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. 2026 Sep 29;15:RP110631. doi: 10.7554/eLife.110631

Dissociable roles of reward prediction error in the contrasting mood dynamics of depression and anxiety

Zhihao Wang 1,2,†, Ting Wang 3,†, Tian Nan 4, Jiahua Xu 5,6, André Aleman 7, Yuejia Luo 4,8,9,10, Bastien Blain 2, Yunzhe Liu 5,6,✉, Pengfei Xu 11,✉
Editors: Andreea Oliviana Diaconescu12, Jonathan Roiser13
PMCID: PMC13623375  PMID: 42809336

Abstract

Mood fluctuations, central to human experience, are profoundly influenced by reward prediction errors (RPE). Although depression and anxiety traditionally exhibit contrasting mood fluctuations, their interrelated nature has made it challenging to pinpoint their specific roles in RPE-induced mood variations. In this study, we employed a computational model of momentary mood within a gambling task, involving 2043 participants across five experiments. Participants also completed a battery of questionnaires designed to allow us to dissociate anxiety- and depression-specific traits through bifactor modeling. Results showed that depression was associated with dampened mood fluctuations due to mood hyposensitivity to RPE. Importantly, this pattern was also found in patients with affective disorders. In contrast, anxiety correlated with heightened mood fluctuations stemming from mood hypersensitivity to RPE in non-clinical participants. Moreover, the shared depression/anxiety component was linked to lower affective baseline and greater risk aversion. Collectively, our results uncover computational dissociation of depression vs. anxiety using RPE-based mood modeling and present multi-dimensional computational signatures for these symptoms, with clinical relevance for management of mood disorders.

Research organism: Human

Introduction

Happiness is a central component of human experience, providing a subjective signal of value and guiding actions aimed at maximizing well-being (Bentham, 1780; Mill, 1859). Yet, well-being is often disrupted, as evidenced by the high prevalence of mood disorders such as depression and anxiety. It is therefore crucial to understand what drives mood fluctuations, and how these processes promote happiness or contribute to mood disorders.

Mood dynamics are strongly influenced by reward prediction error (RPE) – discrepancies between expected and actual outcomes (Eldar and Niv, 2015; Kao et al., 2023; Emanuel and Eldar, 2023; Bennett et al., 2022; Eldar et al., 2016; Rutledge et al., 2014; Otto et al., 2016). This influence is particularly prominent in uncertain environments, such as gambling scenarios, where outcomes frequently deviate from expectations and thereby drive moment-to-moment mood changes (Rutledge et al., 2014; Rutledge et al., 2015; Rutledge et al., 2016a; Blain and Rutledge, 2020; Vanhasbroeck et al., 2021). Although RPE-induced mood fluctuations play a critical role in adaptive behavior (Kao et al., 2023; Eldar et al., 2016; Quoidbach et al., 2019; Taquet et al., 2016), atypical mood dynamics may increase vulnerability to affective disorders (Kao et al., 2023; Broome et al., 2015; Mason et al., 2017; Taquet et al., 2020). Specifically, depression, often associated with blunted emotional responses (Bylsma et al., 2008; Rottenberg et al., 2005), may be linked to dampened mood fluctuations (Rottenberg et al., 2002a; Rottenberg et al., 2002b; Rottenberg and Hindash, 2015; Koval et al., 2012; Rutledge et al., 2017). In contrast, anxiety, characterized by exaggerated responses to uncertainty (Grupe and Nitschke, 2013), might intensify them (Bowen et al., 2006; Bowen et al., 2004). However, distinguishing the unique effects of depression and anxiety on mood dynamics presents a significant challenge, owing to their overlapping symptoms and entangled nature (Stavrakaki and Vargo, 1986; Steer et al., 1995).

Recent work has used bifactor models of the tripartite model of depression and anxiety to clarify their distinct features and differential influences on decision-making (Gagne et al., 2022; Gagne et al., 2020). The tripartite model of anxiety and depression proposes that these two symptom dimensions share a broad general distress or negative affect component while also including symptom-specific components: low positive affect/anhedonia is more specific to depression, whereas physiological hyperarousal is more specific to anxiety (Steer et al., 1995; Simms et al., 2008; Clark and Watson, 1991). Bifactor analysis offers a way to model this structure statistically. In a bifactor model, symptoms load on a general factor reflecting their shared variance and on specific factors capturing residual variance in narrower symptom dimensions after accounting for the general factor. Although bifactor and hierarchical models have long been used in psychometrics, for example intelligence research (Rodriguez et al., 2016; Reise, 2012), their application to anxiety and depression is grounded in the tripartite model and subsequent psychometric work distinguishing general internalizing/distress from symptom-specific dimensions. This framework has recently been extended to computational psychiatry, where shared and specific affective symptom dimensions have been linked to task-derived computational parameters. For example, Gagne et al., 2022 used bifactor analysis to show that depression was associated with weaker prior beliefs, whereas anxiety was associated with a stronger negative bias in belief updating (Gagne et al., 2022). Intriguingly, mood sensitivity to RPE appears to remain intact in both patients with major depressive disorder (MDD) and individuals with high depression scores (Blain and Rutledge, 2020; Rutledge et al., 2017; Csukly et al., 2023), contrary to the hypothesis that depression is associated with reduced RPE-related mood sensitivity (Rutledge et al., 2017). Individuals with anxiety not only show heightened vigilance before an outcome is known but may also assign greater precision to information that resolves uncertainty (Tobias and Ito, 2021; Huang et al., 2017). Such increased precision-weighting could amplify the affective influence of RPEs, leading to larger mood shifts when outcomes deviate from expectations (Villano et al., 2023; Paulus and Yu, 2012). Given evidence suggesting opposite associations of depression and anxiety with mood fluctuations (Rottenberg and Hindash, 2015; Koval et al., 2012; Bowen et al., 2006; Bowen et al., 2004), one possible explanation for the apparent intactness of RPE-related mood sensitivity (Rutledge et al., 2017) is that depression and anxiety exert opposing effects on this sensitivity, thereby counteracting each other. To test this hypothesis, we applied a bifactor model to disentangle these interrelated influences.

