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Occupational sleep medicine: Role of social stressors
Published in S.R. Pandi-Perumal, Meera Narasimhan, Milton Kramer, Sleep and Psychosomatic Medicine, 2017
Pereira Diana, Gerhardt Christin, Maria U. Kottwitz, Elfering Achim
In the modern work context, in which individuals have to focus on getting their work done regardless of the location, being physically away from the workplace does not necessary imply leaving one’s workplace behind in psychological terms.78 At home, many individuals accomplish jobrelated tasks, continue to think about their jobs, ruminate about work-related problems, or reflect on future opportunities.78 Therefore, spending some time off work does not automatically imply that recovery occurs. Cognitive mechanisms can prolong or reactivate psycho-physiological activation due to a stressor or their perception, thereby slowing down or hindering recovery. According to McEwen,82,83 cognitive mechanisms are also likely to result in allostatic load. Moreover, Brosschot et al.79 hypothesized that occupational stressors will only lead to prolonged activation when individuals cognitively perseverate about these stressors; so perseverative cognition should act as a mediator.79 Perseverative cognition, such as the inability to detach psychologically, should be responsible for converting the immediate psychological and physiological concomitants of stressors into the prolonged physiological activation of the body’s systems, which in turn may lead to incomplete or failed recovery and the development of health impairments in the long run.
Somatization, mental health and pain catastrophizing factors associated with risk of opioid misuse among patients with chronic non-cancer pain
Published in Journal of Substance Use, 2020
Sung-Jae Lee, Maryann Koussa, Lillian Gelberg, Keith Heinzerling, Sean D. Young
Past studies looked at associations between opioid misuse and pain catastrophizing scales. This is an important area to examine, since catastrophizing may interfere with the efficacy of treatment strategies including pain coping strategies. In our study, we examined specific PCS subscales and demonstrated that ‘magnification’ and ‘rumination’ were significantly associated with the increased risk of opioid misuse. Rumination is a form of perseverative cognition that focuses on negative content, generally past and present, and results in emotional distress. Rumination may be a distinct dimension of catastrophic thinking (Sullivan, Lynch, & Clark, 2005), which is highly relevant to this study of patients on chronic opioid therapy for non-cancer pain. While rumination can be negatively contributing to patients with chronic pain, past studies indicate that rumination can also be a beneficial psychological process (i.e., at times, rumination may be beneficial when it is specific, concrete, and process-focused) (Watkins, 2009). Therefore, future studies could focus on supporting patients to reframe rumination as a positive strategy.
Examining How Racial Discrimination Impacts Sleep Quality in African Americans: Is Perseveration the Answer?
Published in Behavioral Sleep Medicine, 2018
Lori S. Hoggard, LaBarron K. Hill
Perseverative Cognition (PC), characterized by recurrent patterns of negative, reflective (i.e., rumination) and anticipatory (i.e., worry) thinking (Brosschot, Gerin, & Thayer, 2006; Brosschot, Pieper, & Thayer, 2005), has been identified as a central mechanism potentially linking racism and racial discrimination (RD) to poorer sleep (e.g., Hicken et al., 2013; Steffen & Bowden, 2006). According to this hypothesis, worry (negative affect-laden and uncontrollable thoughts and images; Borkovec, Ray, & Stober, 1998), rumination (passive and self-reflective perseveration on one’s negative emotions and problems; Nolen-Hoeksema, 1991, 2000), and related cognitive processes (i.e., anticipatory stress) all share a common feature: repetitive or recurring negative thoughts. This framework also delineates that such repetitive or recurring thoughts may largely occur outside of conscious awareness (Brosschot, 2010; Brosschot et al., 2010). Research has long indicated that stress-related intrusive thoughts affect multiple domains of sleep, including shorter sleep duration, greater complaints, lower delta sleep ratio, and longer sleep onset latency (Hall et al., 1997; 2000; Kelly, 2002). Moreover, trait worry and rumination have been associated with indicators of poor sleep—including longer sleep onset latency (Pillai, Steenburg, Ciesla, Roth, & Drake, 2014; Takano, Sakamoto, & Tanno, 2014; Zoccola, Dickerson, & Lam, 2009), shorter sleep duration (Nota & Coles, 2014; Takano et al., 2014), and poorer subjective sleep quality (Ottaviani, Medea, Lonigro, Tarvainen, & Couyoumdjian, 2015; Radstaak, Geurts, Beckers, Brosschot, & Kompier, 2014)—as well as with indicators of cardiovascular hyperarousal during sleep (i.e., higher heart rate, lower heart rate variability; Brosschot, Van Dijk, & Thayer, 2007).
Effects of prefrontal transcranial direct current stimulation on autonomic and neuroendocrine responses to psychosocial stress in healthy humans
Published in Stress, 2020
Luca Carnevali, Elena Pattini, Andrea Sgoifo, Cristina Ottaviani
Exposure to psychological stress is a constant characteristic of everyday life in our society, and may adversely affect the mental and physical health of vulnerable individuals. Research into the link between stress and disease outcomes has shown that frequent elevations of physiological responses during the occurrence of stressful events (reactivity hypothesis) and/or persistent emotional or physiological activation during episodes in which stress is cognitively represented, but not necessarily present (perseverative cognition hypothesis; Brosschot, Gerin, & Thayer, 2006), trigger several pathogenic pathways that may ultimately lead to mental and/or somatic disease (Carnevali, Thayer, Brosschot, & Ottaviani, 2018; Treiber et al., 2003). Physiological stress responses include parasympathetic (vagal) withdrawal and sympathetic activation, resulting in increased heart rate (HR) and reduced HR variability (HRV), and activation of the hypothalamic-pituitary-adrenal (HPA) axis, resulting in the secretion of glucocorticoids (in humans mainly cortisol). The Neurovisceral Integration Model posits that the prefrontal cortex (PFC) regulates and inhibits the activity of limbic structures which act to suppress vagal tone and activate sympathetic circuits (Thayer & Lane, 2009). Similarly, animal studies have demonstrated an inhibitory role of the PFC in the regulation of the HPA axis stress response (Gilabert-Juan, Castillo-Gomez, Guirado, Molto, & Nacher, 2013; Herman et al., 2003). Notably, a “bottom-up” pattern of limbic hyperactivity and PFC hypoactivity is observed in mood and anxiety disorders (Britton, Lissek, Grillon, Norcross, & Pine, 2011; Drevets, Price, & Furey, 2008), potentially representing a neural substrate for the persistent autonomic dysfunction that characterizes these disorders (Makovac et al., 2016; Sgoifo, Carnevali, Alfonso, & Amore, 2015).