Emotional regulation and depression: A potential mediator between heart and mind.

Philosophy

A narrative review of the major evidence concerning the relationship between emotional regulation and depression was conducted. The literature demonstrates a mediating role of emotional regulation in the development of depression and physical illness. Literature suggests in fact that the employment of adaptive emotional regulation strategies (e.g., reappraisal) causes a reduction of stress-elicited emotions leading to physical disorders. Conversely, dysfunctional emotional regulation strategies and, in particular, rumination and emotion suppression appear to be influential in the pathogenesis of depression and physiological disease. More specifically, the evidence suggests that depression and rumination affect both cognitive (e.g., impaired ability to process negative information) and neurobiological mechanisms (e.g., hypothalamic pituitary adrenal axis overactivation and higher rates of cortisol production). Understanding the factors that govern the variety of health outcomes that different people experience following exposure to stress has important implications for the development of effective emotion-regulation interventional approaches (e.g., mindfulness-based therapy, emotion-focused therapy, and emotion regulation therapy).

Review Article Emotional Regulation and Depression: A Potential Mediator between Heart and Mind Angelo Compare,1,2 Cristina Zarbo,1 Edo Shonin,3 William Van Gordon,3 and Chiara Marconi1 1 Department of Human and Social Sciences, University of Bergamo, Piazza S. Agostino 2, 24124 Bergamo, Italy 2Human Factors and Technologies in Healthcare Centre, University of Bergamo, Italy 3 Psychology Division, Nottingham Trent University, UK Correspondence should be addressed to Angelo Compare; email@example.com Received 22 September 2013; Revised 17 April 2014; Accepted 23 April 2014; Published 22 June 2014 Academic Editor: Janusz K. Rybakowski Copyright © 2014 Angelo Compare et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. A narrative review of themajor evidence concerning the relationship between emotional regulation and depression was conducted. The literature demonstrates a mediating role of emotional regulation in the development of depression and physical illness. Literature suggests in fact that the employment of adaptive emotional regulation strategies (e.g., reappraisal) causes a reduction of stress-elicited emotions leading to physical disorders. Conversely, dysfunctional emotional regulation strategies and, in particular, rumination and emotion suppression appear to be influential in the pathogenesis of depression and physiological disease. More specifically, the evidence suggests that depression and rumination affect both cognitive (e.g., impaired ability to process negative information) and neurobiological mechanisms (e.g., hypothalamic pituitary adrenal axis overactivation and higher rates of cortisol production). Understanding the factors that govern the variety of health outcomes that different people experience following exposure to stress has important implications for the development of effective emotion-regulation interventional approaches (e.g., mindfulness-based therapy, emotion-focused therapy, and emotion regulation therapy). 1. Introduction Exposure to stress has generally been associated with a wide range of negative outcomes, including decreased well-being and increased incidence of psychological disorders such as posttraumatic stress disorder, generalized anxiety disorder, and major depression [1, 2]. However, some individuals do not develop psychological disorders even when exposed to high levels of stress. It appears, therefore, that when faced with the same stressor, certain individuals demonstrate impaired functionality, while others show remarkable resilience. Stressful events typically elicit significant emotional responses [3, 4]. Accordingly, emotional regulation capacity has been proposed as amediator of stress adjustment [5, 6]. According to this model, exposure to stress leads to the dysregulation of emotions, which in turn elicits negative psychological and physiological health outcomes (e.g., depression and stress-induced cardiomyopathy) (see Figure 1). Whilst emotional regulation capacity has been proposed as amediator in the link between emotion and psychosomatic health, a review of the empirical and theoretical literature that specifically reports on the mediating role of emotional regulation in the development of depression and subsequent additional somatic illness has not been undertaken to date. Thus, the purpose of this paper is to conduct a narrative review about the major evidence concerning the mediating role of the emotional regulation in the link between depression and physical illness. Key theories, methods of assessment, clinical and neurobiological correlates, psychological and physiological mechanisms of action, and treatment approaches are discussed. 2. The Emotional Regulation Emotional regulation, also known as "emotional self-regulation," has been defined by Gross [7] as the set of cognitive Hindawi Publishing Corporation Cardiovascular Psychiatry and Neurology Volume 2014, Article ID 324374, 10 pages http://dx.doi.org/10.1155/2014/324374 2 Cardiovascular Psychiatry and Neurology Stress Emotions emotional regulation capacity Adjustment to stress and resilience dysregulation Physiological diseases Psychological diseases emotional Cognitive Cognitive emotional Cognitive regulation Figure 1: The mediating role of emotional regulation in the relationship between stress and emotions. processes that influence the type of emotional response, as well as how individuals experience and express these emotions. Emotional regulation is a complex process that includes the initiation, the inhibition, or modulation of the following aspects of emotion functioning [8] (see Figure 2): (1) internal emotional states (e.g., the subjective experience of emotion); (2) emotion-related cognitions (e.g., reaction to thoughts about a situation); (3) emotion-related physiological processes (e.g., autonomic arousal, hormonal reactions, etc.); (4) emotion-related behaviors (e.g., facial expressions, verbal responses, etc.). The manner in which individuals are able to manage emotional experience to conform adaptively to a given context appears to be important to mental health [9]. Emotion regulation strategies, such as rumination, can also become maladaptive and significantly impair psychosocial functioning. Therefore, understanding when and why the regulation of emotions becomes harmful is of fundamental importance [10]. This relates to the situational and individual factors that influence cognitive emotion regulation capacity including trait and state levels of psychological, social, and somatic health [11, 12]. Amodel of emotional regulation process, highlighting the crucial role of emotion regulation strategies in determining the relative health-benefit of different responses to emotions, has been proposed by Gross et al. [13]. The process model of emotion regulation has been based upon the "modal model" of emotion, suggesting that a person-situation transaction that compels attention has particular meaning to an individual and gives rise to a coordinated yet flexible multisystem response to the ongoing person-situation transaction [14]. According to the modal model of emotion, emotions arise in a particular sequence that includes four key steps: (i) a Internal emotional states Emotionrelated cognitions Emotionrelated behaviors Emotionrelated physiological processes regulation emotional Cognitive Figure 2: Functioning aspects involved in cognitive emotion regulation. situation (real or imagined) emotionally relevant; (ii) attention directed towards the emotional situation; (iii) appraisal of situation, which means that situation should be evaluated and interpreted; and (iv) emotional response to situation with changes in behavioral, experiential, and physiological response systems. The modal model of emotion suggests moreover the existence of a feedback recursively and dynamic loop from the emotional response to the situation [14]. According to the model of emotional regulation process, there are two overarching control strategies that modulate emotional experience (see Figure 3). (1) Antecedent-Focused Regulation. This regulation strategy occurs at an early stage in the modulation of emotional response [15] and prior to the activation of emotional and behavioral response systems [16]. Antecedent-focused regulation comprises the following types of emotion regulation strategies: (i) selecting the situation (e.g., approaching or avoiding people or situations according to their anticipated emotional impact), (ii) changing the situation (e.g., transforming the environment to alter the emotional impact), (iii) engaging attentional strategies (e.g., focusing attention towards or away from situational circumstances depending upon their emotional potency), and (iv) cognitive change (e.g., reinterpreting the situation to alter its emotional significance). (2) Response-Focused Regulation.This strategy is engaged at a later stage and is focused onmodification of emotional output [10]. In other words, response-focused regulation