Belief traps: Tackling the inertia of harmful beliefs.

Beliefs can be highly resilient in the sense that they are not easily abandoned in the face of counterevidence. This has the advantage of guiding consistent behavior and judgments but may also have destructive consequences for individuals, nature, and society. For instance, pathological beliefs can sustain psychiatric disorders, the belief that rhinoceros horn is an aphrodisiac may drive a species extinct, beliefs about gender or race may fuel discrimination, and belief in conspiracy theories can undermine democracy. Here, we present a unifying framework of how self-amplifying feedbacks shape the inertia of beliefs on levels ranging from neuronal networks to social systems. Sustained exposure to counterevidence can destabilize rigid beliefs but requires organized rational override as in cognitive behavioral therapy for pathological beliefs or institutional control of discrimination to reduce racial biases. Black-and-white thinking is a major risk factor for the formation of resilient beliefs associated with psychiatric disorders as well as prejudices and conspiracy thinking. Such dichotomous thinking is characteristic of a lack of cognitive resources, which may be exacerbated by stress. This could help explain why conspiracy thinking and psychiatric disorders tend to peak during crises. A corollary is that addressing social factors such as poverty, social cleavage, and lack of education may be the most effective way to prevent the emergence of rigid beliefs, and thus of problems ranging from psychiatric disorders to prejudices, conspiracy theories, and posttruth politics.

Towards precision in the diagnostic profiling of patients: leveraging symptom dynamics as a clinical characterisation dimension in the assessment of major depressive disorder.

BACKGROUND: International guidelines present overall symptom severity as the key dimension for clinical characterisation of major depressive disorder (MDD). However, differences may reside within severity levels related to how symptoms interact in an individual patient, called symptom dynamics. AIMS: To investigate these individual differences by estimating the proportion of patients that display differences in their symptom dynamics while sharing the same overall symptom severity. METHOD: Participants with MDD (n = 73; mean age 34.6 years, s.d. = 13.1; 56.2% female) rated their baseline symptom severity using the Inventory for Depressive Symptomatology Self-Report (IDS-SR). Momentary indicators for depressive symptoms were then collected through ecological momentary assessments five times per day for 28 days; 8395 observations were conducted (average per person: 115; s.d. = 16.8). Each participant's symptom dynamics were estimated using person-specific dynamic network models. Individual differences in these symptom relationship patterns in groups of participants sharing the same symptom severity levels were estimated using individual network invariance tests. Subsequently, the overall proportion of participants that displayed differential symptom dynamics while sharing the same symptom severity was calculated. A supplementary simulation study was conducted to investigate the accuracy of our methodology against false-positive results. RESULTS: Differential symptom dynamics were identified across 63.0% (95% bootstrapped CI 41.0-82.1) of participants within the same severity group. The average false detection of individual differences was 2.2%. CONCLUSIONS: The majority of participants within the same depressive symptom severity group displayed differential symptom dynamics. Examining symptom dynamics provides information about person-specific psychopathological expression beyond severity levels by revealing how symptoms aggravate each other over time. These results suggest that symptom dynamics may be a promising new dimension for clinical characterisation, warranting replication in independent samples. To inform personalised treatment planning, a next step concerns linking different symptom relationship patterns to treatment response and clinical course, including patterns related to spontaneous recovery and forms of disorder progression.

Integrating Intra- and Interindividual Phenomena in Psychological Theories.

Psychological science is divided into two distinct methodological traditions. One tradition seeks to understand how people function at the individual level, while the other seeks to understand how people differ from each other. Methodologies that have grown out of these traditions typically rely on different sources of data. While both use statistical models to understand the structure of the data, and these models are often similar, Molenaar (2004) showed that results from one type of analysis rarely transfer to the other, unless unrealistic assumptions hold. This raises the question how we may integrate these approaches. In this paper, we argue that formalized theories can be used to connect intra- and interindividual levels of analysis. This connection is indirect, in the sense that the relationship between theory and data is best understood through the intermediate level of phenomena: robust statistical patterns in empirical data. To illustrate this, we introduce a distinction between intra- and interindividual phenomena, and argue that many psychological theories will have implications for both types of phenomena. Formalization provides us with a methodological tool for investigating what kinds of intra- and interindividual phenomena we should expect to find if the theory under consideration were true.

