Annual Review of Clinical Psychology - Volume 9, 2013

The purpose of this review is (a) to study and systematically review the recent literature examining the co-occurrence and relationships between Axis I psychiatric disorders and Axis II personality disorders, specifically the six originally proposed for the Diagnostic and Statistical Manual of Mental Disorders (DSM)-5, and (b) to consider the clinical utility of the current Axis I and Axis II approach in the DSM-IV-TR and apply findings to state a position on the issue of collapsing together Axis I and Axis II. Community surveys or prospective cohort studies were reviewed as a priority. Our review indicates that the associations between clinical disorders and personality disorders clearly varied within each disorder and across the six personality disorders. Our understanding has advanced, particularly related to the clinical utility of comorbidity, and there may be sufficient evidence to support moving borderline personality disorder to Axis I. However, it seems premature to conclude that comorbidity is best conceptualized by having all disorders in a single category or by deleting disorders so that comorbidity is reduced. Our review suggests some priorities for future research into comorbidity, such as including personality disorders in future multivariate comorbidity models.

Schizophrenia and autism have been linked since their earliest descriptions. Both are disorders of cerebral specialization originating in the embryonic period. Genetic, molecular, and cytologic research highlights a variety of shared contributory mechanisms that may lead to patterns of abnormal connectivity arising from altered development and topology. Overt behavioral pathology likely emerges during or after neurosensitive periods in which resource demands overwhelm system resources and the individual's ability to compensate using interregional activation fails. We are at the threshold of being able to chart autism and schizophrenia from the inside out. In so doing, the door is opened to the consideration of new therapeutics that are developed based upon molecular, synaptic, and systems targets common to both disorders.

Over the past decade, considerable advances have been made in understanding genetic influences on eating pathology. Eating disorders aggregate in families, and twin studies reveal that additive genetic factors account for approximately 40% to 60% of liability to anorexia nervosa (AN), bulimia nervosa (BN), and binge eating disorder (BED). Molecular genetics studies have been undertaken to identify alterations in deoxyribonucleic acid sequence and/or gene expression that may be involved in the pathogenesis of disordered eating behaviors, symptoms, and related disorders and to uncover potential genetic variants that may contribute to variability of treatment response. This article provides an in-depth review of the scientific literature on the genetics of AN, BN, and BED including extant studies, emerging hypotheses, future directions, and clinical implications.

The goal of this review is to provide an overview of biomarkers for Alzheimer's disease (AD), with emphasis on neuroimaging and cerebrospinal fluid (CSF) biomarkers. We first review biomarker changes in patients with late-onset AD, including findings from studies using structural and functional magnetic resonance imaging (MRI), advanced MRI techniques (diffusion tensor imaging, magnetic resonance spectroscopy, perfusion), positron emission tomography with fluorodeoxyglucose, amyloid tracers, and other neurochemical tracers, and CSF protein levels. Next, we evaluate findings from these biomarkers in preclinical and prodromal stages of AD including mild cognitive impairment (MCI) and pre-MCI conditions conferring elevated risk. We then discuss related findings in patients with dominantly inherited AD. We conclude with a discussion of the current theoretical framework for the role of biomarkers in AD and emergent directions for AD biomarker research.

Currently, 8.5% of the US population meets criteria for alcohol use disorders, with a total cost to the US economy estimated at $234 billion per year. Alcohol and tobacco use share a high degree of comorbidity and interact across many levels of analysis. This review begins by highlighting alcohol and tobacco comorbidity and presenting evidence that tobacco increases the risk for alcohol misuse and likely has a causal role in this relationship. We then discuss how knowledge of alcohol and tobacco interactions can be used to reduce alcohol use, focusing on whether (a) smoking status can be used as a clinical indicator for alcohol misuse, (b) tobacco policies reduce alcohol use, and (c) nicotinic-based medications can be used to treat alcohol use disorders.