refers to modifications of the physiological and observable signs of emotions after such emotions have already becomemanifest [15]. Response-focused regulation comprises the following types of regulatory response: (i) suppression of emotion, (ii) inhibition of emotion, (iii) emotion masking, and (iv) emotion intensification [16]. Cardiovascular Psychiatry and Neurology 3 Amygdala OFC Ventral MPFC Dorsal MPFC Figure 3: Amygdala-frontal circuit of emotion regulation. Prefrontal cortex seems to be involved in the modulation of the amygdala reactivity, a critical structure for the generation of negative emotions. During reappraisal, enhanced activation in medial prefrontal cortex (MPFC) is associatedwith attenuation of amygdala activation andwith a reduction of negative affect intensity. Orbitofrontal cortex (OFC) coordinates the interactions between these areas. Antecedent-focused regulation, such as reappraisal, employs cognitive reevaluation strategies in order tomodify situations or reformulate their emotional significance [15]. In particular, reappraisal is a cognitively oriented strategy that allows us to redefine emotional stimuli in unemotional terms or to think about a potential emotion situation in a different way to alter the emotion's impact. Conversely, response-focused regulation, such as suppression, modulates emotional behavior via the inhibition of emotion and external behavioral signals (e.g., facial expression, verbal expressions, hand gestures, etc.). Responsefocused regulation is a less adaptive strategy of regulating emotions and is associated with greater sympathetic activation of the cardiovascular system [12, 17], as well as negative outcomes such as psychopathology, social dysfunction, and depression [18]. In fact, although literature has suggested that reappraisal and suppression are both successful in reducing facial expression, only reappraisal has been shown to decrease internally felt negative emotion [7, 12, 19, 20]. Individuals who typically regulate their emotions through use of suppression report in fact less positive affect, more negative affect, less social support, and more depression [21]. 3. Assessment of Emotional Regulation Measures of emotional regulation typically assess the degree to which people are better able to manage their emotions [22]. The most psychometrically established and commonly employed scales for evaluating emotional regulation are as follows. (1) TheMayer-Salovey-Caruso Emotional Intelligence Test [23]. This scale asks respondents to evaluate the effectiveness of a range of strategies to manage emotions in different scenarios. Responses are compared with those provided by expert researchers in the field. (2) The Emotional Regulation Questionnaire [24]. The emotional regulation questionnaire measures the habitual use of expressive suppression and cognitive revaluation. The scale includes items related to the regulation of both positive and negative emotions [24]. (3) The Emotion Expressivity Scale [25]. This 17-item scale measures the expression and inhibition of emotions. Emphasis is placed on the extent to which respondents suppress their emotions during social interaction [26]. (4) Difficulties with Emotion Regulation Scale (DERS) [27]. The DERS is a brief, 36-item self-report questionnaire designed to assess multiple aspects of emotional dysregulation. Higher scores suggest greater problems with emotion regulation. (5) Emotional Reactivity Scale (ERS) [28]. Emotion reactivity scale (ERS) is a 21-item self-report measure of emotion sensitivity, intensity, and persistence. 4. Emotional Regulation and Depression The strategies people use to regulate their emotions, and in particular negative emotions, appear to be strongly linked to several psychopathologies, such as depression. Depression is a highly prevalent emotion dysregulation disorder that impairs social skills, quality of life, and capacity to label and identify affective states. Referring to the DSM-V [29], the main criteria for a diagnosis of major depressive disorder (MDD) are (i) the presence of depressedmood or a loss of interest or pleasure in daily activities for more than two weeks; (ii) depressed mood that represents a change from the person's baseline; (iii) impairment in social, occupational, and educational functions; (iv) the presence of specific symptoms nearly every day concerning depressed or irritable mood, decreased interest or pleasure in most activities, significant weight change or change in appetite, change in sleep, change in activity, fatigue or loss of energy, feelings of worthlessness or excessive or inappropriate guilt, diminished concentration, and suicidality. In the last decade, evidence implicating specific emotion regulation strategies as risk factors for depression has emerged. Findings from clinical and neuroimaging studies investigating the association between emotional regulation and depression are outlined below (see Table 1). 4 Cardiovascular Psychiatry and Neurology Table 1: Emotional regulation and depression link in clinical and neuroimaging studies. Emotional regulation and depression Clinical studies Neuroimaging studies Depressed patients show (i) inappropriate or ineffective emotion regulation; (ii) difficulties in cognitive control; (iii) difficulties in processing negative material (which leads to greater rumination, less use of reappraisal strategies, and more use of expressive suppression); (iv) negative self-report biases. Depressed patients show (i) dysfunctional stress responses; (ii) decrease in mu-opioid receptor binding potential in the left inferior temporal cortex; (iii) abnormal amygdala activation; (iv) dysfunctional ventral prefrontal cortex activation. 5. Clinical Studies A number of clinical studies have shown that inappropriate or ineffective emotion regulation is a critical component in the development and maintenance of depression and anxiety disorders [30–35]. Depression is also associated with impaired cognitive control such as difficulty in accepting and processing negative material [36]. In turn, this reduced ability to process negative material is associated with increased rumination, impaired cognitive reappraisal, and increased expressive suppression [36]. Clinical studies have also demonstrated that depressed patients are negatively biased in their recognition of emotion, which increases significantly according to diagnostic severity [37]. 6. Neurobiological and Neuroimaging Studies of Circuit of Emotion Regulation Several neurobiological studies have focused on the link between emotional regulation and depression. Evidence implicates dysfunctions in the brain serotonergic system in the pathophysiological mechanism of major depressive disorder (MDD). Knockout mice with targeted deletion of genes involved in the mediation of serotonergic transmission (i.e., removal of tryptophanhydroxylase 2 (Tph2KO)which is a rate-limiting enzyme for serotonin (5-HT) synthesis) have demonstrated the important role played by the brain serotonergic system in emotion dysregulation [38]. Endogenous opioid neurotransmission that activates mu-opioid receptors has also been found to be involved in emotion regulatory processes and is likewise implicated in the etiology of MDD [39]. More specifically, negative mood is associated with statistically significant decreases in mu-opioid receptor binding potential in the left inferior temporal cortex of patients with MDD [39]. Neuroimaging studies have positively correlated MDD and ineffective emotion regulationwith heightened amygdala response [40]. Neuroimaging studies also demonstrate that the prefrontal cortex (PFC) is involved in mediating important higher-order cognitive processes and that the level of activation of the ventral prefrontal cortex reflects the degree of emotionalmodulation and cognitive control on cognitively demanding goal-directed tasks [41]. Dysfunction in this area of the brain has been hypothesized to explain the pathological inability of the brain to regulate and suppress the heightened affective responses to negative affect-eliciting stimuli associated with depression [41]. In fact, PFC activation is strongly influenced by emotional reactions through its functional interaction with the amygdala and the striatal circuitry (areas of the brain involved in emotion and reward processing) [42]. In Figure 3, we describe the amygdala-frontal circuit of emotion regulation. While the amygdala is a critical region to the generation, expression, and experience of negative emotions, some frontal cortical regions are thought to be involved in the modulation of amygdala reactivity and the mediation of effective emotion regulation, with their topdown inhibitory effect on the amygdala. Moreover, stronger coupling exists between amygdala and these areas of the prefrontal cortex (PFC) during conscious emotion regulation, like reappraisal: attenuation of amygdala activation is associated with enhanced activation in ventromedial PFC and dorsal medial PFC [43]. The medial PFC (MPFC) has been linked to the integration between emotion and cognition and to the processes that underlie cognitive reappraisal. A functional distinction has been posited between ventral and dorsalMPFC: ventralMPFC seems to be involved in appraisal for emotional salience of stimuli, while dorsalMPFC seems to be involved in regulation of appropriate behaviors following appraisal. Orbitofrontal cortex (OFC) works as an important relay or coordination region for amygdala andMPFC interactions. Greater functional connectivity between amygdala and OFC/dorsal MPFC during reappraisal is associated with less intensity of negative affect. 