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Chapter 34 Early-Life Socioeconomic Status, Emotion Regulation, and the Biological Mechanisms of Disease across the Lifespan Edith Chen Gregory E. Miller Health disparities—that is, differences in tors, such as access to health care, have disease outcomes by socioeconomic sta- not sufficiently explained existing dispari- tus (SES)—remain one of the most press- ties (Adler, Boyce, Chesney, Folkman, & ing public health issues in our society. For Syme, 1993). In addition, there is growing example, low-SES individuals—meaning consensus that social, and not just biomedi- those who are low in education, income, cal, determinants of disease are important or occupational status—are 2.7 times more to identify (Dankwa-M ullan et al., 2010). likely to have repeated hospitalizations dur- In this chapter, we explore the role that ing a 1-year period than high-SES individu- emotion regulation may play in explaining als (National Center for Health Statistics, health disparities that emerge early in life. 2010), and 3.5 times more likely to suf- We do this by first providing an overview fer activity limitations due to disease than of links between childhood SES and disease high-SES individuals (Braveman, Cubbin, outcomes into adulthood. Second, we exam- Egerter, Williams, & Pamuk, 2010). And by ine whether emotion regulation may serve age 25, those from the lowest SES group are as one explanation for these associations by expected to live 6 fewer years compared to discussing links between emotion regulation those in the highest SES group (Braveman et and physiological processes implicated in al., 2010). disease, as well as meditational evidence for emotion regulation strategies in relationships This issue has become such a widespread between low-SES and these physiological concern that Healthy People 2010, the processes. Third, we discuss the question of national health objectives from the U.S. moderation—that is, whether certain types Department of Health and Human Services of emotion regulation strategies could also (2000), lists eliminating health disparities as serve as protective buffers for a subgroup of one of two overarching goals. In addition, those who are low in SES. Throughout this the National Institutes of Health (NIH) chapter, our premise is that low early life ranked the issue of health disparities third SES fosters certain emotion regulation strat- among its top five priorities (Thomson, egies that emerge during childhood and have Mitchell, & Williams, 2006). implications for physiological processes dur- ing childhood and into adulthood; hence, Explanations for why health dispari- we discuss findings that provide potential ties are so pervasive have been difficult to unearth, because commonly suggested fac- 586
SES, Emotion Regulation, and Mechanisms of Disease 587 explanations for links between childhood hood years increases risk for adverse health SES and both childhood and adult diseases. outcomes later in life. Early Life Environments and Risk In summary, a large body of epidemiolog- for Disease ical evidence demonstrates that low SES dur- We begin by discussing epidemiological evi- ing childhood is associated with a variety of dence that low SES increases risk for disease. poor health outcomes both during childhood Low SES in childhood confers greater risk and into adulthood. In the next section, we for disease, both throughout childhood and explore the idea that one psychological fac- into adulthood. A number of reviews have tor contributing to this association may be documented that the effects of low SES start difficulties with emotion regulation. early, and that low SES during childhood is associated with a number of different The Role of Emotion Regulation as adverse health outcomes, including greater a Pathway Linking SES and Disease asthma morbidity, obesity, and injury rates, In this section, we discuss the idea that and poorer self- and parent-r eports of health emotion regulation may serve as one psy- (Chen, Matthews, & Boyce, 2002; Good- chological pathway linking SES and dis- man, 1999; Starfield, Riley, Witt, & Rob- ease outcomes. To make this argument, we ertson, 2002; Starfield, Robertson, & Wiley, (1) provide a brief overview of associations 2002). between SES and emotion regulation; (2) discuss what types of emotion regulation In addition, the effects of low SES persist strategies are relevant to physiological out- into adulthood (Miller, Chen, & Parker, comes; (3) discuss physiological markers rel- 2011). For example, two reviews of the lit- evant to disease; (4) provide an overview of erature reported that the vast majority of previous research on links between emotion studies found an increased risk of all-cause regulation and physiological outcomes; and mortality in individuals who grew up in low- (5) describe studies that have tested emotion versus high-SES households (Galobardes, regulation as a mediator of SES and physiol- Lynch, & Smith, 2004, 2008). Moreover, ogy relationships. controlling for adult SES did not eliminate these associations, indicating that some- SES and Emotion Regulation thing specific to low SES in childhood con- Emotion regulation refers to strategies to fers risk for early mortality. Another review increase, decrease, or maintain emotional documented a heightened risk of cardiovas- responses (Gross, 2001). Gross’s process cular disease morbidity associated with low model of emotion regulation states that there SES in childhood (Galobardes, Shaw, Law- are various types of emotion regulation strat- lor, Lynch, & Smith, 2006). Again, associa- egies, including antecedent-focused emo- tions held up after researchers controlled for tion regulation, that is, strategies employed adult SES. before emotional responses become fully activated, and response-f ocused emotion These studies are corroborated by quasi- regulation, that is, strategies employed after experimental evidence, such as the viral emotion response tendencies have been acti- challenge paradigm in humans (Cohen, vated (Gross, 1998). Doyle, Turner, Alper, & Skoner, 2004), in which a sample of adults was quarantined In the context of SES, extensive evidence and exposed to rhinoviruses that cause documents that low-SES individuals are colds. Participants who came from low-SES more prone to experience negative emotions, households in childhood were significantly and in turn that these negative emotions more likely to become infected with the rhi- are detrimental for health (for a review, see novirus and to develop cold symptoms com- Gallo & Matthews, 2003; but note that pared to those who came from high child- the evidence of negative emotions actually hood SES households. These associations serving as a mediator of the SES–health held even after researchers controlled for relationship is mixed; Matthews & Gallo, adult SES, suggesting again that experienc- 2011). Nonetheless, in this context, effective ing low SES specifically during the child-
588 HEALTH IMPLICATIONS emotion regulation strategies should reduce nervous system (SNS) become activated with experiences of negative emotions. many psychosocial stressors, releasing hor- mones such as cortisol, epinephrine, and nor- epinephrine (Cannon, 1932; Kemeny, 2003). Implications of Emotion These hormones bind to receptors located on Regulation Strategies a variety of bodily tissues, exerting effects for Physiological Responses on the heart, vasculature, and metabolic Gross (1998) has documented that efforts and immune systems. With respect to acute that fall under antecedent-focused emotion physiological responses, profiles indicative regulation, such as reappraisal, have fewer of lower disease risk include a reduced mag- physiological costs than response-focused nitude of reactivity of these systems and/or emotion regulation strategies, such as sup- a quicker recovery time (quicker return to pression. Hence, in the next sections, we baseline levels) (Krantz & Manuck, 1984; focus on the role that antecedent-focused Linden, Earle, Gerin, & Christenfeld, 1997; emotion regulation plays in linking SES to Linden, Gerin, & Davidson, 2003; McE- physiological and health outcomes. wen, 1998; Schwartz et al., 2003). We note Antecedent-focused emotion regulation that much of the literature reviewed below involves strategies such as reappraisal—that does not directly measure SNS and HPA is, reevaluating a stressful situation in a way activity, but instead focuses on the responses that seeks to reduce its emotional impact. It of end organs such as the heart and blood can also include strategies such as situation vessels. However, because these organs are selection, situation modification, and atten- influenced by SNS and HPA activity, and are tion deployment; together with reappraisal, the source of eventual manifestations of car- all of these strategies occur temporally before diovascular disease (CVD), their responses emotional responses are generated and can to acute stressors are relevant here. alter behavioral, emotional, and physiologi- Over the long term, with excessive and cal response tendencies. Reappraisal is the prolonged exposure to the hormones men- strategy that has been studied most fre- tioned earlier, the structure and function of quently with respect to affective, cognitive, tissues and organs are thought to be altered, and social consequences (Gross, 2001), so in giving rise to pathogenic processes that drive the section below we focus below largely on CVD, such as obesity, insulin resistance, links between reappraisal and physiological systemic inflammation, high blood pressure, processes implicated in disease. endothelial dysfunction, and platelet activa- tion (Brotman, Golden, & Wittstein, 2007; Everson-Rose & Lewis, 2005; Rozanski, Relevant Physiological Markers Blumenthal, Davidson, Saab, & Kubzansky, for Disease 2005). Hence, we also review links between Conceptualizing pathways to disease on emotion regulation strategies and these lon- the biological end entails consideration of ger-term mechanisms. both acute and longer-term physiological Longer-term cumulative physiological responses. Below we provide a brief over- risk has sometimes been encapsulated in view of the types of systems and processes concepts such as allostatic load (McEwen, implicated in chronic diseases—with a focus 1998), which is defined as instances when on diseases linked to inflammation, such as individuals experience stressors repeatedly cardiovascular disease and asthma, so that and have more frequent activation of physi- readers will be familiar with the outcomes ological systems over time; or when physi- we present later on in studies of emotion reg- ological systems do not show adaptation of ulation and physiological processes. In this responses after repeated stressors; or when section, we focus on physiological systems shutdown mechanisms are delayed or insuf- that are capable of being altered by psycho- ficient, leading to prolonged physiological social factors (e.g., stress) and hence could responses over time. The strain on these be plausibly linked to variables such as emo- allostatic systems over years may eventu- tion regulation. ally cause a breakdown of these systems that Acutely the hypothalamic–pituitary– ultimately leads to disease. Empirically, high adrenal (HPA) axis and the sympathetic levels of obesity, insulin resistance, systemic
SES, Emotion Regulation, and Mechanisms of Disease 589 inflammation, blood pressure, endothelial Emotion regulation also mitigates longer- dysfunction, and platelet activation all pre- term pathogenic processes implicated in dict CVD morbidity and mortality (Danesh CVD. For example, better emotion regula- et al., 2005; Guh et al., 2009; Lindmark, tion abilities are linked to lower allostatic Diderholm, Wallentin, & Siegbahn, 2001; load, including higher high-density lipo- Ridker, Hennedens, Buring, & Rifai, 2000; protein (HDL) cholesterol, lower triglycer- Vasan et al., 2001; Yeboah et al., 2009). In ides, and lower basal systolic blood pres- addition, the accumulation of these charac- sure (Kinnunen, Kokkonen, Kaprio, & teristics, in constellations such as allostatic Pulkkinen, 2005). Similarly, reappraisals load or metabolic syndrome, predicts even have been linked to longer-term markers more strongly an increased risk of CVD of immune processes. For example, HIV- later in life (Seeman, Singer, Rowe, Hor- positive individuals who reported finding witz, & McEwen, 1997; Lakka et al., 2002; benefit after experiencing a major negative Morrison, Friedman, & Gray-McGuire, life event showed slower declines in cluster 2007; Ridker, Buring, Cook, & Rifai, 2003; of differentiation 4 (CD4) T cell levels over National Cholesterol Education Program, 2–3 years (indicating a slower progression 2002). to the diagnosis of AIDS) (Bower, Kemeny, Taylor, & Fahey, 1998). Finally, functional Emotion Regulation and Physiological indicators of poor emotion regulation, such and Disease Outcomes as the experience of high levels of depres- We focus here on links specifically between sion and anger, have been associated with the emotion regulation strategy of reap- higher levels of systemic inflammatory praisal and physiological responses, given markers that are implicated in CVD, such as the existing evidence with respect to this interleukin-6 (IL-6) and C-reactive protein strategy. Physiologically, reappraisals reduce (CRP) (Kiecolt-Glaser, McGuire, Robles, & cardiovascular reactivity to acute stressors. Glaser, 2002; Miller, Maletic, & Raison, For example, lower reappraisals of threat 2009). have been associated with reduced blood pressure reactivity during acute stressors Finally, emotion regulation strategies can in both children and adults (El Sheikh & also alter clinical disease outcomes. Reap- Harger, 2001; Maier, Waldstein, & Syn- praisals such as finding benefit after a life- owski, 2003), and lower ambulatory blood threatening event predicts a lower likelihood pressure during daily life social interac- of having a future heart attack (Affleck, Ten- tions (Chen, Matthews, & Zhou, 2007). nen, Croog, & Levine, 1987). Conversely, Similarly, individuals high in the ability to the experience of high levels of negative reappraise stressful situations show reduced affect (arguably an indicator of inadequate vascular reactivity during acutely stress- emotion regulation) has robust associations ful tasks (Mauss, Cook, Chang, & Gross, with CVD-related outcomes (Brosschot, 2007), and lower blood pressure and corti- Gerin, & Thayer, 2006; Everson-Rose & sol responses to an acute stressor (Salovey, Lewis, 2005; Krantz & McCeney, 2002; Stroud, Woolery, & Epel, 2002). Experi- Kubzansky, Kawachi, Weiss, & Sparrow, mental evidence shows that interventions 1998). In addition, how effectively one can aimed at changing appraisals in patient pop- manage emotions (emotional intelligence) ulations produce increases in benefit find- is linked to better general indicators of ing, as well as decreases in serum cortisol physical health (better self-reported health levels from pre- to postintervention (Cruess and fewer illnesses; Goldman, Kraemer, et al., 2000). Finally, consistent with the & Salovey, 1996; Schutte, Malouff, Thor- idea that underlying positive beliefs about steinsson, Bhullar, & Rooke, 2007). Finally, others shape reappraisals and physiological experimental data suggest that interventions responses, those who believe that the world to help individuals process negative emo- is fair (high in just world beliefs) reappraise tions effectively, such as through written dis- an acute stressor as less threatening and closure, produce fewer symptoms and health show less vascular reactivity to the stressor center visits in healthy adults, and improve (Tomaka & Blascovich, 1994). disease indicators in patient populations (Smyth, Stone, Hurewitz, & Kaell, 1999; Smyth, 1998).