This study used a computational model of momentary mood in a gambling task across five experiments involving 2043 participants. Participants also completed a series of questionnaires, enabling bifactor analysis to dissociate the influences of anxiety- and depression-specific traits on mood fluctuations. We measured momentary mood by asking participants, “How happy are you at this moment?” This measure has also been used to index happiness or momentary subjective well-being (Rutledge et al., 2014; Quoidbach et al., 2019; Taquet et al., 2016; Jangraw et al., 2023). Although mood can persist for hours, days, or even weeks (Kao et al., 2023; Emanuel and Eldar, 2023; Eldar et al., 2016; Schiller et al., 2024), momentary mood measured in laboratory settings captures how multiple events accumulate to shape affective state over minutes (Kao et al., 2023; Eldar et al., 2016; Rutledge et al., 2014; Rutledge et al., 2016a; Blain and Rutledge, 2020; Vanhasbroeck et al., 2021; Rutledge et al., 2017; Csukly et al., 2023; Vinckier et al., 2018). Its external validity is supported by associations with depressive symptoms (Blain and Rutledge, 2020; Rutledge et al., 2017). We first validated the tripartite model of depression and anxiety before examining the specific roles of depression and anxiety in mood fluctuations (n=901). Next, we measured mood sensitivity to RPE in a gambling task and investigated its relation to anxiety- and depression-specific traits based on the tripartite model in a laboratory experiment (n=44) and two additional online experiments (n=747 and n=235). In the final experiment (n=116), we tested the generalizability of these findings in a clinical sample of patients with affective disorders, revealing dissociable roles of depression and anxiety in RPE-related mood dynamics.

Results

Experimental protocol

After completing a battery of questionnaires (Gagne et al., 2020; see Materials and methods), participants performed a gambling task with momentary mood ratings (Rutledge et al., 2014; Rutledge et al., 2015; Vanhasbroeck et al., 2021). Within this task, participants were asked to choose between a certain option and a gamble option with two possible outcomes, each occurring with a 50% probability. Participants were instructed to rate their mood every two to three trials (Figure 1). Detailed participant demographics are summarized in Table 1. Choice data (e.g. gambling rates) and mood data (e.g. initial mood, mean mood, and mood variation) showed patterns similar to those reported in previous studies measuring momentary mood during gambling tasks (Figure 1—figure supplements 1 and 2; Rutledge et al., 2015; Rutledge et al., 2016b). We also replicated established effects on momentary mood: mood was higher following gains than following losses, and mood drifted over time (all ps <0.001; Figure 1—figure supplement 3).

Figure 1. Experimental protocol.

(A) Study outline. This study examines how depression and anxiety influence mood fluctuations. The first experiment assesses the bifactor structure that disentangles shared and specific components of depression and anxiety in the psychometric dataset (N=901). The second experiment tests associations between depression- and anxiety-specific traits and RPE-induced mood fluctuations using the questionnaire battery and a gambling task with momentary mood ratings in the laboratory dataset (N=44). The third and fourth experiments replicate the second experiment in online samples (online dataset 1, N=747; online dataset 2, N=235). The fifth experiment tests whether these findings generalize to a clinical dataset of patients with affective disorders (N=61). (B) Mapping between the three factors and 128 items in the bifactor model. (C) Factor loadings of items on the general factor, anxiety-specific factor, and depression-specific factor. (D) Orthogonality among the general, anxiety-specific, and depression-specific factor scores across datasets with complete questionnaire data. (E) Mean correlations between factor scores and questionnaire scores. Overall, the general factor showed high correlations with all questionnaires. The depression-specific factor correlated most strongly with TAIdep and MASQad, whereas the anxiety-specific factor correlated most strongly with the remaining questionnaires. These correlational results supported the bifactor structure of anxiety and depression. (F) Gambling task design. On each trial, participants were asked to choose between a certain option and a gamble option. Once an option was selected, the corresponding outcome was displayed in the center of the screen. The cumulative score was always shown in the upper-right corner. Every two or three trials, participants were asked to complete a self-paced rating of “How happy are you at this moment?” on a slider scale ranging from 0 (very unhappy) to 100 (very happy). (G) Temporal dynamics of happiness ratings for representative individuals with high (top 25%) and low (top 75%) mood variation, healthy datasets, and the clinical dataset. (H) Momentary mood model. (I) Results of momentary mood model for each dataset. MASQaa, the subscale of anxious arousal in the Mood and Anxiety Symptoms Questionnaire; TAIanx, the subscale of anxiety in the Trait Anxiety Inventory; CESD, Center for Epidemiologic Studies Depression Scale; BDI, Beck Depression Inventory; BFIn, the subscale of neuroticism in the Big Five Inventory; PSWQ, Penn State Worry Questionnaire; MASQad, the subscale of anhedonic depression in the Mood and Anxiety Symptoms Questionnaire; TAIdep, the subscale of depression in the Trait Anxiety Inventory; CR, certain reward; EV, expected value; RPE, reward prediction error.

Figure 1.

Figure 1—figure supplement 1. Gambling rate in each dataset.

Figure 1—figure supplement 1.

All datasets showed the same gambling rate pattern, as well as in line with literature.
Figure 1—figure supplement 2. Model-agnostic mood results for all datasets.

Figure 1—figure supplement 2.

All datasets showed the same initial mood overall before the task, mean mood, and mood variation across the task.
Figure 1—figure supplement 3. Replication of the classic mood effects.

Figure 1—figure supplement 3.

(A) Happier after winning than losing. (B) Mood drift across the task.
Figure 1—figure supplement 4. Parameter recovery for the winning model (M1) for the healthy and clinical datasets.

Figure 1—figure supplement 4.

Parameter recovery analysis showed high correlations between the matched simulated and real parameters and low correlations between the mismatched simulated and real parameters.
Figure 1—figure supplement 5. Replication of Rutledge et al., 2017’s findings using BDI (N=1026).

Figure 1—figure supplement 5.

Depression symptom measured by BDI was negatively correlated with the baseline mood parameter. Data was combined from laboratory dataset, online dataset 1, and online dataset 2.
Figure 1—figure supplement 6. Correlations of factor scores from the winning model (the bifactor model) with questionnaire scores for each dataset.

Figure 1—figure supplement 6.

Table 1. Basic demographic details.

Psychometric dataset
(N=901)
Laboratory dataset
(N=44)
Online dataset 1
(N=747)
Online dataset 2
(N=235)
Clinical
dataset
(N=116)
Gender (female) 676 18 500 143 89
Age 22.04±2.10 20.05±1.70 20.90±2.41 21.67±2.52 16.40±3.86
MASQaa 24.70±8.13 22.98±6.14 24.16±7.60 23.92±7.62 43.51±10.51
TAIanx 16.06±4.86 15.00±4.95 15.69±4.97 15.99±5.34 23.35±5.44
CESD 35.28±10.72 33.30±10.73 34.82±10.74 35.06±11.41 55.64±13.04
BDI 11.38±9.35 7.91±8.11 10.04±8.94 10.26±9.18 22.66±17.91
BFIn 33.99±8.82 30.52±8.26 32.82±9.37 32.79±9.81 43.75±9.31
PSWQ 48.28±11.61 46.89±12.52 48.25±12.15 48.36±13.29 59.18±12.87
MASQad 61.49±14.00 60.23±16.63 58.07±15.30 59.57±15.71 77.16±15.39
TAIdep 29.39±5.47 27.32±6.16 27.61±6.27 27.85±6.34 35.97±4.91
Data collection periods 2021.6.22–2021.6.28 2022.6.2–2022.7.5 2022.4.24–2022.5.22 2022.7.22–2022.7.26 2023.3.16–2023.8.4

Descriptive data are presented as mean ± SD.

