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. Author manuscript; available in PMC: 2022 Mar 1.
Published in final edited form as: Int J Eat Disord. 2020 Dec 9;54(3):287–292. doi: 10.1002/eat.23433

Anhedonia, Positive Affect Dysregulation, and Risk and Maintenance of Binge-Eating Disorder

Tyler B Mason 1, Kathryn E Smith 2, Lisa M Anderson 3, Vivienne M Hazzard 4
PMCID: PMC8673784  NIHMSID: NIHMS1655210  PMID: 33295671

Abstract

Low positive affect has been identified as an antecedent of binge-eating episodes among individuals with binge-eating disorder (BED), yet positive affect has received far less attention in eating disorders research than its counterpart, negative affect. In this article, we argue that the low levels of positive affect which occur with anhedonia (i.e., loss of interest or pleasure in activities) may contribute to the onset and maintenance of BED. We introduce a theoretical model in which anhedonia increases risk for BED through its inter-relationships with dysregulated eating and weight gain, and we describe potential direct (e.g., reward-related processes) as well as indirect (e.g., influences on depressive symptoms and physical activity) pathways by which anhedonia may lead to adverse eating- and weight-related outcomes. We also propose a momentary maintenance model in which low positive affect and positive affect dysregulation occurring with anhedonia maintain binge eating directly and indirectly through maladaptive health behaviors, such as decreased physical activity, less healthy eating, and fewer social interactions, which in turn maintain anhedonia. We draw upon outside literatures to present evidence that aligns with the proposed risk and maintenance models and conclude by outlining avenues for future research—including methodological/measurement, theoretical, and clinical research directions.

Keywords: binge-eating disorder, anhedonia, positive affect, theoretical models, maintenance, risk

Anhedonia, defined as a loss of interest or pleasure in activities, involves low levels of positive affect (PA; De Fruyt et al., 2020). While PA has begun to receive some recognition in the eating disorders (EDs) literature (e.g., Coniglio et al., 2019), the role of low PA has historically been overlooked in ED research in lieu of predominant focus on negative affect (Selby et al., 2019). Although little research has explicitly examined the role of anhedonia in binge-eating disorder (BED), some work has investigated the more general and dimensional role of PA. Consistent with affect regulation models of eating pathology, evidence indicates that low PA is an antecedent of binge-eating episodes among individuals with BED (Schaefer et al., 2020). Baseline PA dynamics have also been found to predict BED treatment outcomes, including changes in binge-eating frequency and weight (Mason, Smith, Anderson, et al., 2020; Mason, Smith, Williams-Kerver, et al., 2020). In this article, we propose that anhedonia and PA dysregulation may contribute to risk and maintenance of BED and outline critical methodological/measurement, theoretical, and treatment considerations.

Anhedonia as a Risk Factor for BED

We propose that inter-relationships between anhedonia, dysregulated eating, and weight gain may contribute to the development of BED and outline potential mechanisms. Growing evidence suggests that anhedonia predicts eating- and weight-related outcomes. In adolescents and adults, anhedonia predicted greater weight gain over naturalistic follow-ups (Cho et al., 2018; Ibrahim et al., 2016). Particularly, adults with both high depressive symptoms and high anhedonia were most likely to gain weight (Ibrahim et al., 2016). In a study of adults with overweight/obesity participating in a weight loss intervention, those with anhedonia reported greater binge eating at baseline and follow-up and exhibited poorer weight outcomes (Keränen et al., 2010). Relatedly, social anhedonia (i.e., disinterest in and lack of reward from social interaction) has been demonstrated among individuals with EDs (Barkus & Badcock, 2019). For example, among those with anorexia nervosa and bulimia nervosa, social anhedonia is negatively correlated with hedonic responses to sucrose, though in these populations, evidence suggests fear of weight gain may drive the association more so than decreased ability to derive pleasure from sweet foods (Eiber et al., 2002). To date, there remains limited longitudinal research in this area, and no research exists on the role of social anhedonia in BED and obesity.