590 HEALTH IMPLICATIONS Emotion Regulation as a Mediator ing why low-SES children show heightened inflammatory and cardiovascular responses. The previously discussed literature links In turn, these inflammatory and cardiovas- emotion regulation strategies to physiologi- cular profiles are predictive of later disease. cal, endocrine, and immune processes impli- cated in chronic diseases such as CVD. But is there any evidence that emotion regulation strategies actually mediate the relationship The Role of Emotion Regulation between SES and these biological processes? as Buffer In a series of studies, our research group has In the previous section we discussed how shown evidence for such mediation by focus- emotion regulation strategies serve as one ing on how children and adolescents reap- psychological mediator explaining links praise stressful life situations. between low SES and detrimental profiles of physiological processes relevant to disease. In healthy adolescents, we have shown In this section, we turn to the question of that lower SES is associated with greater whether emotion regulation could also serve cardiovascular reactivity to acute laboratory as a moderator of SES and health outcomes. stressors. We further showed that low-SES Despite the robust associations between low adolescents were less likely to reappraise SES and disease, there remains a subset of ambiguous life situations (e.g., shopping individuals that displays physiologically with an overly attentive sales clerk nearby) healthy profiles despite living under adver- in benign ways. Finally, we documented sity. What can explain this group of individ- that reappraisals of threat statistically medi- uals? That is, what factors might naturally ated the relationship between low SES and protect individuals who grow up in low-SES heightened cardiovascular reactivity (Chen, environments from the physiological toll Langer, Raphaelson, & Matthews, 2004). and accumulation of health problems typi- cally exacted by these environments? Our In patient populations, we have docu- research group has articulated a theory mented similar patterns with disease- about the psychological characteristics that relevant markers. For example, in pediatric may be specifically beneficial to low-SES patients with asthma, we have demonstrated individuals (Chen & Miller, 2012). Emotion that low SES is associated with greater asthma inflammation (e.g., greater produc- tion of cytokines relevant to asthma, higher regulation plays a key role in this theory; eosinophil counts). We further demonstrated hence we discuss its role as a buffer for low- that low SES is associated with being less SES individuals in this chapter. In this sec- likely to reappraise ambiguous life situations tion, we first provide an outline of the shift- in benign ways in this patient population. and-persist theory; then we describe the Finally, we documented that reappraisals of empirical evidence in support of this theory. threat statistically mediated the relationship between low SES and heightened asthma inflammation (Chen, Fisher, Bacharier, & Shift and Persist Strunk, 2003; Chen et al., 2006). The theory begins with the notion that a We further documented that effects of low lifetime of facing constraints with limited SES can be seen at the genomic level. Low options leads those living in a low-SES con- SES children with asthma showed indica- text to place value on the ability to adjust in tions of increased activity of proinflamma- response to stressors through emotion regu- tory gene networks, and these associations lation strategies such as reappraisals (shift- between low SES and gene expression pat- ing). At the same time, in this context, suc- terns were no longer significant once reap- cessful adaptation entails enduring adversity praisals of threat during ambiguous life situ- with strength by finding meaning in difficult ations were statistically controlled (Chen et situations and maintaining optimism in the al., 2009). face of adversity (persisting). We proposed Taken together, this set of studies illus- that this combination of approaches to trates how low-SES individuals are, on aver- dealing with adversity reduces physiologi- age, less able to engage in reappraisals of cal responses to stressful situations acutely, life situations effectively. Furthermore, reap- specifically among those who are low in praisals of threat form one pathway explain- SES, and over the long term mitigates the
SES, Emotion Regulation, and Mechanisms of Disease 591 progression of pathogenic processes leading in emotion regulation to deal with current to chronic diseases such as CVD (Chen & adversities; one also needs also to find Miller, 2012). broader meaning in life and be able to reap- praise the future. Hence the label that we Hence, one of the key components of use, “shift and persist,” is intended to con- this beneficial psychological profile centers note the fact that it is this combination of around the ability to regulate one’s emo- characteristics that will be beneficial to low- tions through reappraisal strategies. Because SES individuals with respect to their health. low-SES individuals on average have fewer In the next section, we discuss evidence sup- opportunities to select or modify their life porting the notion that when low-SES indi- situations (alternative forms of emotion regu- vidual engage in shift and persist, there are lation; Gross, 1998, 2001), reappraisals rep- benefits to the physiological mechanisms resent a realistic approach to emotion regula- that underlie disease. tion in this group. That is, given the myriad day-to-day, largely uncontrollable stressors Empirical Evidence for Shift experienced by many low-SES individuals, and Persist in many instances their best option may be In two studies from our research group, we to control the one thing they can—the self— have documented the benefits of shift and rather than engage in what may turn out to persist specifically for low-SES individuals. be futile attempts to control their environ- In the first study, we assessed childhood ment. By controlling the self, they engage in SES in a national sample of adults. We mea- emotion regulation strategies in which they sured cumulative physiological risk via allo- accept that a stressor has occurred and try to static load, based on 24 different measures change the effect that stressor has on them. across seven physiological systems. Shift They do this by reappraising the meaning of and persist was measured using question- an event, so that the implications for their naires probing reappraisal-related coping lives become less negative. And they adjust styles (shift) and future orientation (persist). their emotional reactions, so that the event We found a three-way interaction between evokes less distress in them. As they come to childhood SES, shift, and persist in predict- see events as having less serious implications ing allostatic load in this sample. Breaking and being less upsetting, the physiological down this three-way interaction revealed responses they elicit are mitigated. Hence, that there was a significant two-way inter- we propose that low-SES individuals uphold action between shift and persist in those as an ideal the goal of utilizing emotion regu- from low childhood SES backgrounds, but lation strategies related to reappraisals when no two-way interaction of shift and persist dealing with stress. The ability to do this suc- among those from high childhood SES back- cessfully comprises the “shift” part of our grounds. The two-way interaction revealed shift-and-p ersist model. that those participants with low childhood SES backgrounds who were high on both Shifting is hypothesized to be neces- shifting and persisting had the lowest allo- sary but not sufficient for buffering low- static load. In contrast, the combination of SES individuals from stressors. In addition shift and persist did not predict allostatic to shifting, we hypothesize that it will be load among those from high-SES childhood important to persist—that is, to endure backgrounds (Chen, Miller, Lachman, Gru- adversity with strength by finding meaning enewald, & Seeman, 2012). in life and maintaining optimism about the future. Finding meaning allows individuals In a second study, using a clinical sample, to understand adversity and to grow from we investigated the effects of shift and per- it. Optimism allows individuals to maintain sist among children diagnosed with asthma, hope about the future, and can be essentially using questionnaires that tapped both reap- thought of as reappraising the future (as praisal styles of coping (for shifting) and opposed to shifting, which entails reapprais- optimism about the future (for persisting). als of events that have already happened). Among those low in SES, the higher their Thus, reappraisals are an important compo- shift-and-persist scores, the lower their nent of both shifting and persisting. asthma inflammation. Also, among low-SES children, higher shift-and-p ersist scores pro- We further postulate that there is some- thing important about the combination— that is, it is not sufficient to be able to engage
592 HEALTH IMPLICATIONS spectively predicted less functional impair- health outcomes across the SES gradient. ment (fewer school absences, less rescue One possibility we suggest here is that on inhaler use) 6 months later, when we con- the psychological end, low-SES children may trolled for baseline levels. In fact, low-SES experience greater difficulties with emotion children who scored high on shift and persist regulation. In particular, low-SES children had inflammatory and clinical profiles more may find themselves less able to reappraise similar to high-SES children with asthma stressful situations in positive ways. In turn, than to low-SES children who scored low in this leads them to be more likely to expe- shift and persist. Shift and persist was not rience negative emotions and physiological related to inflammatory or clinical profiles costs, both acutely and cumulatively, that in high-SES children with asthma (Chen et may contribute to risk for disease over the al., 2011). long term. We note, however, that much of this work is correlational, and cannot be In summary, we find that low-SES indi- used to draw conclusions about causality. viduals who are able to engage in emotion regulation strategies involving reappraisals, We also document that emotion regula- in combination with being optimistic and tion serves an important function in terms future oriented, are the ones who show the of buffering low-SES children from detri- most beneficial physiological profiles and mental physiological profiles. That is, those the least clinical disease impairment. Shift low-SES children who are able to engage in and persist is only beneficial to those who shift and persist (utilizing effective emotion are low in SES, not to those who are high regulation strategies, such as reappraisals in in SES, suggesting that there are context- combination with persisting with hopes and specific determinants of what types of strat- finding meaning with respect to one’s future) egies will be beneficial physiologically for exhibit physiological profiles that are more whom. In particular, for low-SES individu- similar to profiles of high-SES children than als, engaging in reappraisals and focusing on to those of low-SES children who do not the future when encountering current daily engage in shift and persist. These children stressors that are largely uncontrollable may also showed less clinical disease impairment be beneficial. In contrast, for those who are compared to low-SES children who did not high in SES, proactive attempts to eliminate engage in shift and persist. These findings or mitigate stressful situations may be a suggest that shift and persist serves as a nat- more beneficial approach given the greater ural protective factor in low- but not high- resources these individuals tend to have. SES children. In addition, it is important to note that Emotion regulation strategies are an the combination of shift and persist is criti- important factor to consider when inves- cal to physiological profiles among low-SES tigating individual-level psychological individuals. That is, neither shifting nor per- mechanisms underlying SES disparities in sisting alone was predictive of physiological health. These strategies provide an inter- outcomes; rather, it is only when individuals face between children and their broader combine shifting and persisting that one sees social environments, and play an important physiological benefits. This suggests that role in shaping hormonal and inflamma- emotion regulation strategies of reappraisals tory responses to stress. In turn, these acute on their own are not sufficient; rather, they responses appear to have longer-term impli- need to be combined with a focus on the cations for the pathogenic processes that future that emphasizes optimism and mean- underlie chronic diseases across the lifespan. ing in order to derive physiological benefits References among those who are low in SES. Conclusions Adler, N. E., Boyce, W. T., Chesney, M. A., Folk- In summary, health disparities are a press- man, S., & Syme, S. L. (1993). Socioeconomic ing issue in our society, and researchers inequalities in health: No easy solution. Jour- have been working to understand what fac- nal of the American Medical Association 269, tors account for such striking differences in 3140 –3145. Affleck, G., Tennen, H., Croog, S., & Levine, S.
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Chapter 35 Emotion Regulation and Cardiovascular Disease Risk Allison A. Appleton Laura D. Kubzansky My tongue will tell the anger of my heart, Or else my heart concealing it will break. —William Shakespeare, The Taming of the Shrew (Act 4, Scene 3) Cardiovascular disease (CVD) is a leading ering CVD from a developmental or life cause of morbidity and mortality world- course perspective may provide new insights wide (Mendis, Puska, & Norrving, 2011), into disease etiology and suggest novel ave- and it is increasingly clear that disease pro- nues for prevention and intervention efforts. cesses initiate in childhood (Berenson & Srnivasan, 2005; Lloyd-Jones et al., 2009; The notion that emotions are inextrica- National Heart, Lung, and Blood Institute, bly linked to heart health has been part of 2007). Poor cardiovascular health is defined popular discourse for centuries. Terms such as having a combination of unhealthy levels as “broken heart” and “heartsick” invoke of lipids, blood pressure, and glucose, being the well-understood sentiment that while overweight or obese, smoking, being sed- emotions may emanate from within the entary, and having an unhealthy diet. This psyche, emotions move the heart to behave profile is highly prevalent among middle- and respond in predictable ways. Moreover, aged adults in the United States (Folsom et the idea that the control or regulation of al., 2011; Lloyd-Jones et al., 2010) and once emotions also matter for heart health has risk factors are elevated, they are difficult to popularly endured as well, as evidenced ameliorate (Lloyd-Jones et al., 2010). With in the opening quotation. However, while the growing awareness that major CVD risk emotions and cardiovascular health have factors such as atherosclerosis and hyperten- long been recognized as intertwined, the sion are often identifiable many years before exact nature of the relationship is not well the disease is fully manifest, the Ameri- understood. Much epidemiological and psy- can Heart Association recently revised its chological work describes cardiovascular national goals for cardiovascular health pro- risk in association with negative emotions motion to emphasize the identification and (for a review, see Suls & Bunde, 2005), prevention of early life risk factors for CVD and a growing body of work also describes (Lloyd-Jones et al., 2010). As such, consid- the potentially protective effects of posi- 596 tive emotions on cardiovascular health (for
