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. Author manuscript; available in PMC: 2026 Jun 9.
Published in final edited form as: J Psychiatr Res. 2026 May 13;200:38–45. doi: 10.1016/j.jpsychires.2026.05.016

Examining the Independent Effects of Motivational Factors and Withdrawal Mechanisms on Functional Impairment

Michael R Gallagher 1,2,*, Jay C Fournier 2
PMCID: PMC13245140  NIHMSID: NIHMS2178298  PMID: 42143823

Abstract

Motivational factors representing approach and avoidance mechanisms (i.e., behavioral inhibition system, behavioral activation system) have been implicated with depression and anxiety, and have a negative impact on functional outcomes. The independent effects of withdrawal mechanisms, anhedonia and social anxiety, have been established, but are often examined in isolation of one another. The potential modulating or additive relationship between these motivational factors and withdrawal mechanisms remains unclear. Thus, the current study examined the additive and interactive effects of trait level motivational factors and withdrawal mechanisms on impairment in key domains of life. Participants (N =110) with depression and anxiety symptoms ranging from none to severe completed measures of behavioral inhibition (BIS) and behavioral activation (BAS), anhedonia, social anxiety, and functional outcomes. Linear regressions were conducted to assess the interactive and main effects of these factors on life functioning. While no significant interactions emerged, the main effects of anhedonia and social anxiety were stable predictors of life impairment. Additionally, while behavioral inhibition initially exhibited a significant main effect on life impairment in some of the models, this effect appeared to be accounted for by social anxiety; suggesting they measure components of the same underlying construct. These findings suggest that anhedonia and social anxiety are more stable predictors of proximal functional impairment, as we observed no evidence that the interactive relationship between motivational and withdrawal mechanism resulted in worse functioning.

Keywords: anhedonia, anxiety, reward, punishment, functional impairment

1. Introduction

Motivational approach and avoidance systems have long been a focus in depression research (Trew, 2011), as depression has shown to impact real world life functionality (Mehta et al., 2014). Aversive avoidance and appetitive approach are thought to represent two primary motivation systems that underly human behavior and are often measured using the Behavioral Inhibition System (BIS)/Behavioral Activation System (BAS) self-report measure (Carver & White, 1994). Behavioral inhibition captures punishment aversion, or the active avoidance of negative and uncomfortable emotions, and negatively impacts functioning (Hundt et al., 2010). Conversely, behavioral activation involves reward responsivity or one’s reaction to potentially rewarding situations and emotions (Carver & White, 1994), and lower scores are connected to worse functioning (Kasch et al., 2002). The association between BIS/BAS and depression has been extensively examined, and high behavioral inhibition coupled with low behavioral activation scores have been found to predict future depression (Kasch et al., 2002; Rizvi et al., 2016) and distinguish between different presentations of depression (Bijttebier et al. 2009; Hundt et al., 2007). Behavioral inhibition and behavioral activation have also shown to have an impact on normative social functioning behaviors (Hundt et al., 2010), but there appear to be various ways in which behavioral inhibition and behavioral activation can uniquely lead to social withdrawal and result in social impairment.

Anhedonia and social anxiety represent two possible pathways for withdrawal behaviors. Past work examining behavioral activation and inhibition has highlighted the importance of distinguishing between anhedonic depression and anxious depression (Bijttebier et al. 2009). Past studies examining the associations among motivational factors, depression, and anxiety typically focused on how well the motivational factors may predict the onset or severity of depression and anxiety (Coplan et al., 2006; Germans & Kring, 2000; Kimbrel, 2008; McFarland et al., 2006). Little work has examined the combined impact of motivational factors and withdrawal mechanisms on individuals’ functioning across domains of living. Although these withdrawal mechanisms can cause clinically significant distress and impairment at the severe end, frameworks like the Research Domain Criteria (RDoC) and Hierarchical Taxonomy of Psychopathology (HiTOP) suggest that these mechanisms operate on a dimensional continuum and can influence everyday functioning even for those with less severe presentations. These dimensional frameworks suggest that each of these factors represent transdiagnostic dimensions that may modulate each other to influence how individuals navigate their world. Thus, examining the interactions between these dimensional factors will allow for a better understanding of how these mechanisms possibly reinforce and strengthen one another.

