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In their chapter, Bach and Presnall-Shvorin (this volume) introduce guidelines for incorporating empirically-driven trait models of personality pathology, codified in the DSM-5 and ICD-11, into therapeutic practice. Though the authors of this commentary are supportive of the effort to bridge research with clinical practice, they suggest that a mechanistic model which accounts for personality processes underlying descriptive traits could offer greater precision than traits alone. Furthermore, they argue that clinical dysfunction can only be meaningfully defined and treated with an understanding of dynamic, contextualized aspects of personality. To illustrate how a mechanistic model could complement and extend Bach and Presnall’s recommendations, the authors present a case conceptualization using cybernetic theory. Finally, they review how idiographic data gleaned from ambulatory assessment methods provide insight into pathological processes ideal for therapeutic intervention. To achieve a generalizable approach flexible enough to adapt to the individual, they encourage the development of treatment models that go beyond traits to mechanistically link stable and dynamic personality features into a unified framework.
Most of what clinical psychology concerns itself with is directly unobservable. Concepts like neuroticism and depression, but also learning and development, represent dispositions, states, or processes that must be inferred and cannot (currently) be directly measured. Latent variable modeling, as a statistical framework, encompasses a range of techniques that involve estimating the presence and effect of unobserved variables from observed data. This chapter provides a nontechnical overview of latent variable modeling in clinical psychology. Dimensional latent variable models are emphasized, although categorical and hybrid models are touched on briefly. Challenges with specific models, such as the bifactor model are discussed. Examples draw from the psychopathology literature.
The scientific discipline of clinical psychology has witnessed paradigm changes in the prevailing conceptualization of psychopathology and in the rigor of experimental methods to test psychosocial treatments. In parallel, neuroscience approaches to mental illness have become increasingly prominent and technologies to measure psychological constructs over time and across contexts are becoming ubiquitous in psychological research. Altogether, these changes have pushed clinical scientists to incorporate novel research methodologies and analytic approaches. Modern studies of clinical phenomena are often theoretically integrative and assess constructs across levels of measurement, ranging from the molecular to the behavioral. These shifts are fundamental, and necessitate changes in the way modern clinical psychologists design studies, collect data, and draw scientific conclusions. This book is intended to serve as a guide for the next generation of clinical psychologists, who will benefit from greater training in statistics, study design, developmental psychopathology, and multimethod approaches.
This book integrates philosophy of science, data acquisition methods, and statistical modeling techniques to present readers with a forward-thinking perspective on clinical science. It reviews modern research practices in clinical psychology that support the goals of psychological science, study designs that promote good research, and quantitative methods that can test specific scientific questions. It covers new themes in research including intensive longitudinal designs, neurobiology, developmental psychopathology, and advanced computational methods such as machine learning. Core chapters examine significant statistical topics, for example missing data, causality, meta-analysis, latent variable analysis, and dyadic data analysis. A balanced overview of observational and experimental designs is also supplied, including preclinical research and intervention science. This is a foundational resource that supports the methodological training of the current and future generations of clinical psychological scientists.
An ongoing challenge in understanding and treating personality disorders (PDs) is a significant heterogeneity in disorder expression, stemming from variability in underlying dynamic processes. These processes are commonly discussed in clinical settings, but are rarely empirically studied due to their personalized, temporal nature. The goal of the current study was to combine intensive longitudinal data collection with person-specific temporal network models to produce individualized symptom-level structures of personality pathology. These structures were then linked to traditional PD diagnoses and stress (to index daily functioning).
Using about 100 daily assessments of internalizing and externalizing domains underlying PDs (i.e. negative affect, detachment, impulsivity, hostility), a temporal network mapping approach (i.e. group iterative multiple model estimation) was used to create person-specific networks of the temporal relations among domains for 91 individuals (62.6% female) with a PD. Network characteristics were then associated with traditional PD symptomatology (controlling for mean domain levels) and with daily variation in clinically-relevant phenomena (i.e. stress).
Features of the person-specific networks predicted paranoid, borderline, narcissistic, and obsessive-PD symptom counts above average levels of the domains, in ways that align with clinical conceptualizations. They also predicted between-person variation in stress across days.
Relations among behavioral domains thought to underlie heterogeneity in PDs were indeed associated with traditional diagnostic constructs and with daily functioning (i.e. stress) in person-specific networks. Findings highlight the importance of leveraging data and models that capture person-specific, dynamic processes, and suggest that person-specific networks may have implications for precision medicine.
A new fossil site in a previously unexplored part of western Madagascar (the Beanka Protected Area) has yielded remains of many recently extinct vertebrates, including giant lemurs (Babakotia radofilai, Palaeopropithecus kelyus, Pachylemur sp., and Archaeolemur edwardsi), carnivores (Cryptoprocta spelea), the aardvark-like Plesiorycteropus sp., and giant ground cuckoos (Coua). Many of these represent considerable range extensions. Extant species that were extirpated from the region (e.g., Prolemur simus) are also present. Calibrated radiocarbon ages for 10 bones from extinct primates span the last three millennia. The largely undisturbed taphonomy of bone deposits supports the interpretation that many specimens fell in from a rock ledge above the entrance. Some primates and other mammals may have been prey items of avian predators, but human predation is also evident. Strontium isotope ratios (87Sr/86Sr) suggest that fossils were local to the area. Pottery sherds and bones of extinct and extant vertebrates with cut and chop marks indicate human activity in previous centuries. Scarcity of charcoal and human artifacts suggests only occasional visitation to the site by humans. The fossil assemblage from this site is unusual in that, while it contains many sloth lemurs, it lacks ratites, hippopotami, and crocodiles typical of nearly all other Holocene subfossil sites on Madagascar.
We recently reported an association of offspring educational attainment with polygenic risk scores (PRS) computed on parent’s non-transmitted alleles for educational attainment using the second GWAS meta-analysis article on educational attainment published by the Social Science Genetic Association Consortium. Here we test the replication of these findings using a more powerful PRS from the third GWAS meta-analysis article by the Consortium. Each of the key findings of our previous paper is replicated using this improved PRS (N = 2335 adolescent twins and their genotyped parents). The association of children’s attainment with their own PRS increased substantially with the standardized effect size, moving from β = 0.134, 95% CI = 0.079, 0.188 for EA2, to β = 0.223, 95% CI = 0.169, 0.278, p < .001, for EA3. Parent’s PRS again predicted the socioeconomic status (SES) they provided to their offspring and increased from β = 0.201, 95% CI = 0.147, 0.256 to β = 0.286, 95% CI = 0.239, 0.333. Importantly, the PRS for alleles not transmitted to their offspring — therefore acting via the parenting environment — was increased in effect size from β = 0.058, 95% CI = 0.003, 0.114 to β = 0.067, 95% CI = 0.012, 0.122, p = .016. As previously found, this non-transmitted genetic effect was fully accounted for by parental SES. The findings reinforce the conclusion that genetic effects of parenting are substantial, explain approximately one-third the magnitude of an individual’s own genetic inheritance and are mediated by parental socioeconomic competence.