A growing body of research suggests that the construct of emotion regulation is important for understanding the onset, maintenance, and treatment of anxiety disorders. In this review, we provide a selective overview of this emerging field and highlight the major sources of evidence. First, evidence suggests that the construct of emotion regulation can be differentiated from the construct of emotion. Second, there is a large and consistent body of research demonstrating that emotion regulation strategies can modulate emotional responding, and this finding is observed in both behavioral and neuroimaging studies. Third, measures of emotion regulation explain incremental variance in measures of anxiety disorder symptoms not accounted for by measures of negative affect. Although the research implicating emotion regulation in the anxiety disorders is promising, future research will be necessary to further clarify causal mechanisms explaining how emotion regulation confers vulnerability for anxiety disorders and to improve the clarity and consistency of definitions of emotion regulation.

Weight gain remains a well recognized yet difficult to treat adverse effect of many anti-psychotic drugs including agents of the first and second generation. The weight gain liabilities of antipsychotic drugs are partly associated with their ability to increase appetite. Most behavioral interventions for weight control remain of limited efficacy, possibly because they do not specifically target the neuroendocrine factors regulating appetite. Identifying new weight management interventions directly acting on the biochemical and neuroendocrine mechanisms of anti-psychotic induced weight gain may help to improve the efficacy of behavioral weight management programs. Such potentially specific strategies include (1) using diets which do not increase appetite despite calorie restriction; (2) countering thirst as an anticholinergic side-effect; (3) discouraging cannabis use and (4) adding metformin to a behavioral intervention. In view of our currently rather limited treatment repertoire it seems timely systematically to explore such novel options.

Depression is a risk factor for cardiac morbidity and mortality in patients with coronary heart disease, especially in those with a recent history of acute coronary syndrome. To improve risk stratification and treatment planning, it would be useful to identify the characteristics or subtypes of depression that are associated with the highest risk of cardiac events. This paper reviews the evidence concerning several putative depression subtypes and symptom patterns that may be associated with a high risk of morbidity and mortality in cardiac patients, including single-episode major depressive disorder, depression that emerges after a cardiac event, somatic symptoms of depression, and treatment-resistant depression.

Studies consistently report that groups of individuals with major depressive disorder (MDD) demonstrate increased levels of a variety of peripheral inflammatory biomarkers when compared with groups of nondepressed individuals. These findings are often interpreted as meaning that MDD, even in medically healthy individuals, may be an inflammatory condition. In this article, we examine evidence for and against this idea by looking more closely into what the actual patterns of inflammatory findings indicate in terms of the relationship between MDD and the immune system. Data are presented in support of the idea that inflammation only contributes to depression in a subset of patients versus the possibility that the depressogenic effect of inflammatory activation is more widespread and varies depending on the degree of vulnerability any given individual evinces in interconnected physiologic systems known to be implicated in the etiology of MDD. Finally, the treatment implications of these various possibilities are discussed.

Attention-deficit/hyperactivity disorder (ADHD) is a prevalent neurobehavioral disorder affecting 5% to 10% of children. Although considered to be a highly familial disorder, ADHD heritability estimates of 60% to 80% highlight the considerable role that environmental factors may still play in disorder susceptibility. Proposed ADHD environmental risk factors include prenatal substance exposures, heavy metal and chemical exposures, nutritional factors, and lifestyle/psychosocial factors. This paper reviews the literature published in 2010 investigating the association between environmental risk factors and ADHD or related symptomatology. Sources of risk factor exposure and the proposed mechanism by which each exposure is linked to ADHD-related neurobehavioral changes are also reported. Methodologic limitations of the current literature are discussed, and guidelines for future study are proposed. An improved understanding of the role that environmental factors play in ADHD etiology is critical to future ADHD prevention efforts.

Binge eating disorder (BED) is the most prevalent eating disorder in adults, and individuals with BED report greater general and specific psychopathology than non-eating disordered individuals. The current paper reviews research on psychological treatments for BED, including the rationale and empirical support for cognitive behavioral therapy (CBT), interpersonal psychotherapy (IPT), dialectical behavior therapy (DBT), behavioral weight loss (BWL), and other treatments warranting further study. Research supports the effectiveness of CBT and IPT for the treatment of BED, particularly for those with higher eating disorder and general psychopathology. Guided self-help CBT has shown efficacy for BED without additional pathology. DBT has shown some promise as a treatment for BED, but requires further study to determine its long-term efficacy. Predictors and moderators of treatment response, such as weight and shape concerns, are highlighted and a stepped-care model proposed. Future directions include expanding the adoption of efficacious treatments in clinical practice, testing adapted treatments in diverse samples (e.g., minorities and youth), improving treatment outcomes for nonresponders, and developing efficient and cost-effective stepped-care models.

