Annual Review of Clinical Psychology最新文献

In seeking to understand mental health and disease, it is fundamental to identify the biological substrates that draw together the experiences and physiological processes that underlie observed psychological changes. Mitochondria are subcellular organelles best known for their central role in energetics, producing adenosine triphosphate to power most cellular processes. Converging lines of evidence indicate that mitochondria play a key role in the biological embedding of adversity. Preclinical research documents the effects of stress exposure on mitochondrial structure and function, and recent human research suggests alterations constituting recalibrations, both adaptive and nonadaptive. Current research suggests dynamic relationships among stress exposure, neuroendocrine signaling, inflammation, and mitochondrial function. These complex relationships are implicated in disease risk, and their elucidation may inform prevention and treatment of stress- and trauma-related disorders. We review and evaluate the evidence for mitochondrial dysfunction as a consequence of stress exposure and as a contributing factor to psychiatric disease.

This review presents current theory and empirical research that address the interplay between risk and resilience processes among minority youth in the United States. To move the clinical sciences forward in their research and treatment approaches to solving minority-majority health and well-being disparities, ecological, intersectional, and emic (within-group) approaches must be adopted. We discuss the consequences of systematic oppression and marginalization for children in the United States, focusing primarily on research regarding xenophobia, discrimination, and racism. Lastly, we provide examples of recent interventions that take emic approaches to closing minority-majority gaps in developmental outcomes.

There is no accepted definition of the term paraphilia despite its being listed as an essential feature of a class of mental disorders known as the paraphilic disorders. The origin of the term, history of its inclusion as a diagnosis, and logical flaws inherent in the various definitions are discussed in this review. We examine the basis for pathologizing individuals with paraphilias, consider what paraphilias can tell us about how humans develop their sexual interests, and question the usefulness of dividing sexual interests into paraphilias and normophilias. The construct of the paraphilias appears to be poorly conceived and has outlived its usefulness.

Epigenetic mechanisms govern the transcription of the genome. Research with model systems reveals that environmental conditions can directly influence epigenetic mechanisms that are associated with interindividual differences in gene expression in brain and neural function. In this review, we provide a brief overview of epigenetic mechanisms and research with relevant rodent models. We emphasize more recent translational research programs in epigenetics as well as the challenges inherent in the integration of epigenetics into developmental and clinical psychology. Our objectives are to present an update with respect to the translational relevance of epigenetics for the study of psychopathology and to consider the state of current research with respect to its potential importance for clinical research and practice in mental health.

Social Safety Theory hypothesizes that developing and maintaining friendly social bonds is a fundamental organizing principle of human behavior and that threats to social safety are a critical feature of psychological stressors that increase risk for disease. Central to this formulation is the fact that the human brain and immune system are principally designed to keep the body biologically safe, which they do by continually monitoring and responding to social, physical, and microbial threats in the environment. Because situations involving social conflict, isolation, devaluation, rejection, and exclusion historically increased risk for physical injury and infection, anticipatory neural-immune reactivity to social threat was likely highly conserved. This neurocognitive and immunologic ability for humans to symbolically represent and respond to potentially dangerous social situations is ultimately critical for survival. When sustained, however, this multilevel biological threat response can increase individuals' risk for viral infections and several inflammation-related disease conditions that dominate present-day morbidity and mortality.

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.

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.

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.

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.