Both direct and indirect mechanisms may predispose individuals with anhedonia to develop binge eating and gain excess weight. Anhedonia is thought to arise from reductions in dopamine transmission and dysfunction within the reward system, particularly regarding anticipation of reward (wanting), consumption of reward (liking), and learning of reward (Der-Avakian & Markou, 2012; Rømer Thomsen et al., 2015). Outside of EDs and obesity, neuroscience research indicates anhedonia is characterized by reduced reward anticipation and willingness to exert effort to get a reward, decreased liking of rewards, and disruptions in reinforcement learning–i.e., the ability to modify behaviors as a function of reward (Craske et al., 2016; De Fruyt et al., 2020).

Accordingly, studies among individuals with depression have shown that anhedonia is associated with reduced activation in regions associated with value-based decision-making during reward anticipation (Stoy et al., 2011; Ubl et al., 2015), hypoactivity in ventral striatum in the context of positive stimuli (Epstein et al., 2006; Keedwell et al., 2005; Pizzagalli et al., 2009; Wacker et al., 2009), and reduced ventral striatal responding during Pavlovian and instrumental conditioning tasks (Gradin et al., 2011; Kumar et al., 2008). Given this evidence for difficulty with reward learning in anhedonia, one possibility is that individuals with anhedonia have an increased drive to obtain comfort and pleasure from primary reinforcers such as food (versus secondary, or learned, reinforcers) in order to compensate for these deficits and improve affective states, which in turn may increase risk of BED symptoms and weight gain (Giel et al., 2017; Kessler et al., 2016; Reiter et al., 2017).

In addition to potential direct effects of reward dysfunction on appetite regulation, anhedonia may indirectly influence binge eating and obesity development by exacerbating other relevant etiological factors. Research suggests anhedonia, in comparison to other depressive symptoms, is a marker of greater symptom severity and poorer prognosis among individuals with depression (Gabbay et al., 2015; McMakin et al., 2012); as such, anhedonia may compound negative affectivity and depressive symptoms that are known to predict binge-eating pathology and obesity (Luppino et al., 2010; Puccio et al., 2018). Anhedonia also may contribute to lower physical activity, which is central for energy balance, appetite regulation, and neurocognitive functioning (Beaulieu et al., 2018; Cox et al., 2016). Taken together, current evidence suggests anhedonia represents risk for negative eating- and weight-related outcomes, which may be due to altered reward-related processes and secondary effects of anhedonia on other proximal risk factors for binge eating and obesity.

Anhedonia as a Maintenance Factor for BED

Figure 1 depicts a momentary maintenance model of anhedonia and binge eating in BED. This model includes three components: (1) the link between anhedonia and momentary PA; (2) momentary process of low PA, behaviors, and binge eating; and (3) maintenance of binge eating by dysregulated PA. These components are described below.

Figure 1.

Figure 1.

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Momentary maintenance process model of anhedonia and binge eating in binge-eating disorder

Anhedonia and momentary PA.

Anhedonia has demonstrated associations with lower levels of PA and less intense pleasure experiences in ecological momentary assessment (EMA) studies of young adults with versus without anhedonia and adults with major depressive disorder and anhedonia versus controls (Heininga et al., 2017; 2019). Contrary to beliefs that PA reactivity may be blunted in anhedonia (De Fruyt et al., 2020), young adults with anhedonia versus without anhedonia exhibited greater PA variability with no signs of blunted PA reactivity in one EMA study (Heininga et al., 2017), though another EMA study found no differences in PA dynamics between individuals with major depressive disorder and anhedonia compared to controls (Heininga et al., 2019). Moreover, when exploring high-arousal (e.g., energetic) and low-arousal PA (e.g., calm), young adults with anhedonia versus without anhedonia demonstrated greater reactivity to pleasurable experiences in high-arousal PA (Heininga et al., 2017). Taken together, evidence suggests that anhedonia is associated with dysregulation of PA in daily life.