1.1. Behavioral Activation System (BAS) and Social Anxiety

A large amount of research has found social anxiety to be associated with elevated behavioral inhibition (BIS) (Bijttebier et al. 2009; Coplan et al., 2006; Kimbrel, 2008; Kimbrel et al., 2012). Gray and McNaughton (2000) posit that punishment sensitivity, a central element of behavioral inhibition, is the underlying avoidance mechanism that leads to the development of social anxiety – which garnered additional support (Kimbrel, 2008). However, the connection between social anxiety and alterations in behavioral activation (BAS), potentially representing a separate withdrawal pathway, remains largely unknown. Work has begun to examine the relation between anxiety and blunted reward processing (Taylor et al., 2022), and these factors may modulate one another, as both have been shown to lead to impairment (Aderka et al., 2012; Kupferberg et al., 2016; McKnight et al., 2016). For example, if previously pleasurable experiences are already devalued and an individual experiences social anxiety, they may further avoid these prospective uncomfortable yet rewarding situations, leading to further devaluation and avoidance (Taylor et al., 2022). This cycle may account for the connection between diminished behavioral activation and social anxiety found in some past studies (Coplan et al., 2006; Kimbrel et al., 2010, 2012; Morgan et al., 2009), but the nature of these associations remains unclear. One study suggested that low behavioral activation scores may be connected to social withdrawal (Bowker et al., 2017), but others have concluded that behavioral activation and social anxiety are not related (e.g., Kimbrel, 2008). Furthermore, although the effects of behavioral activation and social anxiety on functioning across life domains have been established separately, it is currently unclear whether and how alterations in behavioral activation/reward sensitivity (BAS) and social anxiety may combine to predict functioning. If a combination of low behavioral activation with high social anxiety leads to worse functional life outcomes than either independently, future treatments can be developed to target this potential cycle.

1.2. Behavioral Inhibition System (BIS) and Anhedonia

Prior work on anhedonia as a withdrawal mechanism typically focused on its connection to the behavioral activation system. Both behavioral activation and anhedonia involve features of rewarding processing. Previous studies have found low behavioral activation scores to be predictive of anhedonia and depression (Coplan et al., 2006; Germans & Kring, 2000; Kimbrel et al., 2007), possibly capturing the blunted reward motivation commonly seen in depression (Whitton et al., 2016). Little work has examined associations between behavioral inhibition and anhedonia. Similar to the largely unexplored connection between behavioral activation and social anxiety, behavioral inhibition and anhedonia represent a potentially novel withdrawal pathway that can lead to functional impairment. Some past work has shown a connection between elevated behavioral inhibition scores and depression (Coplan et al., 2006; Hunt et al., 2007). Bijttebier and colleagues interpret these findings within the context of the tripartite model, in which behavioral inhibition may capture the shared general distress between depression and anxiety, whereas behavioral activation is unique to depression (Clark & Watson, 1991). However, others have not found these same associations (McFarland et al., 2006; see Bijttebier et al. 2009 for a review).

Carver & White (1994) posit that heightened punishment aversion, which is driven by biological appetitive processes, leads to behavioral inhibition and avoidance. While punishment may be avoided, the behavioral inhibition is typically coupled with negative emotions and distress. Punishment sensitivity has shown to be a transdiagnostic risk factor across psychological disorders (Claes et al., 2021; Miu et al., 2017). Thus, it is important to consider the potential amplifying effect of motivational factors like behavioral inhibition when measuring and conceptualizing depression.

Regarding anhedonia specifically, it is possible that hypersensitivity to negative outcomes (i.e., high behavioral inhibition, BIS) could impact individuals’ ability to derive enjoyment from pleasurable activities in their lives, leading to withdrawal, functional impairment, and poor life satisfaction. As was the case for behavioral activation and social anxiety, behavioral inhibition and anhedonia have each been established as factors that predict impairments in functioning across domains of life (Barkus & Badcock, 2019; Hundt et al., 2010; Kupferberg et al., 2016). However, the exact nature of the relationship between these two constructs is not understood, especially in the context of functional impairment. If behavioral inhibition and anhedonia interact to predict worse functional outcomes, treatments that target the reinforcing nature of the relationship would be efficacious.