Interpretational issues with the bifactor model: a commentary on 'Defining the p-Factor: An Empirical Test of Five Leading Theories' by Southward, Cheavens, and Coccaro.

Southward, Cheavens, and Coccaro (2022, Psychological Medicine) conducted an ambitious investigation aimed at determining the nature of the general p factor of psychopathology by considering the correlation between the p factor and five candidate constructs. Generally, in this area of research, the bifactor model is preferred to the second order common factor model. In this commentary, we identify several interpretational issues concerning the bifactor model, which are based on a realistic psychometric view of latent variables. These issues may hamper the study of the nature of p factor model using the bifactor model.

Intervening on psychopathology networks: Evaluating intervention targets through simulations.

Identifying the different influences of symptoms in dynamic psychopathology models may hold promise for increasing treatment efficacy in clinical applications. Dynamic psychopathology models study the behavioral patterns of symptom networks, where symptoms mutually enforce each other. Interventions could be tailored to specific symptoms that are most effective at lowering symptom activity or that hinder the further development of psychopathology. Simulating interventions in psychopathology network models fits in a novel tradition where symptom-specific perturbations are used as in silico interventions. Here, we present the NodeIdentifyR algorithm (NIRA) to identify the projected most efficient, symptom-specific intervention target in a network model (i.e., the Ising model). We implemented NIRA in a freely available R package. The technique studies the projected effects of symptom-specific interventions by simulating data while symptom parameters (i.e., thresholds) are systematically altered. The projected effect of these interventions is defined in terms of the expected change in overall symptom activity across simulations. With this algorithm, it is possible to study (1) whether symptoms differ in their projected influence on the behavior of the symptom network and, if so, (2) which symptom has the largest projected effect in lowering or increasing overall symptom activation. As an illustration, we apply the algorithm to an empirical dataset containing Post-Traumatic Stress Disorder symptom assessments of participants who experienced the Wenchuan earthquake in 2008. The most important limitations of the method are discussed, as well as recommendations for future research, such as shifting towards modeling individual processes to validate these types of simulation-based intervention methods.

Formalizing theories of child development: Introduction to the special section.

Here we introduce a Special Section of Child Development entitled "Formalizing Theories of Child Development." This Special Section features five papers that use mathematical models to advance our understanding of central questions in the study of child development. This landmark collection is timely: it signifies growing awareness that rigorous empirical bricks are not enough; we need solid theory to build the house. By stating theory in mathematical terms, formal models make concepts, assumptions, and reasoning more explicit than verbal theory does. This increases falsifiability, promotes cumulative science, and enables integration with mathematical theory in allied disciplines. The Special Section contributions cover a range of topics: the developmental origins of counting, interactions between mathematics and language development, visual exploration and word learning in infancy, referent identification by toddlers, and the emergence of typical and atypical development. All are written in an accessible manner and for a broad audience.

Towards a general modeling framework of resource competition in cognitive development.

The current paper presents an integrated formal model of typical and atypical development based on the mechanisms of mutualism and resource competition. The mutualistic network model is extended with the dynamics of competition for limited resources, such as time and environmental factors. The proposed model generates patterns that resemble established phenomena in cognitive development: the positive manifold, developmental phases, developmental delays and lack of early indicators in atypical development, developmental regression, and "quasi-autism" caused by extreme environmental deprivation. The presented modeling framework fits a general movement towards formal theory construction in psychology. The model is easy to replicate and develop further, and we offer several avenues for future work.

Heterogeneity in Individual Network Analysis: Reality or Illusion?