MASQaa, the subscale of anxious arousal in the Mood and Anxiety Symptoms Questionnaire; TAIanx, the subscale of anxiety in the Trait Anxiety Inventory; CESD, Center for Epidemiologic Studies Depression Scale; BDI, Beck Depression Inventory; BFIn, the subscale of neuroticism in the Big Five Inventory; PSWQ, Penn State Worry Questionnaire; MASQad, the subscale of anhedonic depression in the Mood and Anxiety Symptoms Questionnaire; TAIdep, the subscale of depression in the Trait Anxiety Inventory.

To examine the computational drivers of momentary mood, we used the classic mood model, assuming that momentary mood is modeled as a recency-weighted sum of certain rewards from chosen certain options (CR), expected values of chosen gambles (EV), and RPEs following gamble outcomes (Equation 1; Figure 1H; Rutledge et al., 2014; Vanhasbroeck et al., 2021). RPE was defined as the difference between the obtained outcome and the expected value of the chosen gamble. We also incorporated a drift parameter to account for gradual changes in happiness over time (Jangraw et al., 2023; Vinckier et al., 2018).

Happiness(t)=β0+βCR∑j=1tγt−jCRj+βEV∑j=1tγt−jEVj+βRPE∑j=1tγt−jRPEj+βtt (1)

This model explained momentary moods well across all gambling-task datasets (R2: mean ± SD = 0.67±0.20 for the laboratory dataset, 0.69±0.17 for online dataset 1, and 0.64±0.19 for online dataset 2, and 0.47±0.21 for the clinical dataset; see Appendix 2 and Note 5 for mood model space; see Appendix 1—tables 2 and 4 for mood model comparisons), with good performance for parameter recovery (Figure 1—figure supplement 4). Across all gambling-task datasets, we replicated previous model-based findings on momentary mood (Rutledge et al., 2014; Vanhasbroeck et al., 2021): (1) the RPE weight was significantly higher than the EV weight (ts >3.84, ps <0.001; Figure 1I), suggesting that momentary mood was more strongly influenced by RPEs following gamble outcomes than by the expected value of chosen gamble; (2) the baseline mood parameter β0 was positively correlated with the initial mood ratings (rs >0.25, ps <0.006), supporting the interpretability of this model parameter. We also replicated previous depression-related findings (Rutledge et al., 2017): depression symptom measured by Beck Depression Inventory (BDI) was negatively correlated with the baseline mood parameter β0 (r=–0.173, p<0.001; Figure 1—figure supplement 5). In sum, these confirmatory results support the validity of the questionnaire and task measures, the substantial contribution of RPEs to momentary mood fluctuations, and a robust association between BDI-measured depressive symptoms and the baseline mood parameter.

Depression is associated with dampened mood fluctuations through reduced sensitivity to RPEs

We first examined the association between depression and mood fluctuations, as well as its computational signature. Depression and anxiety often co-occur at the symptom level (Stavrakaki and Vargo, 1986; Clark and Watson, 1991; Briley et al., 2022; Wang et al., 2021), as reflected by a high correlation between depressive symptoms measured by the BDI and anxiety symptoms measured by the anxiety subscale of the Trait Anxiety Inventory (r=0.75, p<0.001). To differentiate the unique influences of anxiety- and depression-specific factors, we applied the validated bifactor structure from the psychometric dataset (Figure 1C) to decompose depression and anxiety symptoms into three orthogonal components: the general factor, anxiety-specific factor, and depression-specific factor (–0.001<rs < 0.001, all ps = 1.000; see Appendix 1 for psychometric properties of the tripartite model of depression and anxiety in our sample; n=901; Figure 1—figure supplement 6).

To examine whether depression-specific factor scores were associated with mood fluctuations, we performed correlation analyses between the depression-specific factor and mood variation, defined as the SD of happiness ratings across trials. We found convergent results across the laboratory dataset, online dataset 1, and online dataset 2. Specifically, depression-specific scores were negatively correlated with mood variation (rs <–0.13, ps <0.041; Figure 2A–C). Model-based correlational analyses further showed negative correlations between depression-specific scores and RPE-related mood sensitivity (βRPE; rs <–0.14, ps <0.019; Figure 2E–G), which remained significant after controlling for gender, age, task earnings, and mood drift (ps <0.035). Bootstrap validation yielded consistent results, indicating that higher depression-specific scores were associated with reduced mood fluctuations and decreased RPE-related mood sensitivity. Given the strong correlation between βRPE and mood variation (rs >0.67, ps <0.001), we further conducted a mediation analysis to examine whether individual differences in RPE-related mood sensitivity statistically accounted for the association between depression loading and mood variation. This analysis was motivated by the hypothesis that depression-related dampening of mood variability may arise, at least in part, from reduced mood sensitivity to RPEs. The results supported our hypothesis (ps <0.015; Figure 2I), suggesting that higher depression-specific scores are associated with dampened momentary mood variation through reduced RPE-related mood sensitivity. See Appendix 1—table 7 for full statistical results for each dataset. To further test whether the association between depression and mood fluctuations was specific to RPE-related mood sensitivity, we regressed depression-specific factor scores on mood sensitivities to CR, EV, and RPE in the combined dataset (N=1026). Only RPE-related mood sensitivity was significantly associated with depression-specific scores (CR: t=0.274, p=0.784; EV: t=–1.069, p=0.285; RPE: t=–3.282, p=0.001; Figure 2K).

Figure 2. Dissociable associations of depression and anxiety with mood fluctuations.

Figure 2.

Correlations of depression- and anxiety-specific factor scores with mood variation and RPE-related mood sensitivity (βRPE) for the laboratory dataset (A, E), online dataset 1 (B, F), online dataset 2 (C, G), and the combined dataset (N=1026; D, H). (I) Reduced RPE-related mood sensitivity statistically mediated the association between depression-specific scores and reduced mood fluctuations. (J) Increased RPE-related mood sensitivity statistically mediated the association between anxiety-specific scores and increased mood fluctuations. (K) Among the mood sensitivity parameters, the depression-specific factor was selectively associated with decreased RPE-related mood sensitivity. (L) Among the mood sensitivity parameters, the anxiety-specific factor was selectively associated with increased RPE-related mood sensitivity. Regression coefficients are shown as bootstrapped mean ± SE. CR, certain reward; EV, expected value; RPE, reward prediction error. *p<0.05.