1.3. The Current Study

Anhedonia and social anxiety represent two withdrawal mechanisms that negatively impact engagement and life satisfaction. Although some past work has established potential pathways between the behavioral inhibition/behavioral activation motivation systems and these withdrawal mechanisms, it remains unclear how these mechanisms combine to impact an individual’s functioning. If reward sensitivity and anxiety result in an avoidance cycle that unravels over time (Taylor et al., 2022), interventions that target this cyclical process would be beneficial. The first step to understanding this process is to determine whether the motivational approach/avoidance factors and withdrawal mechanisms demonstrate independent, additive, or interactive effects on functional outcomes.

The data used in this study are part of a larger study examining the neural correlates of excessive self-consciousness in depression and anxiety. Whereas the larger study focused on negative affectivity, emotion regulation, and self-related processing in depression and anxiety, we were specifically interested in psychosocial functioning across life domains as the main outcome variable in this study. The central aim of the current study was to examine whether the motivation and withdrawal mechanisms are capturing independent associations with life functioning or whether a combination of the mechanisms (e.g., low behavioral activation and high social anxiety) leads to worse functional outcomes. In addition to probing whether the independent effects of behavioral inhibition, behavioral activation, anhedonia, and social anxiety on functional outcomes that have been reported previously would continue to be present when these constructs were examined together, we further hypothesized that 1) behavioral inhibition would moderate the impacts of anhedonia on functional outcomes and that 2) behavioral activation would moderate the impact of social anxiety. Thus, we aim to uncover the additive or amplifying effect of motivational features and withdrawal mechanisms on functional impairment across non-social and social life domains.

2. Methods

2.1. Participants

The data used in this study were part of a sample for a larger neuroimaging study. As part of the exclusion criteria of the larger study, participants were excluded based on previous diagnoses of psychosis or bipolar disorder, substance use disorder, and several other standard neuroimaging exclusion criteria. A total of N = 110 participants were included in the current analyses (Table 1). This sample included participants from the larger parent study who had completed all of the measures included in this study. Participants were recruited into one of two groups. The internalizing group exhibited elevated scores on either the Quick Inventory of Depressive Symptomatology (QIDS-SR score of 6 or greater; Rush et al., 2003) or the Patient-Reported Outcomes Measurement Information System - Anxiety (PROMIS-A T-score of 55 or greater; Pilkonis et al., 2011). The control group had no previous psychiatric history and scores lower than these thresholds. Given the aims of the current study which sought to examine dimensional mechanisms involved in depression and anxiety, the full sample was analyzed dimensionally. All participants provided written consent before participating and the study was approved by the Institutional Review Boards at The Ohio State University and the University of Pittsburgh.

Table 1.

Demographic and Descriptive Statistics

Measure Mean/Count Standard Deviation
Age 22.13 2.95
Sex at Birth Female: 73
Male: 37		 –
Race Asian: 17
Black or African American: 9
Multiple: 8
White: 76		 –
BIS 21.66 4.20
BAS 36.64 6.33
SHAPS 24.65 6.94
LSAS 37.66 28.22
HAM-D 8.70 6.38
HAM-A 7.48 6.34
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Note. BIS = Behavioral Inhibition System, BAS = Behavioral Activation System, SHAPS = Snaith-Hamilton Pleasure Scale, LSAS = Liebowitz Social Anxiety Scale, HAM-D = Hamilton Depression Rating Scale, HAM-A = Hamilton Anxiety Rating Scale.

2.2. Measures

2.1.1. Behavioral Inhibition and Behavioral Activation Scale (BIS/BAS Scale)

Reward and punishment responsiveness were measured with the BIS/BAS scale (Carver & White, 1994). The BIS/BAS scale is a 20 item self-report measure which measures both approach and avoidance activation. Statements are rated on a 4-point Likert scale ranging from 1 (“Strongly Disagree”) to 4 (“Strongly Agree”). The behavioral inhibition system is captured with the 7 item BIS subscale, whereas the 13 item BAS scale consists of three subscales that are often combined into an overall behavioral activation scale (Chen et al., 2023). Higher scores on BIS represent greater punishment aversion/sensitivity, whereas higher scores on the BAS correspond to greater reward responsivity.

