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Details

Autor(en) / Beteiligte
Titel
A twin-family study of self-report symptoms of panic-phobia and somatization
Ist Teil von
  • Behavior genetics, 1995-11, Vol.25 (6), p.499-515
Ort / Verlag
United States
Erscheinungsjahr
1995
Link zum Volltext
Quelle
SpringerLink (Online service)
Beschreibungen/Notizen
  • Self-report symptoms of anxiety are widely used in mental health and social science research as an index of current psychiatric state. Previous twin studies have suggested that genetic factors account for a significant proportion of the variance in these symptoms. To replicate and extend these findings, we examined self-report symptoms of panic-phobia and somatization in the "Virginia 30,000" twin-family sample. Model fitting applied to 80 unique relationships in the twin-family pedigree produced the following major results: (i) genetic effects were significant for both symptom factors, accounting for between 25 and 49% of the total variance, with the exception of symptoms of panic-phobia in females, where they accounted for 15-16% of the variance; (ii) familial environmental effects were absent for symptoms of somatization, while for symptoms of panic-phobia they accounted for a very small proportion of variance in males (< or = 1.2%) and a modest proportion in females (6-17%); (iii) spousal correlations were present for both factors, ranging from +0.05 to +0.20; (iv) genetic factors which influenced symptoms were generally the same in males and females, although their effect was greater in males; (v) heritability estimates were lower in the population-based than in the volunteer sample; and (vi) when test-retest reliability was included in the model, results suggest that genetic factors account for at least half of the stable variance for all symptom factors, except panic-phobia in females. Our results support the validity of previous twin studies of self-report symptoms of anxiety and suggest that genetic factors significantly influence these symptoms but familial-environmental factors play little or no etiologic role.

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