Anxiety is associated with intensified mood fluctuations through increased sensitivity to RPEs

We then examined how anxiety was associated with mood fluctuations. Correlations between the anxiety-specific factor and mood variation were positive in direction across datasets, although they were not statistically significant in several datasets (the laboratory dataset: r=0.10, p=0.531; the online dataset 1: r=0.08, p=0.026; the online dataset 2: r=0.19, p=0.004). Similarly, correlations between the anxiety-specific factor and βRPE were positive in direction but statistically inconsistent across datasets (the laboratory dataset: r=0.04, p=0.820; the online dataset 1: r=0.05, p=0.216; the online dataset 2: r=0.19, p=0.004; Figure 2A–C & and E–G). Because these datasets used comparable task and questionnaire procedures and showed positive effect directions, and because reliable individual differences often require large samples to detect (Marek et al., 2022), we combined the laboratory dataset, online dataset 1, and online dataset 2 (total N=1026). This approach is analogous to an individual-participant-data meta-analytic analysis. We fitted linear mixed-effects models predicting mood variation and βRPE from the three bifactor scores, with dataset included as a random intercept to account for dataset-level variability. For mood variation, the anxiety-specific factor was positively associated with mood variation (t=3.46, p<0.001), whereas the depression-specific factor was negatively associated with mood variation (t=–6.13, p<0.001). For RPE-related mood sensitivity, the anxiety-specific factor was positively associated with βRPE (t=2.60, p=0.009), whereas the depression-specific factor was negatively associated with βRPE (t=–5.30, p<0.001). These associations remained significant after controlling for gender, age, task earnings, and mood drift. In addition, we performed a mini meta-analysis on these correlation coefficients (Goh et al., 2016). Results showed significant positive correlation for both mood variation and RPE-related mood sensitivity (mood variation: Z=3.399, 95 % CI for correlation coefficient r [0.045, 0.166]; RPE-related mood sensitivity: Z=2.618, 95 % CI for correlation coefficient r [0.021, 0.143]), supporting that anxiety is associated with intensified mood fluctuations and increased mood sensitivity to RPE in non-clinical participants. Mediation analysis further showed that heightened mood sensitivity to RPEs statistically mediated the association between anxiety loading and greater mood fluctuations (a×b = 0.055, 95% CI = [0.013, 0.097], p=0.010; Figure 2J). Moreover, linear regression against anxiety-specific factor with mood sensitivity to CR, EV, and RPE as regressors showed RPE-specific mood hyper-sensitivity with anxiety loading (CR: t=–0.36, p=0.718; EV: t=–0.35, p=0.724; RPE: t=2.19, p=0.028; Figure 2L).

To address the possibility that individual differences in subjective scale calibration confounded our findings, we conducted several complementary analyses. For example, individuals with nonlinear utility functions, such as risk-seeking participants, might show disproportionately large mood responses to large versus small wins. We therefore re-analyzed two publicly available datasets using similar risky decision-making tasks with repeated happiness ratings: (n=49; Vanhasbroeck et al., 2021) and the Rutledge smartphone app dataset (n=46,204). See Appendix 3 for details. Collectively, these analyses suggested that individual differences in risk preference did not account for our primary findings regarding distinct mood dynamics in anxiety versus depression. These results further suggest a partial dissociation between decision-related risk preferences and RPE-related mood dynamics. Together, these results suggest that depression and anxiety are associated with opposite patterns of mood dynamics through RPE-specific mood sensitivity.

Differential associations of depression and anxiety with mood fluctuations

To directly test whether depression- and anxiety-specific factors differed in their associations with mood dynamics, we compared the corresponding correlations. These comparisons showed that depression-specific associations were significantly more negative than anxiety-specific associations for both mood variation (laboratory dataset: Z=–1.84, p=0.033; online dataset 1: Z=–5.36, p<0.001; online dataset 2: Z=–3.42, p<0.001) and βRPE (laboratory dataset: Z=–1.77, p=0.038; online dataset 1: Z=–3.67, p<0.001; online dataset 2: Z=–4.00, p<0.001; Figure 2A–C , and E–G). These results support distinct associations of depression- and anxiety-specific factors with RPE-related mood dynamics.

Clinical relevance of reduced RPE-related mood fluctuations in depression

To test whether abnormalities in RPE-driven mood fluctuations can serve as clinically relevant computational markers of depression- and anxiety-related symptom dimensions, we recruited patients with affective disorders (n=116) to complete the same questionnaire battery and gambling task with momentary mood ratings (Figure 1). Demographic, psychological, and clinical characteristics are summarized in Table 1, Appendix 1—table 8. We observed significant negative correlations between depression-specific scores and both mood variation (r=–0.239, p=0.009) and RPE-related mood sensitivity (βRPE; r=–0.216, p=0.020). These associations remained significant after controlling for demographic and clinical covariates, task earnings, and mood drift (ps <0.05). Bootstrap validation yielded consistent results. Mediation analyses further showed that reduced mood sensitivity to RPEs statistically mediated the association between depression-specific scores and lower mood fluctuations (a×b = –0.141, 95% CI = [-0.261,–0.038], p=0.021; Figure 3). However, we did not observe significant correlation with anxiety (mood variation: r=–0.092, p=0.327; βRPE: r=–0.095, p=0.311).

Figure 3. Clinical validation of reduced RPE-related mood sensitivity in depression.

Figure 3.

(A, B) Correlations of depression and anxiety factor score with mood variation and mood parameter of RPE (βRPE) for the clinical dataset. (C) The mediation model among depression, βRPE, and mood variation in the clinical population. The regression coefficients were represented by mean ± SE, which were estimated by bootstrap. RPE, reward prediction error; *p<0.05.

Exploratory associations of the common factor with mood and choice parameters

Given the theoretical relevance of the common factor – often linked to shared symptoms such as somatic complaints, sleep disturbances, and cognitive impairments (Clark and Watson, 1991) – as well as the potential for nonlinear associations with symptom severity, we conducted exploratory analyses to examine its relationship with choice and mood parameters in both healthy and clinical datasets. Choice parameters were estimated using an established approach–avoidance prospect theory model (Rutledge et al., 2015; Rutledge et al., 2016b; Wang et al., 2026), which included loss aversion, domain-specific risk attitude parameters in the gain and loss domains, and value-independent Pavlovian approach and avoidance parameters (see Appendix 7 for details of the computational choice models). In this model, risk attitude was quantified by the exponent parameter α in a prospect-theory-inspired subjective value function. Lower α values reflect greater risk aversion, whereas values closer to or above 1 reflect more linear or risk-seeking valuation.

