Annual Review of Clinical Psychology - Volume 15, 2019

As president of the American Psychological Association in 1998, I organized researchers and practitioners to work on building well-being, not just on the traditional task of reducing ill-being. Substantial research then found that well-being causes many external benefits, including better physical and mental health. Among the applications of Positive Psychology are national psychological accounts of well-being, Positive Psychotherapy, the classification of strengths and virtues, Comprehensive Soldier Fitness, and Positive Education. Positive Psychology has spread beyond psychology into neuroscience, health, psychiatry, theology, and even to the humanities. Positive Psychology has many critics, and I comment on the strongest criticisms. I conclude with the hope that the building of well-being will become a cornerstone of morality, politics, and religion.

We live in an age of psychopharmacology. One in six persons currently takes a psychotropic drug. These drugs have profoundly shaped our scientific and cultural understanding of psychiatric disease. By way of a historical review, we try to make sense of psychiatry's dependency on psychiatric drugs in the care of patients. Modern psychopharmacology began in 1950 with the synthesis of chlorpromazine. Over the course of the next 50 years, the psychiatric understanding and treatment of mental illness radically changed. Psychotropic drugs played a major part in these changes as state hospitals closed and psychotherapy gave way to drug prescriptions. Our review suggests that the success of psychopharmacology was not the consequence of increasingly more effective drugs for discrete psychiatric diseases. Instead, a complex mix of political economic realities, pharmaceutical marketing, basic science advances, and changes in the mental health-care system have led to our current infatuation with psychopharmacology.

Bifactor and other hierarchical models have become central to representing and explaining observations in psychopathology, health, and other areas of clinical science, as well as in the behavioral sciences more broadly. This prominence comes after a relatively rapid period of rediscovery, however, and certain features remain poorly understood. Here, hierarchical models are compared and contrasted with other models of superordinate structure, with a focus on implications for model comparisons and interpretation. Issues pertaining to the specification and estimation of bifactor and other hierarchical models are reviewed in exploratory as well as confirmatory modeling scenarios, as are emerging findings about model fit and selection. Bifactor and other hierarchical models provide a powerful mechanism for parsing shared and unique components of variance, but care is required in specifying and making inferences about them.

Event-related potentials (ERPs) are direct measures of brain activity that can be leveraged for clinically meaningful research. They can relate robustly both to continuous measures of individual difference and to categorical diagnoses in ways that clarify similarities and distinctions between apparently related disorders and traits. ERPs can be linked to genetic risk, can act as moderators of developmental trajectories and responses to stress, and can be leveraged to identify those at greater risk for psychopathology, especially when used in combination with other neural and self-report measures. ERPs can inform models of the development of, and risk for, psychopathology. Finally, ERPs can be used as targets for existing and novel interventions and prevention efforts. We provide concrete examples for each of these possibilities by focusing on programmatic research on the error-related negativity and anxiety, and thus show that ERPs are poised to make greater contributions toward the identification, prediction, treatment, and prevention of mental disorders.

Interoception refers to the process by which the nervous system senses and integrates signals originating from within the body, providing a momentary mapping of the body's internal landscape and its relationship to the outside world. Active inference is based on the premise that afferent sensory input to the brain is constantly shaped and modified by prior expectations. In this review we propose that interoceptive psychopathology results from two primary interoceptive dysfunctions: First, individuals have abnormally strong expectations of the situations that elicit bodily change (i.e., hyperprecise priors), and second, they have great difficulty adjusting these expectations when the environment changes (i.e., context rigidity). Here we discuss how these dysfunctions potentially manifest in mental illness and how interventions aimed at altering interoceptive processing can help the brain create a more realistic model of its internal state.

Implicit cognitive processing is theorized to have a central role in many forms of psychopathology. In the current review, we focus on implicit associations, by which we mean evaluative representations in memory that are difficult to control and do not require conscious reflection to influence affect, cognition, or behavior. We consider definitional and measurement challenges before examining recent empirical evidence for these associations in anxiety, obsessive–compulsive, posttraumatic stress, depressive, and alcohol use disorders. This examination is framed by a brief review of the ways that prominent models of psychopathology represent biased implicit processing of disorder-relevant information. We consider to what extent models reflect more traditional automatic/implicit versus strategic/explicit dual-process perspectives or reflect more recent dynamical systems perspectives in which mental representations are iteratively reprocessed, evolving continuously. Finally, we consider the future research needed to better understand the interactive and temporal dynamics of implicit cognition in psychopathology.