2.2.2. Snaith-Hamilton Pleasure Scale (SHAPS)

Anhedonia was measured via a sum score on the Snaith-Hamilton Pleasure Scale (SHAPS; Snaith et al., 1995). The SHAPS is a well validated measure of anhedonia that measures hedonic tone. Participants are presented with statements regarding enjoyment or pleasure and rate their answers on a 4-point Likert scale ranging from “Strongly Disagree” to “Strongly Agree.” The agree responses are coded as 0, whereas the disagree responses are coded as 1; thus, higher values represent more severe anhedonia.

2.2.3. Liebowitz Social Anxiety Scale (LSAS)

Social anxiety was measured with the Liebowitz Social Anxiety Scale (LSAS; Liebowitz, 1987). The LSAS is a 24 item self-report measure that quantifies self-rated fear and avoidance of various social situations. Higher scores on the LSAS signify greater social anxiety severity.

2.2.4. Longitudinal Interval Follow-up Evaluation-Range Impaired Functioning Tool (LIFE-RIFT)

Life functioning was measured via the Longitudinal Interval Follow-up Evaluation-Range Impaired Functioning Tool (LIFE-RIFT; Leon et al., 1999), a clinician rated measure of functional impairment wherein higher scores signify greater functional impairment. Ratings of social outcomes captured the quality of family and friend relations; ratings of nonsocial outcomes captured functioning in the domains of work, school, and recreation; finally, two global ratings captured the participants global level of life satisfaction and the rater’s global impression of the participants overall level of functioning. Given that many of the participants in the current study had one professional role as either an employee or student, the work and student subscales were combined into a productive activity scale. Productive activity consisted of the average of the work and student variables; however, if one of the variables was missing, productive activity was represented by the variable that was present for that individual. Additionally, given the large correlation and similarity in the language of the satisfaction and global satisfaction subscales (r = 0.84), these two variables were combined into one total life satisfaction subscale.

2.3. Data Analytic Plan

The data analytic plan followed recommendations from past studies that examined the relations between behavioral inhibition/behavioral activation and depression/anxiety (Hundt et al., 2007). Specifically, the joint subsystems hypothesis suggests that behavioral inhibition and behavioral activation should be examined together as they are not independent processes (Corr, 2002) and so both variables were included in all models.1

Linear regressions were conducted to examine the influence of behavioral inhibition/behavioral activation and withdrawal mechanisms on functional impairment via the LIFE-RIFT. The interaction between behavioral inhibition, behavioral activation, and each of the two withdrawal mechanisms, anhedonia or social anxiety, were examined in separate models (Supplemental Tables S1–S5). We examined non-social and social impairment across 5 total LIFE-RIFT scales. This resulted in a total of 10 models, as each of these functional impairment scales were modeled separately for anhedonia and social anxiety. To conform to the joint subsystems hypothesis, and to further explore relationships among behavioral inhibition, behavioral activation, and the withdrawal mechanisms, we probed three-way interactions (e.g., BIS-X-BAS-X-Anhedonia) as exploratory aspects of the model. Age and sex at birth were included in the models as covariates. We had a small amount of missing data (1.52%) and there were no missing data on the measures of behavioral inhibition, behavioral activation, anhedonia, or social anxiety. We used case-wise deletion to handle the small amount of missing LIFE-RIFT data in each of the separate models and report the final sample size in the results for each model. The distributions of each of the dependent variables were examined. Based on the data distribution, we examined model fit of the recreation, friends, and family variables with both a normal and negative binomial distribution to determine the best fitting model. The normal distribution emerged as the better fitting model in each case, regardless of whether anhedonia or anxiety was entered as the withdrawal mechanism. Thus, all regressions were modeled assuming normally distributed residuals.2 Multiple comparisons were addressed using False Discovery Rate (FDR) corrections. In particular, the “p.adjust” function in R was used to obtain FDR corrected p-values, which are reported in the results section as q-values. We report standardized beta coefficients for each of the predictor variables. The data for this study are available at the National Data Archive (Collection #C2945) or upon request.