7. Rumination: A Maladaptive Emotional Regulation Strategy Depressed individuals experience a range of maladaptive cognitions that may lead to underregulation. Rumination, themost commonmaladaptive emotional regulation strategy in depressed individuals, can be defined as an emotional process characterized by repetitive, unwanted, past-oriented negatively inclined thoughts [44, 45]. Rumination is generally considered to be maladaptive and has been implicated in the exacerbation and maintenance of a variety of adverse mental health outcomes, including depression [46, 47]. Rumination is a process related to worry and refers to a cognitive focus on real or imagined upcoming negative events [48]. Worry is a form of fear process and is associated with anxiety, apprehension, and general tension [49]. Rumination and worry are similar in that they are both characterized Cardiovascular Psychiatry and Neurology 5 by repetitive negative thought [45]. For individuals who ruminate or who mentally rehearse past stressful events, the physiological effects of stressors are often more enduring [37] (e.g., continued reflection on a bygone argument may cause stress hormones to continue to circulate in the body long after an argument has ended). The evidence implicates impaired cognitive control as a crucial process underlying ruminative thinking and suggests that it may be an important vulnerability factor for depression [50]. The determinants of rumination are multifaceted. Individual and situational differencesmay play a role in triggering and maintaining ruminative thought [51], and certain individuals are more prone to perseveration than others [44]. The evidence indicates that repeated psychosocial stress in early life has a significant impact on behavior and neural functioning-both of which are risk factors for depression [52]. Furthermore, it has been hypothesized that early-life adversity may result in a reduced capacity for cognitive control in response to a repeated stressor, particularly in individuals who develop maladaptive emotional processing strategies (i.e., trait rumination). In contrast, individuals who were exposed to early-life adversity but developed adaptive emotion processing skills (e.g., high levels of trait mindfulness) typically exhibit enhanced capacity for cognitive control during adulthood [52]. 8. Physiological Mechanisms of Rumination Rumination has been shown to induce prolonged activation of the hypothalamic pituitary adrenal (HPA) axis, and, for those who ruminate excessively or repeatedly, sustained elevations in cortisolmay incur deleterious health consequences [51]. Examples are acute changes in the cardiovascular system and acceleration of atherosclerotic process [53]. The HPA axis is a slow-acting stress response system, whose activation triggers a cascade of events which begins with the secretion of corticotropin-releasing hormone by the hypothalamus and culminates in the release of glucocorticoids (i.e., cortisol) by the adrenal glands into the bloodstream [54]. The HPA axis is a major stress response system that is critical for survival and adaptation and may be particularly relevant in understanding the adverse effects that stressors have on somatic and psychological health. Subsequent and repeated recall of a stressor, which is symptomatic of both rumination and depression, could reactivate the stress response during otherwise nonstressful situations. In fact, evidence suggests that perseverative cognition, such as rumination, may prolong cardiovascular-related physiological activation [55]. Although release of cortisol by theHPA in response to certain stressors may be adaptive in the short term [56], prolonged exposure to cortisol from exaggerated, extended, or repeated activation of the HPA axis is likely to be maladaptive. Indeed, a range of disorders, including cardiovascular disease, have been associated with persistent HPA axis activation [57]. Furthermore, HPA overactivation and elevated basal cortisol levels have been linked to avoidance, withdrawal, and negative emotions such as anxiety and depression [58–63]. Recent studies investigating how the neural correlates of personality regulate emotion processing in the brain have associated the inferior frontal gyrus (IFG) (Brodmann area 45) with trait high levels of rumination [58]. The IFG asserts an important regulatory role in top-down control processes that lead to increases in subcortical activation [64].Therefore, it is reasonable to assume that, by promoting ruminative thinking, emotional suppression is likely to increase positive connectivity between subcortical limbic activation and the IFG. 9. Emotional Regulation Role in the Link between Depression and Illness Literature has suggested that depression, through neurobiological and behavioral processes, may affect physical health and induce physical illness. In particular, depression has been found to be the primary risk factor for cardiac diseases [65]. Depression has been in fact linked to (i) several biological mechanisms, such as inflammatory and immune processes, alterations in activating HPA, variability in heart rate, increased activity of the sympathoadrenal and pituitaryadrenal axes, reduction in circulating endothelial progenitor cells, increase of cortisol and catecholamine levels, alteration of activities of autonomic nervous system, and oxidation processes [66–69] and (ii) several unhealthy lifestyles, such as increased consumption of tobacco, alcohol, and illicit substances, reduced physical activity, overeating, and no medical adherence [68]. Due to the well-known and yet discussed existence of dysfunctional emotional regulation in depression and rumination, a mediating role of emotional regulation in the link between depression and somatic disease may be suggested. Emotional regulation may indirectly affect both the etiology and the prognosis of a physical illness. According to inhibition theory, keeping emotions inside will lead to long-term health problems because it requires continuous physiological work [70]. Several studies have in fact suggested that stronger mood regulation expectancies are associated with lower dysphoria and somatic symptoms in college students and caregivers of chronic diseases [71, 72]. Several studies have shown that different styles of emotion regulation have different relationships with health [12, 73, 74]. In particular, alexithymia, emotional control, and ambivalence have been significantly related to more psychological, social, and physical distress in both healthy and chronically ill populations [75–77]. In contrast, emotional orientation and expression have shown beneficial effects and positive health consequences [78–81]. 10. Psychological Treatments Focusing on Emotional Regulation Current neuroscientific evidence confirms that both emotion and cognition are interacting yet distinct functions which communicate via bidirectional neural connections between the neocortex and emotional centers [82]. These connections allow emotion-related input to modulate cortical activity and cognitive input from the cortex to modulate emotional processing. Understanding how cognitive and emotional 6 Cardiovascular Psychiatry and Neurology systems interact has significant implications for emotion regulation interventions. For example, it has been suggested that intervening at the level of the emotional system itself is a more direct, efficient, and powerful way to override and transform the maladaptive patterns that underlie unhealthy psychological, behavioral, and physiological stress responses [82]. The activation of positive emotions can play a critical role in breaking the stress cycle by effectively transforming stress at its source [83]. Positive emotions have been linked to improved health and increased longevity.They have also been shown to beget increases in cognitive flexibility, creativity, receptivity, innovative problem solving, and psychological resilience in the face of adversity. Furthermore, positive emotions influence interpersonal behavior and promote helpfulness, generosity, and cooperation [61–63]. In other words, positive emotions play a critical role in effective adaptation to life's challenges [84–86]. The literature also suggests that emotional regulation strategies such as positive reappraisal and curtailed rumination exert a protective influence over relapse or exacerbated symptoms in patients with depression and anxiety disorders [87]. Above all, the most common therapies focusing on emotional regulation are presented. 