Emotion Regulation and Cardiovascular Disease Risk 597 a review, see Boehm & Kubzansky, 2012). emotion regulation may play an important Despite this accumulation of evidence, key role in determining CVD risk over the life questions remain, including whether or not course. emotions truly cause CVD, or whether spe- cific emotions are a product of the illness. In this chapter, we first consider the labo- Additional questions revolve around under- ratory and population-based evidence sug- standing the different roles of positive and gesting that emotion regulation may con- negative emotion in determining CVD risk. tribute to CVD risk. The literature linking We suggest that examining CVD risk in emotion regulation to CVD has considered relation to emotion regulation will help to cardiovascular conditions (e.g., cardiovas- address these issues. Thus, in this review we cular disease, hypertension) and the biologi- consider what the extant literature tells us cal markers that are considered indicative of about a relationship between emotion regu- risk of developing CVD in individuals who lation and CVD risk, and identify the poten- are too young to have developed actual dis- tially harmful and health-promoting impact ease. These include indicators of cardiovas- of various emotion regulation strategies in cular function and risk that are measured in this context. response to acute stress, generally obtained from laboratory-based studies (e.g., blood A large literature indicates that both posi- pressure reactivity), predisease conditions tive and negative emotions are relevant in and markers of risk (e.g., hypertension, terms of maintaining cardiovascular health C-reactive protein, metabolic syndrome), or developing CVD (Boehm & Kubzan- and actual measures of disease (e.g., myo- sky, 2012; Suls & Bunde, 2005). Moreover, cardial infarction, death). The term cardio- research has increasingly indicated that vascular disease refers to a group of dis- positive emotional functioning entails more orders of the heart and blood vessels, and than the absence of emotional distress, and encompasses both coronary heart disease that physical and mental health may depend and cerebrovascular disease (Mendis et al., in part on our ability to meet environmen- 2011), the two cardiovascular disease out- tal demands (Kubzansky, Park, Peterson, comes most commonly considered in rela- Vokonas, & Sparrow, 2011). Drawing on tion to emotion. We review work in these these findings, investigators have begun areas, while limiting our discussion to exem- to speculate that beyond the effects of any plar studies that focus on objectively mea- specific emotion, it is the regulation of emo- sured outcomes. Doing so mitigates a com- tion that is critical. Emotion regulation is mon concern about these associations that a higher order feature of emotional func- self-report bias inflates or falsely suggests tioning that involves the monitoring and that emotional factors are causally related management of emotional experience and to health (i.e., more distressed individuals response (Gross, this volume). Emotion report more symptoms). Also, we primarily regulation can be conscious or unconscious consider prospective studies that examine and involve both up- and down-regulation longitudinal data in which emotion regula- of positive and negative emotions. Emotion tion is assessed initially among individuals regulation is learned through socialization who are disease-free, prior to development and experience over time, with childhood of CVD. These study designs help to miti- being an important period of development gate another common concern about these as temperament, biology, and social factors associations: that health conditions actu- interact to build regulatory skills and strate- ally drive emotions rather than the reverse. gies that are then used across the life course We also discuss and apply a developmental (Calkins & Hill, 2007; John & Gross, 2004; perspective to emotion regulation and CVD Rothbart, Sheese, & Posner, and Thompson, risk associations, and consider the evidence this volume). The research findings linking linking childhood emotion regulation to emotions and CVD risk, the importance of CVD risk in adulthood. Finally, we close early life experience in learning to regulate with recommendations for future work. emotion, and the recent evidence indicating Due to space constraints we do not consider that deterioration of cardiovascular health studies of emotion regulation and health risk begins in childhood (Berenson & Srnivasan, behaviors (e.g., smoking) in detail, although 2005), have raised the question of whether we note that such behaviors are considered
598 HEALTH IMPLICATIONS potential pathways through which emotion interest. In this section, we bring together regulation may influence CVD, and rec- important work from each area, integrat- ommend these as areas for future research. ing evidence across disciplines in order to Also, while we focus on studies of emotion expand the evidence base and move the sci- regulation in relation to CVD etiology (i.e., ence forward. development of disease), we recognize that emotion regulation is also likely related to It is important to note that whether the use CVD progression and survival. Finally, it is of an emotion regulation strategy is adap- important to note that while the effects of tive or maladaptive is context-dependent. emotion regulation are likely involved in the However, based on the empirical findings to pathophysiology of many diseases, the evi- date, we argue that the predominant use of a dence to date is strongest for CVD and, as particular set of strategies (e.g., suppression, such, is reviewed specifically in this chapter. inhibition) may carry more cardiovascular health risks than other strategies (e.g., reap- Evidence Linking Emotion praisal, disclosure), even though on occasion Regulation to Cardiovascular the use of such strategies may well be adap- Function and Disease tive. Thus, we acknowledge that there may Over the past several decades, the study be contexts in which strategies such as reap- of emotion regulation and cardiovascular praisal may not always be beneficial, and function and disease has been taken up by strategies such as suppression may be useful. related but traditionally distinct disciplines The larger point is that effective regulation of psychology and epidemiology. Psycholog- (regardless of what regulatory strategy is ical laboratory-based and epidemiological used in any given situation) versus emotion population-based studies have documented dysregulation may have differential effects associations between emotion regulation on cardiovascular disease risk. and cardiovascular function and risk. How- ever, as each discipline has different goals Laboratory‑Based Research and generally relies on different methodolo- Laboratory-based work has found emotion gies, the evidence linking emotion regulation regulation strategies to be associated with to CVD has developed largely in two differ- identifiable patterns in cardiovascular func- ent literatures, with limited crossover. Lab- tion and response to regulatory demands oratory-based studies of emotion regulation that have implications for disease risk (see and cardiovascular function tend to have also Chen & Miller, this volume). The gen- small sample sizes and focus on identifying eral hypothesis guiding work on emotion relevant biological alterations occurring in regulation in this context is that failing association with experimentally manipu- to manage emotions effectively requires a lated use of regulatory strategies. Epidemio- certain degree of psychological and physi- logical studies tend to be observational and ological exertion, and is essentially a form employ large population-based samples, and of stress exposure. Thus, such exertion is focus more on the diagnostic and health risk thought to exact a physiological cost on the implications of dysregulated emotion. More- body, which leads to “wear and tear” and over, epidemiological work includes studies thereby increases vulnerability to disease that explicitly measure emotion regulation over time (Consedine, Magai, & Bonanno, and test associations with cardiovascular 2002; Pennebaker & Beall, 1986). risk (i.e., direct evidence), but these are lim- ited in number. However, more numerous Population-based research tends to focus are studies of cardiovascular risk that do on clinically relevant risk markers (typi- not measure emotion regulation directly but cally measured with resting levels) and inci- assess aspects of emotional functioning (e.g., dence of disease. In contrast, laboratory- negative emotions) that may provide indica- based work often focuses on indicators of tion of poor emotion regulation. We include cardiovascular function and risk that are these studies, because they provide relevant measured in response to acute stress, such but indirect evidence of the relationships of as heart rate and blood pressure reactivity, pulse transmission time, finger pulse ampli- tude, and cardiac interbeat interval. Stress- ful or demanding situations activate the
Emotion Regulation and Cardiovascular Disease Risk 599 hypothalamic–pituitary–adrenal (HPA) axis instructed to suppress, reappraise, or remain and the sympathetic nervous system (SNS), neutral when viewing an anger-eliciting film, resulting in a cascade of related hormones those in the suppression condition exhibited that in turn influence a range of end organ significantly reduced heart rate variability responses, including heart rate and blood compared with baseline, whereas those in pressure. High reactivity is typically inferred the reappraisal condition showed increased by higher heart rate and blood pressure lev- heart rate variability. These studies suggest els, greater increases in sympathetic activa- that actively inhibiting or suppressing emo- tion during acute stress, and slower return to tional expression and experience is associ- baseline levels of these parameters during a ated with deleterious autonomic function- recovery period, after the acute stress expe- ing, which over time may take a toll on the rience has ended. Reactivity has also been cardiovascular system. measured by examining cortisol response to stress (a marker of HPA activation) (Chida Other laboratory-based work has consid- & Hamer, 2008). Heart rate variability is ered whether effects of emotion regulation another parameter this work has considered; strategies over a longer period of time may at rest, lower levels of heart rate variability be associated with beneficial effects on a have been linked with increased risk of devel- variety of other markers of cardiovascular oping CVD (Thayer & Lane, 2007), while health. Many studies have found regula- reduced heart rate variability in response to tory strategies such as emotional disclosure, stress or slower return to resting levels have or the ability to discuss or disclose emo- been linked with autonomic dysregulation tions verbally or in writing, to have posi- (Cohen et al., 2000). Other experimental tive effects on a range of health outcomes, work manipulating emotion regulation has although fewer studies have directly assessed also considered effects on immune-related outcomes related to cardiovascular health. markers or alterations in relevant health In an early experimental study of trauma conditions. disclosure, Pennebaker and Beall (1986) instructed disease-free subjects to write Much work considering emotion sup- in journals over 4 consecutive days about pression and inhibition in these settings has either a traumatic experience or a neutral- found some support for the idea that sup- control event. Compared to controls, those pression may alter acute cardiac response who wrote about a trauma and related emo- in ways that could impair cardiovascular tions made significantly fewer health center health. For example, in two key studies, visits in the 6 months following the disclo- participants were instructed to suppress sure experiment. Such benefits of emotional emotion expression when watching films disclosure have been replicated across a designed to elicit diverse emotions (Gross & variety of samples and with cardiovascular- Levenson, 1993, 1997). Compared to con- related health outcomes. For example, in a trols, those who actively suppressed both randomized controlled trial of expressive positive (amusement) and negative emotion writing among 179 individuals who recently (disgust, sadness) experienced significantly experienced a first-time myocardial infarc- increased activation of the autonomic sys- tion, those randomized to the expressive tem, as measured by a composite variable of writing/emotional disclosure condition had pulse transit time to the finger, finger pulse significantly lower blood pressure, reported amplitude, pulse transit time to the ear, and fewer cardiac symptoms, had fewer medi- figure temperature. Similar patterns of asso- cal appointments, and used less medica- ciation have been observed across a range tion than controls 5 months postinterven- of physiological and health indicators, with tion (Willmott, Harris, Gellaitry, Cooper, more reactivity or risk-related outcomes & Horne, 2011). A recent meta-a nalysis of associated with strategies of suppression 146 experimental disclosure studies among and inhibition (Consedine et al., 2002). One 10,994 participants found a positive and recent study found divergent associations of significant effect (small to moderate in size) emotion suppression and reappraisal with of disclosure specifically on cardiovascular heart rate variability in response to an emo- indicators related to CVD, such as lipids and tion regulation task (Denson, Grisham, inflammation (Frattaroli, 2006). Among the & Moulds, 2011). Among 131 women physiological parameters studied, the stron-
600 HEALTH IMPLICATIONS typically assessed in large-scale studies of gest beneficial effect of emotional disclosure the determinants of CVD. Such epidemio- was evident for specific immune function logical studies generally consider CVD risk parameters. For example, experimental dis- across a set of related outcomes, including closure was associated with lower levels of angina (usually ascertained by self-reported proinflammatory cytokines and C-reactive symptoms), myocardial infarction (usually protein, which in turn predict reduced risk ascertained by hospital records and diagnos- of CVD (Danesh et al., 2004; Pearson et al., tic procedures), and coronary heart disease 2003). death (ascertained by death certificates). Studies of CVD may also consider hyper- While these studies generally suggest tension and stroke as relevant outcomes, potential divergent effects of inhibitive and although we know of no epidemiological expressive forms of regulatory strategies on studies of directly assessed emotion regula- cardiovascular function, other studies do tion that have considered these conditions. not find such differences, and suggest that Incident disease refers to rate of new cases use of either type of strategy requires physi- developing disease rather than the number ological exertion. For example, in a study of of cases in a population at any given time. 190 female college students, women were instructed to suppress emotion, reappraise Existing results are highly congruent emotion, or react naturally (control con- with those from laboratory and experimen- dition) when discussing an upsetting film tal work, and emerging evidence suggests with another participant. Participants in that emotion regulation strategies that fre- both the suppression and reappraisal condi- quently involve suppression or inhibition tions demonstrated larger increases in heart may increase CVD risk, whereas use of rate variability compared to controls (But- other regulatory strategies may reduce CVD ler, Wilhelm, & Gross, 2006). Some stud- risk. For example, one prospective study of ies linking emotion regulation with altered 1,122 older male participants considered cortisol responses in response to stress in the relation between self-regulation and the a laboratory setting have described similar development of CVD. Self-regulation was results whereby suppression and reappraisal assessed when men were disease-free, using are each related to higher cortisol response items from the Minnesota Multiphasic Per- (Lam, Dickerson, Zoccola, & Zaldivar, sonality Inventory assessing one’s ability to 2009). However, in other studies reap- manage impulses, feelings, and behaviors; praisal is associated with less cortisol reac- emotion regulation was identified as a cen- tivity (Chen & Miller, this volume; Salovey, tral feature of this measure of self-r egulation. Stroud, Woolery, & Epel, 2002). Given that Exemplary items used to construct the Self- laboratory-based work explicitly consider- Regulation scale included “I control my ing potential divergent effects of these strat- emotion”; “I am not easily angered”; and egies on a unified and comparable set of “I am usually calm and not easily upset.” cardiovascular-relevant outcomes remains Compared with men who had the lowest limited, additional work is needed to ascer- levels of self-regulation, those with the high- tain whether and how these acute effects est levels had 62% reduced risk of experi- might be informative in regard to long-term encing a nonfatal myocardial infarction or risk. In addition, prospective work would be coronary heart disease (CHD) death over 13 useful to determine whether such patterns of years of follow-up (Kubzansky et al., 2011). exertion affect health over time. Moreover, the association appeared to be additive, because each standard deviation Population‑Based Work increase in self-regulation was associated Direct Evidence with a 20% reduced risk of incident angina, Though capacity to regulate emotions may nonfatal myocardial infarction, and CHD influence cardiovascular health, few have death over the follow-up period. Findings explicitly examined this question in popu- were maintained after adjusting for known lation-based research. While highly prom- coronary risk factors, as well as main effects ising, evidence is limited to a handful of of positive and negative affect. studies, because emotion regulation is not Another study identified control over anger as one mechanism linking anger to