3. Results

3.1. Nonsocial Outcomes

3.1.1. Anhedonia

When anhedonia was included in the model as the withdrawal mechanism, the main effects of behavioral inhibition (B = 0.32, t(97) = 3.22, p = .002, q = .006) and anhedonia (B = 0.33, t(97) = 3.36, p = .001, q = .006) emerged as significant predictors of productivity impairment (Full Model 1: n = 107; F9,97 = 5.71, p < .001). Similarly, both behavioral inhibition (B = 0.45, t(100) = 5.48, p < .001, q < .001) and anhedonia (B = 0.47, t(100) = 5.72, p < .001, q < .001) emerged as significant predictors of life dissatisfaction (Full Model 2: n = 110; F9,100 = 12.63, p < .001). Anhedonia (B = 0.42, t(100) = 4.44, p < .001, q < .001) emerged as a significant predictor of recreation dissatisfaction (Full Model 3: n = 110; F9,100 = 6.63, p < .001). Behavioral inhibition (B = 0.23, t(100) = 2.48, p = .015, q = .073) initially emerged as a predictor of recreation impairment, but it missed the correction threshold. The hypothesized interaction between behavioral inhibition and anhedonia was not significant in any of these nonsocial models (all Bs < 0.11, ps > .17, qs ≥ .30).

3.1.2. Social Anxiety

Social anxiety (B = 0.44, t(97) = 3.36, p = .001, q = .006) emerged as the sole significant predictor of productivity impairment (Full Model 4: n = 107; F9,97 = 5.19, p < .001). This was the only model in which behavioral inhibition (B = 0.12, t(97) = 0.89, p = .38, q = .70) was not a significant predictor of productivity impairment, suggesting that the connection between behavioral inhibition and productivity was captured by the inclusion of social anxiety. The results from the satisfaction model indicated that behavioral inhibition (B = 0.28, t(100) = 2.61, p = .01, q = .03), social anxiety (B = 0.50, t(100) = 4.59, p < .001, q < .001), and sex at birth (B = −0.20, t(100) = −2.52, p = .01, q =. 03) emerged as significant main effects (Full Model 5: n = 110; F9,100 = 11.06, p < .001). In the recreation model, the behavioral activation x social anxiety interaction (B = 0.27, t(100) = 2.16, p = .033, q = .11) was initially significant but did survive the FDR correction. Social anxiety (B = 0.38, t(100) = 3.11, p = .002, q = .03) emerged as the only stable significant predictor in the recreation dissatisfaction model (Full Model 6: n = 110; F9,100 = 6.22, p < .001). The hypothesized interaction between behavioral activation and social anxiety did survive the corrected threshold in any of the nonsocial models (all Bs ≤ 0.27, ps ≥ .03, qs ≥ .11).

3.2. Social Outcomes

3.2.1. Anhedonia

While anhedonia emerged as a consistent indication of social impairment, the role of behavioral inhibition varied depending on the outcome variable. When examining friendship relations, both anhedonia (B = 0.28, t(100) = 2.67, p = .009, q = .044) and behavioral inhibition (B = 0.30, t(100) = 2.89, p = .005, q = .044) emerged as significant predictors (Full Model 7: n = 110; F9,100 = 3.94, p < .001). However, in the family model (Full Model 8: n = 98; F9,88 = 3.13, p = .003), only anhedonia emerged as a significant predictor (B = 0.42, t(88) = 3.79, p < .001, q = .003 for anhedonia; B = 0.10, t(88) = 0.91, p = .37, q = .69 for BIS). The interaction between behavioral inhibition and anhedonia was not significant in either of the social models (all Bs ≤ 0.13, ps ≥ .17, qs ≥ .34).