Prospective studies of adolescents at risk for schizophrenia (high-risk studies) can shed light on the possible premorbid precursors of schizophrenia. Recent studies have provided evidence of neurobehavioral, brain structural, physiologic, and neurochemical deficits in adolescent nonpsychotic high-risk relatives that may date back to childhood or earlier. These results are collectively providing a critical window into the inter-relationships between genetic predisposition, neurodevelopment, and premorbid indicators of risk in schizophrenia. Convergent approaches are inherently powerful in mutually informing each other in enriching the knowledge of the risk factors that predict the eventual onset of schizophrenia. Defining such reliable predictors of the onset of schizophrenia may provide us with the tools to better understand the etiology and pathophysiology of the illness, and may pave the way for innovative methods of treatment and possibly prevention. The authors review the relevant literature in this promising field of inquiry and summarize recent findings from high-risk studies.

Suicide in late life is an enormous public health problem that will likely increase in severity as adults of the baby boom generation age. Data from psychological autopsy studies supplemented with recent studies of suicidal ideation and attempts point to a consistent set of risk factors for the spectrum of suicidal behaviors in late life (suicide ideation, attempts, and deaths). Clinicians should be vigilant for psychiatric illness (especially depression), physical illness, pain, functional impairment, and social disconnectedness. Recent advances in late-life suicide prevention have in common collaborative, multifaceted intervention designs. We suggest that one mechanism shared by all preventive interventions shown to reduce the incidence of late-life suicide is the promotion of connectedness. For the clinician working with older adults, our recommendation is to not only consider risk factors, such as depression, and implement appropriate treatments but to enhance social connectedness as well.

The recent aging trend in the United States has resulted in an exponential growth in the number of informal dementia caregivers. Caring for a family member with dementia has been associated with negative health outcomes likely associated with physiologic changes resulting from stress. Yet caregiving is not always associated with health morbidity. In this review, we highlight resilience factors that appear to have a beneficial relationship with health outcomes. We highlight eleven studies that examined the relationship of one of three broad resilience domains (personal mastery, self-efficacy, and coping style) to caregiver health outcomes. Our main findings were that higher levels of personal mastery and self-efficacy, and increased use of positive coping strategies appear to have a protective effect on various health outcomes in dementia caregivers. Continued research is warranted to help guide prospective directions for caregiver interventions focusing on increasing caregiver resilience and the corresponding impact on caregiver health.

Eating disorders are relatively rare among the general population. This review discusses the literature on the incidence, prevalence and mortality rates of eating disorders. We searched online Medline/Pubmed, Embase and PsycINFO databases for articles published in English using several keyterms relating to eating disorders and epidemiology. Anorexia nervosa is relatively common among young women. While the overall incidence rate remained stable over the past decades, there has been an increase in the high risk-group of 15–19 year old girls. It is unclear whether this reflects earlier detection of anorexia nervosa cases or an earlier age at onset. The occurrence of bulimia nervosa might have decreased since the early nineties of the last century. All eating disorders have an elevated mortality risk; anorexia nervosa the most striking. Compared with the other eating disorders, binge eating disorder is more common among males and older individuals.

In the latter half of the 20th century, research on behavioral treatments for addictions aimed to develop and test effective treatments. Among treatments found to be at least moderately effective, direct comparisons failed to reveal consistent superiority of one approach over another. This ubiquitous finding held true despite underlying theories that differed markedly in their proposed causal processes related to patient change. In the 21st century the focus of treatment research is increasingly on how treatment works for whom, rather than whether it works. Studies of active treatment ingredients and mechanisms of behavioral change, while promising, have yielded inconsistent results. Simple mediation analysis may need to be expanded by inclusion of models testing for moderated mediation, mediated moderation, and conditional indirect effects. Examples are offered as to how these more complex models can lead to increased understanding of the conditions under which specific treatment interventions will be effective and mechanisms of change operative in improving behavioral treatments for addictions.