The use of idiographic research techniques has gained popularity within psychological research and network analysis in particular. Idiographic research has been proposed as a promising avenue for future research, with differences between idiographic results highlighting evidence for radical heterogeneity. However, in the quest to address the individual in psychology, some classic statistical problems, such as those arising from sampling variation and power limitations, should not be overlooked. This article aims to determine to what extent current tools to compare idiographic networks are suited to disentangle true from illusory heterogeneity in the presence of sampling error. To this end, we investigate the performance of tools to inspect heterogeneity (visual inspection, comparison of centrality measures, investigating standard deviations of random effects, and GIMME) through simulations. Results show that power limitations hamper the validity of conclusions regarding heterogeneity and that the power required to assess heterogeneity adequately is often not realized in current research practice. Of the tools investigated, inspecting standard deviations of random effects and GIMME proved the most suited. However, all tools evaluated leave the door wide open to misinterpret all observed variability in terms of individual differences. Hence, the current paper calls for caution in the use and interpretation of new time-series techniques when it comes to heterogeneity.

Overlapping timescales obscure early warning signals of the second COVID-19 wave.

Early warning indicators based on critical slowing down have been suggested as a model-independent and low-cost tool to anticipate the (re)emergence of infectious diseases. We studied whether such indicators could reliably have anticipated the second COVID-19 wave in European countries. Contrary to theoretical predictions, we found that characteristic early warning indicators generally decreased rather than increased prior to the second wave. A model explains this unexpected finding as a result of transient dynamics and the multiple timescales of relaxation during a non-stationary epidemic. Particularly, if an epidemic that seems initially contained after a first wave does not fully settle to its new quasi-equilibrium prior to changing circumstances or conditions that force a second wave, then indicators will show a decreasing rather than an increasing trend as a result of the persistent transient trajectory of the first wave. Our simulations show that this lack of timescale separation was to be expected during the second European epidemic wave of COVID-19. Overall, our results emphasize that the theory of critical slowing down applies only when the external forcing of the system across a critical point is slow relative to the internal system dynamics.

Extended network analysis: from psychopathology to chronic illness.

BACKGROUND: Understanding complex associations between psychopathology and chronic illness is instrumental in facilitating both research and treatment progress. The current study is the first and only network-based study to provide such an encompassing view of unique associations between a multitude of mental and physical health-related domains. METHODS: The current analyses were based on the Singapore Mental Health Study, a cross-sectional study of adult Singapore residents. The study sample consisted of 6616 respondents, of which 49.8% were male and 50.2% female. A network structure was constructed to examine associations between psychopathology, alcohol use, gambling, major chronic conditions, and functioning. RESULTS: The network structure identified what we have labeled a Cartesian graph: a network visibly split into a psychopathological domain and a physical health domain. The borders between these domains were fuzzy and bridged by various cross-domain associations, with functioning items playing an important role in bridging chronic conditions to psychopathology. CONCLUSIONS: Current results deliver a comprehensive overview of the complex relation between psychopathology, functioning, and chronic illness, highlighting potential pathways to comorbidity.

Quantifying resilience of humans and other animals.

All life requires the capacity to recover from challenges that are as inevitable as they are unpredictable. Understanding this resilience is essential for managing the health of humans and their livestock. It has long been difficult to quantify resilience directly, forcing practitioners to rely on indirect static indicators of health. However, measurements from wearable electronics and other sources now allow us to analyze the dynamics of physiology and behavior with unsurpassed resolution. The resulting flood of data coincides with the emergence of novel analytical tools for estimating resilience from the pattern of microrecoveries observed in natural time series. Such dynamic indicators of resilience may be used to monitor the risk of systemic failure across systems ranging from organs to entire organisms. These tools invite a fundamental rethinking of our approach to the adaptive management of health and resilience.

Moderated Network Models.

Pairwise network models such as the Gaussian Graphical Model (GGM) are a powerful and intuitive way to analyze dependencies in multivariate data. A key assumption of the GGM is that each pairwise interaction is independent of the values of all other variables. However, in psychological research, this is often implausible. In this article, we extend the GGM by allowing each pairwise interaction between two variables to be moderated by (a subset of) all other variables in the model, and thereby introduce a Moderated Network Model (MNM). We show how to construct MNMs and propose an ℓ1-regularized nodewise regression approach to estimate them. We provide performance results in a simulation study and show that MNMs outperform the split-sample based methods Network Comparison Test (NCT) and Fused Graphical Lasso (FGL) in detecting moderation effects. Finally, we provide a fully reproducible tutorial on how to estimate MNMs with the R-package mgm and discuss possible issues with model misspecification.

Latent Variable Models and Networks: Statistical Equivalence and Testability.