This article describes the Minnesota Multiphasic Personality Inventory-2-Restructured Form (MMPI-2-RF) and situates the instrument in contemporary psychopathology and personality literature. The historical evolution of the MMPI instruments is highlighted, including how failure to update the test for several decades resulted in increasing disinterest by basic researchers and how the restructuring efforts beginning in the 2000s promised to realign the instrument with basic research. In this regard, the construct validity associated with MMPI-2-RF scores in the context of contemporary dimensional models of psychopathology is considered. Research supporting the applied utility of the MMPI-2-RF scales in a variety of contexts—including mental health screenings, presurgical evaluations, forensic assessment, and public safety screening—is also reviewed. Critiques of the MMPI-2-RF are described and addressed. Finally, a series of recommendations for future updates of the MMPI-2-RF are described along with a path toward the MMPI-3.

Is there a clear line between normal and abnormal mood? Studies of manifest and latent structure provide strong support for a continuum that extends from asymptomatic to subsyndromal to syndromal cases of increasing severity. Subsyndromal symptoms are impairing, predict syndrome onset and relapse, and account for more doctor's visits and suicide attempts than the full syndromes, yet they are not recognized in the current classification. For most research and some clinical activities, dimensional diagnoses are recommended, and examples are offered for how such diagnoses could be made. For clinical activities requiring decisions, a multithreshold model is proposed in which both lower (e.g., mild depression, capturing subsyndromal cases) and upper (e.g., major depression, capturing clinically significant cases) diagnostic categories are used to inform clinical care. Beyond its implications for diagnosis, the dimensionality of depression and anxiety has implications for etiology and for research aimed at understanding how emotions become disrupted in psychopathology.

Psychotherapies may work through techniques that are specific to each therapy or through factors that all therapies have in common. Proponents of the common factors model often point to meta-analyses of comparative outcome studies that show all therapies have comparable effects. However, not all meta-analyses support the common factors model; the included studies often have several methodological problems; and there are alternative explanations for finding comparable outcomes. To date, research on the working mechanisms and mediators of therapies has always been correlational, and in order to establish that a mediator is indeed a causal factor in the recovery process of a patient, studies must show a temporal relationship between the mediator and an outcome, a dose–response association, evidence that no third variable causes changes in the mediator and the outcome, supportive experimental research, and have a strong theoretical framework. Currently, no common or specific factor meets these criteria and can be considered an empirically validated working mechanism. Therefore, it is still unknown whether therapies work through common or specific factors, or both.

One-Session Treatment is a well-established evidence-based treatment for specific phobias in youths that incorporates reinforcement, cognitive challenges, participant modeling, psychoeducation, and skills training into a single, massed session of graduated exposure. This review begins by briefly examining the phenomenology, etiology, epidemiology, and assessment of specific phobias and then pivots to a description of One-Session Treatment. We examine the use of One-Session Treatment with children and adolescents, briefly discussing its components and application, and subsequently review almost two decades of research supporting its efficacy. Finally, we propose future directions for research and practice.

Although the fear response is an adaptive response to threatening situations, a number of psychiatric disorders feature prominent fear-related symptoms caused, in part, by failures of extinction and inhibitory learning. The translational nature of fear conditioning paradigms has enabled us to develop a nuanced understanding of extinction and inhibitory learning based on the molecular substrates to systems neural circuitry and psychological mechanisms. This knowledge has facilitated the development of novel interventions that may augment extinction and inhibitory learning. These interventions include nonpharmacological techniques, such as behavioral methods to implement during psychotherapy, as well as device-based stimulation techniques that enhance or reduce activity in different regions of the brain. There is also emerging support for a number of psychopharmacological interventions that may augment extinction and inhibitory learning specifically if administered in conjunction with exposure-based psychotherapy. This growing body of research may offer promising novel techniques to address debilitating transdiagnostic fear-related symptoms.

Mindfulness meditation is increasingly incorporated into mental health interventions, and theoretical concepts associated with it have influenced basic research on psychopathology. Here, we review the current understanding of mindfulness meditation through the lens of clinical neuroscience, outlining the core capacities targeted by mindfulness meditation and mapping them onto cognitive and affective constructs of the Research Domain Criteria matrix proposed by the National Institute of Mental Health. We review efficacious applications of mindfulness meditation to specific domains of psychopathology including depression, anxiety, chronic pain, and substance abuse, as well as emerging efforts related to attention disorders, traumatic stress, dysregulated eating, and serious mental illness. Priorities for future research include pinpointing mechanisms, refining methodology, and improving implementation. Mindfulness meditation is a promising basis for interventions, with particular potential relevance to psychiatric comorbidity. The successes and challenges of mindfulness meditation research are instructive for broader interactions between contemplative traditions and clinical psychological science.