11. The Emotion-Focused Therapy To be able to effectively regulate emotions, individuals need to be assessed and trained in evidence-based emotion management strategies. In a treatment protocol developed by Greenberg and known as emotion-focused therapy [88], individuals are taught to enhance their awareness of emotion regulation strategies and of emotional processes more generally. Emotion-focused therapy is based on an awarenessenhancing strategy operationalized in an intervention known as process experiential therapy [89], which aims to help people develop emotional intelligence and effective emotion regulation processes. Greenberg [88] proposes three key principles that underlie emotional change. (1) Emotion Awareness.This relates to a greater awareness of emotional experiences and the information they provide, as well as a greater understanding of the behaviors that result from such emotions. Increased emotional awareness promotes the creation of new meanings and helps people to develop new narratives to explain their experiences. (2) Emotion Regulation. In order to reach a state of connection with their own emotional experience, it is necessary to increase people's capacity for selfcalm (e.g., by regulating the heartbeat and breathing). Reduced autonomic and psychological arousal allows people to derive insight and knowledge from their emotional processes and to learn how to handle emergency signals and situations. (3) Changing Emotion with Emotion. A nonadaptive affective state can be transformed into an adaptive one. This change is made possible by relaxation exercises or through the deliberate induction of positive emotions [16]. The main objective of emotion-focused therapy is to help individuals modify internal affective states, the core beliefs that underlie these states, and the behaviors that they elicit. Emphasis is placed on intervening before the emotioneliciting event takes place. This occurs via an increased ability to analyze and be aware of emotions which improves a person's ability to handle internal and external stressors. Emotion-focused therapy has been widely used in interventions aimed at the treatment of depression [16]. 12. The Mindfulness-Based Cognitive Therapy A further innovative interventional approach that has recently been deployed in clinical contexts is that of mindfulness training.Mindfulness derives from Buddhist meditation practice and is fundamentally concernedwith developing and open and unbroken awareness of present moment cognitiveeffective and sensory experience. According to Compare et al. [67], mindfulness effectuates a greater perceptual distance from distorted cognitive and affective processes and this meta-awareness facilitates the regulation (i.e., via the nonreactive observance) of habitual maladaptive responses. Via the regulation of attention, mindfulness empowers participants to cultivate a new relationship with internal and external experiences and in a way that does not encourage avoidance, overengagement, or elaboration [90]. During the last two decades, a credible evidence base has emerged supporting the utilization of mindfulness meditation as an emotion regulation strategy. Indeed, a mindfulness approach known as mindfulness-based cognitive therapy (MBCT) is now advocated by the National Institute for Health and Clinical Excellence (NICE) and the American Psychiatric Association for the treatment of specific forms of depression. Evidence has also shown that increases in levels of dispositional mindfulness are significantly correlated with reductions in avoidance and rumination [91]. Increased breath awareness (a fundamental component of mindfulness meditation) has been shown to reduce autonomic and psychological arousal, and this increased capacity to remain calm can help individuals to respondmore adaptively to internal and external stressors [70]. Negative thinking and ruminative thinking are often employed asmaladaptivemeans of escaping fromnegative affective states such as guilt, depression, and anxiety [71]. The increased levels of self-awareness cultivated during mindfulness practice can confer a greater capacity to label and therefore modulate these affective states [71]. In otherwords, rather than avoiding distressing feelings and thoughts by engaging in ruminative thinking and/or maladaptive behaviors, mindfulness encourages people to objectify any dysfunctional cognitive and affective processes by seeing them as passing phenomena. Another important mechanism by which mindfulness is believed to modulate negative affective states is via the cultivation of self-compassion and compassion. Research has shown that mindfulness leads to a greater awareness of the individuals own suffering and psychological distress, and this helps to instil a greater appreciation of the suffering of others [70, 72]. Accordingly, greater levels of self-compassion and Cardiovascular Psychiatry and Neurology 7 compassion are thought to lead to improvements in pain and emotion tolerance due to individuals being able to assign greater levels of perspective to their emotional and/or somatic pain (i.e., by appreciating that they are not the only person experiencing psychological/somatic distress) [72]. 13. The Emotion Regulation Therapy (ERT) The emotion regulation therapy (ERT) is a recent treatment for generalized anxiety disorder (GAD) that integrates components of cognitive-behavioral, acceptance, dialectical, mindfulness-based, experiential, and emotion-focused treatments [92, 93]. The ERT is based on the emotion dysregulation model of GAD that suggests that GAD subjects have difficulties in the modulation of emotions, showing difficulty in identifying, describing, and clarifying the motivational content of emotion. GAD subjects utilize in fact worry as a maladaptive cognitive control strategy in order to reduce and control an aversive or uncertain emotional state. ERT aims, then, to enhance knowledge, acceptance, utilization, and management of emotions addressing cognitive, emotional, and contextual factors that may contribute to maladaptive responses. ERT program includes 20 sessions of 50–60 minutes, divided in 16 weeks and four phases. The first phase focuses on psychoeducation aboutGAD, functional patterns of worry and emotions in various situations, and self-monitoring of worry episodes. The second phase focuses on the development of somatic awareness and emotion regulation skills.The third phase focuses on the application of skills during exposure to emotionally evocative themes. The fourth and final phase focuses on terminating the therapeutic relationship, relapse prevention, and future goals [35]. The main aim of ERT for GAD subjects is to learn the ability to effectively increase or decrease attendance to emotional experience, tolerate distress, and adapt to social environment. In specific, ERT aims to teach GAD subjects to: (i) identify, differentiate, and describe their emotions; (ii) increase both acceptance of affective experience and ability to adaptively manage emotions; (iii) decrease use of emotional avoidance strategies, such as worry; (iv) increase ability to utilize emotional information in identifying needs, making decisions, guiding thinking, motivating behavior, and managing interpersonal relationships and other contextual demands [35]. 14. Conclusions Based on an extensive examination of the empirical and theoretical literature related to emotional regulation, it appears that a strong association exists between emotional regulation and depression and that emotional regulation mediates the role between depression and further psychological and/or somatic illness. It is concluded that when adaptive emotional regulation strategies (e.g., reappraisal) are employed, there is reduced likelihood of stress-elicited emotions leading to mental or physical disorders. Although there is some evidence that suggests the involvement of frontal cortical regions in the modulation of amygdala reactivity towards emotion regulation, interregional connectivity between amygdala and prefrontal cortex in the context of affect regulation remains unknown. Further studies are needed to better explain the neural circuit connecting amygdala and PFC in emotion regulation. Conversely, emotional dysregulation (e.g., rumination, suppression, etc.) appears to be influential in the pathogenesis of psychological disease, such as depression. More specifically, the evidence suggests that depression and rumination affect both cognitive (e.g., difficulty in processing negative information) and neurobiological mechanisms (e.g., HPA axis overactivation and higher rates of cortisol production). Given the height link between depression, emotional regulation, and somatic diseases, future research and clinical studies should focus on the specific role of emotional regulation in affecting both depression and somatic diseases in order to highlight the specific mental and biological processes that lead to illness. Understanding the factors that govern the variety of health outcomes that different people experience following exposure to stress will have important implications for the identification and ongoing validation of effective emotion-regulation interventional approaches (e.g., mindfulness-based therapy, emotion-focused therapy, emotion regulation therapy, etc.). Conflict of Interests The authors declare that there is no conflict of interests regarding the publication of this paper. References [1] B. S. Dohrenwend and B. P. Dohrenwend, "Overview and prospects for research on stressful life events," in Stressful Life Events: Their Nature and Effects, B. S. Dohrenwend and B. P. Dohrenwend, Eds., p. 313, Wiley, New York, NY, USA, 1974. [2] K. S. Kendler, L. M. Karkowski, and C. A. Prescott, "Causal relationship between stressful life events and the onset of major depression,"The American Journal of Psychiatry, vol. 156, no. 6, pp. 837–841, 1999. [3] R. S. Lazarus, Stress and Emotion: A New Synthesis, Springer, New York, NY, USA, 1999. [4] I. G. Sarason, J. H. Johnson, and J. M. Siegel, "Assessing the impact of life changes: development of the life experiences survey," Journal of Consulting and Clinical Psychology, vol. 46, no. 5, pp. 932–946, 1978. [5] C. J. McCarthy, R. G. Lambert, and N. P. Moller, "Preventive resources and emotion regulation expectancies as mediators between attachment and college students' stress outcomes," International Journal of Stress Management, vol. 13, no. 1, pp. 1– 22, 2006. [6] D. Schwartz and L. J. Proctor, "Community violence exposure and children's social adjustment in the school peer group: the mediating roles of emotion regulation and social cognition," Journal of Consulting and Clinical Psychology, vol. 68, no. 4, pp. 670–683, 2000. [7] J. J. Gross, "Antecedentand response-focused emotion regulation: divergent consequences for experience, expression, and physiology," Journal of Personality and Social Psychology, vol. 74, no. 1, pp. 224–237, 1998. 