To improve robustness and reduce the risk of false positives, we focused on findings that were consistent across datasets. Model comparisons using BIC consistently favored linear over nonlinear models for associations between the common factor and mood and choice parameters (Table 2). Specifically, we observed significant negative associations between the common factor and two key variables: the baseline mood parameter and gain-domain risk attitude (Figure 4). Notably, these parameters were not consistently related to either the depression-specific or anxiety-specific factor across healthy and clinical datasets (depression ×baseline mood parameter: r=–0.12, p<0.001 for the healthy datasets and r=–0.08, p=0.934 for the clinical dataset; anxiety ×baseline mood parameter: r=–0.14, p<0.001 for the healthy datasets and r=–0.15, p=0.104 for the clinical dataset; depression ×risk attitude for gain: r=–0.02, p=0.505 for the healthy datasets and r=–0.00, p=0.961 for the clinical dataset; anxiety ×risk attitude for gain: r=0.01, p=0.846 for the healthy datasets and r=0.04, p=0.688 for the clinical dataset). These findings suggest that higher common-factor scores, reflecting general internalizing psychopathology, are associated with a lower affective baseline and greater gain-domain risk aversion, consistent with the idea that the common factor captures transdiagnostic features shared across mood and anxiety disorders.

Table 2. Exploratory analysis for the common factor.

Models Healthy datasets (n=1026) Clinical dataset (n=116)
BIC Results BIC Results
β0 ~ common –830.23 b=–0.03, t=–6.54, p<0.001, 95% CI = [-0.042–0.022] –113.74 b=–0.03, t=–2.05, p=0.043, 95% CI = [-0.052–0.001]
β0 ~ common + common2 –823.74 –110.91
αgain ~ common 551.76 b=–0.03, t=–3.08, p=0.002, 95% CI = [-0.049–0.011] 101.7 b=–0.11, t=–3.24, p=0.002, 95% CI = [-0.172–0.041]
αgain ~ common + common2 553.73 106.12

Note: For healthy datasets, we added datasets as random variables. β0, the mood baseline parameter; αgain, risk attitude for gain.

Figure 4. Consistent negative associations of the common factor with mood baseline and gain-domain risk attitude across datasets.

Figure 4.

(A) Negative association between the common factor and the baseline mood parameter. (B) Negative association between the common factor and gain-domain risk attitude. Regression coefficients are shown as mean ± SE. *p<0.05.

Discussion

Although atypical mood dynamics are considered central features of depression and anxiety (Rottenberg et al., 2002a; Rottenberg and Hindash, 2015; Bowen et al., 2006; Bowen et al., 2004), little is known about their underlying computational mechanisms. Our study offers computational insights into the distinct associations of depression and anxiety with mood fluctuations. By orthogonally decomposing shared and specific symptom variance in depression and anxiety, we were able to distinguish their specific associations with mood dynamics. Depression-specific symptoms were associated with dampened mood fluctuations through reduced mood sensitivity to RPEs, whereas anxiety-specific symptoms were linked to intensified mood fluctuations through increased mood sensitivity to RPEs in non-clinical datasets. Notably, the depression-related reduction in RPE-related mood sensitivity was replicated in patients with affective disorders, highlighting its potential clinical relevance as an affective computational marker. Moreover, the shared depression–anxiety component was linked to a lower affective baseline and greater risk aversion.

Depression and anxiety, though often coexisting (Stavrakaki and Vargo, 1986; Steer et al., 1995), show contrasting associations with mood dynamics, consistent with their distinct affective profiles (Koval et al., 2012; Bowen et al., 2006; Bowen et al., 2004). Our computational model not only replicates the important role of RPEs in mood dynamics but also highlights the divergent mediating roles of RPE-related mood sensitivity in the associations of depression and anxiety with mood fluctuations. The opposite associations of depression and anxiety with mood sensitivity to RPEs complement previous findings of apparently intact RPE-related mood sensitivity in depression (Blain and Rutledge, 2020; Rutledge et al., 2017; Csukly et al., 2023). These findings further underscore the necessity of decomposing shared and specific components of depression and anxiety in studies of mood dynamics, which can enhance our understanding of their distinct associations with emotion processing and cognitive flexibility. This point is consistent with bifactor-based work showing that shared and specific symptom dimensions can have different computational correlates. For example, Gagne et al., 2020 showed that bifactor-derived symptom dimensions differentially relate to maladaptation to environmental volatility (Gagne et al., 2020), complementing previous findings that trait anxiety is associated with inflexible adjustment to volatility (Gagne et al., 2020). Although the present study did not include neuroimaging, the observed computational dissociation may map onto partially distinct neural systems involved in reward learning, mood updating, and affective psychopathology. RPE processing has been consistently linked to striatal–midbrain dopaminergic reward-learning circuits (Rutledge et al., 2014; Schultz et al., 1997). The integration of these reward-learning signals into subjective mood and value-based decision-making may further involve the ventral medial prefrontal cortex and orbitofrontal cortex (Vinckier et al., 2018). In addition, the anterior insula may be particularly relevant for integrating feedback-related signals with affective and interoceptive states (Rutledge et al., 2014; Vinckier et al., 2018), potentially linking RPE processing to anxiety- and depression-related mood dynamics. Consistent with this view, Cecchi et al., 2022 used intracranial EEG to show that feedback-related neural activity tracks mood fluctuations and risky choice. Future neuroimaging studies should test whether depression-related reductions and anxiety-related increases in RPE-related mood sensitivity are associated with altered interactions among striatal, prefrontal, and insular circuits.

This study bridges research on affective dynamics and reward-based decision-making in depression. Anhedonia, a core symptom of depression, refers to a reduced ability to experience pleasure (Hall et al., 2024). In affective science, researchers have used experience-sampling methods over several weeks or months (Emanuel and Eldar, 2023; Eldar et al., 2016; Bowen et al., 2006; Pulcu et al., 2022), showing dampened mood fluctuations in depression (Rottenberg and Hindash, 2015; Koval et al., 2012). In parallel, decision-making and learning research has often adopted laboratory-based learning or gambling tasks, revealing alterations in reward processing in individuals with depression (Pike and Robinson, 2022; Bishop and Gagne, 2018). However, how altered reward processing translates into aberrant momentary hedonic experience remains largely unknown. Our study employed a gambling task with momentary mood ratings, allowing us to examine reward- and RPE-related mood dynamics. Consistent with both affective-science and reward-learning accounts (Rottenberg et al., 2005; Koval et al., 2012), this study provides evidence that depressive symptoms are associated with reduced mood sensitivity to RPEs.

