This systematic review aimed to compare acceptance and commitment therapy (ACT) andcognitive behavioral therapy (CBT) as a treatment for anxiety disorders by means of asystematic review of the existing literature. Studies were identified by searching thedatabases of PsycINFO and PubMed. RCT studies comparing CBT and ACT as treatmentsfor anxiety disorders were included in the study. Seven studies met the inclusions criteria. Allseven studies showed that both CBT and ACT significantly improved psychological health.No statistically significant differences between the two treatment modalities was evident. Theresults suggest that ACT can be used as a viable treatment for individuals suffering fromanxiety disorder. / Denna systematiska litteraturstudie ämnar jämföra Acceptance and commitment therapy (ACT) och Kognitiv beteendeterapi (KBT) för behandling av ångestsyndrom. RCT studier med avsikt att jämföra KBT och ACT som behandlingsintervention identifierades genomsökningar på databaserna PsycINFO och PubMed samt inkluderades i uppsatsen. Artikelsökningen resulterade i 7 studier som matchade inklusionskriterierna. Samtliga studier påvisade att KBT och ACT signifikant förbättrade deltagarnas psykiska hälsa. Dock så återfanns ingen signifikant skillnad i en gruppjämförelse mellan behandlingsinterventionerna. Resultatet från denna systematiska litteraturstudie visar på att det finns en medelhög till högvetenskaplig evidens som pekar på små till inga skillnader mellan ACT och KBT på ångestsyndrom. ACT kan potentiellt användas som en likvärdig alternativ till guldstandarden KBT för behandling av ångestrelaterad problematik.

Background: Emotion regulation has been identified as a major contributor to the development of psychopathology and, by extension, to understanding the positive effects of various psychotherapy mechanisms. Little work has been done, however, on the extent to which individual components of emotion regulation operate as prognostic factors in psychological treatment. Context sensitivity and reflective functioning are emerging as important aspects of adaptive emotion regulation capacity and may be related to a portion of patient therapy outcome when investigated as a patient characteristic. Design and Participants: A sample of 130 adults seeking treatment for depression and anxiety through a digital psychotherapy provider were recruited to participate. Individuals presenting with comorbid severe mental illness or psychosis, significant substance abuse concerns, active suicidal ideation, and active manic states were excluded from participation. Methods: Participants completed individual difference measures for Five-factor Personality, reflective functioning (i.e., Reflective Functioning Questionnaire; RFQ), and the context sensitivity (i.e., Context Sensitivity Index; CSI), and were followed over three months of psychotherapy. Clinical outcomes were measured with diagnosis-specific symptom measures such as the PHQ-9 for depression and the GAD-7 for anxiety at baseline and then every 3 weeks for the duration of treatment. Results: Participants reported significant improvement in depression and anxiety symptoms after three months of treatment (p < .001). CSI and RFQ scores were unassociated with baseline symptom severity. Certainty about others’ thoughts, an RFQ subscale, was inversely associated with outcome (p < .05). CSI scores were unassociated with treatment outcome at 3 months. Lack of insight, an RFQ subscale, significantly improved as a result of treatment when baseline symptoms were high (p < .05). Conclusions: Reflective functioning may be a promising patient characteristic for explaining a modest portion of treatment outcome. Lack of emotional insight improved meaningfully as a result of treatment for individuals with more severe depression and anxiety at baseline. Further research is needed to investigate aspects of emotion regulation as a route towards better understanding outcome in psychotherapy.

The common mental disorders (CMDs) which include non-psychotic depression and anxiety-related disorders aggregate mental illnesses commonly seen together without assuming clear diagnostic boundaries. Thus, it provides an excellent platform for a symptom-level investigation of common suffering in regions where the current Western-based diagnostic categories may not apply. This current study investigates the symptom networks of CMDs among adult primary care patients in India, using data from a clinical trial testing the effectiveness of a collaborative stepped-care intervention led by lay health counselors. Network modeling was used to investigate a) symptom centralities, b) boundaries between depression and anxiety-related disorders, and c) baseline differences in network configurations across gender, public versus private health care settings, and treatment response over one-year of follow-up. Intense anxiety/panic and fatigue were the most central symptoms overall. While panic and depressed mood were the most central in public health care settings, fatigue and depressed mood were most central in private settings. Overall, findings indicate central symptoms might differ across cultures and socioeconomic groups. To the knowledge of this current author, this is the first study investigating the symptom networks of CMDs among primary care patients in India.

No description available.