8 Cardiovascular Psychiatry and Neurology [8] R. Siegler, How Children Develop, Exploring Child Develop StudentMedia Tool Kit ScientificAmericanReader toAccompany How Children Develop, Worth, New York, NY, USA, 2006. [9] J. J. Gross and R. F. Muñoz, "Emotion regulation and mental health," Clinical Psychology: Science and Practice, vol. 2, no. 2, pp. 151–164, 1995. [10] S. A. Moore, L. A. Zoellner, and N. Mollenholt, "Are expressive suppression and cognitive reappraisal associated with stressrelated symptoms?" Behaviour Research and Therapy, vol. 46, no. 9, pp. 993–1000, 2008. [11] J. L. Abelson, I. Liberzon, E. A. Young, and S. Khan, "Cognitive modulation of the endocrine stress response to a pharmacological challenge in normal and panic disorder subjects," Archives of General Psychiatry, vol. 62, no. 6, pp. 668–675, 2005. [12] J. J. Gross, "Emotion regulation: affective, cognitive, and social consequences," Psychophysiology, vol. 39, no. 3, pp. 281–291, 2002. [13] J. J. Gross, "The emerging field of emotion regulation: an integrative review," Review of General Psychology, vol. 2, no. 3, pp. 271–299, 1998. [14] J. J. Gross and R. A. Thompson, "Emotion regulation: conceptual foundations," in Handbook of Emotion Regulation, J. J. Gross, Ed., Guilford Press, New York, NY, USA, 2011. [15] P. R. Goldin, K. McRae, W. Ramel, and J. J. Gross, "The neural bases of emotion regulation: reappraisal and suppression of negative emotion," Biological Psychiatry, vol. 63, no. 6, pp. 577– 586, 2008. [16] D. Villani, A. Grassi, and G. Riva, Tecnologie Emotive: Nuovi Media per Migliorare la Qualità della Vita e Ridurre lo Stress, LED, Milano, Italy, 2011. [17] H. A. Demaree, B. J. Schmeichel, J. L. Robinson, J. Pu, D. E. Everhart, and G. G. Berntson, "Upand down-regulating facial disgust: affective, vagal, sympathetic, and respiratory consequences," Biological Psychology, vol. 71, no. 1, pp. 90–99, 2006. [18] A. A. Grandey, "Emotion regulation in the workplace: a new way to conceptualize emotional labor," Journal of Occupational Health Psychology, vol. 5, no. 1, pp. 95–110, 2000. [19] J. J. Gross andR.W. Levenson, "Emotional suppression: physiology, self-report, and expressive behavior," Journal of Personality and Social Psychology, vol. 64, no. 6, pp. 970–986, 1993. [20] J. J. Gross and R. W. Levenson, "Hiding feelings: the acute effects of inhibiting negative and positive emotion," Journal of Abnormal Psychology, vol. 106, no. 1, pp. 95–103, 1997. [21] O. P. John and J. J. Gross, "Individual differences in emotion regulation," in Handbook of Emotion Regulation, J.J. Gross, Ed., Guilford Press, New York, NY, USA, 2007. [22] S. Côté, A. Gyurak, and R.W. Levenson, "The ability to regulate emotion is associated with greater well-being, income, and socioeconomic status,"Emotion, vol. 10, no. 6, pp. 923–933, 2010. [23] J. D. Mayer, P. Salovey, and D. R. Caruso, Manual for the MSCEIT (Mayer-Salovey-Caruso Emotional Intelligence Test), Multi-Health Systems, Toronto, Canada, 2002. [24] J. J. Gross andO. P. John, "Individual differences in two emotion regulation processes: implications for affect, relationships, and well-being," Journal of Personality and Social Psychology, vol. 85, no. 2, pp. 348–362, 2003. [25] A. M. Kring, D. A. Smith, and J. M. Neale, "Individual differences in dispositional expressiveness: development and validation of the Emotional Expressivity Scale," Journal of Personality and Social Psychology, vol. 66, no. 5, pp. 934–949, 1994. [26] J. W. Burns, P. J. Quartana, and S. Bruehl, "Anger management style moderates effects of emotion suppression during initial stress on pain and cardiovascular responses during subsequent pain-induction," Annals of Behavioral Medicine, vol. 34, no. 2, pp. 154–165, 2007. [27] K. L. Gratz and L. Roemer, "Multidimensional assessment of emotion regulation and dysregulation: development, factor structure, and initial validation of the difficulties in emotion regulation scale," Journal of Psychopathology & Behavioral Assessment, vol. 26, no. 1, pp. 41–54, 2004. [28] M. K. Nock, M. M. Wedig, E. B. Holmberg, and J. M. Hooley, "The emotion reactivity scale: development, evaluation, and relation to self-injurious thoughts and behaviors," Behavior Therapy, vol. 39, no. 2, pp. 107–116, 2008. [29] American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disorders, American Psychiatric Publishing, Arlington, Va, USA, 5th edition, 2013. [30] D. H. Barlow, L. B. Allen, and M. L. Choate, "Toward a unified treatment for emotional disorders," Behavior Therapy, vol. 35, no. 2, pp. 205–230, 2004. [31] L. Campbell-Sills, D. H. Barlow, T. A. Brown, and S. G. Hofmann, "Acceptability and suppression of negative emotion in anxiety and mood disorders," Emotion, vol. 6, no. 4, pp. 587– 595, 2006. [32] L. Campbell-Sills, D. H. Barlow, T. A. Brown, and S. G. Hofmann, "Effects of suppression and acceptance on emotional responses of individuals with anxiety and mood disorders," Behaviour Research and Therapy, vol. 44, no. 9, pp. 1251–1263, 2006. [33] T. B. Kashdan and M. F. Steger, "Expanding the topography of social anxiety. An experience-sampling assessment of positive emotions, positive events, and emotion suppression,"Psychological Science, vol. 17, no. 2, pp. 120–128, 2006. [34] T. B. Kashdan, V. Barrios, J. P. Forsyth, and M. F. Steger, "Experiential avoidance as a generalized psychological vulnerability: comparisons with coping and emotion regulation strategies," Behaviour Research and Therapy, vol. 44, no. 9, pp. 1301–1320, 2006. [35] D. S. Mennin, "Emotion regulation therapy: an integrative approach to treatment-resistant anxiety disorders," Journal of Contemporary Psychotherapy, vol. 36, no. 2, pp. 95–105, 2006. [36] J. Joormann and I. H. Gotlib, "Emotion regulation in depression: relation to cognitive inhibition," Cognition and Emotion, vol. 24, no. 2, pp. 281–298, 2010. [37] M. Punkanen, T. Eerola, and J. Erkkilä, "Biased emotional recognition in depression: perception of emotions in music by depressed patients," Journal of Affective Disorders, vol. 130, no. 1-2, pp. 118–126, 2011. [38] N. Araragi and K. Lesch, "Serotonin (5-HT) in the regulation of depression-related emotionality: insight from 5-HT transporter and tryptophan hydroxylase-2 knockout mouse models," Current Drug Targets, vol. 14, no. 5, pp. 549–570, 2013. [39] S. E. Kennedy, R. A. Koeppe, E. A. Young, and J. Zubieta, "Dysregulation of endogenous opioid emotion regulation circuitry in major depression in women," Archives of General Psychiatry, vol. 63, no. 11, pp. 1199–1208, 2006. [40] G. Perlman, A. N. Simmons, J. Wu et al., "Amygdala response and functional connectivity during emotion regulation: a study of 14 depressed adolescents," Journal of Affective Disorders, vol. 139, no. 1, pp. 75–84, 2012. [41] Y. I. Sheline, D. M. Barcha, J. L. Price et al., "The default mode network and self-referential processes in depression," Cardiovascular Psychiatry and Neurology 9 Proceedings of the National Academy of Sciences of the United States of America, vol. 106, no. 6, pp. 1942–1947, 2009. [42] S. Aznar and A. B. Klein, "Regulating prefrontal cortex activation: an emerging role for the 5-HT2A serotonin receptor in the modulation of emotion-based actions?" Molecular Neurobiology, vol. 48, no. 3, pp. 841–853, 2013. [43] S. J. Banks, K. T. Eddy, M. Angstadt, P. J. Nathan, and K. Luan Phan, "Amygdala-frontal connectivity during emotion regulation," Social Cognitive and Affective Neuroscience, vol. 2, no. 4, pp. 303–312, 2007. [44] J. M. Smith and L. B. Alloy, "A roadmap to rumination: a review of the definition, assessment, and conceptualization of this multifaceted construct," Clinical Psychology Review, vol. 29, no. 2, pp. 116–128, 2009. [45] E. R. Watkins, "Constructive and unconstructive repetitive thought," Psychological Bulletin, vol. 134, no. 2, pp. 163–206, 2008. [46] S. Nolen-Hoeksema, J. Morrow, and B. L. Fredrickson, "Response styles and the duration of episodes of depressed mood," Journal of Abnormal Psychology, vol. 102, no. 1, pp. 20– 