In addition to supporting the proposed role of anxiety in intensified mood fluctuations (Grupe and Nitschke, 2013; Bowen et al., 2006; Bowen et al., 2004), our study provides a computational account of this phenomenon: anxiety was associated with heightened mood sensitivity to RPEs. Notably, the anxiety-related effects were less robust than the depression-related effects and were detectable only in the pooled dataset (n=1026); therefore, they require further replication in larger samples. Anxiety symptoms are often marked by exaggerated anticipatory responses to uncertainty and excessive affective reactivity (Grupe and Nitschke, 2013). Because RPEs quantify the discrepancy revealed when uncertain outcomes are resolved, our findings suggest a potential pathway through which anxiety may shape mood responses to uncertainty resolution – by amplifying affective responses to unexpected outcomes. In this way, individuals with higher anxiety may exhibit a stronger need to resolve uncertainty (Browning et al., 2015), which could contribute to increased mood reactivity to RPEs. Our findings differ from those of Browning et al., 2015, who reported reduced adaptation of learning rates to environmental volatility in anxiety. However, the two findings may reflect different aspects of uncertainty processing: while Browning et al., 2015 focused on learning-rate adaptation in response to environmental volatility, our study targets affective responsiveness to outcome-level prediction errors. Thus, anxious individuals may exhibit reduced cognitive flexibility in belief updating yet increased emotional reactivity to prediction errors, highlighting a possible dissociation between cognitive and affective systems. Notably, the pattern of heightened RPE sensitivity observed in the pooled non-clinical dataset was not observed in the clinical sample. On the one hand, this discontinuity may reflect that the clinical sample was underpowered to detect anxiety-specific effects, especially given the high comorbidity between anxiety and depression in affective disorders (Appendix 1—table 8). Based on the effect size observed in the non-clinical datasets (r=0.079), we estimated that a sample size of 1226 would be required to detect this effect with 80% statistical power using a two-tailed test with α=0.05. This estimate is substantially larger than the current clinical sample size (n=116). On the other hand, it may reflect a disruption of mood homeostasis in clinical populations (Paulus and Yu, 2012; Paulus, 2007). In non-clinical individuals, counterbalancing associations of depression- and anxiety-related traits with mood variation may help maintain emotional equilibrium. In contrast, affective disorders may involve a loss of such regulatory balance, reducing the ability to stabilize mood in the face of competing depression- and anxiety-related affective signals.

The common factor – reflecting general internalizing psychopathology – was consistently associated with both a lower affective baseline (i.e. affective setpoint) and greater gain-domain risk aversion. Regarding baseline mood, previous large-scale studies have established a reliable association between a lower affective setpoint and elevated depressive symptoms in both individuals scoring high on the BDI and patients diagnosed with MDD (Rutledge et al., 2017). Extending this work, our bifactor approach decomposed shared and specific symptom variance in depression and anxiety into three orthogonal components and revealed that only the common factor, rather than the depression- or anxiety-specific components, was significantly associated with a lower affective baseline. This finding suggests that the shared general distress component, rather than depression- or anxiety-specific symptom variance, is more closely related to individuals’ affective baselines (Kao et al., 2023). With respect to decision-making, prior literature using risky decision-making tasks without feedback has linked pathological anxiety to greater risk aversion (Charpentier et al., 2017). In line with this, our results from a risky decision-making task with feedback suggest that the common factor, rather than anxiety-specific variance per se, is more consistently associated with risk aversion. This suggests that heightened gain-domain risk aversion may be a transdiagnostic feature of internalizing psychopathology, rather than being uniquely attributable to anxiety. Notably, model comparison favored linear over nonlinear associations, indicating that even subclinical levels of general internalizing symptoms are measurably associated with affective baseline and gain-domain risk processing. Taken together, these findings underscore the importance of incorporating general internalizing dimensions into computational models of affect and choice.

Several limitations of the present study should be noted. First, although anxiety- and depression-related associations differed consistently, the anxiety-specific associations themselves were less robust across datasets. This pattern may raise the possibility of confounding by scale-related variability – that is, individual differences in how participants calibrate or use mood rating scales. Because both mood variability and βRPE are derived from subjective ratings, such scale-use differences could disproportionately affect weaker anxiety-specific effects. Our additional analyses, including analyses of two publicly available datasets with similar paradigms (Vanhasbroeck et al., 2021, n=49; Rutledge et al., n=46,204), did not support this explanation (see Appendix 3). Nevertheless, future studies would benefit from task designs that better control for scale sensitivity and elicit stronger mood responses to risky outcomes, possibly by incorporating more emotionally salient or high-stakes decision contexts. Second, our symptom assessment focused specifically on anxiety and depression. This choice was motivated by our primary hypotheses, but it limits our ability to evaluate the specificity of the observed associations. Recent work has shown that individuals with suicidal thoughts and behaviors exhibit reduced mood sensitivity to CR, but not to RPEs (Wang et al., 2026), suggesting that the current RPE-related effects are not driven by suicide-related processes. However, because we did not assess other psychiatric dimensions, such as compulsivity or schizophrenia-spectrum symptoms, we cannot determine whether the current findings are specific to anxiety- and depression-related symptom dimensions or instead reflect broader transdiagnostic psychopathology or nonspecific response-related variance. Future studies should include measures covering a wider range of psychiatric dimensions, such as internalizing, externalizing, inattentive/neurodevelopmental, mood/anxiety, and withdrawal dimensions identified by Wise et al., 2026, to better characterize whether links among symptom dimensions, RPE sensitivity, and mood variability are disorder-specific or transdiagnostic.

In conclusion, our findings emphasize the distinct associations of depression and anxiety with mood fluctuations, underlining the importance of partitioning shared and specific symptom variance in affective science. In particular, the robust association between depression and reduced RPE-related mood sensitivity may inform the development of computationally informed, mechanism-based interventions for affective disorders, offering a promising direction for future research and clinical translation.

Materials and methods

A total of 2634 participants via online platforms (questionnaires from https://www.wjx.cn and tasks from https://www.naodao.com) took part in five experiments, including a psychometric experiment, a laboratory experiment, and two online replication experiments. Participants were recruited through participant pools and study advertisement. For online experiments, interested participants accessed the study through an online link and completed the questionnaires and task remotely. For the laboratory experiment, participants completed the study in a controlled laboratory setting. The study was approved by the Ethics Committee of Beijing Normal University (approve number: ICBIR_A_0016_028). Written or electronic informed consent was obtained from all participants before participation. Participants were paid a basic participation fee and a performance-based bonus, and the payment structure was explained before the experiment.

Participants

Data from 1145 participants was collected in the psychometric experiment. Participants were excluded if (1) they failed any of the attentional checks (four items); (2) they made the same choices for all items; (3) they responded with extreme inconsistency in two similar questionnaires (difference in z-scores out of ± 2). The final sample for the psychometric dataset consisted of 901 participants. We recruited 59, 1087, and 343 participants for the laboratory experiment, the online experiment 1, and the online experiment 2, respectively. Participants were excluded if (1) they failed any of the attentional checks in questionnaires (four items), (2) they failed any of the catch trials (four trials), and (3) they responded too fast (reaction time for decision <200 ms) in more than 10% of the 90 trials. The final sample for the laboratory dataset, the online dataset 1, and the online dataset 2 included 44, 747, and 235 participants, separately. See Table 1 for demographic information and data collection periods. Because online data collection may raise concerns about AI-generated responses, we note that artificial intelligence tools, such as ChatGPT, became widely known to the public in November 2022, whereas all online experiments in the present study were conducted before November 2022 (see Table 1). Therefore, these data were unlikely to have been substantially affected by participants’ use of AI tools.