Emotion Regulation and Cardiovascular Disease Risk 601 cardiovascular risk (for a review, see Ded- “I try to suppress my anger but would like ert, Calhoun, Watkins, Sherwood, & Beck- to let others know how I feel”) was associ- ham, 2010). In a study of Finnish adults (n = ated with midlife metabolic syndrome. The 7,933), several dimensions of anger expres- authors found that mood repair and mood sion and control were assessed in relation to maintenance were significantly associated incident CVD events (myocardial infarction, with reduced risk of metabolic syndrome, stroke) over 10–15 years of follow-up (Hauk- whereas emotional ambivalence was associ- kala, Konttinen, Laatikainen, Kawachi, & ated with higher risk of metabolic syndrome Uutela, 2010). Anger control was character- at age 42. This study suggests that effective ized by items related to the extent to which regulation of emotion may protect cardio- anger is regulated (e.g., “I control my tem- vascular health, and emotion dysregula- per”), and anger expression was character- tion may contribute to CVD risk. However, ized by how people generally react when this study did not account for prior physi- feeling angry (e.g., “I express my anger”). cal health or other relevant covariates such While experiences of anger per se were not as socioeconomic status that could provide associated with CVD, participants report- alternative explanations for the associations ing the lowest levels of anger control had observed. 35% significantly higher risk of experienc- ing a fatal or nonfatal cardiovascular event A recent study by our group also observed in the subsequent 10–15 years compared to divergent associations of different emo- those with the highest levels of anger control tion regulation strategies as assessed by the (Haukkala et al., 2010). These findings were Emotion Regulation Questionnaire (Gross maintained even after researchers took into & John, 2003) with C-reactive protein account demographic and coronary risk fac- (CRP). CRP, an inflammatory risk marker tors, as well as depressive symptoms. While for CVD, is associated with atherosclerosis not specifically addressing how the anger is and incident coronary events (Danesh et al., regulated (e.g., suppressed, situation reap- 2004; Pearson et al., 2003). CRP is often praised), this study suggests that the occur- used as a predisease marker of CVD by ref- rence of negative emotions such as anger erencing a diagnostic cut point identified by may not be sufficient to induce risk. Instead, the Centers for Disease Control and Preven- it is the failure to regulate the emotion effec- tion (CDC)/American Heart Association tively that may help explain anger and CVD (Pearson et al., 2003). We examined reap- risk associations. praisal (i.e., altering how one thinks about an emotion-eliciting situation in order to Another study of 181 Finnish men and change its emotional impact) and suppres- women observed cross-sectional associa- sion (i.e., inhibiting emotional expression tions of adaptive and maladaptive emotion in response to an emotion eliciting event). regulation with metabolic syndrome (Kin- Among 379 U.S. adults, an increase of one nunen, Kokkonen, Kaprio, & Pulkkinen, standard deviation in reappraisal was signif- 2005). Metabolic syndrome, which is char- icantly associated with 20% lower odds of acterized by hypertension, elevated lipid having levels of CRP at or above the CDC/ levels, central adiposity (a measure of body American Heart Association’s high risk cut fat distribution), and insulin resistance, point (Appleton, Buka, Loucks, Gilman, & is a well-established risk marker for CVD Kubzansky, 2013). Conversely, a one stan- (Expert Panel on Detection Evaluation and dard deviation increase in suppression was Treatment of High Blood Cholesterol in significantly associated with 44% higher Adults, 2001). In this study, the authors odds of having systemic inflammation levels examined whether use of certain emotion indicating high CVD risk. Similarly, some regulation strategies including mood repair preliminary analyses by our research group (e.g., “I am imagining something nice to using the same sample found reappraisal keep my mood up”) and mood mainte- and suppression also be patterned differen- nance (e.g., “I would not want to change tially with 10-year risk of developing CVD this mood”) were associated with meta- in midlife (Appleton, Loucks, Buka, & Kub- bolic syndrome at age 42. The authors also zansky, unpublished data). This emerging examined whether emotional ambivalence body of work provides the first direct pop- (a specific form of emotion dysregulation; ulation-based evidence that emotion regula-
602 HEALTH IMPLICATIONS tion may contribute significantly to cardio- of distress marked by dysregulated emotion vascular health. in response to trauma, has also been linked to incident cardiovascular events in mili- Indirect Evidence tary veteran and community-based civilian While the evidence base explicitly linking populations (for a review, see Dedert et al., emotion regulation to CVD in the general 2010). Taken together, these studies suggest population is small, much indirect evidence significantly increased cardiovascular risk comes from studies of poor emotional func- associated with experiencing chronic nega- tioning and negative affective states, which tive emotion and poor emotional function- are characterized in part by dysregulated ing that likely derives in part from maladap- emotion (Kubzansky et al., 2011; Taylor, tive emotion regulation. Lerner, Sage, Lehman, & Seeman, 2004). Chronic distress is thought to influence car- Whereas experiencing chronic negative diovascular health by way of repeated and emotions may indicate dysregulation, posi- excessive activation of the stress response tive emotional functioning may be consid- and impaired adaptation, which over time ered a marker of effective emotion regula- may contribute to damaging the cardio- tion. A recent review of studies of positive vascular system (McEwen, 2003), and also psychological well-being and cardiovascu- risk behaviors associated with poor men- lar health identified a consistent protective tal health (e.g., smoking) (Everson-Rose & effect of positive emotions and psychological Lewis, 2005). Work in this area has pri- attributes related to more frequent occur- marily focused on three negative affective rence of positive emotions (e.g., optimism); states in association with CVD risk: anger, findings also suggested that positive emo- anxiety, and depression (Chida & Steptoe, tions and related factors are associated with 2009; Suls & Bunde, 2005). Though epide- health-related behaviors that reduce risk of miological studies often consider depression CVD (e.g., increased physical activity) and and anxiety as representing single emotions, more resilient biological function (e.g., less in fact they reflect complex constellations systemic inflammation) (Boehm & Kub- of chronic elevations of maladaptive cogni- zansky, 2012). The evidence of CVD buff- tions, behaviors, and emotions, of which ering attributable to positive functioning is dysregulated emotion is one feature (Laza- most well established for optimism (Boehm rus, 1991). However, given the importance & Kubzansky, 2012; Peterson & Bossio, of dysregulated emotion in these affective 2000). For example, in a study of 97,253 states, we review studies linking them to participants of the Women’s Health Initia- CVD, because we speculate that an emo- tive, women with high levels of dispositional tion regulation perspective could add insight optimism had significantly lower risk of inci- to understanding their observed associa- dent CHD and CHD mortality compared tions. Studies reviewed in this section do to those with low levels of optimism over not explicitly measure emotion regulation; 8 years of follow-up, even after controlling we therefore characterize them as providing for health risk behaviors, obesity, lipids, and indirect evidence that dysregulated emotion depressive symptoms (Tindle et al., 2009). may contribute to CVD. Another domain of healthy psychological In a review of 37 studies examining pro- functioning that may promote cardiovascu- spective associations of negative emotions lar health is emotional vitality, which can with incident CHD events in initially healthy be defined as feeling energetic or full of pep, individuals, high anger was associated and having a sense of positive well-being and with 1.5- to threefold higher risk of CHD; emotional self-c ontrol characterized in part chronic anxiety was associated with 1.5- to by effective emotion regulation (Kubzansky sevenfold higher risk of CHD; and clinically & Thurston, 2007; Rozanski & Kubzansky, relevant levels of depression was associated 2005). In a study of 6,025 healthy men and with more than a 2.5-fold elevated risk, with women ages 25–74 years at baseline, those gradations in risk evident according to levels with the highest levels of emotional vitality of depressive symptoms (Kubzansky, 2007). had 19% reduced risk of developing CHD Posttraumatic stress disorder, a severe form over 15 years of follow-up compared to those with the lowest levels of emotional vital- ity (Kubzansky & Thurston, 2007). Effects
Emotion Regulation and Cardiovascular Disease Risk 603 were maintained after researchers took into sion (Howren, Lamkin, & Suls, 2009), and account known coronary risk factors, as chronic and acute stress (Janicki-Deverts, well as depression and psychological prob- Cohen, Matthews, & Cullen, 2008; Steptoe, lems. Taken together, these studies suggest Hamer, & Chida, 2007). that positive emotional and psychological functioning protect cardiovascular health, Moreover, beyond simply indicating the providing indirect evidence that effective absence of deterioration, the ability to regu- emotion regulation may increase cardiovas- late emotions effectively appears to enhance cular resilience. cardiovascular health actively. Similar to mechanisms associated with dysregulation, Mechanisms by Which Emotion effective emotion regulation may promote Regulation Influences CVD cardiovascular health by not only preventing Emotion regulation may affect CVD risk deteriorative processes but also promoting through both physiological and behav- restorative health behaviors and biological ioral pathways. As noted earlier, dysregu- functioning. Important to note is that dete- lated emotion is associated with increased riorative and restorative processes are not likelihood of engaging in deleterious always on a continuum (for a more detailed cardiovascular-r elated health behaviors such discussion, see Boehm & Kubzansky, as smoking, unhealthy diet, and low physical 2012). Relevant health-p romoting behaviors activity (Kiecolt-Glaser, McGuire, Robles, include engaging in more opportunities for & Glaser, 2002). Emotion dysregulation is rest and restoration (Rozanski & Kubzan- also associated with deteriorative biological sky, 2005), frequent consumption of fruits functioning in terms of the development of and vegetables, improved problem solving, obesity (Blaine, 2008), high levels of cho- and mobilization of social support (Eisen- lesterol and blood pressure, atherosclerosis, berg, Hofer, & Vaughan, 2007). Whereas and inflammation (Appleton, Buka, et al., dysregulated emotion may heighten HPA 2013; Boehm & Kubzansky, 2012). Labo- and SNS activity and initiate a cascade of ratory-based studies (see earlier sections for physiological risks for CVD, effectively examples) suggest that effects may occur via regulated emotion may prevent such activ- heightened or repeated activation of stress– ity and further enhance healthy cardiovas- response systems, including the HPA and cular functioning, although few studies have SNS. Such overactivation has been linked to directly tested this hypothesis. In one of a variety of potentially damaging biological the few empirical tests conducted, a recent alterations, including hemodynamic forces study (reviewed earlier) found support for such as increased turbulence and shear this hypothesis by demonstrating that reap- stress leading to impaired endothelial func- praisal was associated with lower inflam- tion, and flow-related arterial injury leading matory risk and suppression was associated to increased atherogenesis, as well as altered with elevated inflammatory risk (Appleton, electrical stability of the heart and increased Buka, et al., 2013). Other forms of healthy inflammation (Kubzansky & Kawachi, psychological functioning that have been 2000). For example, heightened HPA and identified as possible markers of adaptive SNS activity and resultant stress hormones emotion regulation (e.g., positive well-being, (e.g., corticosteroids, catecholamines) initi- optimism) have also been linked to relevant ate an inflammatory response characterized biological markers, such as slower rates of by the production of a number of inflamma- progression of carotid atherosclerosis and tory markers, including CRP (Black & Gar- better endothelial function (Boehm & Kub- butt, 2002). Inflammation is of increased zansky, 2012; Ikeda et al., 2011). interest in studies of emotion regulation and CVD, because it is strongly implicated Important to consider is that emotion in the pathophysiology of CVD (Danesh regulation strategies are used at different et al., 2004; Pearson et al., 2003) and has points during the emotion-generative pro- also been linked with several factors related cess (Gross, 2001; Gross & John, 2003; to emotion regulation, including depres- John & Gross, 2004), and strategies can be employed at any stage. Thus, it may be that the effect of the emotion regulatory strategy on physiological activation, inflammation, and subsequent CVD risk is due in part to
604 HEALTH IMPLICATIONS the timing of use of each strategy. For exam- adults during their middle to later adult- ple, reappraisal is antecedent-focused, which hood, a time when CVD is likely to become means that it is employed before the emo- manifest, many studies indicate that loss of tion occurs and involves changing cognitive cardiovascular health can begin in childhood appraisals about the situation, which then and progress over the life course (Berenson prevents or reduces the intensity of nega- & Srnivasan, 2005). Studies of emotion tive emotions (Gross, 2001; Gross & John, regulation and CVD among adults are ill 2003; John & Gross, 2004). Therefore, equipped to answer important etiological HPA or SNS dysregulation may be avoided, questions as to when these processes emerge potentially leading to lower levels of systemic and begin to exert damaging or health- inflammation, which in turn may lower promoting effects. Given that emotion regu- CVD risk. On the other hand, suppres- lation strategies are learned over time, with sion, a response-focused strategy employed childhood being a major period of develop- after the emotion has occurred, involves ment (Calkins & Hill, 2007; John & Gross, the modification of behavioral manifesta- 2004), a more explicit consideration of these tions of the emotion (Gross, 2001; Gross & relationships over the life course may be John, 2003; John & Gross, 2004). Though highly fruitful. In this section, we argue that individuals may appear outwardly tranquil, the way forward in emotion regulation and chronic negative emotions and associated CVD research is to move toward framing HPA and SNS dysregulation may continue and evaluating hypotheses from a develop- internally unchecked, ultimately contribut- mental or life course perspective. Doing so ing to increased systemic inflammation and may not only answer important scientific CVD risk. Moreover, suppression has been questions but also suggest novel avenues for found to require significant mental exer- the prevention of CVD. tion (Consedine et al., 2002; Gross, 2001). Thus, the act of suppression may further tax Applying a Developmental Perspective body systems and contribute to elevations in Children are typically born with many of systemic inflammation and CVD risk. Emo- the requisite components of ideal cardiovas- tion regulation theory and research suggest cular health. They generally have healthy that regulating the emotion earlier in the blood pressure, lipid, and glucose levels; emotion-generative process may be more they do not smoke and have the potential effective than doing so in the later, response- for developing an ideal body weight, and focused stage of the process (Gross, 2001). healthy dietary and physical activity prac- As such, while the appropriateness of any tices. So how does the loss of cardiovascu- given strategy is context dependent, consis- lar health occur, and when does it begin to tent reliance on response-focused (e.g., sup- become evident? What role does emotion pression) versus antecedent-oriented (e.g., regulation play in the loss or promotion of reappraisal) regulation may differentially cardiovascular health over time? We believe impact biological processes and long-term the answers to these questions are related CVD risk. in part to achieving a key socioemotional developmental milestone during childhood: The Way Forward attaining emotion regulation skills. The confluence of evidence from laboratory- and population-based research strongly sug- Emotion regulation is not primarily an gests that the association between emotion inborn trait. Rather, it is a set of strategies regulation and CVD is not spurious. More- learned through socialization and expe- over, risk and protective associations have rience over time, with childhood being a been consistently observed across a variety key period of development (John & Gross, of emotion regulation indicators, signify- 2004). Temperament, maturation, and ing that emotion dysregulation may increase social experiences shape core emotion regu- CVD risk, whereas effective emotion regu- lation competencies during childhood, with lation may lower it. While all the evidence refinements occurring over the lifespan in reviewed thus far has been obtained with accordance with new experiences (Calkins & Hill, 2007; John & Gross, 2004; Zeman, Cassano, Perry-Parrish, & Stegall, 2006).