Objective: This study examined whether overt and relational peer victimization were associated with the severity of Social Phobia (SoP) symptoms and whether frequent victimization was more common among youth with SoP as compared to youth with other anxiety disorders. In addition, the study examined whether self-esteem, peer beliefs, and emotional lability were linked to internalizing symptoms above and beyond overt and relational victimization severity. Method: Participants were 90 youth (47 boys, 43 girls; M age = 11.06 years; SD = 3.09) and their parents. Youth had been referred to an outpatient child and adolescent anxiety disorders clinic. Measures included (a) a semi-structured diagnostic interview, (b) youth self-report forms assessing peer victimization, anxiety, depressive symptoms, loneliness, and global self-worth, and (c) parent-report forms assessing anxiety and emotion regulation. Results: Results showed a concurrent positive association between peer victimization and self-reported social anxiety, with relational victimization providing unique information above and beyond overt victimization. Peer victimization was not associated with a specific diagnosis, but was related to multiple internalizing problems (negative beliefs about the peer group accounted for some of this relation). Conclusions: Peer victimization is important to assess for and consider in the treatment of childhood and adolescent anxiety disorders. Peer victimization is associated with social anxiety symptoms, and relational victimization, in particular, is associated with internalizing problems among youth with anxiety disorders. Victimization appears to be associated with symptomatology rather than diagnosis. / Psychology

Research from the information processing and temperament literatures has proposed dysfunction within systems of attention, including early attentional orientation (bottom-up) and later executive control of attention (top-down), in contribution toward the development of anxiety disorders. This study investigated the moderating role of attentional control on the relationship between threat-related attention bias and youth anxiety severity. Participants were 107 treatment-seeking youth (7-17 years, Mage = 11.17 years, SD = 3.06; 41.4% male) who met diagnostic criteria for an anxiety disorder. Multimodal assessment (behavioral, youth-, and parent-report) of attention control, threat-related attention bias, and anxiety severity was conducted. Hierarchical regression analyses provided little support for attention control as a moderator of the relationship between threat-related attention bias and anxiety severity. However, attention control was identified as a more salient predictor of anxiety severity than threat-related attention bias. Measures of attention were identified as distinct from parent-reported symptoms of attention-deficit/hyperactivity disorder (ADHD) and depression for youth. Similarly, measures of attention and anxiety severity for youth were not related to parenting behavior or parental attention control but were influenced by parents’ self-reported symptoms of anxiety and depression. Implications for future research and clinical work are discussed. / Psychology