The developmental origins of health and disease hypothesis applied to neurodevelopmental outcomes asserts that the fetal origins of future development are relevant to mental health. There is a third pathway for the familial inheritance of risk for psychiatric illness beyond shared genes and the quality of parental care: the impact of pregnant women's distress—defined broadly to include perceived stress, life events, depression, and anxiety—on fetal and infant brain–behavior development. We discuss epidemiological and observational clinical data demonstrating that maternal distress is associated with children's increased risk for psychopathology: For example, high maternal anxiety is associated with a twofold increase in the risk of probable mental disorder in children. We review several biological systems hypothesized to be mechanisms by which maternal distress affects fetal and child brain and behavior development, as well as the clinical implications of studies of the developmental origins of health and disease that focus on maternal distress. Development and parenting begin before birth.

Children's development is largely dependent on caregiving; when caregiving is disrupted, children are at increased risk for numerous poor outcomes, in particular psychopathology. Therefore, determining how caregivers regulate children's affective neurobiology is essential for understanding psychopathology etiology and prevention. Much of the research on affective functioning uses fear learning to map maturation trajectories, with both rodent and human studies contributing knowledge. Nonetheless, as no standard framework exists through which to interpret developmental effects across species, research often remains siloed, thus contributing to the current therapeutic impasse. Here, we propose a developmental ecology framework that attempts to understand fear in the ecological context of the child: their relationship with their parent. By referring to developmental goals that are shared across species (to attach to, then, ultimately, separate from the parent), this framework provides a common grounding from which fear systems and their dysfunction can be understood, thus advancing research on psychopathologies and their treatment.

The gut microbiome is implicated in the pathophysiology of a wide range of psychological disorders. Preclinical studies have provided us with key insights into the mechanisms by which the microbiome influences bidirectional gut–brain communication. There are many signaling pathways involved, including the hypothalamic–pituitary–adrenal axis, immune modulation, tryptophan and serotonin metabolism, bile acid transformation, microbial production of neuroactive compounds, and regulation of the endocannabinoid system. The complex and widespread influence of the microbiome on many physiological and psychological processes has generated a keen interest in its therapeutic potential for depression, anxiety, autism, and other psychiatric disorders. It has been shown that the microbiome composition of people suffering with such conditions differs significantly from that of healthy controls, and although the area is in its infancy, interventional studies that alter a person's microbiome through the use of probiotics, prebiotics, or dietary change can alleviate psychopathological symptoms.

This article reviews the interactions of estrogen changes and psychosocial stress in contributing to vulnerability to major depressive disorder (MDD) in women. Estrogen modulates brain networks and processes related to changes in stress response, cognition, and emotional dysregulation that are core characteristics of MDD. Synergistic effects of estrogen on cognitive and emotional function, particularly during psychosocial stress, may underlie the association of ovarian hormone fluctuation and depression in women. We propose a model of estrogen effects on multiple brain systems that interface with stress-related emotional and cognitive processes implicated in MDD and discuss possible mechanisms through which reproductive events and changes in estrogen may contribute to MDD risk in women with other concurrent risk factors.

Suicide is the second leading cause of death worldwide for adolescents. Despite decades of research on correlates and risk factors for adolescent suicide, we know little about why suicidal ideation and behavior frequently emerge in adolescence and how to predict, and ultimately prevent, suicidal behavior among youths. In this review, we first discuss knowledge regarding correlates, risk factors, and theories of suicide. We then review why adolescence is a period of unique vulnerability, given changing biology and social network reorganization. Next, we present a conceptual model through which to interpret emerging findings in adolescent suicide research. We suggest that a promising area for future research is to examine adolescent suicide as a failure of biological responses to acute stress in the proximal moments of a suicidal crisis. After reviewing initial evidence for this conceptualization, we review future directions for studies on adolescent suicide.

