期刊
JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY
卷 61, 期 9, 页码 979-987出版社
WILEY
DOI: 10.1111/jcpp.13183
关键词
Obsessive-compulsive disorder; anxiety sensitivity; adolescence; aetiology; genetics
资金
- W T Grant Foundation
- University of London Central Research fund
- UK Medical Research Council (MRC) [G81/343, MR/M021475/1, G120/635]
- MRC Clinical Research Training Fellowship [MR/N001400/1]
- National Institute for Health Research (NIHR) Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and King's College London
- Johnson's Baby
- MRC [G120/635, MR/N001400/1, MR/M021475/1] Funding Source: UKRI
Background Anxiety sensitivity, the tendency to fear the symptoms of anxiety, is a key risk factor for the development anxiety disorders. Although obsessive-compulsive disorder was previously classified as an anxiety disorder, the prospective relationship between anxiety sensitivity and obsessive-compulsive symptoms (OCS) has been largely overlooked. Furthermore, a lack of genetically informative studies means the aetiology of the link between anxiety sensitivity and OCS remains unclear. Methods Adolescent twins and siblings (N = 1,579) from the G1219 study completed self-report questionnaires two years apart assessing anxiety sensitivity, OCS, anxiety and depression. Linear regression models tested prospective associations between anxiety sensitivity and OCS, with and without adjustment for anxiety and depressive symptoms. A phenotypic cross-lagged model assessed bidirectional influences between anxiety sensitivity and OCS over time, and a genetic version of this model examined the aetiology of these associations. Results Anxiety sensitivity was prospectively associated with changes in OCS, even after controlling for comorbid anxiety and depressive symptoms. The longitudinal relationship between anxiety sensitivity and OCS was bidirectional, and these associations were predominantly accounted for by nonshared environmental influences. Conclusions Our findings are consistent with the notion that anxiety sensitivity is a risk factor for OCS during adolescence, but also suggest that experiencing OCS confers risk for heightened anxiety sensitivity. The reciprocal links between OCS and anxiety sensitivity over time are likely to be largely mediated by nonshared environmental experiences, as opposed to common genes. Our findings raise the possibility that interventions aimed at ameliorating anxiety sensitivity could reduce risk for OCS, and vice versa.
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