28, 1993. [47] L. Rood, J. Roelofs, S. M. Bögels, S. Nolen-Hoeksema, and E. Schouten, "The influence of emotion-focused rumination and distraction on depressive symptoms in non-clinical youth: a meta-analytic review," Clinical Psychology Review, vol. 29, no. 7, pp. 607–616, 2009. [48] T. D. Borkovec, W. J. Ray, and J. Stöber, "Worry: a cognitive phenomenon intimately linked to affective, physiological, and interpersonal behavioral processes," Cognitive Therapy and Research, vol. 22, no. 6, pp. 561–576, 1998. [49] T. D. Borkovec, E. Robinson, T. Pruzinsky, and J. A. DePree, "Preliminary exploration of worry: some characteristics and processes," Behaviour Research and Therapy, vol. 21, no. 1, pp. 9–16, 1983. [50] I. Demeyer, E. de Lissnyder, E. H. W. Koster, and R. de Raedt, "Rumination mediates the relationship between impaired cognitive control for emotional information and depressive symptoms: a prospective study in remitted depressed adults," Behaviour Research and Therapy, vol. 50, no. 5, pp. 292–297, 2012. [51] P. M. Zoccola and S. S. Dickerson, "Assessing the relationship between rumination and cortisol: A review," Journal of Psychosomatic Research, vol. 73, no. 1, pp. 1–9, 2012. [52] L. Wang, N. Paul, S. J. Stanton, J. M. Greeson, and M. J. Smoski, "Loss of sustained activity in the ventromedial prefrontal cortex in response to repeated stress in individuals with early-life emotional abuse: implications for depression vulnerability," Frontiers in Psychology, vol. 4, article 320, 2013. [53] D. J. Brotman, S. H. Golden, and I. S. Wittstein, "The cardiovascular toll of stress,"The Lancet, vol. 370, no. 9592, pp. 1089–1100, 2007. [54] K. D. Rudolph, W. Troop-Gordon, and D. A. Granger, "Individual differences in biological stress responses moderate the contribution of early peer victimization to subsequent depressive symptoms," Psychopharmacology, vol. 214, no. 1, pp. 209– 219, 2011. [55] J. F. Brosschot, W. Gerin, and J. F. Thayer, "The perseverative cognition hypothesis: a review of worry, prolonged stressrelated physiological activation, and health," Journal of Psychosomatic Research, vol. 60, no. 2, pp. 113–124, 2006. [56] G. P. Chrousos and P. W. Gold, "The concepts of stress and stress system disorders: overview of physical and behavioral homeostasis," Journal of the American Medical Association, vol. 267, no. 9, pp. 1244–1252, 1992. [57] B. McEwen, T. Seeman, R. Davidson, K. Scherer, and H. Goldsmith, "Stress and affect: applicability to the concepts of allostasis and allostatic load," inHandbook of Affective Sciences, Oxford University Press, New York, NY, USA, 2003. [58] K. A. Buss, R. J. Davidson, N. H. Kalin, and H. H. Goldsmith, "Context-specific freezing and associated physiological reactivity as a dysregulated fear response," Developmental Psychology, vol. 40, no. 4, pp. 583–594, 2004. [59] C. K. Fortunato, A. E. Dribin, D. A. Granger, and K. A. Buss, "Salivary alpha-amylase and cortisol in toddlers: differential relations to affective behavior," Developmental Psychobiology, vol. 50, no. 8, pp. 807–818, 2008. [60] M. R. Gunnar and D. M. Vazquez, "Stress neurobiology and developmental psychopathology," in Developmental Psychopathology, D. Cicchetti andD.Cohen, Eds.,Wiley,NewYork, NY, USA, 2006. [61] M. R. Gunnar, S. Wewerka, K. Frenn, J. D. Long, and C. Griggs, "Developmental changes in hypothalamus-pituitaryadrenal activity over the transition to adolescence: normative changes and associations with puberty," Development and Psychopathology, vol. 21, no. 1, pp. 69–85, 2009. [62] N. H. Kalin, S. E. Shelton, M. Rickman, and R. J. Davidson, "Individual differences in freezing and cortisol in infant and mother rhesus monkeys," Behavioral Neuroscience, vol. 112, no. 1, pp. 251–254, 1998. [63] I. M. Goodyer, J. Herbert, A. Tamplin, and P. M. E. Altham, "Recent life events, cortisol, dehydroepiandrosterone and the onset of major depression in high-risk adolescents,"The British Journal of Psychiatry, vol. 177, pp. 499–504, 2000. [64] E. C. Fabiansson, T. F. Denson, M. L. Moulds, J. R. Grisham, and M. M. Schira, "Don't look back in anger: neural correlates of reappraisal, analytical rumination, and angry rumination during recall of an anger-inducing autobiographical memory," NeuroImage, vol. 59, no. 3, pp. 2974–2981, 2012. [65] A. Compare, C. Zarbo, G. M. Manzoni et al., "Social support, depression, and heart disease: a ten year literature review," Frontiers in Psychology, vol. 4, article 384, 2013. [66] A. Compare, E. Germani, R. Proietti, and D. Janeway, "Clinical psychology and cardiovascular disease: an up-to-date clinical practice review for assessment and treatment of anxiety and depression," Clinical Practice and Epidemiology in Mental Health, vol. 7, pp. 148–156, 2011. [67] A. Compare, R. Bigi, P. S. Orrego, R. Proietti, E. Grossi, and A. Steptoe, "TypeDpersonality is associatedwith the development of stress cardiomyopathy following emotional triggers," Annals of Behavioral Medicine, vol. 45, no. 3, pp. 299–307, 2013. [68] K.Maier, D. Chatkoff, andM.M. Burg, "Cardiopatia coronarica e depressione: prevalenza, prognosi, fisiopatologia e trattamento," in Mente e Cuore. Clinica Psicologica della Malattia Cardiaca, E. Molinari, A. Compare, and G. Parati, Eds., pp. 93– 107, Springer, Milano, Italy, 2007. [69] C. B. Nemeroff and P. J. Goldschmidt-Clermont, "Heartache and heartbreak-the link between depression and cardiovascular disease," Nature Reviews Cardiology, vol. 9, no. 9, pp. 526–539, 2012. [70] J. W. Pennebaker and H. C. Traue, "Inhibition and psychosomatic processes," inEmotion, Inhibition, andHealth, H. C. Traue and J. W. Pennebaker, Eds., Hogrefe Huber, Seattle, Wash, USA, 1993. 10 Cardiovascular Psychiatry and Neurology [71] H. J. Brashares and S. J. Catanzaro, "Mood regulation expectancies, coping responses, depression, and sense of burden in female caregivers of Alzheimer's patients," Journal of Nervous and Mental Disease, vol. 182, no. 8, pp. 437–442, 1994. [72] I. Kirsch, J. Mearns, and S. J. Catanzaro, "Mood-regulation expectancies as determinants of dysphoria in college students," Journal of Counseling Psychology, vol. 37, no. 3, pp. 306–312, 1990. [73] J. J. Gross and O. P. John, "Mapping the domain of expressivity: multimethod evidence for a hierarchical model," Journal of Personality and Social Psychology, vol. 74, no. 1, pp. 170–191, 1998. [74] C. L. Gohm and G. L. Clore, "Four latent traits of emotional experience and their involvement in well-being, coping, and attributional style," Cognition and Emotion, vol. 16, no. 4, pp. 495–518, 2002. [75] L. Solano, M. Costa, L. Temoshok et al., "An emotionally inexpressive (Type C) coping style influences HIV disease progression at six and twelvemonth follow-ups,"Psychology and Health, vol. 17, no. 5, pp. 641–655, 2002. [76] J. S. Tucker, D. K. Winkelman, J. N. Katz, and B. L. Bermas, "Ambivalence over emotional expression and psychological well-being among rheumatoid arthritis patients and their spouses," Journal of Applied Social Psychology, vol. 29, no. 2, pp. 271–290, 1999. [77] R. Verissimo, R. Mota-Cardoso, and G. Taylor, "Relationships between alexithymia, emotional control, and duality of life in patients with inflammatory bowel disease," Psychotherapy and Psychosomatics, vol. 67, no. 2, pp. 75–80, 1998. [78] A. L. Stanton, S. Danoff-Burg, C. L. Cameron et al., "Emotionally expressive coping predicts psychological and physical adjustment to breast cancer," Journal of Consulting and Clinical Psychology, vol. 68, no. 5, pp. 875–882, 2000. [79] J. M. Smyth, "Written emotional expression: effect sizes, outcome types, and moderating variables," Journal of Consulting and Clinical Psychology, vol. 66, no. 1, pp. 174–184, 1998. [80] S. K. Lutgendorf and P. Ullrich, "Cognitive processing, disclosure, and health: Psychological and physiological mechanisms," in The Writing Cure: How Expressive Writing Promotes Health and Emotional Well-Being, S. J. Lepore and J. M. Smyth, Eds., American Psychological Association, Washington, DC, USA, 2002. [81] J.W. Pennebaker, E. Zech, and B. Rimé, "Disclosing and sharing emotion: Psychological, social, and health consequences," in Handbook of Bereavement Research: Consequences, Coping, and Care, M. S. Stroebe, R. O. Hansson, W. Stroebe, and H. Schut, Eds., American Psychological Association, Washington, DC, USA, 2001. [82] R. McCraty and D. Tomasino, "Coherence-building techniques and heart rhythm coherence feedback: new tools for stress reduction, disease prevention and rehabilitation," in Clinical Psychology and Heart Disease, E. Molinari, A. Compare, and G. Parati, Eds., Springer, Milano, Italy, 2006. [83] C. R. Snyder and S. J. Lopez, Handbook of Positive Psychology, Oxford University Press, New York, NY, USA, 2002. [84] B. L. Fredrickson, "The role of positive emotions in positive psychology: the broaden-and-build theory of positive emotions," American Psychologist, vol. 56, no. 3, pp. 218–226, 2001. [85] R.McCraty andD.Childre, "Thegrateful heart: the psychophysiology of appreciation," in The Psychology of Gratitude, R. A. Emmons and and M. E. McCullough, Eds., Oxford University Press, New York, NY, USA, 2004. [86] A. M. Isen, "Positive affect," in Handbook of Cognition and Emotion, T. Dalgleish and M. Power, Eds., John Wiley & Sons, New York, NY, USA, 