Emotion Regulation and Cardiovascular Disease Risk 605 This developmental or life course perspective ally exclusive, it is possible that emotion reg- can help us understand how achieving this ulation skills originating during childhood developmental milestone specifically influ- shape developing brain architecture and ences CVD risk in adulthood. For example, biological systems, as well as contribute to children who develop patterns of dysregu- behaviors that together and independently lated emotion regulation (e.g., impulsivity, influence later cardiovascular risk. Thus, poor attention, depressed mood) generally developing poor emotion regulation skills continue to exhibit such patterns through during childhood may have lifelong cardio- adolescence and adulthood (Brame, Nagin, vascular consequences by negatively altering & Tremblay, 2001; Caspi, Moffitt, & New- biological systems during sensitive periods man, 1996; Dekker et al., 2007). Thus, as of development and through accumulated they age, children with such patterns of reg- damage over time. For example, persistent ulation are more likely to initiate and main- psychological distress (i.e., dysregulated tain a range of risk-related health behaviors emotion) is associated with activation of the (e.g., cigarette smoking, sedentary behav- HPA axis (Luppino et al., 2010). Prolonged ior, poor diet) that over time may contrib- HPA activity is thought to up-regulate hor- ute to disease development and progression mones that influence appetite and promote (Shonkoff & Phillips, 2000). weight gain (Luppino et al., 2010). As such, poor childhood emotion regulation may Developmental or life course epidemiol- alter developing metabolic processes during ogy is the study of chronic disease risk in a sensitive period of development, which in terms of the long-term effects of health- turn may increase risk of obesity and other relevant experiences that occur during gesta- conditions linked with increased suscep- tion, childhood, adolescence, and adulthood tibility to developing CVD (e.g., elevated (Ben-Shlomo & Kuh, 2002). Experiences inflammation, dyslipidemia) later in life. can be biological, behavioral, environmen- Conversely, learning effective emotion regu- tal (physical and social), and psychological lation skills early in life may prevent such in nature. Emotion regulation can be consid- risk and promote resiliency by helping to ered one such factor that may have positive buffer such deleterious stress reactivity and or negative health implications over time. prevent such damage to biological systems. From this perspective, emotion regulation Also, psychological distress/dysregulated may affect disease risk mainly in two ways. emotion is associated with behaviors related First, a latency model suggests that both to higher risk of obesity that may emerge adverse and health-promoting experiences even in childhood (and continue through during particular sensitive or critical periods adolescence and into adulthood), such as of development will have lasting effects on emotional eating, consumption of calorie- health and functioning, with effects emerg- dense foods, and decreased physical activity ing years or decades after the initial experi- (Blaine, 2008), whereas adaptive emotional ence (Ben-Shlomo & Kuh, 2002; Shonkoff, functioning is associated with greater like- Boyce, & McEwen, 2009). Such a model lihood of engaging in health-promoting implies that early prevention and interven- behaviors (Boehm & Kubzansky, 2012). tion are crucial. Second, an accumulation model specifies that the number and dura- While the American Heart Association’s tion of experiences cumulatively add up to national goals for cardiovascular health affect health, again, often with a significant promotion emphasize that cardiovascular amount of time passing before the effects risk originates early in life and urge study manifest as health outcomes (Ben-Shlomo of early-life antecedents (Lloyd-Jones et al., & Kuh, 2002; Shonkoff et al., 2009). This 2010), considering emotion regulation and perspective suggests multiple windows of CVD risk from a developmental perspec- opportunity for prevention and intervention, tive is highly novel. While there is a grow- because an accumulation model would sug- ing literature on child emotion regulation gest that positive and negative factors cumu- and adult CVD risk, we do not know how latively build to determine disease resilience early in life these processes may be evident, and risk, respectively. because research examining emotion regula- tion and biological markers of CVD risk are Because both latency and accumulation of scant. We turn now to the emerging empiri- risk explanations are plausible and not mutu-
606 HEALTH IMPLICATIONS cal evidence linking childhood emotion reg- a prospective study of 2,278 Australian boys ulation to adult CVD risk. and girls, found that child behavior prob- lems (a marker of emotional dysfunction) at Evidence Linking Child Emotion ages 5 and 14 years were associated with 4.6 Regulation to Adult CVD Risk higher risk (95% confidence interval (CI): Among the limited set of prospective stud- 2.36, 9.06) of obesity at age 21, once they ies on associations between child emotion controlled for maternal demographic and regulation and adult CVD risk, most have lifestyle variables, child dietary patterns, TV focused on upstream risk markers for CVD, viewing, family meals, and physical activity. such as obesity and inflammation, rather In a study of 2,209 Finnish boys, Duarte than on objectively measured clinical end- et al. (2010) found that both moderate and points of disease (e.g., myocardial infarc- high levels of conduct problems (which may tion, stroke). This may be due to (1) limited also mark severely dysregulated emotion) availability of prospectively assessed infor- at age 8 years were associated with two- to mation on childhood emotional functioning threefold higher risk of overweight and obe- in cohort studies that were initiated decades sity at ages 18–23, compared to low levels of ago, and (2) the relative youth of participants conduct problems. These associations were in the longitudinal cohorts that have col- maintained when the researchers controlled lected information on child emotional func- for hyperactivity and sociodemographic tioning and adult health, so that actual CVD variables. outcomes have not yet developed. Moreover, most studies assess primarily poor emo- Similar findings have been observed in tional functioning, behavior problems, or studies of childhood emotional functioning psychological disorders. These conditions and systemic inflammation in adulthood. can be considered markers of or proxies for For example, in a prospective study of 379 dysregulated emotion, but they do not pro- U.S. adults, multiple domains of child emo- vide direct assessments of emotion regula- tional functioning (directly assessed by a tion. As discussed previously in our review study psychologist when participants were of studies of depression and anxiety with age 7) were examined in association with CVD risk, we do not conflate poor emotion CRP levels in middle adulthood. Poor child regulation with psychopathology. Instead, self-regulation (i.e., unrestrained, impulsive we acknowledge that child behavior dis- behavior) and distress proneness (i.e., emo- orders and emotional functioning reflect a tionally labile, easily frustrated) were each complex set of factors that include problems associated with elevated CRP levels 35 years with emotion regulation. Thus, these stud- later, after researchers controlled for demo- ies are suggestive, and we encourage future graphics, being born small for gestational work to measure child emotion regulation age, child health status, child body mass explicitly in relation to later cardiovascu- index, and child IQ (Appleton et al., 2011). lar risk. That said, findings from life course Associations were robust, because poor studies of child emotional functioning and child emotional functioning was associated behavior problems, and adult CVD risk are with 2.3- to 3.9-fold greater odds of having congruent with associations observed in CRP levels at or above the CDC/American studies of adults and suggest that cardiovas- Heart Association’s cut point for being at cular risk may have developmental origins in high-risk for CVD (Pearson et al., 2003). child emotion regulation. Moreover, there was evidence that these associations were mediated by adult weight For example, while the direction of the status and modified by early life socioeco- relation between emotional functioning and nomic status (Appleton et al., 2011, 2012). obesity is debated and is likely to be bidi- In other words, poor childhood emotional rectional (Atlantis & Baker, 2008; Luppino functioning increased inflammatory risk et al., 2010), several studies have found that in adulthood by way of higher body mass poor child emotional functioning contrib- index, and such associations were more utes to the development of obesity in adult- robust for children growing up in poorer hood (Duarte et al., 2010; Goodwin et al., environments than for those from higher 2008; Mamun et al., 2009). Mamun et al., in level socioeconomic environments (see also Chen and Miller, this volume, for a more
Emotion Regulation and Cardiovascular Disease Risk 607 detailed discussion of the interrelationships risk. For men, no association was observed between socioeconomic status and adversity, for attention regulation and 10-year CVD emotion regulation, and health). In a study risk, but each standard deviation increase of 526 male participants of the Dunedin, in child distress proneness was significantly New Zealand cohort, Odgers et al. (2007) associated with 17% higher risk. These examined childhood conduct problem levels associations were maintained when we con- assessed repeatedly from ages 7–26 years in trolled for childhood cardiovascular health, association with various physical health out- body mass index, chronic conditions, IQ, comes at age 32, including CVD risk factor socioeconomic status, being born small for clustering (a composite of factors including gestational age, and demographic factors. overweight, high blood pressure, and dys- Next, in another prospective study within regulated lipid levels, among others) and this sample, we considered the role of atten- inflammation, as measured by CRP. Com- tion regulation in association with the devel- pared to those with low levels, boys with opment of a favorable cardiovascular health persistently high levels of conduct problems profile at age 42 (Appleton et al., 2013). This had 2.9 higher odds (95% CI: 1.3–6.2) of profile is characterized by low blood pres- having high-risk CRP in adulthood. Adult- sure, low body mass index, healthy lipid hood CVD risk factor clustering was also levels, not smoking, and not having diabetes higher in those with persistent conduct prob- (Daviglus et al., 2004; Lloyd-Jones, Dyer, lems than in better functioning children, but Wang, Daviglus, & Greenland, 2007). A one the association was not significant (Odgers standard deviation increase in child atten- et al., 2007). tion regulation was significantly associated with 40% higher odds of having favorable While measures of behavior problems can cardiovascular health in midlife. Of note, be considered markers of emotion dysregu- this association was maintained when we lation, they ultimately provide somewhat adjusted for early life cardiovascular health, limited insight into the broader relationship socioeconomic status, and potential psy- between emotion regulation and CVD risk, chosocial and behavioral pathway variables since they measure emotional functioning from adulthood. These studies suggest that at only one end of the spectrum rather than earlier acquisition of effective emotion regu- considering the range of functioning. Few lation may reduce risk of CVD and promote life course studies have considered whether early development of healthy cardiovascular adaptive or effective emotion regulation in functioning. childhood is associated with reduced CVD risk in adulthood. This is a critical gap in the Summary and Recommendations literature. To address this issue, our research for Future Work group has conducted two preliminary stud- Taken together, the evidence from labo- ies that examine the potential cardiovascu- ratory- and population-based studies in lar benefit of effective emotion regulation in adulthood and over the life course suggest childhood. that poor emotion regulation may impair cardiovascular function and increase risk, First, in a prospective study of 377 U.S. whereas effective emotion regulation may adult men and women, we examined asso- reduce risk and promote cardiovascular ciations of effective and poor emotion health. Moreover, evidence is accumulating functioning, assessed by a study psycholo- that CVD may have developmental origins gist when participants were age 7, with the in child emotion regulation that influence 10-year risk of developing CVD in their 40s trajectories of risk or resilience earlier than (Appleton, Loucks, Buka, Rimm, & Kub- was previously considered. However, as is zansky, 2013). For women, a one standard evident from this examination of the litera- deviation increase in child attention regula- ture, research in this area is still limited, and tion (ability to stay focused, considered an additional work is needed to address critical effective regulatory strategy) was marginally remaining issues. For example, studies that associated with 8% reduced risk (p = .09) of explicitly measure emotion regulation in developing CVD in the next 10 years, and a one standard deviation increase in distress proneness (considered poor functioning) was significantly associated with 31% higher
608 HEALTH IMPLICATIONS conjunction with cardiovascular health and at modifying risk during this time are not functioning over time (and across a range of yet well established. In general, public health outcomes) will help to identify when these and biomedicine have not focused on the processes emerge and exert damaging or sensitivity of child emotion development to health-promoting effects. In addition, stud- help safeguard cardiovascular or other forms ies that consider not only dysregulation but of lifelong health, or prioritized emotional also effective emotion regulation in relation development for resource allocation as a to CVD outcomes would provide clearer way to reduce disease burden in adulthood. understanding of the spectrum of effects. Because we believe research in this area will Moreover, epidemiological research should continue to indicate the central importance be informed by experimental findings, and of developing emotion regulatory capacity, vice versa, to ensure that causal inferences we suggest that greater resources be dedi- are accurate and to guide efficient explo- cated to promoting the acquisition of healthy ration of how effects may occur. Research emotion regulation strategies throughout on pathways, behavioral and biological, life, with a particular emphasis on early life also remain limited but could facilitate dis- stages. tinguishing between latency and cumula- tive effects, thereby indicating key periods However, to our knowledge, programs for targeting prevention and intervention designed to promote the development of strategies. In fact, the earlier reported find- healthy emotion regulation skills among ings that effects of emotion regulation were children in the general population are scant. modified by socioeconomic status are par- Work in this area is generally intervention- ticularly intriguing, suggesting that effects focused rather than prevention-oriented. of emotion regulation on health may well Thus, efforts target pediatric populations be modifiable (Appleton et al., 2012). It may with identified mental health problems, with be that when more resources are available the aim of building or improving emotion to children who are somewhat dysregu- regulation skills. For example, contextual lated, regulatory capacity can be improved, emotion regulation therapy, a developmen- thereby leading to better health over the life tally based treatment approach for pediat- course (for related discussion of this issue, ric depression, involves learning to manage see Chen and Miller, this volume). emotional distress by identifying contexts that elicit maladaptive emotional responses, We suggest that work in this area is excit- then incorporating more adaptive responses ing and worth pursuing, because it has a that can be used even in challenging situa- number of important implications, both for tions (Kovacs & Lopez-Duran, 2012). This understanding emotion regulation more gen- approach is developmentally focused, which erally and for thinking about it as a lifelong means that therapeutic approaches are critical asset. Capacity to regulate emotions age-appropriate and tailored to the child’s may have more far-reaching effects than developmental stage. Moreover, there are a have previously been identified, and timing number of effective school-based programs of acquisition of this capacity may matter for designed to prevent anxiety and promote physical health and perhaps other outcomes emotional resilience in children through as well. Thus, capacity to regulate emotion is cognitive-behavioral therapy and other important not only as an outcome in its own forms of psychotherapy (for a review, see Neil right, but also as a determinant of health, & Christensen, 2009). Such programs might which suggests it could play an important provide the basis for thinking about preven- role in health-r elated prevention strategies. tion strategies that could be implemented on a larger scale, either in population-based True prevention of CVD must involve the studies or with high-risk populations. Thus, prevention of the development of CVD risk prevention programs could consider incor- factors in the first place. This “primordial porating these and other skills-building prevention” has become increasingly more techniques typically used in traditional interesting in public health and medicine psychological treatments for child emotion (Lloyd-Jones et al., 2010). While experts dysregulation (e.g., guided practice in using in cardiovascular health largely acknowl- adaptive strategies, role playing, paren- edge that childhood is a life stage particu- tal involvement) in the design of programs larly amenable to CVD prevention, efforts
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Chapter 36 Emotion and Self‑Regulation Failure Dylan D. Wagner Todd F. Heatherton As most people can attest, conquering vices enson, 1994). It has been suggested that one and changing bad habits are difficult. Even function of emotion is to indicate whether when the motivation to change is strong, individuals are succeeding or failing to meet self-control failures are common. Subjec- their goals (Carver & Scheier, 1990). There- tively, it often feels as though our capacity fore, just as it would be fatally maladaptive to self-regulate waxes and wanes in the face for an organism to have the ability to turn of new temptations, changing moods, and off thirst, it would be just as detrimental to fatigue. Contemporary investigations into be able to completely shut down emotions. the causes of self-regulation failure have However, there are times when our emo- demonstrated that the ability to self-regulate tions interfere with our goals or may lead us can be undermined by a variety of threats to further distress, such as when our mood that act by impairing awareness, exhausting causes us to violate social norms (i.e., being limited resources, or increasing the salience tragically depressed on a first date or over- of temptations. Perhaps the most potent of joyed at a funeral). Thus, it is often in our these threats is negative affect. When peo- best interests to be able to regulate our affec- ple experience emotional distress, be it in tive states. the form of a bad mood, disappointment, or social rejection, they often find it more In this chapter, we take the view that reg- difficult to resist temptations or to sup- ulating emotions relies on much of the same press unwanted impulses and may engage cognitive and neural machinery as regulating in various forms of self-defeating behaviors other responses (e.g., thoughts, behaviors, (for a review, see Baumeister, 1997). How- impulses) with the understanding that, all ever, the relationship between emotions and things being equal, emotions are more dif- self-control is by no means all one-way; too ficult to suppress or inhibit. Unlike behav- much self-regulation over a period of time iors, thoughts, or cravings, all of which tend can increase emotional reactivity, as well as to have a clear target of regulation (e.g., “I impair an individual’s ability to regulate his must not grab the cigarette and light it”), or her emotions. affect is typically more diffuse, with no clear action to regulate. Indeed, one of the central Much like the experience of hunger or findings of research on emotion regulation thirst, emotions serve to motivate behavior is that direct, response-focused attempts to and predispose individuals toward certain suppress the outward expression of emotion actions (e.g., Keltner & Gross, 1999; Lev- are more cognitively taxing and less success- 613