PA, behaviors, and binge eating.

The broaden-and-build theory (Fredrickson, 2001) suggests that subjective experiences of PA expand one’s attentional scope and promote engagement in behaviors that further engender PA. Consistent with this theory, evidence from general samples show bi-directional associations between momentary PA and adaptive behaviors, such that higher PA predicts healthy eating (e.g., increased fruit/vegetable intake), physical activity, and social interactions, and these behaviors predict higher subsequent PA (Conner et al., 2015; Liao et al., 2015; Liu et al., 2019; Mason et al., 2019). Conversely, individuals with BED typically engage in less healthy eating patterns, consume fewer healthy foods, engage in less physical activity, and have more interpersonal difficulties (e.g., Brugner et al., 2019; Engel et al., 2009; Hrabosky et al., 2007; Masheb et al., 2011), which may serve to maintain lower overall and within-day PA. Binge eating may be used as a way to momentarily increase PA in individuals with BED. Consistently, in a recent EMA study of adults with BED, trajectories of PA surrounding binge eating showed that, on average, PA decreased prior to binge eating and stabilized following binge eating, providing evidence for a PA-enhancing effect of binge eating in BED (Schaefer et al., 2020).

PA dysregulation and binge-eating maintenance.

In addition to low PA being associated with binge eating, data suggests elevated levels of PA compared to one’s average level interact with other state or trait risk factors to predict binge eating (Smith et al., 2019; 2020). That is, individuals with BED may engage in binge eating when PA is lower than their average level as well as when PA is higher than their average level. Therefore, rather than engaging in healthy behaviors to maintain PA, at moments when individuals with BED experience higher-than-usual PA, they may be more likely to engage in binge eating as a way to maintain PA, given that they may not experience PA from many other activities due to underlying anhedonia. Binge eating for PA maintenance may be learned through repeated instances of binge eating increasing low levels of momentary PA. Consistently, a laboratory study found preliminary support for this explanation, such that women with BED with greater baseline expectations that food is rewarding consumed more calories after a PA induction (Dingemans et al., 2009).

Future Directions for Research

Methodological/measurement directions.

Testing and extending the proposed models represent vital steps toward increasing understanding of the role of anhedonia in BED. Much research in the ED field focuses on composite measures of depressive symptoms, but it is key to specifically include measures that assess anhedonia and PA dynamics (including intensity, instability, differentiation, and inertia; Trull et al., 2015). Also, future work should utilize intensive longitudinal designs (e.g., EMA) to examine maintenance mechanisms of binge eating implicated in proposed models of BED. EMA studies may offer critical insights regarding momentary processes, including altered reward learning and maladaptive patterns of positive reinforcement in the maintenance of binge eating.

It is critical for EMA analyses to disaggregate PA into between- and within-subjects components (Curran & Bauer, 2011) to study associations between low and high PA compared to one’s average. Given assertions in our model that both high and low PA may predict binge eating, non-linear models will be important to evaluate. In addition, studies should incorporate sensors and measures to objectively capture PA-promoting behaviors (e.g., accelerometers, 24-hour dietary recalls, electronically activated recorders). Further, longitudinal multi-wave EMA designs will enable researchers to examine changes in anhedonia, behaviors, and reward-related processes, and the extent to which these mechanisms represent BED prevention and treatment targets.

Consistent with calls for elucidation of risk factors across various levels of analysis, future research should also evaluate biological factors associated with anhedonia and altered reward processes that may contribute to the development and maintenance of binge eating. In particular, identifying neurobiological mechanisms may provide insight regarding promising treatment targets for individuals with BED. For instance, findings from mood disorders field suggest that anhedonia is associated with altered dopaminergic function that may influence reward learning and related processes (Cooper et al., 2018). Recent developments in neurobiological, pharmacological, and computational approaches provide the opportunity to examine dopaminergic deficits that might contribute to the neurobiological factors underlying anhedonia-related reward deficits in BED (Cooper et al., 2018). Given evidence outside of BED samples suggesting that behavioral and neural responses may differ when processing primary (e.g., food) vs. secondary (e.g., money) rewards (e.g., Amlung et al., 2016; Herpertz et al., 2015; Valentine & O’Doherty, 2009), elucidating the extent to which anhedonia in BED is specific to aberrant processing of primary versus secondary rewards will be another important future direction. Identifying neurobiological factors that contribute to elevated anhedonia and maintain altered reward processes offers the potential to identify candidate biological factors that could be targeted to bolster treatment outcomes for BED.