Molecular genetic research, building on genetic epidemiology, has provided the field of psychiatry with a host of exciting advances. It is now clear beyond any reasonable doubt that genetic inheritance influences liability to develop almost every major psychiatric disorder. Rapid progress in identifying genes contributing to psychiatric liability, recently accelerated by the advent of approaches such as genome-wide association studies and chromosomal microarray analysis, raises a critical question for psychiatric practice and training: how will molecular genetics alter the practice of psychiatry for front-line clinicians? The premise of the present review is that our growing knowledge regarding the roles of copy number variants in behavioral disorders will soon require revision of standards of evaluation and care for psychiatric patients.

Until recently, the search for genes contributing to Alzheimer's disease (AD) had been slow and disappointing, with the notable exception of the APOE ε4 allele, which increases risk and reduces the age at onset of AD in a dose-dependent fashion. Findings from genome-wide association studies (GWAS) made up of fewer than several thousand cases and controls each have not been replicated. Efforts of several consortia—each assembling much larger datasets with sufficient power to detect loci conferring small changes in AD risk—have resulted in robust associations with many novel genes involved in multiple biological pathways. Complex data mining strategies are being used to identify additional members of these pathways and gene–gene interactions contributing to AD risk. Guided by GWAS results, next-generation sequencing and functional studies are under way with the hope of helping us better understand AD pathology and providing new drug targets.

During the past two decades, the Child Psychiatry Branch at the National Institute of Mental Health has conducted a longitudinal study (including long-term prospective follow-up) of childhood-onset schizophrenia, a rare form of the disorder. Critical to this research has been accurate diagnosis. Outpatient screening has accurately diagnosed 55% of the 121 childhood-onset schizophrenia patients in the study to date. However, inpatient observation including drug-free observation has proven crucial to ruling out 96 children with alternative diagnoses who had been provisionally admitted for inpatient study. Standardized clinical ratings from outpatient screening only predicted 62% of these nonschizophrenia patients. Historically, medication-free observation was standard clinical care for difficult and unusual patients; this should be employed when possible in similar situations.

Major depressive disorder (MDD) is a common psychiatric illness with high levels of morbidity and mortality. Despite intensive research during the past several decades, the neurobiological basis and pathophysiology of depressive disorders remain unknown. Genetic factors play important roles in the development of MDD, as indicated by family, twin, and adoption studies, and may reveal important information about disease mechanisms. This article describes recent developments in the field of psychiatric genetics, with a focus on MDD. Early twin studies, linkage studies, and association studies are discussed. Recent findings from genome-wide association studies are reviewed and future directions discussed. Despite all efforts, thus far, no single genetic variation has been identified to increase the risk of depression substantially. Genetic variants are expected to have only small effects on overall disease risk, and multiple genetic factors in conjunction with environmental factors are likely necessary for the development of MDD. Future large-scale studies are needed to dissect this complex phenotype and to identify pathways involved in the etiology of MDD.

Current psychiatric disorders classifications are based exclusively on categorical models, which were designed to increase the reliability of the diagnosis. However, this system has some limitations and various psychiatric disorders may be classified using a dimensional approach, which is more appropriate when no clear boundaries exist between entities or when examining various features on a continuum. Thus, the forthcoming DSM-V appears to undertake a hybrid approach, by including categorical models associated with dimensions. We aimed to review examples of dimensions or symptom clusters, associated with a categorical approach, which could be useful in refining bipolar disorder classification. We selected predominant polarity, psychotic symptoms, inhibition/activation behavioral level and emotional reactivity to define mood episodes, impulsivity/suicidality/substance misuse and cognitive impairment. The selection was based on the fact that these dimensions or symptom clusters are currently discussed to be implemented in the DSM-V and/or may orientate towards the choice of specific treatments and represent more homogeneous and thus more appropriate sub-groups for research purpose. In the future, there will be a need to identify biomarkers that can definitively validate the use of these criteria.