3.2.2. Social Anxiety

As was the case in the non-social models, when social anxiety was substituted into the social models, social anxiety was the only significant predictor (B = 0.45, t(100) = 3.51, p < .001, q = .007) for friendship relations (Full Model 9: n = 110; F9,100 = 5.16, p < .001). Similarly, social anxiety was the only significant predictor (B = 0.44, t(88) = 3.08, p = .003, q = .01) for family relations (Full Model 10: n = 98; F9,88 = 2.52, p = .013). Behavioral inhibition was not significantly associated with either of the social outcomes (Bs ≤ 0.11, ps > .40, qs ≥ .69). The behavioral activation x social anxiety interaction was not significant in any of the social models (all Bs ≤ 0.14, ps ≥ .35, qs ≥ .70).

3.3. Final Omnibus Models

Additional analyses were conducted to further probe the potential independent effects of anhedonia and social anxiety on the five measurements of functional impairment. The significant predictor variables from each of the previous models were entered as independent variables, along with age and sex at birth. For example, behavioral inhibition, anhedonia, and social anxiety emerged as significant main effect predictors of productivity impairment in the respective models; thus, they were entered simultaneously into a new regression model. Results revealed that anhedonia (B = 0.29, t(101) = 2.90, p = .005, q = .04, ηp2 = 0.07) was a significant predictor of productivity impairment (see Figure 1); social anxiety did not meet the correction threshold (B = 0.25, t(101) = 2.08, p = .04, q = .08, ηp2 = 0.04). Behavioral inhibition (B = 0.18, t(101) = 1.58, p = .12, q = .18, ηp2 = 0.02) was no longer a significant predictor of productivity impairment (Omnibus Model 1: F5,101 = 10.80, p < .001).

Figure 1. Productivity Impairment.

Figure 1

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Note. Higher scores on the productivity index correspond to greater functional impairment in the student and/or employment domains. Anhedonia and social anxiety were mean centered. Points were jittered for better visualization.

The next model examined the significant predictor variables (behavioral inhibition, anhedonia, and social anxiety) associated with global functioning. Anhedonia (B = 0.35, t(104) = 4.13, p < .001, q < .006, ηp2 = 0.14), social anxiety (B = 0.26, t(104) = 2.57, p = .01, q = .02, ηp2 = 0.06), and behavioral inhibition (B = 0.30, t(104) = 3.28, p = .001, q = .003, ηp2 = 0.09) scores were all predictive of life dissatisfaction (Omnibus Model 2: F5,104 = 24.27, p < .001; see Figure 2).

Figure 2. Life Dissatisfaction.

Figure 2

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Note. Higher scores on the dissatisfaction index correspond to greater overall life dissatisfaction and global impairment. BIS = Behavioral Inhibition System. Anhedonia, social anxiety, and BIS were mean centered. Points were jittered for better visualization.

Anhedonia and social anxiety were entered as surviving independent variables in the recreation model. Both anhedonia (B = 0.36, t(105) = 3.72, p < .001, q = .002, ηp2 = 0.12) and social anxiety (B = 0.34, t(105) = 3.48, p < .001, q = .002, ηp2 = 0.10) remained as independent significant predictors of recreation dissatisfaction (Omnibus Model 3: F4,105 = 16.03, p < .001; see Figure 3).

Figure 3. Recreation Impairment.

Figure 3

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Note. Higher scores on the recreation index represent greater impairment/dissatisfaction in recreational activities. Anhedonia and social anxiety were mean centered. Points were jittered for better visualization.

For the social models, we observed different patterns for functioning in friendship- and family-relationships (see Figure 4). Regarding functioning in friendship relationships (Omnibus Model 4: F5,104 = 9.43, p < .001), only social anxiety (B = 0.45, t(104) = 3.67, p < .001, q = .002, ηp2 = 0.11) remained significant when anhedonia and behavioral inhibition were examined simultaneously (B = 0.12, t(104) = 1.17, p = .24, q = .49, ηp2 = 0.01 for anhedonia; B = 0.04, t(104) = 0.40, p = .69, q = .69, ηp2 = 0.002 for BIS). For impairments in family relationships (Omnibus Model 5: F4,93 = 7.58, p < .001), only anhedonia remained as a stable predictor (B = 0.32, t(93) = 2.75, p = .007, q = .02, ηp2 = 0.08), whereas social anxiety did not meet the FDR cutoff (B = 0.23, t(93) = 2.01, p = .047, q = .08, ηp2 = 0.04).

