A central feature of Major Depressive Disorder (MDD) is the tendency to respond to sadness with rumination, a maladaptive emotion regulation strategy that has been shown to predict the duration and severity of depressive episodes (McLaughlin and Nolen-Hoeksema, 2011 and Nolen-Hoeksema et al., 2008). The response styles theory (Nolen-Hoeksema et al., 2008) defines depressive rumination as a method of processing negative events by repetitively focusing on feelings of distress as well as the potential antecedents or repercussions of these feelings. A substantial body of research has demonstrated negative behavioral and emotional consequences of depressive rumination. Compared to more adaptive emotion regulation strategies, such as distraction, ruminative responses to sad mood diminish problem solving, increase engagement in maladaptive behaviors, and hinder recovery from negative events (Lyubomirsky and Tkach, 2004 and Nolen-Hoeksema et al., 2008). Most notably, experimental research has shown that when individuals are in a sad mood state, rumination leads to more self-reported sadness compared to distraction (Feldner, Leen-Feldner, Zvolensky, & Lejuez, 2006). Depressive rumination, therefore, is believed to directly contribute to the pervasive low mood associated with depressive episodes (Morrow & Nolen-Hoeksema, 1990). In contrast to the considerable research examining the emotional and behavioral effects of depressive rumination, relatively little is understood about the consequences of depressive rumination on physical health, and in particular, on neuroendocrine functioning.
Recent theories posit that the maladaptive consequences of some forms of repetitive thought, including stressor-focused and depressive rumination, extend beyond emotional wellbeing to physical wellbeing (Brosschot, Gerin, & Thayer, 2006; see review by Watkins, 2008). Specifically, the continual processing or contemplation of a depressing or stressful event is predicted to alter individuals’ biological functioning. The neuroendocrine system plays a primary role in our body's biological functioning (Patchev & Patchev, 2006). A central component of the neuroendocrine system is the hypothalamic-pituitary-adrenal (HPA) axis, a primary index of which is the hormone cortisol. Whereas moderate cortisol fluctuation facilitates adaptive responses to environmental changes, excess cortisol production – often stemming from chronic HPA axis activity – can be detrimental (Dedovic et al., 2009, Gold et al., 2002 and Sephton and Speigel, 2003). Prolonged cortisol secretion leads to neurotoxicity in areas of the brain responsible for regulating emotions and coping effectively with distress (McEwen, 2006). Excessive cortisol secretion also has been shown to increase risk for medical conditions, including cancer, diabetes, and arthritis (McEwen, 1998), making it critical to understand factors associated with greater cortisol secretion.
Initial work in nonclinical populations has provided evidence for a connection between stressor-focused rumination and cortisol elevations (see review by Zoccola & Dickerson, 2012). Extending these findings to a sample of depressed adolescence, Stewart, Mazurka, Bond, Wynne-Edwards, (2013) found that trait depressive rumination was associated with elevated cortisol levels during the recovery period, whereas the tendency to use more adaptive emotion regulation strategies (e.g., distraction/problem solving) was associated with faster cortisol decline. The one study to use an experimental manipulation exposed participants to a sad mood induction and then randomly assigned them to a depressive rumination or distraction condition (Kuehner, Huffziger, & Liebsch, 2009). Results showed less cortisol decline in the rumination condition among students with high versus low depression symptoms. The effect of experimentally induced depressive rumination on cortisol levels, however, has never been examined within a clinically depressed sample.
The current study aimed to extend past research by examining the effects of induced depressive rumination versus distraction on cortisol secretion in clinically depressed and healthy control participants. Participants were exposed to a forced-failure paradigm, which was designed to place them in a sad mood state prior to the emotion regulation induction (Hammen, 2005). Participants then were randomly assigned to the depressive rumination or distraction condition. Salivary cortisol was measured when participants entered the lab, and during forced failure, emotion regulation, and post-emotion regulation periods. Overall, we expected cortisol levels to decline across the experiment as participants habituated to the stress of coming into the laboratory (Marceau, Dorn, & Susman, 2012). However, we expected depressive rumination to interrupt this cortisol decline. Specifically, we predicted that both depressed and healthy control participants in the depressive rumination condition would demonstrate less cortisol decline compared to individuals in the distraction condition. In addition, we expected that the effects of depressive rumination would be stronger in the group with clinical depression.