There is overwhelming evidence that sleep is crucial for memory consolidation. Patients with schizophrenia and their unaffected relatives have a specific deficit in sleep spindles, a defining oscillation of non-rapid eye movement (NREM) Stage 2 sleep that, in coordination with other NREM oscillations, mediate memory consolidation. In schizophrenia, the spindle deficit correlates with impaired sleep-dependent memory consolidation, positive symptoms, and abnormal thalamocortical connectivity. These relations point to dysfunction of the thalamic reticular nucleus (TRN), which generates spindles, gates the relay of sensory information to the cortex, and modulates thalamocortical communication. Genetic studies are beginning to provide clues to possible neurodevelopmental origins of TRN-mediated thalamocortical circuit dysfunction and to identify novel targets for treating the related memory deficits and symptoms. By forging empirical links in causal chains from risk genes to thalamocortical circuit dysfunction, spindle deficits, memory impairment, symptoms, and diagnosis, future research can advance our mechanistic understanding, treatment, and prevention of schizophrenia.

The nomenclature of personality disorders in the 11th revision of the International Classification of Diseases and Related Health Problems represents the most radical change in the classification history of personality disorders. A dimensional structure now replaces categorical description. It was argued by the Working Group that only a dimensional system was consistent with the empirical evidence and, in the spirit of clinical utility, the new system is based on two steps. The first step is to assign one of five levels of severity, and the second step is to assign up to five prominent domain traits. There was resistance to this structure from those who feel that categorical diagnosis, particularly of borderline personality disorder, should be retained. After lengthy discussion, described in detail here, there is now an option for a borderline pattern descriptor to be selected as a diagnostic option after severity has been determined.

Pain and substance use are highly prevalent and co-occurring conditions that continue to garner increasing clinical and empirical interest. Although nicotine and tobacco, alcohol, and cannabis each confer acute analgesic effects, frequent or heavy use may contribute to the development and progression of chronic pain, and pain may be heightened during abstinence. Additionally, pain can be a potent motivator of substance self-administration, and it may contribute to escalating use and poorer substance-related treatment outcomes. We integrated converging lines of evidence to propose a reciprocal model in which pain and substance use are hypothesized to interact in the manner of a positive feedback loop, resulting in the exacerbation and maintenance of both conditions over time. Theoretical mechanisms in bidirectional pain–substance use relations are reviewed, including negative reinforcement, social cognitive processes, and allostatic load in overlapping neural circuitry. Finally, candidate transdiagnostic factors are identified, and we conclude with a discussion of clinical implications and future research directions.

There is substantial evidence that heightened anxiety vulnerability is characterized by increased selective attention to threatening information. The reliability of this anxiety-linked attentional bias has become the focus of considerable recent interest. We distinguish between the potential inconsistency of anxiety-linked attentional bias and inconsistency potentially reflecting the psychometric properties of the assessment approaches used to measure it. Though groups with heightened anxiety vulnerability often exhibit, on average, elevated attention to threat, the evidence suggests that individuals are unlikely to each display a stable, invariant attentional bias to threat. Moreover, although existing assessment approaches can differentiate between groups, they do not exhibit the internal consistency or test-retest reliability necessary to classify individuals in terms of their characteristic pattern of attentional responding to threat. We discuss the appropriate uses of existing attentional bias assessment tasks and propose strategies for enhancing classification of individuals in terms of their tendency to display an attentional bias to threat.

Mental disorders are increasingly conceptualized as biomedical diseases, explained as manifestations of genetic and neurobiological abnormalities. Here, we discuss changes in the dominant explanatory accounts of psychopathology that have occurred over time and the driving forces behind these shifts, lay out some real-world evidence for the increasing ascendancy of biomedical explanations, and provide an overview of the types of attitudes and beliefs that may be affected by them. We examine theoretical and conceptual models that are relevant to understanding how biomedical conceptualizations might affect attitudes and beliefs about mental disorders, and we review some empirical evidence that bears on this question. Finally, we examine possible strategies for combatting potential negative effects of biomedical explanations and discuss important conclusions and directions for future research.

Despite psychological scientists’ increasing interest in replicability, open science, research transparency, and the improvement of methods and practices, the clinical psychology community has been slow to engage. This has been shifting more recently, and with this review, we hope to facilitate this emerging dialogue. We begin by examining some potential areas of weakness in clinical psychology in terms of methods, practices, and evidentiary base. We then discuss a select overview of solutions, tools, and current concerns of the reform movement from a clinical psychological science perspective. We examine areas of clinical science expertise (e.g., implementation science) that should be leveraged to inform open science and reform efforts. Finally, we reiterate the call to clinical psychologists to increase their efforts toward reform that can further improve the credibility of clinical psychological science.