Figure 4. Social Impairment.

Figure 4

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Note. The left panel displays the family domain and the right panel represents the friendship domain. Higher scores in both figures represent greater relationship impairment/dissatisfaction in the respective domain. Anhedonia and social anxiety were mean centered. Points were jittered for better visualization.

4. Discussion

The current study aimed to investigate the potential independent or interactive effects of motivation and withdrawal mechanisms on life functioning in a sample with normal to abnormal levels of functioning, consistent with a dimensional approach to characterizing psychopathology. Motivational factors and withdrawal mechanisms have all been independently associated with negative outcomes and impairment (Aderka et al., 2012; Kupferberg et al., 2016; McKnight et al., 2016; Mehta et al., 2014). Mixed results previously emerged regarding the potential relations between behavioral activation and social anxiety, as well as behavioral inhibition and anhedonia. The long-term goal of this line of work is to understand how the potential cycle between motivation and withdrawal unfolds over time. Thus, the first step taken in this study was to examine these trait level motivation and withdrawal factors cross-sectionally, to assess whether they have independent effects.

4.1. Anhedonia

Anhedonia consistently emerged as a significant predictor of functional impairment, and behavioral inhibition was also associated with functional impairment in several of the models. These results suggest that a lack of interest or inability to experience pleasure may negatively impact life functioning in work/school performance, satisfaction, enjoyment, and relationship quality. Additionally, those who have heightened behavioral inhibition (i.e., punishment sensitivity) may operate “on edge” or be more prone to avoid certain situations, resulting in impairment. These findings support past work that depression and behavioral inhibition (i.e., punishment aversion) negatively influence functioning (Aderka et al., 2012; Kupferberg et al., 2016; McKnight et al., 2016; Mehta et al., 2014).

Behavioral activation was not a significant predictor in any of the models, suggesting that anhedonia may be capturing a mechanism independent of the reward responsiveness that is operationalized by the behavioral activation subscale. This aligns with the conceptualization that behavioral activation reflects only a part of anhedonia and reward processing more broadly. Behavioral activation may only capture the appetitive approach (“wanting”) aspect of reward (Carver & White, 1994), whereas anhedonia captures both anticipatory (“wanting”) and consummatory (“liking”) features of reward processing (Admon & Pizzagalli, 2015). Another potential explanation is that the withdrawal mechanisms (e.g., anhedonia) are stronger proximal predictors of impairment.

4.2. Social Anxiety

Social anxiety emerged as a consistent predictor of impairment for each of the functional outcomes examined. The substitution of social anxiety into the productivity, recreation, and friendship models resulted in behavioral inhibition no longer being a significant predictor. Kimbrel (2008) posits that behavioral inhibition is the underlying motivational mechanism that leads to the development of social anxiety. Thus, it is likely that behavioral inhibition and social anxiety explain overlapping variance in functional outcomes, as they were positively correlated (r = 0.65) and appear to measure similar anxiety responsiveness mechanisms. Social anxiety appears to be the more proximal stable predictor for measures of life functioning.

The omnibus analyses including all surviving predictor variables also revealed that anhedonia and social anxiety remained as significant predictors of productivity impairment, recreation disinterest, and life dissatisfaction. Interestingly, whereas social anxiety emerged as the only remaining significant predictor of friendship impairment, anhedonia was the only surviving predictor of familial strain. These omnibus analyses support the notion that anhedonia and social anxiety represent unique withdrawal mechanisms that independently impact life outcomes. Behavioral inhibition and behavioral activation do not appear to amplify these effects.

We found that anhedonia and social anxiety are both predictors of functional impairment, but they appear to offer unique information that may be useful for clinicians. For example, anhedonia and social anxiety both predict recreation impairment and life dissatisfaction. In these cases, clinicians can encourage patients to engage in recreational and leisure activities as part of the treatment plan, which has shown to reduce depression and anxiety (Harvey et al., 2010; Puyat et al., 2020). Despite the overlap between anhedonia and social anxiety, these mechanisms also appear to influence different types of social relationships. Our findings suggest that anhedonia, a lack of interest and motivation, negatively impacts family relations. Family relations tend to be the most immediate and proximal relationships, as interactions with family members are more frequent in day-to-day life (Zhaoyang et al., 2018). Social anxiety is associated with friendship strain. Friendships typically revolve around more public social encounters (Roth & Peng, 2024), which are likely to be impacted by social anxiety. Thus, it may be important to target the specific mechanism leading to the particular kind of social impairment the individual is experiencing.