614 HEALTH IMPLICATIONS ful than antecedent-focused methods such sexual behavior (Bousman et al., 2009; Rob- as distraction and reappraisal (Richards erts et al., 2012), excessive Internet usage & Gross, 2000). Although there may very (LaRose, Lin, & Eastin, 2003), and aggres- well be advantages to considering emotion sion (Berkowitz, 1989). Although multiple regulation as a separate domain (i.e., Gross, emotions can be considered negative or posi- 2002), for the present discussion we consider tive in valence, the extant literature on the it fruitful to think of emotion regulation as role of affect in self-regulation seldom disso- another type of self-regulation, thereby ren- ciates them. Here, too, we employ the broad dering it subject to the same vulnerabilities categories of negative and positive affect, and threats as other forms of self-control noting that these necessarily subsume many (see Heatherton & Wagner, 2011). different emotion categories. In the following sections, we examine the The role of negative affect in initiating relationship among emotions, emotion regu- self-regulation failure has also been stud- lation, and self-regulation failure. We focus ied in experimental settings using a variety primarily on intrinsic forms of emotion reg- of affect induction procedures. Generally, ulation, in which individuals regulate their these procedures involve exposure to sad own internal affective states, rather than or aversive stimuli in the form of images, on extrinsic emotion regulation, in which music, or movie clips. Other commonly used individuals attempt to influence the emo- techniques include writing about negative tions of others through affect displays or life events (i.e., a funeral) or reading a series other means. Along with an overview of the of increasingly negative self-r eferential state- mechanisms whereby emotions can derail ments, such as in the Velten (1968) mood self-regulation, we also consider the case of induction procedure. Much of this work has misregulation, for example, when individu- been conducted within the realm of drug als seek out temptations (e.g., food, drugs and alcohol addiction, where negative affect or alcohol) as a misguided strategy to repair has long been known to be the most potent their mood or escape from aversive self- cause of relapse (e.g., Marlatt & J. Gor- awareness resulting from overindulgence don, 1985). In smokers and other substance of these same temptations. In addition, we abusers, inducing negative affect in the review findings that regulation of emotions laboratory has been shown to increase sub- exerts a cost on self-regulatory capacity and, stance cravings (Childress et al., 1994; Fox, conversely, that engaging in effortful self- Bergquist, Hong, & Sinha, 2007; Tiffany & regulation can impair emotion regulation. Drobes, 1990; Willner & Jones, 1996) and Finally, we highlight recent research sug- the intensity of substance use (McKee et al., gesting that emotional reactivity is increased 2011) when compared to neutral or positive when self-regulatory resources are depleted. mood inductions. The Role of Negative Affect Chronic dieters are another population in Self‑Regulation Failure that has received considerable attention with When dieters, substance abusers, or sexual regards to the relationship between nega- offenders are asked to describe their rea- tive affect and self-regulation failure (i.e., sons for engaging in harmful behaviors (e.g., disinhibited eating). Inducing negative emo- binge eating, sexual aggression, smoking, tional states in dieters increases eating both and drug use) they overwhelmingly report in comparison to non-dieters, but also to that their actions were triggered by negative dieters in a neutral mood (e.g., Baucom & affect (Haedt-Matt & Keel, 2011; Kassel, Aiken, 1981; Heatherton, Striepe, & Wit- Stroud, & Paronis, 2003; Pithers, Kashima, tenberg, 1998; Herman & Polivy, 1975). For Cumming, Beal, & Buell, 1988; Sinha, instance, Heatherton, Herman, and Polivy 2007). Among the general population, (1991) induced negative affect either by giv- negative affect is similarly associated with ing participants negative performance feed- impulsive and self-defeating behaviors, such back during a cognitive task or by instruct- as alcohol consumption (Witkiewitz & Vil- ing them that they would have to prepare a larroel, 2009), gambling (Raviv, 1993), risky speech that would be given in the presence of their peers. In order to measure overeat- ing, participants were asked to participate in an unrelated taste-test of various flavors
Emotion and Self-Regulation Failure 615 of ice cream, which, unbeknownst to them, we consider a number of mechanisms that had been weighed prior to the task so that have been proposed to explain the disinhib- the amount of ice cream consumed could be iting effects of negative affect. Many of these calculated afterwards. In both cases, dieters mechanisms target specific aspects of self- ate significantly more ice cream than non- regulation, so it is important at this stage to dysphoric subjects. Moreover, this occurred briefly review some of the core components even when negative affect was induced by involved in theories of self-regulation. having participants anticipate a future task (i.e., public speaking). Similar findings have Although the details vary, most models of been found for social drinkers, in whom fear self-r egulation can be said to deal with three of future social evaluations increases alcohol basic components. The first involves a target consumption relative to participants who state that is to be attained. This can be a were not going to be evaluated (Higgins & goal, such as the goal to quit smoking or to Marlatt, 1975). avoid contaminating the palate with cheap wines, but this may also be a set of standards, Social rejection is another method of such as rules of conduct (i.e., whenever pos- inducing negative affect that has a rich his- sible, avoid drinking and teaching). The tory of being associated with behavioral second component involves an awareness of disinhibition, aggression, and violent crimes one’s actions, often referred to as monitor- (e.g., high school shootings; Leary, Kow- ing. In cybernetic models of self-regulation alski, Smith, & Phillips, 2003). Labora- (e.g., Carver & Scheier, 1981), monitoring tory studies in which subjects are induced involves comparing current behavior with to feel socially excluded have found that the desired goal state and signaling any dis- being rejected increases aggression (DeWall, crepancy. Monitoring is a particularly vul- Twenge, Bushman, Im, & Williams, 2010; nerable component of self-regulation, as a Twenge, Baumeister, Tice, & Stucke, 2001; failure to monitor ongoing behavior neces- Warburton, Williams, & Cairns, 2006) sarily entails an inability to catch (and there- and reduces the willingness to help others fore control) unwanted actions. The final (Twenge, Baumeister, DeWall, Ciarocco, & component is regulation itself. Upon identi- Bartels, 2007). For example, when given the fying a thought or an emotion that conflicts opportunity to decide how much hot sauce with his or her goals, that person must be to administer to a group of people who capable of implementing a strategy to inhibit had previously been identified as disliking or otherwise disarm the unwanted impulse. spicy foods, rejected individuals assigned Limited capacity models of self-regulation four times more hot sauce than nonrejected (Baumeister & Heatherton, 1996) empha- peers (Warburton et al., 2006). With respect size the ways in which this component oper- to self-regulation failures, social exclusion ates like a muscle and is therefore subject to has been shown to have the same effects as improvement through training and also to other negative affect inductions, leading to breakdowns through fatigue. Figure 36.1A overeating (Baumeister, DeWall, Ciarocco, depicts a model of self-regulation wherein & Twenge, 2005; Oaten, Williams, Jones, monitoring, limited capacity resources, and & Zadro, 2008) and reduced persistence on goals interact with the strength of impulses difficult tasks (Baumeister et al., 2005). Thus and temptations, ultimately determining it seems that, as with negative affect, social self-regulatory success or failure. rejection can lead to self-regulation failure, although with an added dose of aggression. In the following sections we turn to some of the proposed mechanisms for how nega- Why Does Negative Affect Impair tive affect may impair self-control. As we Self‑Control? shall see, negative affect appears to have So far we have reviewed various lines of the pernicious ability to operate on each evidence demonstrating that negative affect of the aforementioned components of self- can precipitate a variety of maladaptive regulation. Acting like poison tendrils, it behaviors, most of which are indicative of reaches into all aspects of self-control (Fig- poor self-control. In the following sections ure 36.1B), interfering with monitoring, exhausting the capacity to regulate behav- ior, and increasing the strength of desires and temptations.
616 HEALTH IMPLICATIONS A. SELF-REGULATION GOALS AND STANDARDS TEMPTATIONS AND DESIRES MONITORING CAPACITY SUCCESS (working memory, (ego depletion, FAILURE (food, drugs, media use, etc.) self-awareness) strength) B. SELF-REGULATION GOALS AND STANDARDS TEMPTATIONS AND DESIRES MONITORING CAPACITY SUCCESS (working memory, (ego depletion, FAILURE (food, drugs, media use, etc.) increases self-awareness) strength) misregulation increases impulse strength decreases monitoring decreases capacity failure increases negative affect Negative Affect FIGURE 36.1.╇ (A) Under normal circumstances, when a person is faced with temptations, successful self-rÂ
Emotion and Self-Regulation Failure 617 & Cannon, 1992). Results from a recent eties) will impair task-relevant monitoring. functional neuroimaging study of chronic Perhaps nowhere has this mechanism been dieters offer further evidence that negative better studied than in research on the phe- affect may serve to increase the rewarding nomenon of stereotype threat. This work has properties of appetitive stimuli—in this case shown that reminding women of negative of appetizing foods. Following a negative stereotypes about their gender, or reminding or neutral mood induction, chronic diet- African Americans of negative stereotypes ers were exposed to appetizing food cues about their race, can lead them to underper- during functional neuroimaging (Wagner, form on math or intelligence tests (Spencer, Boswell, Kelley, & Heatherton, 2012). Rela- Steele, & Quinn, 1999; Steele & Aronson, tive to nondieters, dysphoric dieters showed 1995). Studies demonstrate that this decre- increased brain activity in the orbitofrontal ment in performance is at least in part due cortex, a brain area implicated in represent- to a reduction in working memory capacity, ing the rewarding value of appetizing foods. which is thought to result from concurrent Moreover, activity in the orbitofrontal cor- attempts to regulate affect (Johns, Inzlicht, tex and ventral striatum was correlated with & Schmader, 2008). This phenomenon has a measure of how distressing subjects found been shown to “spill over” into nonstereo- the negative mood induction, suggesting that typed domains, as shown in work by Inzli- increases in reward-related brain activity to cht and Kang (2010), who demonstrate that food cues were dependent on the strength inducing stereotype threat in women results of the negative emotional state (Wagner et in disinhibited eating of unhealthy foods. al., 2012). Taken together, these findings Further evidence that working memory from both human and animal studies sug- is impacted by negative affect comes from gest that negative affect may sensitize people studies in which inducing emotional dis- to rewards, thereby rendering temptations tress through the anticipation of an upcom- more difficult to regulate. ing evaluation (e.g., public speaking) leads to poorer performance on working mem- Negative Affect Reduces Monitoring ory tests (Schoofs, Preuss, & Wolf, 2008). through Cognitive Load Indeed, one imaging study found that ste- Another mechanism whereby negative affect reotype threat leads to increased activity may reduce self-control is by impairing the in brain regions associated with affect (i.e., monitoring component of self-regulation. ventral anterior cingulate cortex) but not in Specifically, research demonstrates that areas that support working memory (Krendl, when dieters overeat following a negative Richeson, Kelley, & Heatherton, 2008). In mood induction, they are less aware than this case, the authors argued that it is likely nondieters of the precise amount of food that emotional distress resulting from ste- they have consumed (Heatherton, Polivy, reotype threat has downstream effects on Herman, & Baumeister, 1993). Reasons for working memory. this reduced awareness vary from a moti- vated desire to escape from negative affect Outside of the realm of negative affect, (see the next section) to an increase in cogni- research on the effects of cognitive load tive load as a result of ruminating over one’s on self-regulation have shown that cogni- mood. In this section we focus on the pos- tive loads impairs a variety of controlled sibility that experiencing negative affect can behaviors, from suppressing thoughts (Weg- lead to increased working memory load as ner & Erber, 1992) to inhibiting food con- people ruminate over their negative mood sumption in dieters (Ward & Mann, 2000). and neglect to monitor their behavior (Fig- Mann and Ward (2007) proposed an atten- ure 36.1B). tional myopia theory of cognitive load, which posits that cognitive load restricts the As monitoring entails the ability to main- range of attention to targets in the imme- tain goals and standards in working memory diate environment, thereby rendering indi- (Hofmann, Schmeichel, & Baddeley, 2012), viduals vulnerable to a variety of external it follows that a concurrent working mem- cues. To the extent that negative affect ory load (e.g., attempting to regulate mood increases cognitive load through rumina- or ruminating over one’s performance anxi- tion or attempts to regulate affect (Johns et al., 2008), a similar attentional myopia may
618 HEALTH IMPLICATIONS occur when people are experiencing a nega- Managing Negative Affect Depletes tive emotional state. Self‑Regulatory€Strength Over the last decade, considerable evidence Another means by which cognitive load has been gathered in favor of a strength model can bring about self-Âr
Emotion and Self-Regulation Failure 619 study by Vohs and Heatherton (2000) this Taken together, the results of the studies is precisely what was found when dieters reviewed in this section offer both behav- who were asked to inhibit their expression ioral and neural evidence that engaging in of sadness while watching an emotionally self-regulation, be it in the emotional or evocative video subsequently overindulged the cognitive domain, leads to transient themselves in appetizing ice cream. impairments in subsequent self-regulation attempts. Thus, with respect to our poison Although the bulk of the research on self- tendrils model of negative affect, ongoing regulatory depletion and emotion examines attempts to regulate negative affect serve how emotion regulation can produce sub- to reduce self-regulatory capacity, thereby sequent self-regulation failure on nonemo- increasing the likelihood of self-regulation tional tasks, studies shows that this effect failure (Figure 36.1B). Moreover, these find- goes both ways, such that engaging in effort- ings suggest that it is important to consider ful self-regulation also impairs subsequent the individual’s prior self-regulatory con- attempts at emotion regulation. The first text, as having to engage in other forms of researchers who looked at this question had self-regulation can lead to transient impair- participants engage in a thought suppression ments of emotion regulation, which may task, followed by an emotion regulation task exacerbate the effects of negative affect on that required participants to inhibit express- self-regulation. ing emotions evoked by an emotional video (Muraven, Tice, & Baumeister, 1998). They Depleting Self‑Regulatory Strength found that participants whose resources Intensifies Emotions and Impulses had been depleted by the thought suppres- Although early models of self-regulation sion task were subsequently less successful at tacitly assumed that the strength of impulses inhibiting their emotions. In another study, and emotions remain essentially unchanged Schmeichel (2007) extended these findings during self-regulation failure, recent theo- to more traditional tasks of executive func- ries suggest that impulses and emotions tion. In this experiment, participants com- may increase in strength when self-control pleted a complex working memory task, is depleted (e.g., Heatherton & Wagner, followed by an emotion inhibition task. As 2011; Schmeichel, Harmon-Jones, & Har- in the Muraven et al. (1998) study, partici- mon-Jones, 2010; Vohs et al., submitted). pants whose self-regulatory resources were For instance, the recent study by Vohs and depleted by the complex working memory colleagues demonstrated that when partici- task were impaired at suppressing their emo- pants are in a depleted state, they experi- tions relative to a nondepleted control group ence stronger cravings for appetizing food, (Schmeichel, 2007). as well as rate emotions and pain as being felt more acutely than do nondepleted par- More recently, the interplay between self- ticipants). The results of the brain imaging regulatory strength and emotional regula- study by Wagner and Heatherton (2013) tion was investigated using functional neu- bear some similarities to these findings. roimaging (Wagner & Heatherton, 2013). Although the results of this study were inter- In this study, participants were assigned to preted in terms of emotion dysregulation fol- either a depletion condition, in which they lowing depletion, it is equally plausible that completed a difficult attention control task, self-regulatory depletion served to amplify or a control condition. Next, all participants people’s experience of affect, resulting in viewed a series of emotional scenes differ- greater amygdala activity in response to ing in valence. Compared to control par- negative scenes, thus making emotion regu- ticipants, those who were depleted exhib- lation more difficult. ited greater neural activity in the amygdala, a region involved in the perception and This relatively new line of research sug- detection of emotion, when viewing nega- gests that self-regulatory depletion not only tive emotional scenes. Moreover, depleted harms subsequent attempts at self-control participants exhibited reduced connectiv- but also increases the strength of emotions ity between the amygdala and prefrontal and desires. For the current discussion this regions implicated in top-down control, sug- suggests that managing ongoing negative gesting a failure to engage in emotion regu- lation (Wagner & Heatherton, 2013).
