Article

Structure of genetic and environmental risk factors for dimensional representations of DSM-IV anxiety disorders

Department of Mental Health, Norwegian Institute of Public Health, Box 4404 Nydalen, 0403 Oslo 3, Norway.
The British journal of psychiatry: the journal of mental science (Impact Factor: 7.34). 10/2009; 195(4):301-7. DOI: 10.1192/bjp.bp.108.059485
Source: PubMed

ABSTRACT Twin data permit decomposition of comorbidity into genetically and environmentally derived correlations. No previous twin study includes all major forms of anxiety disorder.
To estimate the degree to which genetic and environmental risk factors are shared rather than unique to dimensionally scored panic disorder, generalised anxiety disorder, phobias, obsessive-compulsive disorder and post-traumatic stress disorder.
Data obtained from 2801 young-adult Norwegian twins by means of the Composite International Diagnostic Interview were analysed with the Mx program.
A multivariate common factor model fitted best. The latent liability to all anxiety disorders was substantially more heritable (54%) than the individual disorders (23% to 40%). Most of the genetic effect was common to the disorders. Genes contributed just over 50% to the covariance between liabilities.
The five anxiety disorders all share genetic and environmental risk factors. This has implications for the revision of the anxiety disorder section in DSM-V.

0 Followers
 · 
125 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: Obsessive-compulsive disorder (OCD) has long been an enigma in the psychopathology of anxiety. This chapter describes the clinical features of obsessions and compulsions, and how they differ from related clinical phenomena such as pathological worry, normal intrusive thoughts, and rumination. It presents three clinical vignettes that illustrate the widely varying symptom profile of OCD. The DSM-5 debate on the removal of OCD from the anxiety disorders classification based on issues of differential diagnosis and comorbidity is discussed and this is followed by a brief review of epidemiology and clinical features of OCD. The chapter also talks about theory and research on the etiology of OCD with a focus on genetics, neurophysiology, and cognitive-behavioral theory and research on OCD. Four distinct symptom subtypes identified based on structural analysis of self-report and symptom interviews are described. The chapter concludes with summary remarks and future directions for advancing our understanding of the disorder.
    THE WILEY HANDBOOK OF ANXIETY DISORDERS, Edited by Paul Emmelkamp and Thomas Ehring, 01/2014: pages 497–534; John Wiley & Sons, Ltd.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Anxiety symptoms and syndromes are common in bipolar disorders, occurring in over half of all subjects with bipolar disorder type I. Despite methodological and diagnostic inconsistencies, most studies have shown a robust association between the presence of a broadly defined comorbid anxiety disorder and important indices of clinical morbidity in bipolar disorder, including a greater number of depressive episodes, worse treatment outcomes, and elevated risk of attempting suicide. Anxiety symptoms and/or syndromes often precede the onset of bipolar disorder and may represent a clinical phenotype of increased risk in subjects with prodromal symptoms. Although the causal relationship between anxiety and bipolar disorders remains unresolved, the multifactorial nature of most psychiatric phenotypes suggests that even with progress towards more biologically valid phenotypes, the "phenomenon" of comorbidity is likely to remain a clinical reality. Treatment studies of bipolar patients with comorbid anxiety have begun to provide preliminary evidence for the role of specific pharmacological and psychotherapeutic treatments, but these need to be confirmed in more definitive trials. Hence, there is an immediate need for further research to help guide assessment and help identify appropriate treatments for comorbid conditions.
    Current Psychiatry Reports 02/2015; 17(2):540. DOI:10.1007/s11920-014-0540-2 · 3.05 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: This review brings together recent research from molecular, neural circuit, animal model, and human studies to help understand the neurodevelopmental mechanisms underlying social anxiety disorder. Social anxiety disorder is common and debilitating, and it often leads to further psychopathology. Numerous studies have demonstrated that extremely behaviorally inhibited and temperamentally anxious young children are at marked risk of developing social anxiety disorder. Recent work in human and nonhuman primates has identified a distributed brain network that underlies early-life anxiety including the central nucleus of the amygdala, the anterior hippocampus, and the orbitofrontal cortex. Studies in nonhuman primates have demonstrated that alterations in this circuit are trait-like in that they are stable over time and across contexts. Notably, the components of this circuit are differentially influenced by heritable and environmental factors, and specific lesion studies have demonstrated a causal role for multiple components of the circuit. Molecular studies in rodents and primates point to disrupted neurodevelopmental and neuroplastic processes within critical components of the early-life dispositional anxiety neural circuit. The possibility of identifying an early-life at-risk phenotype, along with an understanding of its neurobiology, provides an unusual opportunity to conceptualize novel preventive intervention strategies aimed at reducing the suffering of anxious children and preventing them from developing further psychopathology.
    American Journal of Psychiatry 08/2014; 171(11). DOI:10.1176/appi.ajp.2014.14040449 · 13.56 Impact Factor

Full-text (2 Sources)

Download
51 Downloads
Available from
May 23, 2014