Trait Affect, Emotion Regulation, and the Generation of Negative and Positive Interpersonal Events.

Positive and negative trait affect and emotion regulatory strategies have received considerable attention in the literature as predictors of psychopathology. However, it remains unclear whether individuals' trait affect is associated with responses to state positive affect (positive rumination and dampening) or negative affect (ruminative brooding), or whether these affective experiences contribute to negative or positive interpersonal event generation. Among 304 late adolescents, path analyses indicated that individuals with higher trait negative affect utilized dampening and brooding rumination responses, whereas those with higher trait positive affect engaged in rumination on positive affect. Further, there were indirect relationships between trait negative affect and fewer positive and negative interpersonal events via dampening, and between trait positive affect and greater positive and negative interpersonal events via positive rumination. These findings suggest that individuals' trait negative and positive affect may be associated with increased utilization of emotion regulation strategies for managing these affects, which may contribute to the occurrence of positive and negative events in interpersonal relationships.

Cognitive Attributions in Depression: Bridging the Gap between Research and Clinical Practice.

Individuals seeking treatment for depression often are struggling with maladaptive cognitions that impact how they view themselves and the world. Research on cognitive attributions that underlie depressed mood focuses on the phenomenon of negative cognitive style, in which depressed people tend to view undesirable occurrences in life as having internal, stable, and global causes. Based on research, clinicians have developed various techniques that seek to modify depressive attributions in order to alleviate symptoms of depression. In this article, the authors review the literature on attributions in depression, present clinically relevant interventions based on empirical support, provide case examples, and summarize future directions and recommendations for researchers and practitioners.

The Relationship Between Family Functioning and Adolescent Depressive Symptoms: The Role of Emotional Clarity.

Emotion regulation has been implicated in the etiology of depression. A first step in adaptive emotion regulation involves emotional clarity, the ability to recognize and differentiate one's emotional experience. As family members are critical in facilitating emotional understanding and communication, we examined the impact of family functioning on adolescent emotional clarity and depressive symptoms. We followed 364 adolescents (ages 14-17; 52.5% female; 51.4 % Caucasian, 48.6% African American) and their mothers over 2 years (3 time points) and assessed emotional clarity, depressive symptoms, and adolescents' and mothers' reports of family functioning. Emotional clarity mediated the relationship between adolescents' reports of family functioning and depressive symptoms at all time points cross-sectionally, and according to mothers' reports of family functioning at Time 1 only. There was no evidence of longitudinal mediation for adolescents' or mothers' reports of family functioning. Thus, family functioning, emotional clarity, and depressive symptoms are strongly related constructs during various time points in adolescence, which has important implications for intervention, especially within the family unit.

Deficits in Emotional Clarity and Vulnerability to Peer Victimization and Internalizing Symptoms Among Early Adolescents.

Peer victimization is a significant risk factor for a range of negative outcomes during adolescence, including depression and anxiety. Recent research has evaluated individual characteristics that heighten the risk of experiencing peer victimization. However, the role of emotional clarity, or the ability to understand one's emotions, in being the target of peer victimization remains unclear. Thus, the present study evaluated whether deficits in emotional clarity increased the risk of experiencing peer victimization, particularly among adolescent girls, which, in turn, contributed to prospective levels of depressive and anxiety symptoms. In the present study, 355 early adolescents (ages 12-13; 53% female; 51% African American) who were part of the Adolescent Cognition and Emotion project completed measures of emotional clarity, depressive symptoms, and anxiety symptoms at baseline, and measures of peer victimization, depressive symptoms, and anxiety symptoms at follow-up. Moderation analyses indicated that deficits in emotional clarity predicted greater peer victimization among adolescent girls, but not adolescent boys. Moderated mediation analyses revealed that deficits in emotional clarity contributed to relational peer victimization, which, in turn, predicted prospective levels of depressive and anxiety symptoms among adolescent girls, but not boys. These findings indicate that deficits in emotional clarity represent a significant risk factor for adolescent girls to experience relational peer victimization, which, in turn, contributed to prospective levels of internalizing symptoms. Thus, prevention programs should target deficits in emotional clarity to prevent peer victimization and subsequent internalizing symptoms among adolescent girls.

