The Hierarchical Taxonomy of Psychopathology (HiTOP) has emerged out of the quantitative approach to psychiatric nosology. This approach identifies psychopathology constructs based on patterns of co-variation among signs and symptoms. The initial HiTOP model, which was published in 2017, is based on a large literature that spans decades of research. HiTOP is a living model that undergoes revision as new data become available. Here we discuss advantages and practical considerations of using this system in psychiatric practice and research. We especially highlight limitations of HiTOP and ongoing efforts to address them. We describe differences and similarities between HiTOP and existing diagnostic systems. Next, we review the types of evidence that informed development of HiTOP, including populations in which it has been studied and data on its validity. The paper also describes how HiTOP can facilitate research on genetic and environmental causes of psychopathology as well as the search for neurobiologic mechanisms and novel treatments. Furthermore, we consider implications for public health programs and prevention of mental disorders. We also review data on clinical utility and illustrate clinical application of HiTOP. Importantly, the model is based on measures and practices that are already used widely in clinical settings. HiTOP offers a way to organize and formalize these techniques. This model already can contribute to progress in psychiatry and complement traditional nosologies. Moreover, HiTOP seeks to facilitate research on linkages between phenotypes and biological processes, which may enable construction of a system that encompasses both biomarkers and precise clinical description.

Traditionally, personality has been conceptualized in terms of dimensions of human experience – habitual ways of thinking, feeling, and behaving. By contrast, psychopathology has traditionally been conceptualized in terms of categories of disorder – disordered thinking, feeling, and behaving. The empirical literature, however, routinely shows that psychopathology does not coalesce into readily distinguishable categories. Indeed, psychopathology tends to delineate dimensions that are relatively similar to dimensions of personality. In this special issue of Personality Neuroscience, authors took up the challenge of reconceptualizing personality and psychopathology in terms of connected and interrelated dimensions, and they considered the utility of pursuing neuroscientific inquiry from this more integrative perspective. In this editorial article, we provide the relevant background to the interface between personality, psychopathology, and neuroscience; summarize contributions to the special issue; and point toward directions for continued research and refinement. All told, it is evident that quantitatively derived, integrative models of personality–psychopathology represent a particularly promising conduit for advancing our understanding of the neurobiological foundation of human experience, both functional and dysfunctional.

Many of the characteristics cited in Hibbing et al.'s account are ineffective predictors of economic conservatism. However, these same characteristics are often associated with differences not only in social conservatism but also in religiousness and authoritarianism. Hibbing et al. may have offered a useful explanation of traditionalism and attitudes toward change across domains rather than of general political attitudes.

Individuals high in the personality trait Openness to Experience appear to engage spontaneously (during wake) in processes of elaborative encoding similar to those Llewellyn identifies in both dreaming and the ancient art of memory (AAOM). Links between Openness and dreaming support the hypothesis that dreaming is part of a larger process of cognitive exploration that facilitates adaptation to new experiences.

Charney's dismissal of well-established methods in behavioral genetic research is misguided. He claims that studies of heritability and genetic association depend for their validity on six assumptions, but he cites no sources to support this claim. We explain why none of the six assumptions is strictly necessary for the utility of either method of genetic analysis.

Despite the substantial heritability of nearly all psychological traits, it has been difficult to identify specific genetic variants that account for more than a tiny percentage of genetic variance in phenotypes. Common explanations for this “missing heritability” include massive polygenicity, rare variants, epigenetics, epistasis, and gene–environment interactions. Gene–trait (G × T) interaction is another concept useful for understanding the lack of obvious genetic main effects. Both genes and environments are distal contributors to human behavior, but the brain is the proximal driver of behavior. The effect of any single genetic variant is dependent on the configuration of the brain in which it is expressed. One method to begin studying how single genes interact with variations in the rest of the brain is to investigate G × T interactions. A psychological trait reflects a characteristic pattern of psychological function (and, therefore, of brain function), which has its origin in the cumulative effects of both the genome and the environment. A trait therefore describes variation in the broad organismic context in which any single gene operates. We describe the nature and significance of G × T interactions for understanding psychopathology and normal trait variation, which are illustrated with empirical examples.

Cramer et al. articulate a novel perspective on comorbidity. However, their network models must be compared with more parsimonious latent variable models before conclusions can be drawn about network models as plausible accounts of comorbidity. Latent variable models have proven generative in studying psychopathology and its external correlates, and we doubt network models will prove as useful for psychopathology research.

It is established that reading and reading-related processes are heritable; genes thus play an important role in the foundation of individual differences in reading. In this article, we focus on one facet of reading–comprehension. Comprehension is a higher order cognitive skill that requires many other cognitive processes for it to unfold completely and successfully. One such process is executive functioning, which has been associated with genetic variation in the catechol-O-methyltransferase (COMT) gene. Genotypes and haplotypes of four single nucleotide polymorphisms in COMT were investigated in 179 incarcerated adolescent delinquents. Four hierarchical logistic regression models predicting the presence/absence of comprehension difficulties were fitted to the data; genetic variation in COMT and the presence/absence of maternal rejection were investigated as main effects and as effects acting interactively. Three out of four interaction terms were found to be important predictors of individual differences in comprehension. These findings were supported by the results of the haplotype analyses, in which the four investigated polymorphisms were considered simultaneously.

Dreams represent threat, but appear to do so metaphorically more often than realistically. The metaphoric representation of threat allows it to be conceptualized in a manner that is constant across situations (as what is common to all threats begins to be understood and portrayed). This also means that response to threat can come to be represented in some way that works across situations. Conscious access to dream imagery, and subsequent social communication of that imagery, can facilitate this generalized adaptive process, by allowing the communicative dreamer access to the problem solving resources of the community.

[Revonsuo; Solms]