Theoretical directions.

Overall, theoretical models focused on BED are lacking, and theoretical models in the ED field do not explicitly include anhedonia and PA (Pennesi & Wade, 2016). This leaves an urgent need to incorporate recent research on anhedonia and potential deficits in reward processes within risk and maintenance models of BED. Research is needed to empirically identify the causal pathways by which anhedonia may increase risk for BED. While reward system dysfunction (both reward surfeit and deficit models) has been proposed to account for overconsumption and excess weight, neither the surfeit or deficit model has demonstrated unequivocal support across the literature. Future research should investigate the extent to which binge eating may initially result from heightened reward responsiveness to food (potentially due to anhedonia-related reward dysfunction) but over time, lead to down-regulation of dopamine receptors within reward regions and compound risk of future binge eating and weight gain (Stice et al., 2010). Further, in addition to elucidating the role of PA and anhedonia, future theoretical and empirical research should consider interactional associations between negative affect and PA.

With respect to potential indirect mechanisms, future research should investigate the roles exacerbation of depressive symptoms and decreased physical activity may play. In addition, research on social anhedonia should examine whether having a detached or uninterested interpersonal style may increase interpersonal problems and thereby act as an additional indirect pathway, as interpersonal problems are considered a central component within the interpersonal model of binge eating (Wilfley et al., 2002). In addition to refining our proposed risk model of anhedonia and BED, future research is needed to examine possible moderators of BED risk among those with anhedonia. Further, we call for more research on maintenance models of BED, which are lacking. Specifically, research is needed to test each of the processes we outline in our momentary maintenance model of binge eating in BED. Finally, while the models in the current paper focus on how anhedonia promotes and maintains BED, anhedonia may occur across EDs (Tchanturia et al., 2012) and thus future research should elucidate how these models may apply to other EDs. Also, future research should examine bi-directionality of associations; that is, how BED symptoms promote and maintain anhedonia, as noted in Figure 1.

Treatment directions.

The proposed risk and maintenance models may also provide a guiding framework for treatment planning and intervention development for BED. For instance, if findings support the role of anhedonia as a risk and/or prognostic factor, clinicians should assess for elevated anhedonia prior to treatment. In the case that future research supports the proposed mechanistic maintenance model, this would inform treatment development efforts. For example, efforts to adapt PA-focused interventions (e.g., PA treatment for depression and anxiety; Craske et al., 2019) may prove particularly beneficial for individuals who demonstrate deficits in reward anticipation, consumption, and/or learning processes posited to contribute to BED. Finally, identifying neurobiological processes underlying altered reward processes may also inform the development of brain-based interventions (e.g., non-invasive neuromodulation, pharmacological interventions).

Conclusions

Initial evidence suggests that anhedonia contributes to risk and maintenance of BED. However, systematic research is needed to better understand the role of anhedonia-related reward processes in BED. To address gaps, we have proposed the first risk and maintenance models of BED, providing foundation for future research examining anhedonia-related models of BED.

Acknowledgments

This work was funded partially by the National Institute of Diabetes and Digestive and Kidney Diseases (Award Number K01DK124435) and the National Institute of Mental Health (Award Numbers K23MH123910 and T32MH082761).

Footnotes

The authors have no conflicts of interest to disclose.

Data Availability Statement: Data sharing is not applicable to this article as no new data were created or analyzed in this study.

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