyzes. There is a particular need to find factors that are important in the changes in adolescence. Until now, genetic designs have not been used much and it is good to make more use of them in research into the interaction between environment and genes.

Introduction

Comorbidity is the relationship between two diagnoses. A problem with this method is that symptoms are then seen as passive indicators of hidden disorders. Comorbidity then comes from a single cause that causes the two disorders. In clinical psychology, however, it is true that symptoms are not seen as passive indicators of disorders, but that they themselves can cause other symptoms. There is a direct relationship between symptoms. There is no single cause for comorbidity, but there are a number of ways to comorbidity, and which way that is varies per person. A network approach has been developed for mental disorders and comorbidity. In this approach, symptoms are not seen as indicators of hidden disorders, but as components of a network. Comorbidity comes from a direct relationship between symptoms of multiple disorders. Half (47.4%) of all symptoms in the DSM4 are directly or indirectly connected to a main component. This component of connected symptoms has the characteristics of a "small world".

Results

Study 1: Setting up and analyzing the DSM-IV network

All symptoms from the DSM-IV were represented as nodes. There is a connection between nodes when two symptoms are both among the criteria of a particular disorder. Symptoms of the same disorder get a direct connection, while indirect connections arise when two symptoms both have a shared symptom. Two symptoms have no connection if there is no possibility of moving from one symptom to another through other symptoms.

We expect that symptom groups in the DSM are causally related to each other. Symptoms cluster more together than one can expect based on chance. Half of all symptoms therefore have a connection with each other. And the paths to get from one symptom to another are relatively short.

The degree of a node indicates how many connections the node has with other nodes. The degree distribution of a network provides important information about the network structure. The degree distribution of the DSM network is exponential. This can be seen as a "single-scale network". The symptom with the highest degree is insomnia, followed by psychomotor unrest, psychomotor disorder and depressive mood.

Another important characteristic of knots is their "betweenness". This measures the probability that a node lies between two other nodes. The four symptoms with the highest "betweenness" are irritation, distractibility, anxiety and depression.

Study 2: Empirical data for the network structure

The "small world" feature means that symptom activation is quickly spread throughout the network. The network model explains a significant part of the comorbidity within the DSM-IV. If one has one symptom from the DSM-IV, chances are that he / she will also develop another symptom from the DSM. The average shortest path length between two disorders is equal to the expected number of paths a person has to take to achieve a symptom of disorder A from a symptom of disorder B. The higher this path length is, the further two disorders lie apart in the network.

Study 3

The previous two analyzes show that path lengths and empirical comorbidity values ​​were correlated if one would expect if symptoms had a network structure. However, disorders are time dependent. They are dynamic, and sometimes there is a time criterion for how long the symptoms should be present as a minimum. The network model takes this into account. To show how the network can predict comorbidity, a simulation was performed for two disorders to show that the comorbidity values ​​are consistent with empirical data. Symptom dynamic is an increase in the chance of a certain symptom, when someone has more neighbor symptoms. If someone has depression and a loss of interest, the chance of having suicidal thoughts is higher than for someone who has a loss of interest, but no depression. Even though the simulated networks are incomplete, the results do provide evidence for the possibility that a network model can reproduce empirical data.

Discussion

The "missing heritability" indicates that the individual differences in vulnerability to develop a disorder are for the most part genetically determined. However, only a small part of the genetic variance can be traced to identified gene changes.

The strength of the symptom connections in a network can partly be explained genetically, but it is probably not the case that all connections in a disorder are influenced by the same genes in all people.

Introduction

Depression affects three interpersonal processes, namely problems with social skills, reactions of others to depression and dysfunctional family relationships.

Social skills deficits and depressions

According to Lewinsohn behavioral therapy, people with depression have reduced social skills, which means they miss out on positive reinforcers from the environment. This will make the depression worse. Interpersonal reactions to someone else's depressive behavior are sympathetic at first, but soon rejective. Poor social skills are therefore a cause, but also a consequence of depression.

Social skills of people with depression are often scored through a self-report. Evidence has been found by Segrin that people with depression score their own social skills more negatively than others would. However, a study by Lewinsohn indicated that people with depression look at their own skills more realistically than non-depressed people. Non-depressed people would overestimate their own social skills. This pattern is called the depressive realism effect.

It remains therefore unclear whether a self-report is reliable enough to determine the social skills of a depressed person. Nevertheless, in the majority of cases, depressed people score their own social skills lower than non-depressed people do.