1999. [87] J. Min, J. J. Yu, C. Lee, and J. Chae, "Cognitive emotion regulation strategies contributing to resilience in patients with depression and/or anxiety disorders," Comprehensive Psychiatry, vol. 54, no. 8, pp. 1190–1197, 2013. [88] L. Greenberg, Emotion-Focused Therapy, Coaching Client to Work through Their Feelings, APA, Washingtopn, DC, USA, 2002. [89] L. S. Greenberg, L. N. Rice, and R. Elliot, Facilitating Emotional Change: The Moment-by-Moment Process, Guilford, New York, NY, USA, 1993. [90] S. R. Bishop, M. Lau, S. Shapiro et al., "Mindfulness: a proposed operational definition," Clinical Psychology: Science and Practice, vol. 11, no. 3, pp. 230–241, 2004. [91] S. Kumar, G. Feldman, and A. Hayes, "Changes in mindfulness and emotion regulation in an exposure-based cognitive therapy for depression," Cognitive Therapy and Research, vol. 32, no. 6, pp. 734–744, 2008. [92] D. S. Mennin, R. G. Heimberg, C. L. Turk, and D. M. Fresco, "Applying an emotion regulation framework to integrative approaches to generalized anxiety disorder,"Clinical Psychology: Science and Practice, vol. 9, no. 1, pp. 85–90, 2002. [93] D. S. Mennin, C. L. Turk, R. G. Heimberg, and C. N. Carmin, "Focusing on the regulation of emotion: A new direction for conceptualizing and treating generalized anxiety disorder," in Cognitive Therapy over the Lifespan: Evidence and Practice, M. A. Reinecke and D. A. Clark, Eds., pp. 60–89, Cambridge University Press, New York, NY, USA, 2004. Submit your manuscripts at http://www.hindawi.com Stem Cells International Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 MEDIATORS INFLAMMATION of Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 Behavioural Neurology Endocrinology International Journal of Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 Disease Markers Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 BioMed Research International Oncology Journal of Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 Oxidative Medicine and Cellular Longevity Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 PPAR Research The Scientific World Journal Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 Immunology Research Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 Journal of Obesity Journal of Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 Computational and Mathematical Methods in Medicine Ophthalmology Journal of Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 Diabetes Research Journal of Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 Research and Treatment AIDS Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 Gastroenterology Research and Practice Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 Parkinson's Disease Evidence-Based Complementary and Alternative Medicine Volume 2014 Hindawi Publishing Corporation http://www.hindawi.com


A Quandary of Wokeness

Philosophy

Article A Quandary of Wokeness M. Oreste Fiocco Department of Philosophy, University of California, Irvine, CA, USA; email@example.com Submitted: 16 June 2021, accepted: 31 January 2022, published: 29 April 2022 Abstract: Being woke, that is, being aware of the appalling injustices borne by many in American society because of certain identities or features and wanting to act to redress these injustices, seems to put one in a quandary: either one can accept a role in the struggle against injustice that seems obviously inefficacious or, if one insists on doing more, one must, it seems, engage in epistemic imperialism, thereby wronging some of those one is endeavoring to help. Keywords: sexual orientation; race; gender; identity; wokeness; epistemic imperialism How to cite: Fiocco, M.O. A Quandary of Wokeness. Journal of Controversial Ideas 2022, 2(1), 10; doi:10.35995/jci02010010. © 2022 Copyright by the author. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY 4.0) license. I am a straight, white, cis man and I am woke. I characterize myself in these terms sincerely, without the least resentment or irony. In characterizing myself as woke, I mean that I am aware of the appalling injustices borne by people in American society because of their sexual orientation, race, gender, and other features. This awareness comes through observation, and the effort to empathize with people whose experiences it is impossible for me actually to share. It incites me to want to try to redress these injustices. Surely, there is much I can do, given that I am privileged in several dimensions, secure both in my position and financially, and have the conviction that action must be taken. If you want to undo injustice, you can find, through conversation and various media, lists of suggested actions to take. Some of these are not really helpful: Donate! Volunteer! (Yes, but to whom, with whom? Organizations are based on different principles, with competing priorities and objectives. On what grounds do you choose?) Some suggestions are more helpful: Call out bigotry! Intervene! I am willing to do both. Acting on these suggestions, however, depends on happenstance and, at best, addresses only a few instances of recurrent problems. Most lists of suggested actions include the exhortation to educate oneself. If you do this, you will acquire a sense of the complexity of the problems of injustice, whose bases are not merely in the overt actions of individuals, but in an insidious system. This system, in a society ostensibly founded on equality and embracing equal opportunity: incarcerates blacks at over 5 times the rate of non-Hispanic whites-so although blacks 1 Journal of Controversial Ideas 2022, 2(1), 10; 10.35995/jci02010010 make up only 13% of the total population, they are 40% of those incarcerated;1 allows a woman to make, on average, 78ȼ for every dollar a man does;2 leads to only 22% of Latinx adults having some sort of college degree-whereas 47% of adult whites do (thus, as of 2017, degree attainment levels of Latinx adults were about 10% lower than the attainment levels of whites in 1990).3 This system, working via mechanisms overlooked or ignored, can oppress even against the intentions of those who would succor. If you want to make momentous changes, ones more widespread and lasting than real but ephemeral ones in your immediate environment, you must smash the system. But here it is by no means clear how to proceed. The injurious system is manifest, the means of undoing it are elusive. If you are appropriately woke and educated, you will be conscious of discordant voices-including ones from those most harmed by the system-on the point of what needs to be done. There is disagreement about how the system works, on how much of it should be dismantled, on how to go about dismantling it, on what should replace it and even on how to understand those bearing its negative effects. Awareness of this variety of inconsistent opinions leads to irresolution that inhibits engagement. This is my current state. I have been bothered by this irresolution. Recently, I began to recognize its source in these conversations of discordant voices. A scene in Regina King's film, One Night in Miami, was revelatory. King's film is a fictional account of the night Muhammad Ali (Cassius Clay at the time) upset Sonny Liston to first become heavyweight champion of the world. In the scene I found so illuminating, Malcolm X is portrayed as castigating Sam Cooke for not doing enough in the struggle for racial justice. Cooke is fiercely indignant at the accusation that he is not contributing appropriately to the struggle and the two men argue. This film, of course, is not a documentary, so this argument might not have occurred. Yet you can easily believe it did, and that other similar ones, between those who live and might die by the struggle, take place every day. Any familiarity with discussions of race in America reveals a host of contrary judgments and directives. Therefore, for you to act without arbitrariness-in good faith and with commitment-to assist in redressing the problems of racial injustice seems to require evaluation of these incompatible views, in order to accept some and thereby reject others. Such evaluation seems to require, at the very least, clear accounts of the central concepts and distinctions-for example, blackness, Latinx, Asian, Asian-American, person of color, etc.-and some account of what is to be done in light of these. But I have no such accounts. More importantly, given the incompatibility of the views, I am not in the position to obtain these accounts without disregarding or overruling the views of some I aim to help, and such dismissal, an assertion of dominance, seems to be something like epistemic imperialism. Even if I am able-which is contentious-to say, for instance, what blackness is, who am I to say what is to be done in the best interests of those who are black, when doing so requires me to disregard some of those who identify as black? My irresolution is not limited to the domain of racial injustice. I have a very good friend, Kathleen Stock, who is vilified as a TERF (that is, a trans-exclusionary radical feminist). I understand her positions-for which she has been persecuted-and the conscientiousness and compassion that motivates them. Yet I have other very good 1 https://www.prisonpolicy.org/reports/rates.html. 2 https://upload.wikimedia.org/wikipedia/commons/f/f8/Equal_Pay_Infographic.pdf. (Source: Women's Bureau, U.S. Department of Labor). 