I think exploring the etiology of illness bears significant importance in that causes of a disorder provide a great deal of information on treatment approaches. For instance, in treating a depression, a therapist can make an individualized approach to a patient, depending on the etiology. It makes more sense when the therapeutic approach to exogenous depression is differentiated from the one to endogenous depression. Admittedly, there are not many cases that causes are well identified in mental disorder. Furthermore, one primary risk factor does not necessarily account for outbreak of a disorder even though it is identified. In this regard, I do agree with the authors, Kendler, Kuhn & Prescott(2004), that exploring how distinct risk factors interact in the etiology illness is an essential topic to be addressed.
In order to test interaction among risk factors-the personality trait of neuroticism, sex, and adversity resulting from exposure to stressful life events(p.631)-, the authors tested out both additive and multiplicative models. And two types of interaction effects were found. The first is between neuroticism and adversity. Individuals with high neuroticism were more sensitive to the depressogenic effect of adversity. This finding is also empirically supported with previous research and can be explained by a stress-vulnerability model. The second is between adversity and sex. The effect of high adversity on onset of depression episodes was pronounced regardless of sex. However, the effect of low adversity on onset of depression episodes was pronounced only in women. This finding is not consistent with previous research.
I think the authors did not provide a good explanation of the interacting effect between sex and adversity. Initially, they tried to distinguish the research by pointing out that their work examined sex differences in reaction to the level of threat posed by stressful live events, instead of to the presence versus absence of them(p.631). In spite of the none-typical, but strong finding of interaction effect between sex and adversity, the authors only suggested that the origins of the sex effect in risk for major depression may lie in the considerably high risk in women for episodes that are unrelated to the experience of high-treat events(p.635). They should have explained more the link between the differentiated measurement by ‘posed threat' and the interaction effect. Also, they could have explored the possibility of a population-based sample resulting in the difference, so that the following replication study might clearly address this question.
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Good points about the sex difference--I agree. I would like to see perhaps a set of alternative models clearly stated that would point the way toward explaining this interaction effect.
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