Thesis (PhD)--Stellenbosch University, 2014. / ENGLISH ABSTRACT: The etiology of anxiety disorders remains incompletely understood. Clear evidence for a genetic component has been proposed; however, there is also an increasing focus on environmental factors and the interaction between these and the genetic components that may mediate (anxiety) disorder pathogenesis. No single gene or genetic component has been explicitly identified as being involved in the development of anxiety disorders. This is most likely due to a number of reasons, which include, for example, the heterogeneity of anxiety disorders, the contribution of environmental factors and methodological limitations (e.g. small sample size) of research studies. Until now, genetic association studies usually focused on one particular psychiatric disorder at a time. However, with the difficulty in identifying susceptibility genes and/or loci in heterogeneous disorders like obsessive-compulsive disorder and other conditions in the anxiety spectrum, it is perhaps timely to consider multivariate genetics and epidemiological studies in a number of disorders sharing a core characteristic – such as anxiety. In addition to genetic underpinnings, a number of environmental variables have also been identified as risk factors for pathological anxiety, including adverse life events like childhood physical and sexual abuse. The hypothesis for this project is that a pre-existing genetic vulnerability (or genetic risk) interacts with the impact of adverse life events to result in the development of one or more anxiety disorder(s). Considering phenotypic overlap amongst the anxiety disorders, it is likely that diverse networks of genes and/ or interacting pathways are responsible for the phenotypic manifestations observed. Sprague Dawley rats exhibiting behaviours indicative of anxiety in the context of environmental stressors (maternal separation and restraint stress) were used as model for the identification of novel susceptibility genes for anxiety disorders in humans. The striatum has previously been implicated as a candidate in the brain architecture of anxiety pathogenicity, and is also a site exhibiting a high degree of synaptic plasticity. The synaptic plasticity pathway was investigated using the dorsal striatum of the rat brain and several genes were identified to be aberrantly expressed in “anxious” rats relative to controls (Mmp9, Bdnf, Ntf4, Egr2, Egr4, Grm2 and Arc). In humans, it was found that the severity of early adversity was significantly and positively associated with the presence of an anxiety disorder in adulthood. When the human homologues of the susceptibility candidate genes that were identified using the animal model were screened in a human cohort of patients with obsessive-compulsive disorder (OCD), panic disorder (PD) or social anxiety disorder (SAD) (relative to controls), five single nucleotide polymorphisms (SNPs) were found to be significantly associated with these conditions. Four of these SNPs were also found to significantly interact with the severity of childhood trauma. Haplotype analysis of variants within the identified susceptibility candidates revealed novel haplotype associations, four of which are located in the MMP9 gene. Notably, this the first study to link these particular mutations in the MMP9 gene with anxiety disorders and this finding is consistent with previous work suggesting that MMP9 is involved in conditions like cardiovascular disease and cancer which have been associated with increased prevalence of anxiety disorders. In conclusion, this project yielded important findings pertaining to the etiology of anxiety disorders. The use of a combined anxiety disorders cohort (OCD, PD and SAD) may suggest that the associations found here may hold true for anxiety disorders in general and not only for a particular clinically delineated condition. Childhood trauma was confirmed as an increased susceptibility risk for anxiety disorders. Also, this research contributed several novel susceptibility genes (MMP9, EGR2, EGR4, NTF4, and ARC), five significant SNP associations, four significant SNP-environment interactions and five haplotype associations (within MMP9 and BDNF) as candidates for anxiety pathogenicity. The identified polymorphisms and haplotypes were demonstrated to be associated with susceptibility to anxiety disorders in a gene-environment correlation and gene-environment interaction. / AFRIKAANSE OPSOMMING: Die oorsake van angssteurings word steeds nie volledig verstaan nie. Daar is duidelike bewyse vir 'n genetiese komponent, maar daar is ook toenemende fokus op omgewingsfaktore en die interaksie tussen hierdie omgewingsfaktore en genetiese komponente by angssteurings. Geen enkele geen of genetiese komponent is al geïdentifiseer as diè wat betrokke is by die ontwikkeling van angssteurings nie. Dit is waarskynlik weens 'n aantal redes, wat byvoorbeeld, die heterogeneïteit van angssteurings, die bydrae van omgewingsfaktore en metodologiese beperkings (bv. klein steekproef) van die navorsingstudies, insluit. Verder het genetiese assosiasiestudies tot nou toe gewoonlik net op een spesifieke psigiatriese versteuring op 'n slag gefokus. Maar, gegewe die uitdaging om vatbaarheidsgene en / of loci in heterogene steurings soos obsessief – kompulsiewe steuring (OKV) en ander toestande op die angsspektrum te identifiseer, is dit tyd om genetiese en kliniese studies in ‘n aantal steurings - met ‘n oorvleuende kern-element soos angs -, gesamentlik te oorweeg. Bykomend tot die genetiese boustene, is ‘n aantal omgewingsveranderlikes soos traumatiese lewenservarings tydens die kinderjare as risikofaktore vir patologiese angs geidentifiseer. Die hipotese vir hierdie projek is dat daar 'n interaksie tussen genetiese kwesbaarheid (of genetiese risiko) en traumatiese lewensevarings is en dat dit tot die ontwikkeling van 'n / veelvoudige angssteuring(s) kan lei. Inaggenome die fenotipiese oorvleueling tussen die angssteurings, is dit waarskynlik dat diverse netwerke van gene en / of interaktiewe geen-paaie vir die manifestasie van hierdie toestande verantwoordelik is. Sprague Dawley-rotte met gedragswyses aanduidend van angs, in die konteks van omgewingstressore (d.i. skeiding van die ma-rot en bedwang-stres [restraint stress]), is as model gebruik vir die identifisering van nuwe vatbaarheidsgene vir angssteurings in mense. Die striatum is voorheen as ‘n kandidaat in die brein-argitektuur van patologiese angs voorgehou, en is ook ‘n plek met ‘n hoë mate van sinaptiese plastisiteit. Die sinaptiese plastisiteit is ondersoek deur te fokus op die dorsale striatum van die rotbrein en daar is verskeie gene gevind wat anders is in “angstige” rotte in vergelyking met kontroles (Mmp9, Bdnf, Ntf4, Egr2, Egr4, Grm2 en Arc). In mense is daar gevind dat die ernstigheidsgraad van vroeë trauma beduidend en positief met die teenwoordigheid van ‘n angssteuring tydens volwassenheid verband hou. Toe die menslike ekwivalente van die vatbaarheidsgene wat met die dieremodel geïdentifiseer is in ‘n mens-kohort met obsessief-kompulsiewe steuring (OKS), panieksteuring (PS) en sosiale angssteuring (SAS) ondersoek is, is gevind dat daar 5 enkele nukleotied polimorfismes (ENPs) is wat met die toestande verband hou. Daar is ook gevind dat vier van hierdie ENPs beduidend verband hou met die ernstigheidsgraad van trauma tydens die kinderjare. Haplotipe analise van variante binne die geïdentifiseerde vatbaarheidsgene het op nuwe haplotipe assosiasies – waarvan 4 op die MMP9-geen geleë is – gedui. Hierdie is dus die eerste studie wat gevind het dat dié spesifieke mutasies van die MMP9-geen met angssteurings verband hou. Hierdie bevinding strook met vorige werk wat daarop dui dat die MMP9-geen by toestande soos kardiovaskulêre siekte en kanker wat ook met verhoogde voorkoms van angssteurings verband hou, betrokke is. Ter afsluiting kan ons sê dat hierdie projek belangrike bevindinge oor die oorsake van angssteurings gemaak het. Die gebruik van ‘n gekombineerde angssteurings-kohort (OKS. PS en SAS) kan moontlik suggereer dat die assosiasies wat ons hier gevind het, waar is vir alle angssteurings en nie net vir ‘n spesifieke afgebakende toestand nie. Traumatiese ervarings tydens die kinderjare is ook bevestig as ‘n risiko vir die ontwikkeling van angssteurings. Hierdie navorsing het ook verskeie nuwe vatbaarheidsgene (MMP9, EGR2, EGR4, NTF4, en ARC), 5 beduidende ENP assosiasies, 4 beduidende ENP-omgewings-interaksies en 5 haplotipe assosiasies (by MMP9 en BDNF) geïdentifiseer as moontlike kandidate wat ‘n rol speel by die ontstaan van patologiese angs. Daar is ook gevind dat die geïdentifiseerde polimorfismes en haplotipes met vatbaarheid vir angssteurings in ‘n geen-omgewing- korrelasie en geen-omgewing- interaksie verband hou. Stellenbosch University http://scholar.sun.ac.za

