Why the study?
Youths at high risk for depression struggle to repair sad moods, and atypical sympathetic arousal may contribute to these mood repair problems.
Does familial risk for depression affect sympathetic arousal during sad mood induction and repair in never-depressed youths?
Does familial risk for depression affect sympathetic arousal during sad mood induction and repair in never-depressed youths?
Youths at high familial risk for depression exhibit atypical patterns of sympathetic arousal during emotional processing, which may impair their ability to regulate sad mood.
Answers are grounded in this paper and cite their sources.
May inform early identification of mood regulation issues in at-risk youth; hypothesis-generating and requires prospective trials before clinical use.
Youths at high risk for depression have been shown to have problems in repairing their own sad mood. Given that sympathetic arousal has been implicated both in the experience and regulation of affect, an atypical pattern of arousal may be one of the factors that contribute to mood repair problems. In the current study, we measured sympathetic arousal of never-depressed youths at high (n = 56) and low (n = 67) familial risk for depression during sad mood induction and instructed mood repair. Sympathetic arousal was indexed by skin conductance level (SCL) and cardiac pre-ejection period (PEP); mood repair outcome was indexed by self-rated affect. High-risk youths demonstrated increased SCL during sadness induction, which persisted during mood repair; low-risk youths evidenced increased SCL only during mood repair. Shortened PEP was evident only among high-risk youths and only during mood repair. Furthermore, shortened PEP during mood induction predicted less successful mood repair in the low-risk but not in the high-risk group. The findings suggest that: (a) depression-prone youths differ from control peers in patterns of sympathetic responses to emotional stimuli, which may impair their ability to relieve sadness, and (b) activation patterns differ across subsystems (SCL vs. PEP) of sympathetic activity, in conjunction with depression risk status.
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Daches et al. (2020) studied this question.
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