Annual Review of Clinical Psychology最新文献

Bipolar disorder is a lifelong mood disorder characterized by extreme mood swings between mania and depression. Despite fitness costs associated with increased mortality and significant impairment, bipolar disorder has persisted in the population with a high heritability and a stable prevalence. Creativity and other positive traits have repeatedly been associated with the bipolar spectrum, particularly among unaffected first-degree relatives and those with milder expressions of bipolar traits. This suggests a model in which large doses of risk variants cause illness, but mild to moderate doses confer advantages, which serve to maintain bipolar disorder in the population. Bipolar disorder may thus be better conceptualized as a dimensional trait existing at the extreme of normal population variation in positive temperament, personality, and cognitive traits, aspects of which may reflect a shared vulnerability with creativity. Investigations of this shared vulnerability may provide insight into the genetic mechanisms underlying illness and suggest novel treatments.

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.

The goal of this review is to enable clinical psychology researchers to more rigorously test competing hypotheses when studying risk factors in observational studies. We argue that there is a critical need for researchers to leverage recent advances in epidemiology/biostatistics related to causal inference and to use innovative approaches to address a key limitation of observational research: the need to account for confounding. We first review theoretical issues related to the study of causation, how causal diagrams can facilitate the identification and testing of competing hypotheses, and the current limitations of observational research in the field. We then describe two broad approaches that help account for confounding: analytic approaches that account for measured traits and designs that account for unmeasured factors. We provide descriptions of several such approaches and highlight their strengths and limitations, particularly as they relate to the etiology and treatment of behavioral health problems.

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.

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.

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.