This study examined the mediating role of Maladaptive Emotion-focused coping (MEFC) on the relationship between Early Maladaptive Schemas (EMS), anxiety and depression.

Research shows that anxiety disorders are common and problematic in children. Treatment studies demonstrate that cognitive-behavioural interventions for children can successfully minimise these problems. Further, when implemented as early intervention or prevention programs, these interventions can prevent the onset of anxiety problems in 7 to 14 year olds and reduce existing levels of anxiety. This type of preventive approach has enormous potential for improving community mental health in a low cost model of service delivery. Yet, to develop this as a viable service model, these programs need to be evaluated under 'real world' conditions as opposed to specialist university clinical teams. In this research, the long-term effectiveness of an ecological model of the prevention of anxiety disorders for children was conducted. In the first study, teachers (N = 17) were trained intensively in the principles of anxiety and the FRIENDS anxiety prevention program (Barrett, Lowry-Webster & Holmes, 1999). Measures were taken of the PROXIMAL effects of training on the knowledge and self-efficacy of participating teachers at two points in time. Compared to teachers in a control group (N= 17) and a group comprised of psychologists regarded as experts in the FRIENDS anxiety program (N= 22), trained teachers demonstrated significant increases in the levels of knowledge and self-efficacy at time two. These increases approached levels exhibited by experts in terms of knowledge, and were not significantly different from experts in their levels of self-efficacy to implement the FRIENDS program following training. This study also explored the quality or fidelity of program implementation by these trained teachers (INTERMEDIATE EFFECTS). Results demonstrated that trained teachers implemented the program with high levels of integrity in accordance with the FRIENDS intervention manual. The second study sought to investigate the outcomes for participating children in terms of actually preventing and reducing existing levels of anxiety. Also of interest was the impact this intervention had on levels of depression. Participants were 594 children aged 10-13 years from 7 schools in Brisbane Australia. Children, and parents reported on children's social, emotional and behavioural characteristics at three-assessment points over 12 months. Results were examined universally (for all children) and for children who scored above the clinical cut-off for anxiety at pre-test. Results revealed that children in the FRIENDS intervention group reported fewer anxiety symptoms regardless of their risk status at posttest. In terms of reported levels of depression, only the high anxiety group who completed the FRIENDS intervention evidenced significant improvements at posttest. The results indicated that intervention gains were maintained over a period of 12 months, as measured by self-reports and diagnostic interviews. Moreover, evidence of a prevention effect was also demonstrated, with a significantly greater percentage of children in the control group progressed to "at risk" or "remained at risk" compared to children in the intervention group. Additionally, 85% of children in the intervention group who were scoring above the clinical cut-off for anxiety and depression were diagnosis free in the intervention condition at 12-month follow-up, compared to only 31.2% of children in the control group. Implications of these findings are examined, alongside limitations of the study and directions for future research.

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2006. / Härtill 4 uppsatser.