Chapter 10: Summary and General Discussion

This chapter discusses the implications of the results of the studies described in this thesis. First, a summary is given of the results of the previous chapters. Summary As a prelude to the subsequent analyses, Chapter two addressed the co-morbidity between anxiety and depression, by reviewing empirical evidence regarding mechanisms that might underlie the frequent co-morbidity within anxiety disorders, and between anxiety disorders and depression. The theory of Gray & McNaughton (2000) was taken as a frame of reference. Gray & McNaughton (2000) hypothesized that the anxiety disorders as well as depression are distinct entities with the co-morbidity explained by 1) recursive interconnections linking the brain regions involved in fear, anxiety and panic and 2) heritable personality traits such as neuroticism underlying anxiety as well as depression. Their theory can be translated into the co-morbidity models of Klein and Riso (1993) and Neale and Kendler (1995). These models describe causes for co-morbidity in general, which can be formally tested in longitudinal or twin-family designs. Co-morbidity due to recursive interconnections linking brain regions can be viewed as one disorder being an epiphenomenon of the other, i.e. multiformity. Co-morbidity due to neuroticism being a heritable risk factor for anxiety as well as depression can be interpreted as co-morbidity due to a partly shared genetic etiology. Twin and family studies investigating these models for anxiety, depression and neuroticism, were reviewed. To compare the outcomes systematically, genetic and environmental correlations between disorders were calculated for 23 twin studies and the results of 12 family studies were summarized according to the method of Klein & Riso (1993). Twin studies showed that co-morbidity within anxiety disorders and between anxiety disorders and depression is explained