3 https://edtrust.org/wp-content/uploads/2014/09/Latino-Degree-Attainment_FINAL_4-1.pdf. 2 Journal of Controversial Ideas 2022, 2(1), 10; 10.35995/jci02010010 friends who challenge the former, firmly rejecting her views. I also understand their positions, and appreciate the care and values underlying them. The positions here are irreconcilable, and so the actions each side prescribes to mitigate the unacceptable injustices associated with gender are simply incompatible. Given my awareness of this, principled action seems to require clear accounts of the central concepts (e.g., woman, transgender, nonbinary, etc.). But, again, I am not in the position to acquire these without a seeming epistemic imperialism. Even if I am able-which is contentious-to say, for instance, what it is to be a woman, who am I to say what is to be done in the best interests of women, when doing so requires me to disregard some of those who identify as women? The difficulties here are deeper than familiar ones of acting with imperfect knowledge or in light of your own competing values. Each of us must always act without complete knowledge of all factors germane to that action, as we balance values that might motivate incompatible actions. For limited beings, such agency cannot be faulted. Here, however, there is this problem, which seems unavoidable, of epistemic imperialism. To be an epistemic imperialist is to employ concepts or other theoretical apparatus recognized to be incompatible with some person's concepts (or other theoretical apparatus) in order to address issues of mutual importance, in particular, when devising courses of action that bear on that person. To act with respect to someone in light of an account of things-including, perhaps, themselves-that one recognizes they do not accept, is to belittle that person by dismissing their own understanding of things; in so doing, one acts as if the other is not a significant epistemic agent and, hence, what they might value or how they might structure their lives is irrelevant. Such canceling, via this sort of epistemic dominance, is a harm. Thus, if you assert that pork is edible by (openly) serving bacon to someone known to maintain a kosher diet or to be vegan, you disregard, in an inappropriate way, how that person sees things and, by so doing, disregard that person themselves (presenting your own reasons for eating pork while serving it does not alleviate the harm). Not every disagreement leads to epistemic imperialism. There can and must be civil exchanges in which opposing views are presented, compared, and the reasons for holding one of the views examined. Epistemic imperialism occurs after-or in lieu of-such an exchange of reasons, when disagreement remains and, insisting on one's own view, one acts to, say, get someone off a university campus or out of a certain restroom. Moreover, one is not an epistemic imperialist merely by adopting (and acting on) a view of some phenomenon about which one does not have first-hand experience and, hence, which others might, in some sense, know better. In most cases, the pertinent features of that phenomenon are sufficiently accessible that one can form justified beliefs about it, and act justifiably with respect to it, even without such intimate experience. So, for instance, I may have justified beliefs about abortion, and act in light of these, without ever having been pregnant. In cases of addressing injustice to certain groups or kinds, however, many people hold that the matter is different. In these cases, some believe that distinctive mental experiences available only to those who are members of that group (or instances of that kind) are constitutive of that group. Thus, what it is to be a member of that group is to have those very experiences. These constitutive experiences then inform the interests and needs of members of that group, thereby determining how they ought to be treated. Of course, this account of group membership is disputed by many, including those who self-identify as members of the relevant group. A different account of who is in a group has consequences for the interests and needs of that group, and so determines a different course with respect to how they ought to be treated. Crucially, even where there is not 3 Journal of Controversial Ideas 2022, 2(1), 10; 10.35995/jci02010010 this sort of dispute regarding who is in a group, there are always disagreements among members of a group about what actions ought to be taken to best promote their interests. I (indeed anyone) must adopt some account of group membership or course of action; presumably, ones that best align with my own epistemic principles and values. In doing so, I overrule the views-and consequently debase the values of-at least somemembers of the group I am endeavoring to help. This is epistemic imperialism. Given the divisions among members of any group, such imperialism is unavoidable, insofar as I would try to elevate a group that is being treated unjustly. So maybe, in light of all this, my role as a straight, white, cis man is not to instigate change. If principled action requires epistemic imperialism, then maybe my role is merely to appreciate alternative perspectives. This, though, would leave out powerful allies in the effort to eradicate injustice. Perhaps I should act only against those things that anyone, regardless of their more sophisticated views of race or gender, would regard as objectionable. I can do this, but it is a course that is extremely limited. It does seem that my role in this effort should not be simply passive or piecemeal. If, as seems the case, straight white cis men are the hegemonic group in America and the primary beneficiaries of the current system, then those among us who find this system unconscionable must have more to do to bring it down. This leads to a quandary: One in my position can accept a peripheral role in the struggle against injustice, one that seems obviously inefficacious. Or, if one insists on doing more, one must, it seems, engage to some extent in epistemic imperialism, canceling, and thereby wronging, some of those one is endeavoring to help. Neither course is consistent with being woke, that is, with the awareness of both the magnitude of the problems of injustice-and the essential role of all those who have endured injustice in determining how best to address these problems. Some might think the solution here is obvious. The bases of injustice in our society, they hold, are not the divisions between races and genders and other identities, but rather the material conditions arising from the disparities between the haves and the have nots. To redress injustice, you must eliminate the riling disparities; any action intended to address societal injustice not directed at these is misguided. I wholeheartedly accept the former claim, not the latter. Races, genders, orientations, and other means by which persons identify themselves are real and, therefore, fundamental4 parts of the world-no less real than cell phones, baseball, or money (which are no less real than trees, photosynthesis, or hydrogen atoms). As such, they can be, and do seem to be, sources of irreducible problems that require consideration and response. To dismiss these identities or the distinctions on which they are based, then, is not an adequate reaction to the quandary. I present this quandary not because I think it justifies some agenda. On the contrary, the main concern here is that I lack an agenda when one for those like me is urgently needed. I could participate in a march with other supporters of the Black Lives Matter movement (which I have); attend courses designed to make me more aware of the pervasiveness of injustice in our society (which I have), I could take a pledge, promoted by my employer, to uphold certain values of equality and eschew practices contrary to them (which I have). I could make every effort-which I do-to teach my children to judge people only by the content of their character, for our destiny is indeed tied up with all those 4 See my "Each Thing Is Fundamental: Against Hylomorphism and Hierarchical Structure," American Philosophical Quarterly 56 (2019): 289–301. 4 Journal of Controversial Ideas 2022, 2(1), 10; 10.35995/jci02010010 who are mistreated; our freedom is indeed inextricably bound to theirs.5 These actions, though, seem feeble. I am strong; certainly there is more that I can do. But what? I earnestly seek advice. Note, however, before you offer advice: although the foregoing considerations put me in a quandary, they very likely put you in one, too. Acknowledgments: I would like to express my sincere gratitude to the following people for very helpful discussion during the writing and revising of this paper: Sven Bernecker, Bill Brewer, Ian Coller, Jeff Helmreich, Dan Korman, Ari Koslow, Jeff McMahan, David Malament, J.B. Manchak, Duncan Pritchard, Kate Ritchie, Maya Rupert, Nathan Salmon, Matt Soteriou, Kathleen Stock, Elanor Taylor, and TiffanyWilloughby-Herard. One should not infer that those acknowledged agree with everything-or anything-that I say herein. 5 This is, of course, an allusion to Martin Luther King, Jr.'s "I Have a Dream" speech.