Measurements of anxiety and depression

In line with previous literature orthogonally decomposing anxiety and depression (Gagne et al., 2022; Gagne et al., 2020), participants completed a set of Chinese version questionnaires of anxiety and depression. These measurements included the Mood and Anxiety Symptoms Questionnaire (MASQ; 62 items; Liu et al., 2015), the Trait subscale of the State-Trait Anxiety Inventory (TAI; 20 items; Shek, 1988), the BDI (21 items; Shek, 1990), the Penn State Worry Questionnaire (PSWQ; 16 items; Zhong et al., 2009), the Center for Epidemiologic Studies Depression Scale (CESD; 20 items; Jiang et al., 2019), and the Big Five Inventory-2 (BFI; 60 items; Zhang et al., 2022). Each item in the TAI, BDI, and CESD was rated on a four-point Likert scale, while a five-point Likert rating scale was used for the MASQ, PSWQ, and BFI. There were four items for attentional checks, which required the participants to make a specific choice and were embedded in the entire measurements, for example “please select the second option for this item”.

Patients with affective disorders

We also recruited 121 patients with affective disorders, including MDD, anxiety disorder, and bipolar disorder. After excluding participants with no variance in mood ratings, the final sample included 116 patients. See Table 1, Appendix 1—table 8 for details.

Experimental procedure

Participants were asked to make a choice between a certain option and a gamble (50% probability for each outcome) and to rate their momentary moods. Before the task protocol, participants were asked to rate their current happiness that we consider as their initial mood. At the beginning of the task, participants were endowed with 500 points. Each trial started with two options (a gamble option and a certain option) that presented randomly on each side (Figure 1F). Upon response, the chosen option would be highlighted in yellow for 0.5 s. Then the corresponding outcome at the screen center was presented for 1 s, followed by a fixation cross with a random duration (0.6~1.4 s). If the gamble was chosen, participants had equal probability to obtain each outcome. The obtained outcome would be accumulated to their total score, which was presenting at the top-right concern. Every two to three trials, participants rated “how happy are you at this moment” from 0 (very unhappy) to 100 (very happy) by moving a slider anchoring at midpoint (i.e. 50). Upon identifying their current mood, a fixation cross was presented with a random duration (0.6–1.4 s). Please note that the slider in the laboratory experiment was anchoring at the midpoint, that is 50. To exclude the potential anchoring effect, we did not set an anchor in the online replication experiment to check the robustness of our findings. This task consisted of 90 randomly presented trials, including 30 mixed trials, 30 gain trials, and 30 loss trials. In mixed trials, participants made a choice between a certain amount 0 and a gamble with a gain amount {40, 45, or 75} and a loss amount determined by a multiplier {0.2, 0.34, 0.5, 0.64, 0.77, 0.89, 1, 1.1, 1.35, or 2} on the gain amount. In gain trials, there was a certain gain amount {35, 45, or 55} and a gamble with 0 and a gain amount determined by a multiplier {1.68, 1.82, 2, 2.22, 2.48, 2.8, 3.16, 3.6, 4.2, or 5} on the certain gain amount. In loss trials, there were a certain loss amount {−35,–45, or –55} and a gamble with 0 and a loss amount determined by a multiplier {1.68, 1.82, 2, 2.22, 2.48, 2.8, 3.16, 3.6, 4.2, or 5} on the certain loss amount. Many amounts and multipliers were used to accommodate a wide range of risk and loss sensitivity, as in previous literature (Rutledge et al., 2014; Rutledge et al., 2015). We also set four trials embedded in the entire task for attentional checks. For example, participants were asked to make a choice between a certain gain 20 and a gamble 35/55, where the correct response for this trial was the gamble choice. All experimental procedures were programmed using Psychopy3 (2021.2.3) builder and hosted on https://www.naodao.com.

Model fitting

We fit model parameters by using the method of maximum likelihood estimation (MLE) with fmincon function of MATLAB (version R2015a) at the individual level. To avoid local minimum, we ran this optimization function with random starting locations 50 times. Bayesian information criteria (BIC) were used to compare model fits.

Mediation model

The mediation model was conducted using a sequence of regression steps. First, a regression of the independent variable depression on the dependent variable mood variation was performed; Second, a regression of the independent variable depression on the mediator variable βRPE was performed; Next, a regression of the independent variable depression and the mediator variable βRPE on the dependent variable mood variation was performed; Finally, the indirect and total effects were estimated.

Statistical analysis

We performed correlations among depression/anxiety factor scores, behavioral indices, and parameters using Matlab R2015a. To further validate our main correlational results, the percentile bootstrap CIs were estimated using the R package ‘boot’ and 5000 bootstrap resamples. We used an online calculator (https://www.psychometrica.de/correlation.html) to examine differences between two correlation coefficients. All reported tests are two-tailed. We set the significance level at P=0.05.

Acknowledgements

This study was funded by the National Natural Science Foundation of China (32671404, 32500929, 32271093 and 32371104), the National Science and Technology Innovation 2030 Major Program (2022ZD0205500), Beijing Natural Science Foundation (Z230010), Ministry of Education Humanities and Social Sciences (25YJC190023), Shenzhen Philosophy and Social Sciences Planning Project (SZ2026C011), Shenzhen Medical Academy of Research and Translation (C2601022), National Human Genetic Resources Sharing Service Platform (2005DKA21300), and the Fundamental Research Funds for the Central Universities (2243300005).

Appendix 1

Psychometric properties of the bifactor model of anxiety and depression in the Chinese population

We tested the validation of the tripartite model of anxiety and depression in the Chinese population (n=901). All participants were asked to complete a set of anxiety- and depression-related questionnaires (see Materials and methods), as previous literature on the tripartite model (Bentham, 1780; Mill, 1859). To examine the underlying factor structure, the entire sample was equally divided into two datasets according to the participants’ number for exploratory and confirmatory factor analysis (EFA dataset, the first part, 1–450; CFA dataset, the second part, 451–901), respectively. For the EFA dataset, we determined the number of factors based on theoretical considerations (i.e. the tripartite model of anxiety and depression Eldar and Niv, 2015; Kao et al., 2023; Emanuel and Eldar, 2023) and scree plot. Results showed that our data was best explained by three factors (40.24%). We then used the three-factor bifactor model to decompose the item-level covariance matrix into a general factor and two specific factors. The ‘Psych’ package in R was used to perform Schmid-Leiman (SL) orthogonalization procedure to obtain factor loadings for each item. Specifically, the SL procedure used oblique factor analysis and higher order factor analysis based on the lower order factor correlations to extract the shared higher order factor (the common factor). Factor scores for each participant were calculated using the Anderson-Rubin method, which is a weighted-least squares solution that maintains the orthogonality of the common score and each specific factor score. Results of factor loadings indicated that the common factor had high loadings (>0.4) for multiple anxiety-related and depression-related items and moderately high loadings (>0.2) across almost all items (Figure 1D). One specific factor had high loadings (>0.4) on items related to anhedonia while another specific factor had high loadings (>0.4) on items related to worry and anxious arousal (Figure 1D).