Individuals with schizotypal personality disorder (SPD) share genetic, phenomenologic, and cognitive abnormalities with people diagnosed with schizophrenia. To date, 15 structural MRI studies of the brain have examined size, and 3 diffusion tensor imaging studies have examined white matter connectivity in SPD. Overall, both types of structural neuroimaging modalities have shown temporal lobe abnormalities similar to those observed in schizophrenia, while frontal lobe regions appear to show more sparing. This intriguing pattern suggests that frontal lobe sparing may suppress psychosis, which is consistent with the idea of a possible neuroprotective factor. In this paper, we review these 18 studies and discuss whether individuals with SPD who both resemble and differ from schizophrenia patients in their phenomenology, share some or all of the structural brain imaging characteristics of schizophrenia. We attempt to group the MRI abnormalities in SPD into three patterns: 1) a spectrum of severity—abnormalities are similar to those observed in schizophrenia but not so severe; 2) a spectrum of region—abnormalities affecting some, but not all, brain regions affected in schizophrenia; and 3) a spectrum of compensation—abnormalities reflecting greater-than-normal white matter volume, possibly serving as a buffer or compensatory mechanism protecting the individual with SPD from the frank psychosis observed in schizophrenia.

There is consistent evidence that the principal etiology of schizophrenia involves predisposing genetic factors. Recent years have seen several new insights in the genetics of schizophrenia. Several chromosomal regions show significant evidence that they contain schizophrenia susceptibility genes. A clinically relevant genetic subtype of schizophrenia (22q deletion syndrome) has been identified. There is new evidence that spontaneous mutations may play a role. There are new recommendations for genetic counseling. The progress to date suggests that understanding of a neurodevelopmental pathway from genetic susceptibility to schizophrenia will soon be fundamentally altered by molecular genetic advances in this complex disease.

Cigarette smoking is a major public health problem that causes more than 5 million deaths annually worldwide. Cigarette smoking is especially common among individuals with psychiatric comorbidity, including individuals with primary psychiatric disorders and other addictions. Effective behavioral and pharmacologic treatments for smoking cessation are available. Behavioral treatments including brief (< 3 minutes) counseling by physicians are effective. Seven first-line pharmacologic treatments are currently available: five nicotine replacement therapies, bupropion, and varenicline. In addition, clonidine and nortriptyline are second-line treatments for smoking cessation. These treatments increase the chances of quitting smoking by two- to threefold, supporting their use in smokers who are motivated to quit. However, effective treatments for many subpopulations, including smokers with psychiatric comorbidities as well as adolescent, pregnant, or postpartum smokers, remain to be developed and represent an important challenge.

The capacity to deliver some forms of behavioral treatment via computers may prove to be a small revolution in the delivery of mental health care. Although early research on the efficacy of these approaches has yielded mixed results, this new strategy offers tremendous potential to provide empirically supported therapies to many individuals who would never access psychiatric care, to extend the time and expertise of clinicians, and to offer improved care and monitoring. However, the great promise of computer-assisted therapies may be diminished if their benefits are overstated or if they are broadly released or disseminated before being carefully evaluated using the same methodologic standards that are requirements for evaluating clinician-delivered therapies. In this article, we review the current status of empiric support for computer-assisted therapies, advocating for enhanced rigor to identify those that are most effective, as well as the need to more thoroughly assess possible adverse effects, recognizing that even a modestly effective computer-assisted intervention could have enormous impact.

Alcohol and other drug use among adolescents has been a public health problem for decades. Although some substance use may be developmentally routine, a concerning number of adolescents meet criteria for a substance use disorder and could greatly benefit from a quality treatment experience. However, parents and health care providers want evidence of the efficacy of adolescent-specific treatment programs. This review summarizes four factors surrounding the efficacy of current adolescent treatment programs: 1) adolescent-specific treatment services; 2) the variety of therapeutic modalities; 3) relapse and recovery rates; and 4) the need for evidence-based, quality assessments and research. Current adolescent treatment efforts are summarized, and the recent literature regarding the efficacy of adolescent treatment and recovery rates is discussed.

Information and communication technologies offer clinicians the opportunity to work with patients to manage chronic conditions, including addiction. The early research on the efficacy of electronic treatment and support tools is promising. Sensors have recently received increased attention as key components of electronic treatment and recovery management systems. Although results of the research are very promising, concerns at the clinical and policy level must be addressed before widespread adoption of these technologies can become practical. First, clinicians must adapt their practices to incorporate a continuing flow of patient information. Second, payment and regulatory systems must make adjustments far beyond what telemedicine and electronic medical records have required. This paper examines potential roles of information and communication technologies as well as process and regulatory challenges.