4.3. Limitations and Future Directions

The sample consisted of a broad internalizing sample, as well as healthy controls. Consistent with frameworks that highlight the importance of examining psychopathology through a dimension approach, such as RDoC and HiTOP, we examined the data as a dimensional sample. However, it is possible that the interaction effects may have been more likely to emerge at one or the other end of the severity ranges represented in the sample. Future research should examine the motivational factors and withdrawal mechanisms in community and healthy samples. It is also possible the interactive effects were not able to be identified due to a lack of power. Future work may benefit from examining whether the current results replicate in a larger sample. Another limitation is the cross-sectional design of this study, as the effects were not able to be examined over the course of time or with treatment. Since this was not a developmental study, the exact timeline of the onset of these mechanisms is unknow; thus, it is not possible to know which of the elevations emerged first. A last limitation is that the functional measures included as the outcome variables were captured by clinician interview and may be subject to recall biases. Future work should compare the current findings with functional self-report measures and performance-based functional measurements to examine the generalizability of the findings to various forms of psychosocial functioning.

This work was the first step in unraveling the potential reinforcing cycle between behavioral activation/inhibition and withdrawal mechanisms. Disentangling the onset, course, and potentially detrimental cyclical nature of these factors can lead to the development of timely interventions that accurately target the most central symptoms. This study helped establish the independent nature of these effects on functional outcomes, as social anxiety and anhedonia appear to be the more stable proximal predictors of current functional impairments. Future work should examine the time course of these factors, as well mediation or path effects. A more fine-grained examination of functioning may require the utilization of ecological momentary assessments to establish a reliable timeline and monitor symptom fluctuations. Additional work would also benefit from examining these factors within a network to identify the most central or influential mechanisms over the functional outcomes. One result of such work could be that treatments are targeted to affect the most influential symptoms to reduce the factors most responsible for impaired functioning across domains.

5. Conclusion

We examined the potential independent and interactive effects of motivational factors and withdrawal mechanisms on functional life outcomes. We found that anhedonia and social anxiety emerged as stable predictors of current life impairment. Additionally, while behavioral inhibition appears to influence functional outcomes, this impact is often no longer present when examined concurrently with social anxiety, suggesting they represent similar constructs, and that social anxiety may be the more proximal risk factor for poor functioning. Thus, the withdrawal mechanisms, anhedonia and social anxiety, may be more effective risk predictors of functional impairment. While it is important to understand the motivational features that underly behavior, measures of anhedonia and social anxiety appear to offer reliable, yet unique and independent, measurement predictions of functional impairment across different life domains. This work addresses a gap in the literature by providing evidence for the independent impact of withdrawal and motivational mechanisms on functional impairment. Future work should examine how these transdiagnostic factors of depression and anxiety exacerbate and build on each other over time.

Supplementary Material

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Funding

Research reported in this study was supported by the National Institute of Mental Health (R01 MH112758; PI: JCF). The funding source had no involvement in the study design, collection, analysis, or decision to submit the article for publication.

Footnotes

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We conducted secondary analyses where only BIS, BAS, and BIS x BAS interaction were included as predictors (Supplemental materials S6–S7).

2

The models for recreation, friends, and family were modeled with the normal and negative binomial distributions to determine model fit. The pattern of findings is largely unchanged regardless of the distribution. See supplemental materials for the full list of fit values.

Declaration of Competing Interests

JCF receives royalties from Guilford Press. We do not have any other declarations of interest to disclose.

Data Availability Statement

The data for this study are available at the National Data Archive (Collection #C2945) or upon request.

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Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Supplementary Materials

1
NIHMS2178298-supplement-1.pdf (473.2KB, pdf)

Data Availability Statement

The data for this study are available at the National Data Archive (Collection #C2945) or upon request.

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