620 HEALTH IMPLICATIONS affect may not only reduce self-regulatory affect, people report consuming their favor- capacity but also lead to a concurrent ite substance (e.g., food, alcohol, or drugs) or increase in the intensity of currently experi- engaging in their favorite activity (e.g., shop- enced affect, thereby amplifying its deleteri- ping, television, gambling) precisely because ous effects on all aspects of self-regulation, they believe it will make them feel better (e.g., as indicated by the path between depletion Faber & Christenson, 1996; Rook, 1987; and negative affect in Figure 36.1B. Sayette, 1993). Thus, when stuck in a nega- tive emotional state, people will shirk their Mood Repair and Escaping long-term goals in order to address the more Negative Affect Take Precedence immediate need to feel better. One particu- over Long‑Term Goals larly disconcerting example of mood repair One likely explanation for why people turn following negative affect comes from a study to eating, smoking, and drinking in times in which participants were asked to rate the of emotional distress is that they believe personalities of ethnic ingroup and outgroup such activities can restore their mood (Say- members. Participants who were induced to ette, 1993). Indeed, even in nonhuman ani- experience negative affect—as a result of mals, consuming pleasurable foods has been negative performance feedback on an osten- shown to reduce neuroendocrine markers sibly unrelated test—subsequently rated the of distress (Foster et al., 2009). In humans, ethnic outgroup members more negatively research has shown that merely being than did control subjects (Fein & Spencer, exposed to appetizing stimuli (e.g., food, 1997). Moreover, it was found that this ten- drugs, alcohol) can activate positive hedonic dency to denigrate outgroup members led to thoughts (Hofmann, van Koningsbrug- increased self-esteem in the negative affect gen, Stroebe, Ramanathan, & Aarts, 2010; group, suggesting that participants deni- Sayette & Hufford, 1997). For instance, in grated outgroup members in order to make dieters, exposure to descriptions of appetiz- themselves feel better. Likewise, when peo- ing foods has been shown to spontaneously ple experience social rejection, they become activate more hedonic thoughts about the more willing to take illicit drugs or waste pleasurable aspects of eating than descrip- money on goods that are liked by their peers, tions of neutral foods (Papies, Stroebe, & but not necessarily by themselves, if doing so Aarts, 2007). This attention to the pleasur- increases their chances at fitting in (Mead, able aspects of temptations can have serious Baumeister, Stillman, Rawn, & Vohs, 2011). consequences, especially in cases of alcohol Other examples involve the effect of nega- and substance use in which withdrawal from tive affect on spending. In these studies, neg- the substance elicits negative affect that is ative affect has been shown to increase par- relieved only by further substance use. It ticipant’s willingness to pay more for goods, has been suggested that this need to cope as well as sell things they already own for with—and escape from—negative affect less money (Lerner, Small, & Loewenstein, produced by withdrawal is one of the central 2004). These findings were taken to indicate motivations underlying addiction (Baker, that people see buying new things or selling Piper, McCarthy, Majeskie, & Fiore, 2004). old things as a way of changing their current Moreover, through prolonged conditioning state and thereby escape negative affect. of substance use and improved mood, any experience of negative affect—whether due Although attempting to repair one’s mood to specific triggers or merely the vicissitudes through engaging in pleasurable activities of daily life—can trigger the desire for drugs such as eating may seem like a good tem- or alcohol (Baker et al., 2004; Childress et porary strategy to alleviate negative affect, al., 1994). studies show that this form of mood repair is often a case of misregulation. Unlike other Given people’s belief that consuming food forms of self-regulation failure, misregu- and alcohol or engaging in pleasurable activ- lation is not so much a lack of self-control ities will improve their mood, is there any as the use of self-control in a misguided— empirical evidence that people employ this and often futile—attempt to improve one’s strategy when experiencing negative affect? state (Baumeister & Heatherton, 1996). For Studies examining a wide range of behav- instance, studies show that although diet- iors show that, upon experiencing negative ers may binge-eat in an attempt to improve their mood, they often end up feeling worse
Emotion and Self-Regulation Failure 621 after eating than they did before (for a meta- escaping self-awareness becomes an effec- analysis, see Haedt-Matt & Keel, 2011). tive strategy for reducing negative affect. However, attempts to reduce self-a wareness Finally, a study by Tice and colleagues come at the expense of the ability to focus (2001) elegantly demonstrated that cer- on long-term goals and an increased vulner- tain cases of disinhibited behavior are due ability to temptations in the immediate envi- entirely to a motivated attempt to improve ronment. For example, dieters who experi- affective states. In this study, participants ence a self-esteem threat are more likely were induced to experience negative affect, than nondieters to overeat (Heatherton et but in one group they were given a pill al., 1993). Likewise, following self-esteem and told that it would freeze their mood. threats, people drink more alcohol (Hull & Whereas participants who did not receive Young, 1983), watch more television (Mos- the mood-freezing pill exhibited typical kalenko & Heine, 2003) and avoid sitting in signs of self-regulation failure, such as eat- front of mirrors (Twenge, Catanese, & Bau- ing unhealthy foods or procrastinating with meister, 2003). pleasurable activity before a task, those who took the mood-freezing pill showed no signs With respect to our model, this suggests of disinhibition (Tice et al., 2001). Thus, that, in some instances, negative affect inter- when participants believed engaging in plea- feres with the machinery of self-regulation surable activities could not improve their (e.g., monitoring or capacity), but in other negative emotional state, they ceased trying circumstances, people chose to indulge in to change their mood by indulging in these temptations as a means of repairing their activities. mood. This form of misregulation may tem- porarily relieve negative affect, but once the The case of misregulation is particularly awareness sets in that people have failed at interesting, because it suggests that self- their regulatory goals, further negative affect regulation failure following negative affect ensues, thus jeopardizing future attempts is not always due to a failure in the machin- at self-regulation (see also Heatherton and ery of self-r egulation; rather it reflects a con- Polivy’s [1992] spiral model describing the scious shift in priorities as people focus on relationship between negative affect and improving their immediate affective state chronic dieting). at the expense of their long-term regulatory goals. Indeed, it has been suggested that Are All Negative Emotions sometimes people actually use self-control Equally Likely to Cause to bring about personal harm, such as when Self‑Regulation Failure? they smoke or use drugs to fit in and make In many of the studies we have reviewed, friends (Rawn & Vohs, 2011). However, negative affect refers primarily to any these short-term strategies often lead to unpleasurable or aversive emotional state, more negative affect as people move further thus subsuming a variety of emotional and further away from their goals, such as categories—from frustration to shame when dieters overeat to improve their mood to social rejection. In some cases, nega- but then finds themselves further from their tive affect is assessed through self-reports, goal of weight loss (Heatherton & Polivy, whereas in others the emotional state is 1992). experimentally induced, affording more control over the specific emotions produced. Intimately related to the notion of mis- That being said, differences between nega- regulation is research on escape from self- tive emotion types are seldom reported, with awareness (Baumeister, 1991; Heatherton & two exceptions. The first involves research Baumeister, 1991). In contrast to the mood in chronic dieters demonstrating that nega- repair hypothesis outlined earlier, escape tive affect inductions that specifically target theory posits that self-awareness is aver- an individual’s self-esteem (e.g., negative sive for people who possess negative self- performance feedback, social rejection) are views (see Higgins, 1987). Unfortunately, more effective at producing disinhibited eat- for those with negative self-views, increas- ing (Heatherton et al., 1991, 1993, 1998; ing self-a wareness does not help them regu- Lattimore & Maxwell, 2004) than induc- late, because self-awareness itself can lead to negative affect as people’s attention becomes focused on their perceived shortcomings (Mor & Winquist, 2002). For these people,
622 HEALTH IMPLICATIONS tions targeting physical distress (e.g., fear of the opportunity to indulge in temptations electric shock; Heatherton et al., 1991; Her- or pleasurable activities. Emotion can, man & Polivy, 1975). however, color behavior in other ways. For instance, in Schwarz’s (1990) feelings as The second exception involves research on information model, an individual’s current the consequences of being socially excluded. emotional state can be used as information As described earlier, social rejection can in making evaluative judgments or resolving lead to poorer task performance, selfishness, ambiguities. For example, following a nega- aggression, and increased eating in dieters. tive mood induction, people tend to judge Paradoxically, however, other studies indi- their current happiness and life satisfaction cate that inducing feelings of social rejection less positively than when in a positive mood can increase affiliative behaviors (Maner, (Schwarz & Clore, 1983). Other research DeWall, Baumeister, & Schaller, 2007; Wil- shows that people in a negative mood tend liams & Sommer, 1997), as well as improve to elaborate on information, demonstrat- memory for social information (Gardner, ing more accurate performance on tasks Pickett, & Brewer, 2000). One explanation requiring attention to details (reviewed in for this discrepancy is that socially rejected Schwarz, 1990). Other theorists have sug- people are adaptively deploying both pro- gested that emotions signal the need for self- tective and affiliative strategies, such that regulation. For instance, Carver and Scheier when the opportunity for forging new social (1990) argued that positive emotions signal bonds appears low (as in some experiments) that a person is achieving his or her goal they react with selfish and occasionally hos- (e.g., successfully dieting), whereas nega- tile behaviors, whereas when there is an tive emotions arise when a person is mov- opportunity for meaningful social contact, ing away from his or her goal (e.g., gaining they instead switch to an affiliative strat- weight during a diet). From this perspective, egy in an attempt to repair their self-esteem then, negative affect should serve to increase (e.g., Baumeister, Brewer, Tice, & Twenge, rather than thwart efforts at self-regulation. 2007; Maner et al., 2007; Smart Richman The discrepancy between the preceding the- & Leary, 2009). Indeed, a recent imaging ories and the evidence reviewed in this chap- study found that interpersonal distress led ter can be resolved if we consider when in to increased mental engagement for posi- time these effects are likely to take place. In tive social stimuli (as indexed by activity in this chapter we have primarily focused on medial prefrontal cortical regions associated the role of negative affect in eliciting self- with mentalizing) and decreased engagement regulation failure “in the moment,” when for negative social stimuli (Powers, Wagner, people are confronted with the immediate Norris, & Heatherton, 2013). Although need to regulate themselves, such as when these reactions to social rejection have only faced with temptations. Over longer time tangential bearing on self-regulation failure, frames, outside of these “hot” moments, they do highlight the complexity of the rela- negative affect may very well serve to moti- tionship between negative affect and self- vate individuals to change their current state regulation, demonstrating that reactions to for the better (Heatherton & Polivy, 1992). negative affect can strategically vary accord- ing to the individual’s goals. As described The Role of Positive Affect in the previous sections, what can appear in Self‑Regulation Success to be a failure to maintain self-control may and Failure instead be a strategy to repair mood through In the preceding sections we have focused consuming foods or alcohol, or engaging in solely on the role of negative affect in self- pleasurable activities at the expense of other regulation failure, with scant mention of its regulatory goals. opposite, positive affect. This is largely for two reasons: First, researchers have often Can Negative Affect Ever Increase neglected positive affect in favor of negative Self‑Regulation Success? affect (see Ashby, Isen, & Turken, 1999); Much of the work discussed here has exam- second, of the research that does consider ined the influence of affect on self-regulation positive affect, there is less evidence that it in “hot” contexts, such as when faced with
