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Notably, there were several tests impaired in both of our depressed groups, indicating that depression is a common contributing factor.
At the 6 month follow-up, depression scores had significantly improved in both depressed groups (p < 0.001), but the improvement did not differ between groups (21 ± 8 [CAU] vs 22 ± 10 [SCR], NS).
Furthermore, LEIDS-R scores mediate the relationship between neuroticism and depressive symptomatology in both never-depressed and previously depressed groups (Barnhofer & Chittka 2010).
In our study, we found that the healthy control groups had higher SSRS scores than the depressed groups, which implies that social support might prevent depression.
The recent unexpected finding of decreased rejection rates in individuals with clinical depression [12] makes sense from the current account given that depressed groups typically show lower PA and higher NA [13].
Both depressed groups had significantly higher baseline RDQ rumination and self-rated depressive symptoms than the control group (all p <.001).
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We first compared depressed and non-depressed groups using chi-squared and Mann–Whitney U-tests.
It reliably distinguishes between previously depressed and never-depressed groups and also correlates highly with CR as measured with a mood induction procedure (Van der Does 2002).
Analyses of variance were used to determine the differences between the depressed and the non-depressed groups on the depression, anxiety, quality of life and social support measures.
Analyses revealed that even without the depression subscale there was a significant difference between the depressed and non-depressed groups on PSI scores (t (159) = -6.13, p <.001).
In patients, no differences in basal cortisol levels were found between the depressed and non-depressed groups.
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