Around 19% of US adults smoke cigarettes, and smoking remains the leading avoidable cause of death in this country. Without treatment only ∼5% of smokers who try to quit achieve long-term abstinence, but evidence-based cessation treatment increases this figure to 10% to 30%. The process of smoking cessation comprises different pragmatically defined phases, and these can help guide smoking treatment development and evaluation. This review evaluates the effectiveness of smoking interventions for smokers who are unwilling to make a quit attempt (motivation phase), who are willing to make a quit attempt (cessation phase), who have recently quit (maintenance phase), and who have recently relapsed (relapse recovery phase). Multiple effective treatments exist for some phases (cessation), but not others (relapse recovery). A chronic care approach to treating smoking requires effective interventions for every phase, especially interventions that exert complementary effects both within and across phases and that can be disseminated broadly and cost-effectively.

This review examines neuroimaging and neurocognitive findings on alcohol-related toxicity in adolescents. Teens who meet criteria for alcohol use disorders, as well as those who engage in subdiagnostic binge drinking behaviors, often show poorer neurocognitive performance, alterations in gray and white matter brain structure, and discrepant functional brain activation patterns when compared to nonusing and demographically matched controls. Abnormalities are also observed in teens with a family history of alcoholism, and such differences in neuromaturation may leave youths at increased risk for the development of an alcohol use disorder or increased substance use severity. More prospective investigations are needed, and future work should focus on disentangling preexisting differences from dose-dependent effects of alcohol on neurodevelopment. Intervention strategies that utilize neuroimaging findings (e.g., identified weaknesses in particular neural substrates and behavioral correlates) may be helpful in both prevention and intervention campaigns for teens both pre- and postinitiation of alcohol use.

Health disparities (differences in health by socioeconomic groups) are a pressing issue in our society. This article provides an overview of a multilevel approach that seeks to understand the mechanisms underlying health disparities by considering factors at the individual, family, and neighborhood levels. In addition, we describe an approach to connecting these factors to various levels of biological processes (systemic inflammation, cellular processes, and genomic pathways) that drive disease pathophysiology. In the second half of the article, we address the question of why some low-socioeconomic-status (low-SES) individuals manage to maintain good physical health. We identify naturally occurring psychosocial factors that help buffer these individuals from adverse physiological responses and pathogenic processes leading to chronic disease. What is protective for low-SES individuals is not the same as what is protective for high-SES individuals, and this needs to be taken into account in interventions aimed at reducing health disparities.

After sketching how my own interest and research into bullying problems began, I address a number of potentially controversial issues related to the definition and measurement of such problems. The importance of maintaining the distinctions between bullying victimization and general victimization and between bullying perpetration and general aggression is strongly emphasized. There are particular problems with the common method of peer nominations for purposes of prevalence estimation, comparisons of such estimates and mean levels across groups and time, and measurement of change. Two large-scale projects with time series data show that several recent claims about cyber bullying made in the media and by some researchers are greatly exaggerated and lack scientific support. Recent meta-analyses of the long-term outcomes for former bullies and victims provide convincing evidence that being involved in such problems is not just a harmless and passing school problem but something that has serious adjustment and public health consequences that also entail great costs to society. Another section presents my view of why the theme of bullying took quite some time to reach the peer relations research community in the United States and the role of a dominant research tradition focusing on “likeability” in this account. In a final section, I summarize some reasons why it may be considered important and interesting to focus both research and intervention on bully/victim problems.

Recovery (also known as the “recovery orientation,” “recovery vision,” or “recovery philosophy”) has been the dominant paradigm shaping current mental health policy for the past decade. It is claimed to be a revolutionary departure from the past and a guide to policy that will transform outcomes of severe mental illness. This review looks critically at the history of recovery and examines the ways in which this history has shaped the values, beliefs, and practices of current recovery-based policies. Recovery is a treatment philosophy that emerged from the ruins of deinstitutionalization and the psychopharmaceutical revolution. Yet paradoxically, recovery reflects many of the same ideas that made deinstitutionalization and the era of psychopharmacology possible. Further, history reveals how the recovery movement is deeply indebted to and embedded within the sociocultural values of neoliberalism that have shaped public policy since the presidential election of Ronald Reagan in 1980.