Networks are gaining popularity as an alternative to latent variable models for representing psychological constructs. Whereas latent variable approaches introduce unobserved common causes to explain the relations among observed variables, network approaches posit direct causal relations between observed variables. While these approaches lead to radically different understandings of the psychological constructs of interest, recent articles have established mathematical equivalences that hold between network models and latent variable models. We argue that the fact that for any model from one class there is an equivalent model from the other class does not mean that both models are equally plausible accounts of the data-generating mechanism. In many cases the constraints that are meaningful in one framework translate to constraints in the equivalent model that lack a clear interpretation in the other framework. Finally, we discuss three diverging predictions for the relation between zero-order correlations and partial correlations implied by sparse network models and unidimensional factor models. We propose a test procedure that compares the likelihoods of these models in light of these diverging implications. We use an empirical example to illustrate our argument.

The network structure of schema modes.

A fundamental question in psychotherapy is whether interventions should target client problems (i.e., problem-focused approaches) or client strengths (i.e., strength-focused approaches). In this study, we first propose to address this question from a network perspective on schema modes (i.e., healthy or dysfunctional patterns of co-occurring emotions, cognitions, and behaviours). From this perspective, schema modes mutually influence each other (e.g., healthy modes reduce dysfunctional modes). Recent evidence suggests that changes in modes that are strongly associated to other modes (i.e., central modes) could be associated with greater treatment effects. We therefore suggest research should investigate the relative centrality of healthy and dysfunctional modes. To make an exploratory start, we investigated the cross-sectional network structure of schema modes in a clinical (comprising individuals diagnosed with paranoid, narcissistic, histrionic, and Cluster C personality disorders) and non-clinical sample. Results showed that, in both samples, the Healthy Adult was significantly less central than several dysfunctional modes (e.g., Undisciplined Child and Abandoned and Abused Child). Although our study cannot draw causal conclusions, this finding could suggest that weakening dysfunctional modes (compared to strengthening the Healthy Adult) might be more effective in decreasing other dysfunctional modes. Our study further indicates that several schema modes are negatively associated, which could suggest that decreasing one might increase another. Finally, the Healthy Adult was among the modes that most strongly discriminated between clinical and non-clinical individuals. Longitudinal and experimental research into the network structure of schema modes is required to further clarify the relative influence of schema modes.

The network approach to psychopathology: a review of the literature 2008-2018 and an agenda for future research.

The network approach to psychopathology posits that mental disorders can be conceptualized and studied as causal systems of mutually reinforcing symptoms. This approach, first posited in 2008, has grown substantially over the past decade and is now a full-fledged area of psychiatric research. In this article, we provide an overview and critical analysis of 363 articles produced in the first decade of this research program, with a focus on key theoretical, methodological, and empirical contributions. In addition, we turn our attention to the next decade of the network approach and propose critical avenues for future research in each of these domains. We argue that this program of research will be best served by working toward two overarching aims: (a) the identification of robust empirical phenomena and (b) the development of formal theories that can explain those phenomena. We recommend specific steps forward within this broad framework and argue that these steps are necessary if the network approach is to develop into a progressive program of research capable of producing a cumulative body of knowledge about how specific mental disorders operate as causal systems.

Toward incorporating genetic risk scores into symptom networks of psychosis.

BACKGROUND: Psychosis spectrum disorder is a heterogeneous, multifactorial clinical phenotype, known to have a high heritability, only a minor portion of which can be explained by molecular measures of genetic variation. This study proposes that the identification of genetic variation underlying psychotic disorder may have suffered due to issues in the psychometric conceptualization of the phenotype. Here we aim to open a new line of research into the genetics of mental disorders by explicitly incorporating genes into symptom networks. Specifically, we investigate whether links between a polygenic risk score (PRS) for schizophrenia and measures of psychosis proneness can be identified in a network model. METHODS: We analyzed data from n = 2180 subjects (controls, patients diagnosed with a non-affective psychotic disorder, and the first-degree relatives of the patients). A network structure was computed to examine associations between the 42 symptoms of the Community Assessment of Psychic Experiences (CAPE) and the PRS for schizophrenia. RESULTS: The resulting network shows that the PRS is directly connected to the spectrum of positive and depressive symptoms, with the items conspiracy and no future being more often located on predictive pathways from PRS to other symptoms. CONCLUSIONS: To our knowledge, the current exploratory study provides a first application of the network framework to the field of behavior genetics research. This allows for a novel outlook on the investigation of the relations between genome-wide association study-based PRSs and symptoms of mental disorders, by focusing on the dependencies among variables.