Emotion and Self-Regulation Failure 623 plays a strong part in self-regulation failures Conclusion or successes, at least in the types of contexts discussed in this chapter. For example, com- Negative affect may very well be the most pared to positive moods, negative moods and potent disinhibitor of restrained behavior. events are typically found to be more memo- When people feel worthless, depressed, or rable and are experienced more intensely rejected, they are more likely to engage in (see Baumeister, Bratslavsky, Finkenauer, & a variety of self-defeating behaviors. Fol- Vohs, 2001). Moreover, in the mood induc- lowing negative affect, dieters overeat, for- tion studies reviewed earlier, of those that mer smokers smoke, and alcoholics fall into have directly compared negative and posi- relapse. More generally, people become more tive affect, negative always trump positive likely to procrastinate, to be selfish or hos- (Willner & Jones, 1996; Tiffanny & Drobes, tile, and even go so far as to denigrate out- 1990). Thus, it appears that negative affect group members. Negative affect appears to is generally a much more potent force than accomplish this pernicious feat by poisoning positive affect in self-r egulation failure. all facets of self-r egulation (see Figure 36.1): Does positive affect promote self- sensitizing people to rewards and tempta- regulation success? There is some research tions, decreasing monitoring of behavior, suggesting that positive affect can serve reducing self-regulatory capacity, and caus- to momentarily increase self-regulation ing people to focus on repairing their mood strength. For instance, when people hold at the expense of abandoning their goals and the goal of self-improvement in mind, posi- giving in to their impulses and desires. tive affect inductions lead to increased Although it often appears that our self- use of self-control (Fishbach & Labroo, control is entirely at the mercy of our emo- 2007). Based on these results, Fishbach and tions, it is also the case that emotion regu- Labroo suggest that positive affect pushes lation can be derailed by prior attempts at people to strive toward a currently acti- self-regulation in the cognitive domain. For vated goal. If that goal happens to be about instance, engaging in effortful self-regulation self-improvement, then self-regulation may tasks can exhaust self-regulatory resources, follow; however, if the goal is mood regu- thereby jeopardizing subsequent emo- lation, then self-regulation may suffer to tion regulation attempts. Moreover, recent the degree that it is opposed to maintain- research has shown that when people are ing a positive mood. Another study show- cognitively depleted by prior attempts at self- ing beneficial effect of positive affect on regulation, emotions and impulses appear to self-regulation found that inducing positive increase in potency, rendering them a more affect restored self-regulation capacity fol- forceful adversary to self-c ontrol. lowing self-regulatory depletion (Tice, Bau- The interplay among emotions, emotion meister, Shmueli, & Muraven, 2007). This regulation, and self-regulation has been dis- finding suggests that the capacity to engage cussed as though each of the myriad ways in self-control is at least partially moderated that emotions can hijack self-control work by affect. In fact, to the degree that partici- independently of the others. However, it is pants in the Tice et al. study hold the goal to far more likely that the multiple routes to succeed at the tasks laid out by the experi- self-regulation failure are themselves inter- menters, then the results of Fishbach and active. For instance, negative affect can Labroo (2007) would suggest that the posi- lead to a desire to escape negative states by tive affect induction reversed the effects of reducing self-awareness and also to engage self-regulatory depletion by pushing subjects in pleasurable activities, even if these activi- to expend whatever resources they had left ties conflict with long-term goals. Together, in the service of the goal of succeeding at the these may serve to increase the pull of imme- task. It is worth pointing out that although diately available rewards, because the ability these studies suggest that positive affect can to monitor behavior is lessened as the focus increase self-control under certain circum- shifts to pleasure. Negative affect may also stances, it is likely that under a different set place a load on working memory indepen- of circumstances (e.g., at a bar), with a dif- dent of the desire to escape self-awareness, ferent goal in mind (e.g., celebrating with thus further reducing the ability to monitor friends), positive affect may lead to greater behavior. Throw in the fact that prior self- celebratory excess. regulatory effort may leave the individual
624 HEALTH IMPLICATIONS in a depleted state in which both resources Baumeister, R. F. (1991). Escaping the self: Alco- for further self-control are lacking and the strength of impulses and temptations holism, spirituality, masochism, and other is increased, and it is a small miracle that flights from the burden of selfhood. New people are not constantly acting out their York: Basic Books. fantasies, drinking, smoking, or indulg- Baumeister, R. F. (1997). Esteem threat, self- ing every gastronomic desire. If the studies regulatory breakdown, and emotional distress reviewed in this chapter paint a dire picture, as factors in self-d efeating behavior. Review of it is important to note that emotion is not all General Psychology, 1(2), 145–174. bad: For instance, it has been demonstrated Baumeister, R. F., Bratslavsky, E., Finkenauer, that experiencing positive emotions can C., & Vohs, K. D. (2001). Bad is stronger than improve self-regulation by helping to buffer good. Review of General Psychology, 5(4), against the depleting effects of prior tasks 323–370. (Tice et al., 2007). Baumeister, R. F., Bratslavsky, E., Muraven, M., & Tice, D. M. (1998). Ego depletion: Is the In this chapter we reviewed evidence sug- active self a limited resource? Journal of Per- gesting that negative emotions are a potent sonality and Social Psychology, 74(5), 1252– cause of self-regulation failure and we have 1265. proposed a simple poison tendrils model in Baumeister, R. F., Brewer, L. E., Tice, D. M., & which negative affect invades and disrupts Twenge, J. M. (2007). Thwarting the need to nearly every aspect of self-regulatory func- belong: Understanding the interpersonal and tion. Moreover, results from a variety of inner effects of social exclusion. Social and behavioral and neural studies suggest that Personality Psychology Compass, 1(1), 506– the relationship between emotions and self- 520. regulation is dynamic and interactive, such Baumeister, R. F., DeWall, C. N., Ciarocco, N. that emotion-induced self-regulation fail- J., & Twenge, J. M. (2005). Social exclusion ure serves not only to intensify currently impairs self-regulation. Journal of Personality experienced emotions and desires but also and Social Psychology, 88(4), 589–604. to increase negative affect as the individual Baumeister, R. F., & Heatherton, T. (1996). Self- moves further and further away from his regulation failure: An overview. Psychological or her goals. Negative affect is thus a par- Inquiry, 7(1), 1–15. ticularly potent threat to self-regulation, Berkowitz, L. (1989). Frustration–aggression because it not only reduces the capacity for hypothesis: Examination and reformulation. control (increased working memory load, Psychological Bulletin, 106(1), 59–73. reduced self-awareness and monitoring) but Bousman, C. A., Cherner, M., Ake, C., Leten- it may also lead to increases in the strength dre, S., Atkinson, J. H., Patterson, T. L., et al. of experienced desires and emotions, render- (2009). Negative mood and sexual behavior ing them all the more difficult to resist. among non-m onogamous men who have sex with men in the context of methamphetamine References and HIV. Journal of Affective Disorders, 119(1–3), 84–91. Ashby, F. G., Isen, A. M., & Turken, A. U. (1999). Campbell Teskey, G., Kavaliers, M., & Hirst, M. A neuropsychological theory of positive affect (1984). Social conflict activates opioid analge- and its influence on cognition. Psychological sic and ingestive behaviors in male mice. Life Review, 106(3), 529–550. Sciences, 35(3), 303–315. Carver, C. S., & Scheier, M. (1981). Attention and Baker, T. B., Piper, M. E., McCarthy, D. E., Majeskie, M. R., & Fiore, M. C. (2004). self-regulation: A control-theory approach to Addiction motivation reformulated: An affec- human behavior. New York: Springer-Verlag. tive processing model of negative reinforce- Carver, C. S., & Scheier, M. F. (1990). Origins ment. Psychological Review, 111(1), 33–51. and functions of positive and negative affect: A control-p rocess view. Psychological Review, Baucom, D. H., & Aiken, P. A. (1981). Effect of 97(1), 19–35. depressed mood in eating among obese and Childress, A. R., Ehrman, R., McLellan, A. nonobese dieting and nondieting persons. T., MacRae, J., Natale, M., & O’Brien, C. Journal of Personality and Social Psychology, P. (1994). Can induced moods trigger drug- 41(3), 577–585. related responses in opiate abuse patients?
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Author Index Aaker, J. L., 288 Aksan, N., 160, 313 Alper, C. M., 571, 587 Aarts, H., 244, 350, 354, 356, Akutsu, S., 325 Als, H., 277 Albert, D., 9, 189, 284 Altamirano, L. J., 127 362, 366, 367, 620 Alberts, H. J. E. M., 352 Alvarez, J., 405 Abe, K., 435 Alcaine, O. M., 84, 403, 470 Amar, S., 562 Abela, J. R., 405 Aldao, A., 127, 135, 271, 327, Amaral, D. G., 537 Aber, J. L., 116, 309 Ambady, N., 259 Abler, B., 11, 65, 82, 145, 325, 396, 398, 399, 401, 404, 405, Amiaz, R., 355 417, 418, 474, 483, 492, 496 Amir, M., 241, 242 326, 327 Aldridge, J. W., 96, 471 Amir, N., 424, 513, 514, 516, Abramovitz, A., 498 Alea, N., 207 Abramson, L. Y., 383 Aleman, A., 141, 148, 532 517, 520, 522, 523 Abu-Lughod, L., 288 Alexander, R. D., 225 Amir, T., 524 Ackerman, B. P., 163 Algom, D., 132 Amit, I., 576 Adams, C. E., 480, 557 Alicata, D., 435 Amodio, D. M., 362 Adams, C. M., 95 Allan, C. L., 69 An, S. K., 52 Adams, G., 285 Allan, N. P., 164, 166 Anderson, A. K., 14, 252, 352, Adamson, L., 277 Allen, A. B., 379, 480, 557 Addis, D. R., 104 Allen, A. H., 81 530, 548, 556, 557 Addis, M., 497 Allen, J. P., 192, 225, 228 Anderson, B., 46 Adler, N. E., 586 Allen, J. S., 195 Anderson, C., 325 Affleck, G., 589 Allen, L. B., 496 Anderson, C. L., 370 Aglioti, S. M., 497 Allen, M., 556 Anderson, C. S., 497 Agras, W., 483 Allen, N. B., 187, 188, 190, 191, Anderson, E., 450 Ahadi, S. A., 159, 165, 308, 310 352 Anderson, J. R., 28 Ahrens, A. H., 383 Allman, J. M., 460 Anderson, M. C., 104 Aiken, P. A., 116, 117, 614 Alloy, L. B., 383, 416 Anderson, P. L., 552 Ainslie, G., 99 Allport, G. W., 252, 306 Anderson, S. W., 143 Ainsworth, M. D. S., 226, 229, Almeida, D. M., 209, 210, 211, Andersson, G., 469 212 Andover, M. S., 530 237, 273, 277 Alonso-Alonso, M., 355 Andrade, E. B., 141, 193 Akerstedt, A. M., 212 Andrade, J., 348 Akiyama, T., 403 629
630 Author Index Andrew, C., 66 B Bariola, E., 189, 190, 191, 322, Andrews-Hanna, J. R., 450, 457, 328 Baars, B. J., 350 460 Babuscio, T., 439 Barkley, R. A., 98 Ang, C., 522 Baccus, J. R., 384, 511 Barlow, D. H., 14, 62, 134, 135, Angstadt, M., 83, 145 Bacharier, L. B., 590 Ansell, E., 384 Baddeley, A. D., 348, 617 370, 377, 393, 394, 395, 396, Anstiss, V., 353 Badiani, A., 429 397, 401, 406, 417, 424, 461, Antonenko, O., 11, 341 Badre, D., 28, 33, 472, 477 469, 470, 473, 479, 481, 496, Antoni, M. H., 575, 576 Baer, R. A., 548, 552, 557, 559 498, 499, 508, 519, 529, 533, Antonucci, T. C., 210 Baerensten, K. B., 557 551 Appleton, A. A., 596, 601, 603, Baert, S., 422, 424, 518 Barnard, P. J., 529, 530, 536, 537 Baeyens, C., 499, 500 Barndollar, K., 366 606, 607, 608 Baeyens, F., 256, 353 Barnes, R. D., 353 Apter, A., 399 Bagby, R. M., 329 Barnett, W. S., 167 Arbuckle, N. L., 260 Bailey, M. T., 576 Barnhofer, T., 560 Arch, J. J., 399, 551 Baime, M. J., 552 Baron, R. M., 226 Arellano, C. M., 276 Baker, C. I., 24 Baron, R. S., 227 Arevalo, J. M., 575 Baker, L., 226 Barrett, L. F., 5, 12, 13, 14, 24, Ariely, D., 141, 369 Baker, M., 606 26, 27, 28, 29, 176, 223, 224, Arkowitz, H., 476 Baker, N., 352 252, 289, 447, 448, 449, 450, Armony, J. L., 537 Baker, R., 396, 399 451, 452, 453, 454, 455, 456, Arnsten, A. F. T., 230, 536 Baker, S. C., 97 459, 460, 461, 508 Arntz, A., 494, 495 Baker, T. B., 432, 616, 620 Barrig, P. S., 309 Aron, A. R., 28, 33, 227, 273 Bakermans-Kranenburg, M. J., Barrios, V., 370 Aron, E. N., 273 Barry, R. A., 167 Aronson, E., 381 63, 229, 510 Barsalou, L. W., 14, 447, 448, Aronson, J. A., 98, 141, 617 Bakker, M. P., 164 449, 451, 452, 453, 458, 462 Asensio, S., 435 Baldwin, M. W., 384, 511, 512, Bartels, A., 226 Ashby, F. G., 622 Bartels, J. M., 615 Asher, E. R., 226 513, 521 Bartholomew, K., 243 Ashley, V., 509 Ball, T. M., 398, 399, 400, 401, Bartholow, B., 45 Askegaard, S., 346 Bartley, M., 241 Aslin, R. N., 121 402 Bassett, H. H., 181 Asmussen, L., 187 Balzarotti, S., 325, 326, 327, 330 Bastian, B., 385 Asnaani, A., 398, 529 Banaji, M. R., 254, 352 Bates, J. E., 113, 158, 159, 161, Aspinwall, L. G., 291 Band, G. P. H., 53 167, 305, 307, 310, 315 Astin, J. A., 548, 552 Bandler, R., 26 Bateson, G., 296 Atlantis, E., 606 Bandstra, N. F., 165 Baucom, D. H., 116, 117, 614 Atlas, L. Y., 36, 66 Bandura, A., 361 Baum, A., 575 Attwood, A. S., 351, 523 Banjeree, R., 296 Baumeister, R. F., 111, 116, 117, Auerbach, R. P., 405 Banks, S. J., 83, 145 128, 131, 132, 135, 230, 321, August, G. J., 431 Bannister, T., 241 348, 349, 350, 354, 355, 362, Auksztulewicz, R., 104 Banton, T., 222 366, 378, 381, 386, 472, 474, Aupperle, R. L., 471, 473, 476 Bar, M., 176, 223, 450, 475 613, 615, 616, 617, 618, 619, Austin, S. N., 259 Barbas, H., 61, 459 620, 621, 622, 623 Avenanti, A., 497 Barber, B., 188 Baumgartner, T., 227 Avery, S. N., 81 Barber, J. P., 539 Bayles, K., 113 Avihou-Kanza, N., 239 Barbey, A., 448 Beach, S. R., 276 Avivi, Y. E., 471 Barch, D. M., 98, 230, 311, 474 Beal, L. S., 614 Axelrod, S. R., 533 Barden, J., 256 Beall, S. K., 598, 599 Aycock, J., 213 Bargas-Avila, J., 354 Beard, C., 514, 516, 517, 520, Ayduk, O., 93, 111, 112, 118, Barger, S. D., 574 521, 523, 524 Bargh, J. A., 31, 77, 254, 255, Beauchaine, T. P., 491 119, 127, 129, 158, 161, 162, Beaulieu-Pelletier, G., 379 190, 312, 378, 431, 479, 556 288, 366, 367, 377 Beauregard, M., 64, 84, 311 Azuma, H., 285, 294 Bar-Haim, Y., 63, 510, 511, 512, 518, 521
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