The cyclical nature of depressed mood and future risk: Depression, rumination, and deficits in emotional clarity in adolescent girls.

Deficits in emotional clarity, the understanding and awareness of one's own emotions and the ability to label them appropriately, are associated with increased depressive symptoms. Surprisingly, few studies have examined factors associated with reduction in emotional clarity for adolescents, such as depressed mood and ruminative response styles. The present study examined rumination as a potential mediator of the relationship between depressive symptoms and changes in emotional clarity, focusing on sex differences. Participants included 223 adolescents (51.60% female, Mean age = 12.39). Controlling for baseline levels of emotional clarity, initial depressive symptoms predicted decreases in emotional clarity. Further, rumination prospectively mediated the relationship between baseline depressive symptoms and follow-up emotional clarity for girls, but not boys. Findings suggest that depressive symptoms may increase girls' tendencies to engage in repetitive, negative thinking, which may reduce the ability to understand and label emotions, a potentially cyclical process that confers vulnerability to future depression.

Exploring the Association Between Obsessive-Compulsive Symptoms and Loneliness: Consideration of Specificity and Gender.

Loneliness, or perceived social isolation, is associated with a range of adverse physical and emotional outcomes. In particular, feeling lonely has been linked with anxiety, anger, stress, and depressive symptoms. Although loneliness has been extensively investigated with respect to depression and social anxiety, few studies have considered the relationship between loneliness and obsessive-compulsive symptoms (OCS). Loneliness may be particularly relevant to OCS given the social stigma associated with obsessions and compulsions along with high comorbidity between OCS and depression. The overarching aim of this investigation was to examine the relationship between OCS and loneliness in a young adult sample (N = 395) recruited from a large university. Participants completed self-report measures of OCS, loneliness, depression, and social anxiety. Higher levels of OCS were associated with greater perceived loneliness, and this relationship remained significant despite controlling for depression and social anxiety. OCS had a significant association with the isolation facet of loneliness, and loneliness in turn was uniquely associated with obsessions and checking symptoms. Gender differences were examined, which indicated that females with high OCS endorsed the greatest levels of loneliness. Implications for clinical research and treatment are discussed.

Common and rare alleles of the serotonin transporter gene, SLC6A4, associated with Tourette's disorder.

To evaluate the hypothesis that functionally over-expressing alleles of the serotonin transporter (SERT) gene (solute carrier family 6, member 4, SLC6A4) are present in Tourette's disorder (TD), just as we previously observed in obsessive compulsive disorder (OCD), we evaluated TD probands (N = 151) and controls (N = 858). We genotyped the refined SERT-linked polymorphic region 5-HTTLPR/rs25531 and the associated rs25532 variant in the SLC6A4 promoter plus the rare coding variant SERT isoleucine-to-valine at position 425 (I425V). The higher expressing 5-HTTLPR/rs25531 LA allele was more prevalent in TD probands than in controls (χ(2) = 5.75; P = 0.017; odds ratio [OR], 1.35); and, in a secondary analysis, surprisingly, it was significantly more frequent in probands who had TD alone than in those who had TD plus OCD (Fisher's exact test; P = 0.0006; OR, 2.29). Likewise, the higher expressing LAC haplotype (5-HTTLPR/rs25531/rs25532) was more frequent in TD probands than in controls (P = 0.024; OR, 1.33) and also in the TD alone group versus the TD plus OCD group (P = 0.0013; OR, 2.14). Furthermore, the rare gain-of-function SERT I425V variant was observed in 3 male siblings with TD and/or OCD and in their father. Thus, the cumulative count of SERT I425V becomes 1.57% in OCD/TD spectrum conditions versus 0.15% in controls, with a recalculated, family-adjusted significance of χ(2) = 15.03 (P < 0.0001; OR, 9.0; total worldwide genotyped, 2914). This report provides a unique combination of common and rare variants in one gene in TD, all of which are associated with SERT gain of function. Thus, altered SERT activity represents a potential contributor to serotonergic abnormalities in TD. The present results call for replication in a similarly intensively evaluated sample. © 2013 Movement Disorder Society.

Anxiety and affective disorder comorbidity related to serotonin and other neurotransmitter systems: obsessive-compulsive disorder as an example of overlapping clinical and genetic heterogeneity.