A network approach on the relation between apathy and depression symptoms with dementia and functional disability.

BACKGROUND: Studies on the association between depression and dementia risk mostly use sum scores on depression questionnaires to model symptomatology severity. Since individual items may contribute differently to this association, this approach has limited validity. METHODS: We used network analysis to investigate the functioning of individual Geriatric Depression Scale (GDS-15) items, of which, based on studies that used factor analysis, 3 are generally considered to measure apathy (GDS-3A) and 12 depression (GDS-12D). Functional disability and future dementia were also included in our analysis. Data were extracted from 3229 participants of the Prevention of Dementia by Intensive Vascular care trial (preDIVA), analyzed as a single cohort, yielding 20,542 person-years of observation. We estimated a sparse network by only including connections between variables that could not be accounted for by variance in other variables. For this, we used a repeated L1 regularized regression procedure. RESULTS: This procedure resulted in a selection of 59/136 possible connections. GDS-3A items were strongly connected to each other and with varying strength to several GDS-12D items. Functional disability was connected to all three GDS-3A items and the GDS-12D items "helplessness" and "worthlessness". Future dementia was only connected to the GDS-12D item "memory problems", which was in turn connected to the GDS-12D items "unhappiness" and "helplessness" and all three GDS-3A items. CONCLUSION: Network analysis reveals interesting relationships between GDS items, functional disability and dementia risk. We discuss what implications our results may have for (future) research on the associations between depression and/or apathy with dementia.

Affluence boosted intelligence? How the interaction between cognition and environment may have produced an eighteenth-century Flynn effect during the Industrial Revolution.

Cognition played a pivotal role in the acceleration of technological innovation during the Industrial Revolution. Growing affluence may have provided favourable environmental conditions for a boost in cognition, enabling individuals to tackle more complex (industrial) problems. Dynamical systems thinking may provide useful tools to describe sudden transitions like the Industrial Revolution, by modelling the recursive feedback between psychology and environment.

Reductionism in retreat.

We address the commentaries on our target article in terms of four major themes. First, we note that virtually all commentators agree that mental disorders are not brain disorders in the common interpretation of these terms, and establish the consensus that explanatory reductionism is not a viable thesis. Second, we address criticisms to the effect that our article was misdirected or aimed at a straw man; we argue that this is unlikely, given the widespread communication of reductionist slogans in psychopathology research and society. Third, we tackle the question of whether intentionality, extended systems, and multiple realizability are as problematic as claimed in the target article, and we present a number of nuances and extensions with respect to our article. Fourth, we discuss the question of how the network approach should incorporate biological factors, given that wholesale reductionism is an unlikely option.

The Gaussian Graphical Model in Cross-Sectional and Time-Series Data.

We discuss the Gaussian graphical model (GGM; an undirected network of partial correlation coefficients) and detail its utility as an exploratory data analysis tool. The GGM shows which variables predict one-another, allows for sparse modeling of covariance structures, and may highlight potential causal relationships between observed variables. We describe the utility in three kinds of psychological data sets: data sets in which consecutive cases are assumed independent (e.g., cross-sectional data), temporally ordered data sets (e.g., n = 1 time series), and a mixture of the 2 (e.g., n > 1 time series). In time-series analysis, the GGM can be used to model the residual structure of a vector-autoregression analysis (VAR), also termed graphical VAR. Two network models can then be obtained: a temporal network and a contemporaneous network. When analyzing data from multiple subjects, a GGM can also be formed on the covariance structure of stationary means-the between-subjects network. We discuss the interpretation of these models and propose estimation methods to obtain these networks, which we implement in the R packages graphicalVAR and mlVAR. The methods are showcased in two empirical examples, and simulation studies on these methods are included in the supplementary materials.