| The association between atopic disorders and depression: The Northern Finland 1966 Birth Cohort Study | ||
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It is evident that depression is associated also with a wide range of physical illnesses other than atopic disorders (Horrobin & Bennet 1999, Evans & Charney 2003, Katon 2003). As reviewed by Horrobin & Bennet (1999) and Katon (2003), studies of patients with e.g., diabetes mellitus, coronary artery disease, and certain neurologic illnesses have reported higher rates of major depression than in patients without these disorders. A recent meta-analysis of studies of major depression in patients with diabetes showed that the odds of major depression in the diabetes group was twice (OR = 2.0, 95%CI 1.8–2.2) that of the nondiabetic group (Anderson et al. 2001, Katon 2003). Further, rates of major depression have been shown to vary between 17% and 27% in patients with coronary artery disease (for a review, see Rudisch & Nemeroff 2003). In addition, the prevalence of major depression has been found to be 20%–30% and 16%–30% in patients with Parkinson’s disease and multiple sclerosis, respectively (for a review, see Katon 2003).
The relationship between depression and certain physical illnesses is probably bidirectional in nature: physical illness may be a risk factor for depression because of psychosocial stressors, functional impairment, and other biological mechanisms on the one hand, but, on the other, depression may serve as an etiologic factor in the onset and course of somatic illness as reviewed by Evans & Charney (2003). Even though the physical illness may have a direct pathophysiologic effect on the brain (i.e., multiple sclerosis), or have indirect physiologic effects (i.e., increasing cytokine levels that affect the brain), the exact mechanisms behind the associations between physical illnesses and depression have largely remained unclear (Horrobin & Bennet 1999, Joynt et al. 2003, Katon 2003). It is also possible that both certain somatic illnesses and depression are attributable to some third factor, being behind the pathophysiology of both disorders (Horrobin & Bennet 1999).