Abstract

Objectives: converging research suggests that mindfulness training exerts its therapeutic effects on depression by reducing rumination. Theoretically, rumination is a multifaceted construct that aggregates multiple neurocognitive aspects of depression, including poor executive control, negative and overgeneral memory bias, and persistence or stickiness of negative mind states. Current measures of rumination, most-often self-reports, do not capture these different aspects of ruminative tendencies, and therefore are limited in providing detailed information about the mechanisms of mindfulness. Methods: we developed new insight into the potential mechanisms of rumination, based on three model-based metrics of free recall dynamics. These three measures reflect the patterns of memory retrieval of valenced information: the probability of first recall (Pstart) which represents initial affective bias, the probability of staying with the same valence category rather than switching, which indicates strength of positive or negative association networks (Pstay), and probability of stopping (Pstop) or ending recall within a given valence, which indicates persistence or stickiness of a mind state. We investigated the effects of Mindfulness-Based Cognitive Therapy (MBCT; N = 29) vs. wait-list control (N = 23) on these recall dynamics in a randomized controlled trial in individuals with recurrent depression. Participants completed a standard laboratory stressor, the Trier Social Stress Test, to induce negative mood and activate ruminative tendencies. Following that, participants completed a free recall task consisting of three word lists. This assessment was conducted both before and after treatment or wait-list. Results: while MBCT participant’s Pstart remained relatively stable, controls showed multiple indications of depression-related deterioration toward more negative and less positive bias. Following the intervention, MBCT participants decreased in their tendency to sustain trains of negative words and increased their tendency to sustain trains of positive words. Conversely, controls showed the opposite tendency: controls stayed in trains of negative words for longer, and stayed in trains of positive words for less time relative to pre-intervention scores. MBCT participants tended to stop recall less often with negative words, which indicates less persistence or stickiness of negatively valenced mental context. Conclusion: MBCT participants showed a decrease in patterns that may perpetuate rumination on all three types of recall dynamics (Pstart, Pstay, and Pstop), compared to controls. MBCT may weaken the strength of self-perpetuating negative associations networks that are responsible for the persistent and “sticky” negative mind states observed in depression, and increase the positive associations that are lacking in depression. This study also offers a novel, objective method of measuring several indices of ruminative tendencies indicative of the underlying mechanisms of rumination.

Highlights

  • Major depressive disorder (MDD) is a debilitating mood disorder that affects almost 19 million adults in the USA at any given time (Regier et al, 1998) and almost 20% of the USA population over a lifetime (Blazer et al, 1994; Kessler et al, 2005)

  • We examined three measures of free recall dynamics: the probability of first recall (Pstart), probability of stopping (Pstop), and probability of staying rather than switching (Kahana, 2012), which we adapted to study the effects of valence on recall dynamics

  • GENERAL DISCUSSION We examined for the first time model-based measures of recall dynamics that could give insights into the mechanisms underlying

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Summary

Introduction

Major depressive disorder (MDD) is a debilitating mood disorder that affects almost 19 million adults in the USA at any given time (Regier et al, 1998) and almost 20% of the USA population over a lifetime (Blazer et al, 1994; Kessler et al, 2005). MDD is recurrent and progressive, with the likelihood of recurrence exceeding 80% (Judd, 1997; Mueller et al, 1999). A weak PFC results in a hyperactive amygdala (Siegle and Hasselmo, 2002; Siegle et al, 2007b), and an increase in sympathetic hyperarousal and high levels of cortisol (for a review, see Jindal et al, 2003), resulting in damage to the hippocampus (Sheline et al, 1996, 1999; Bremner et al, 2000; Mervaala et al, 2000; Steffens et al, 2011)

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