The role of rumination in illness trajectories in youth: linking trans-diagnostic processes with clinical staging models

Abstract

Research in developmental psychopathology and clinical staging models has increasingly sought to identify transdiagnostic biomarkers or neurocognitive deficits that may play a role in the onset and trajectory of mental disorders and could represent modifiable treatment targets. Less attention has been directed at the potential role of cognitiveemotional regulation processes such as ruminative response style. Maladaptive rumination (toxic brooding) is a known mediator of the association between gender and internalizing disorders in adolescents and is increased in individuals with a history of early adversity. Furthermore, rumination shows moderate levels of genetic heritability and is linked to abnormalities in neural networks associated with emotional regulation and executive functioning. This review explores the potential role of rumination in exacerbating the symptoms of alcohol and substance misuse, and bipolar and psychotic disorders during the peak age range for illness onset. Evidence shows that rumination not only amplifies levels of distress and suicidal ideation, but also extends physiological responses to stress, which may partly explain the high prevalence of physical and mental co-morbidity in youth presenting to mental health services. In summary, the normative developmental trajectory of rumination and its role in the evolution of mental disorders and physical illness demonstrates that rumination presents a detectable, modifiable trans-diagnostic risk factor in youth.

Physical symptom complaints, cognitive emotion regulation strategies, self‐compassion and diabetes distress among adults with Type 2 diabetes

“…Past interventions have also shown promise to alter and improve perceived distress in diverse people with Type 2 diabetes [24] and Type 1 diabetes [25]. In chronic illness samples, negative cognitive emotion strategies have been linked to increases in distress and depressive symptoms [26], with rumination specifically associated with increases in emotional distress and depression, as well as dysregulation of the hypothalamic-pituitary-adrenal axis, which may represent a biological mechanism underlying relationships to poor health outcomes [9,27]. Our study further underscores the importance of negative cognitive emotion regulation and negative self-compassion as potential intervention targets to ameliorate diabetes distress.…”

Attenuated intrinsic connectivity within cognitive control network among individuals with remitted depression: Temporal stability and association with negative cognitive styles

“…Consistent with this possibility, one study found attenuated connectivity within the CCN among adolescent girls at high risk due to having a parental history of depression, although this study did not evaluate cognitive vulnerability features (Clasen et al, 2014). Given that aberrant CCN functioning may underlie cognitive factors that are known to confer risk for MDD onset or relapse (e.g., Abela and Hankin, 2011;Alloy et al, 2006;Langenecker et al, 2007aLangenecker et al, , 2014Stange et al, 2014Stange et al, , 2016; for a review, see Alloy et al, 2016), longitudinal clinical staging studies are needed to determine whether deficits in CCN connectivity confer similar risk, may represent an early scar of illness, or a combination thereof (Grierson et al, 2016;Peters et al, 2015). To this end, recent studies have demonstrated that greater CCN task-based activation (including dorsolateral prefrontal cortex and inferior parietal lobule) during inhibitory control predicted a greater likelihood of responding to antidepressant treatment for MDD (Gyurak et al, 2016;Langenecker et al, 2007a).…”

Feasibility and Acceptability of the ‘HABIT’ Group Programme for Comorbid Bipolar and Alcohol and Substance use Disorders

“…Taken as a whole, many researchers have suggested the need for further revisions to interventions for BD-ASUD (Power, Nishimi, & Kizer, 2005;El-Guebaly, 2012;Kallestad et al, 2016), and that some evidence for additional adaptations may come to light from a greater understanding of the underlying shared risk factors for persistence of ASUD and BD (Grierson, Hickie, Naismith, & Scott, 2016). For example, functioning and quality of life in both BD and ASUD can be impaired by residual mood, anxiety and sleep symptoms (Judd et al, 2003;Gerra et al, 2014;Wang et al, 2014).…”

“…These symptoms can be partially ameliorated by pharmacotherapy, but it is increasingly clear that psychological interventions, especially cognitive, behavioural or self-regulation approaches, may be more efficient (McMurrich et al, 2012;Naqvi et al, 2015;Strickland, Reynolds, & Stoops, 2016). Also, symptoms of BD and ASUD may all be precipitated or maintained by dysfunctional cognitive emotional regulation (CER), particularly a negative ruminative response style (Gruber et al, 2011;Caselli et al, 2013;de Silveira & Kauer-Sant'Anna, 2015;Grierson et al, 2016). The exacerbation of mood disorder or ASUD may be, in part, driven by negative rumination.…”