Individuals with obsessive-compulsive disorder (OCD) have also been shown to have comorbid lifetime diagnoses of major depressive disorder (MDD; rates greater than 70%), bipolar disorder (rates greater than 10%) and other anxiety disorders (e.g. panic disorder, post-traumatic stress disorder (PTSD)). In addition, overlap exists in some common genetic variants (e.g. the serotonin transporter gene (SLC6A4), the brain-derived neurotrophic factor (BDNF) gene), and rare variants in genes/chromosomal abnormalities (e.g. the 22q11 microdeletion syndrome) found across the affective/anxiety disorder spectrums. OCD has been proposed as a possible independent entity for DSM-5, but by others thought best retained as an anxiety disorder subtype (its current designation in DSM-IV), and yet by others considered best in the affective disorder spectrum. This review focuses on OCD, a well-studied but still puzzling heterogeneous disorder, regarding alterations in serotonergic, dopaminergic and glutamatergic neurotransmission in addition to other systems involved, and how related genes may be involved in the comorbidity of anxiety and affective disorders. OCD resembles disorders such as depression, in which gene × gene interactions, gene × environment interactions and stress elements coalesce to yield OC symptoms and, in some individuals, full-blown OCD with multiple comorbid disorders.

Rare missense neuronal cadherin gene (CDH2) variants in specific obsessive-compulsive disorder and Tourette disorder phenotypes.

The recent finding that the neuronal cadherin gene CDH2 confers a highly significant risk for canine compulsive disorder led us to investigate whether missense variants within the human ortholog CDH2 are associated with altered susceptibility to obsessive-compulsive disorder (OCD), Tourette disorder (TD) and related disorders. Exon resequencing of CDH2 in 320 individuals identified four non-synonymous single-nucleotide variants, which were subsequently genotyped in OCD probands, Tourette disorder probands and relatives, and healthy controls (total N=1161). None of the four variants was significantly associated with either OCD or TD. One variant, N706S, was found only in the OCD/TD groups, but not in controls. By examining clinical data, we found there were significant TD-related phenotype differences between those OCD probands with and without the N845S variant with regard to the co-occurrence of TD (Fisher's exact test P=0.014, OR=6.03). Both N706S and N845S variants conferred reduced CDH2 protein expression in transfected cells. Although our data provide no overall support for association of CDH2 rare variants in these disorders considered as single entities, the clinical features and severity of probands carrying the uncommon non-synonymous variants suggest that CDH2, along with other cadherin and cell adhesion genes, is an interesting gene to pursue as a plausible contributor to OCD, TD and related disorders with repetitive behaviors, including autism spectrum disorders.

Phenomenological features and clinical impact of affective disorders in OCD: a focus on the bipolar disorder and OCD connection.

BACKGROUND: Given the general population prevalence rates of obsessive compulsive disorder (OCD) and the affective disorders, one would expect the co-occurrence of these syndromes to be rare. Yet findings by our group and others have revealed extremely high rates of comorbidity in OCD with both depressive disorders (DD; 50%) and bipolar disorder (BPD; 10%). The current investigation sought to further clarify the role affective disorder comorbidity-particularly that with BPD-may play in the clinical expression of OCD. METHOD: A total of 605 individuals with OCD were evaluated with the Structured Clinical Interview for DSM-IV. The sample included three groups: BPD (bipolar I or II; N = 79, 13.1%), DD (major depression or dysthymia; N = 388, 64.1%), and NAD (no affective disorder comorbidity; N = 138, 22.8%). Group-wise comparisons were conducted on comorbidity patterns, impairment measures, and clinical features of OCD. RESULTS: Analyses revealed a graded severity pattern, with the BPD group as the most severe, followed by the DD group, and finally the NAD group. Severity was reflected by the total number of Axis I disorders (P<.01), the number of psychiatric hospitalizations (P<.001), impairment measures (Ps<.05), and OCD symptoms (P<.01). It is worth noting that the impairment and OCD symptom severity findings were not attributable to the higher level of nonmood disorder comorbidities in the BPD and DD groups. RESULTS: Those individuals with comorbid affective disorders, particularly BPD, represent a clinically severe group compared to those without such comorbidity. Clarifying the phenomenological features of OCD-affective disorder comorbidity has important etiological and treatment implications.