Social skills of people with depression can also be determined by the friends of those with depression. People with depression have lower social skills in their social interactions than people without depression. So apparently there is something in the social behavior of people with depression that stands out among their friends, resulting in a lower assessment of the social skills of those with depression.

Eye contact

People with depression make less eye contact with their conversation partners than non-depressed people do. The facial expressions of people with depression are less spontaneous and lively than people without depression.

Facial expressions

Depressed people have more control over their facial expressions and suppress a smile easier. This makes it more difficult for the other person to evaluate the facial expression of the depression. Decreased social skills are not only visible through problems with appropriate and effective implementation of social behavior, but also through understanding the behavior of others. Depressed people have a negative bias in which they see neutral facial expressions of others as negative and have more difficulty recognizing a happy face. People with depression therefore have difficulty looking happy and recognizing a happy face.

Posture

People with depression nod less during a conversation. They also use fewer hand gestures while telling a story.

Language

People with depression talk slower, softer, less, have more and longer pauses and respond more slowly to the behavior of others. They are more negative towards acquaintances than to strangers.

According to Lewinsohn's behavioral theory about depression, impaired social skills are a cause of depression. There is conflicting evidence for this. An alternative possibility is that poor social skills are the result of depression. The scar hypothesis states that people have noticed during a depressive period that they had reduced social skills, so that these reduced social skills increase the risk of a new depression in the future. A third possibility for the relationship between poor social skills and depression is that poor social skills contribute to the cause of depression or are a type of vulnerability factor in the development of depression.

Those who have poor social skills and stressful environmental experiences have an increased chance of getting a depression. Having poor social skills makes people vulnerable to stressful events.

In line with the social skills deficit hypothesis, most people have problems with social skills when they are in depression. Poor social skills can be seen as a cause of depression, as a consequence of depression and as a vulnerability factor for developing depression.

Interpersonal responses to depression

Coyne's interpersonal interaction model is based on the influence of reactions of others on people with depression. Depressive behavior causes a negative reaction in others. In the beginning people will show sympathy, but after a while this will turn into irritation. This takes care of the depressed person and sees this as rejection. This rejection maintains the depression.

Excessive Reassurance Seeking

Coyne has observed that a lot of communication from a depressed person is aimed at confirming the relationship with the other. The search for reassurance often occurs with depressed people. This is irritating to the others and therefore provokes rejection. People with depression are so often looking for confirmation because they have low self-esteem and have experienced many negative things. According to the circumplex model, interpersonal behavior elicits a certain expected response from others. If someone does not respond according to this expectation, this causes a negative affect for the other. If the partner of the person who is depressed gives the depressed person attention and confirmation, the partner expects the depressed person to do something with this. If the depressed person responds by seeking confirmation, the partner's motivation runs out to help and support the depressed person even longer.

Emotional Contagion

The group of friends of a depression is often more irritated than people without a depressive acquaintance.

Interpersonal Rejection of People with Depression

People with depression are more likely to be rejected by others. Men in particular are rejected. Strangers are rejected rather than acquaintances. According to the self-verification theory, people are motivated to maintain their self-image in order to increase their sense of control. For someone who is depressed this can be seen in the fact that people with depression mainly pay attention to negative feedback from others, because this info confirms their self-image. This ensures the maintenance of the depression.

Family relations and depression

Certain interactions within a family will increase the risk factors for getting a depression. Emotional abuse in the family creates a fear of criticism and rejection. Rose and Abramson (1992) stated that emotional abuse is very harmful to the child's self-image. If this self-image is repeatedly brought down by the parent, it will lead to a vulnerability to the development of depression. In the case of physical and sexual abuse, this association also exists, but it is less strong, because the child's self-image is not directly brought down by the parent.

There is a strong mutual relationship between depression and marital problems. Spouses with a depressed partner have a lot of problems with this and also have a greater chance of getting a depression. The interaction between men and women is often negative, conflicts are handled poorly. Another factor that reinforces the relationship between depression and marital problems is the fact that young people with depression marry too quickly. They see marriage as a solution for their depressive feelings.

Women are more sensitive than men to the symptoms of depression, leading to a worse marriage. A bad marriage leads to a worsening of depressive feelings among men and women. Having depression causes many problems with upbringing. As a result, children with a depressed father / mother have a greater chance of depression.

Conclusion

People are social animals. Social relationships play a major role in emotion regulation. If something goes wrong within such a relationship, it has a major negative impact on human emotions. The other way around also works. If someone is depressed, this will have a negative impact on interpersonal relationships. There are two interpersonal processes that can increase the risk of developing depression. First, it is having poor social skills. Secondly, having poor self-esteem through upbringing with abuse.