In the CFA dataset, all items were allowed to load onto the common factor. Each item was also allowed to load onto either the anxiety-specific factor or the depression-specific factor. The assignment for each item was depended on whether the loading on each specific factor was greater than 0.2 in the EFA dataset. After item assignments, factor loadings were re-estimated with diagonally weighted least squares estimation (DWLS). This method only allowed each item to load on the loaded factor in the EFA dataset (>0.2), because it is more appropriate for ordinal data and less sensitive to deviations from normality, as compared with maximum likelihood estimation (Bennett et al., 2022). We implemented this procedure with the specification of an orthogonal solution using the ‘Lavaan’ package in R. The quality of the fit was evaluated by the comparative fit index (CFI), Tucker-Lewis index (TLI), root mean square error of approximation (RMSEA), and standardized root-mean-square residual (SRMR). Results showed excellent goodness-of-fit indices (CFI = 0.989, TLI = 0.989, RMSEA = 0.046, SRMR = 0.061). We additionally performed the same analysis for the CFA dataset as in the EFA dataset to access the similarity between different datasets. That is, we conducted an unconstrained (i.e., exploratory, but not confirmatory) bifactor analysis in the CFA dataset. The resulting factor loadings were highly congruent with the factor loadings in the EFA dataset (cosine-similarity was 0.99 for the common factor loadings, 0.99 for the depression-specific factor loadings, and 0.98 for the anxiety-specific factor loadings). As predicted by the factor structure, the common factor scores are orthogonal to each specific factor score (Figure 1C&E).

To verify the factor structure underlying anxiety and depression, our model space also included a three-factor high-order model and a simple three-factor model. Comparison of model fit revealed that the bifactor model outperformed other models (Appendix 1—table 1), confirming the bifactor structure underlying anxiety and depression. In addition, the common factor showed high correlations with all questionnaires (rs >0.69; Figure 1F), except the anxious arousal subscale of the Mood and Anxiety Symptoms Questionnaire (MASQaa; r=0.16). The anxiety-specific factor was mainly contributed by the anxiety subscale of the State-Trait Anxiety Inventory (TAIanx, r=0.60), the neuroticism of the Big Five Inventory-2 (BFIn, r=0.41), the Penn State Worry Questionnaire (PSWQ, r=0.41), MASQaa (r=0.86), the Beck Depression Inventory (BDI; r=0.52), and the Center for Epidemiologic Studies Depression Scale (CESD; r=0.54), while the depression-specific factor was mainly contributed by the depression subscale of the State-Trait Anxiety Inventory (TAIdep, r=0.52) and the anhedonia depression subscale of the Mood and Anxiety Symptoms Questionnaire (MASQad; r=0.58). Correlations between factors and questionnaires showed the same pattern in different datasets (Figure 1—figure supplement 6). These results indicated good construct validity of this bifactor model of anxiety and depression. Together, these results validated the bifactor model of anxiety and depression in the Chinese population and supported the classic tripartite model. Regarding the application, the bifactor model was initially derived and validated using the larger psychometric dataset (n=901). For subsequent analyses, we applied this validated bifactor solution by computing factor scores using the loadings obtained from the original psychometric sample. This operation was consistent with recent literature of computational psychiatry (Eldar et al., 2016).

In addition, the ratio of 450 participants to 128 items in the EFA split-half sample, approximately 3.5:1, is below some conventional sample-size recommendations for EFA, including the often-cited recommendation of five participants per item (Rutledge et al., 2014). However, the split-half EFA yielded a stable factor structure, and the independent CFA further supported the robustness of this solution. Moreover, reliable EFA solutions may be obtained even with relatively small samples when the data are well-conditioned, such as when factor loadings are high, the number of factors is small, and each factor is defined by multiple items (Otto et al., 2016). These conditions were largely met in our data.

For factor score extraction, we followed prior work using bifactor modeling in computational psychiatry (Rutledge et al., 2015) and extracted factor scores with the Anderson–Rubin method, implemented using psych::factor.scores with method = "Anderson". This approach yields standardized and mutually orthogonal factor scores, which is particularly appropriate for our subsequent correlation analyses because it avoids multicollinearity among the general, depression-specific, and anxiety-specific factors. As a robustness check, we also extracted factor scores using the Bartlett method from an oblique bifactor model, which allowed the depression- and anxiety-specific factors to correlate. In the combined dataset (n=1026), anxiety- and depression-specific scores were significantly correlated when extracted using the Bartlett method (r=0.638, p<0.001), whereas, as expected, they were effectively uncorrelated when extracted using the Anderson–Rubin method (r<0.001, p=1.000). This comparison suggests that the Anderson–Rubin method is more appropriate for our analytic aim of isolating the unique contributions of shared and symptom-specific variance because it separates the general distress/internalizing factor from residual anxiety- and depression-specific components. Thus, we retained the Anderson–Rubin factor scores in the main analyses. We further analyzed non-orthogonalized full depression and anxiety scores to assess the robustness of our results. When full depression and anxiety scores were entered in separate linear mixed-effects models predicting RPE-related mood sensitivity, with dataset included as a random intercept, the anxiety association was not significant (anxiety: b=0.002, t=1.130, p=0.259; depression: b=–0.008, t=–3.732, p<0.001). By contrast, when the full non-orthogonalized anxiety and depression scores were entered simultaneously in the same linear mixed-effects model, the original pattern was replicated: anxiety and depression showed opposing associations with RPE-related mood sensitivity (anxiety: b=0.012, t=4.619, p<0.001; depression: b=–0.017, t=–5.851, p<0.001). This pattern is consistent with a mutual suppression effect: shared variance between anxiety and depression may obscure their unique associations when examined separately, whereas simultaneous regression reveals their opposing symptom-specific associations. These results support our interpretation that RPE-related mood sensitivity is linked to the separable anxiety- and depression-specific components.

Appendix 1—table 1. Psychometric model comparisons.

Models CFI TLI RMSEA SRMR
Bifactor model 0.989 0.989 0.046 0.061
Three-factor model 0.794 0.789 0.200 0.205
High-order model 0.981 0.981 0.060 0.072

Appendix 1—table 2. Mood model comparisons.

Model number # of parameters Δ BIC
Laboratory dataset N=44 Online dataset 1 N=747 Online dataset 2 N=235 Clinical dataset N=116
Model #1 6 0 0 0 0
Model #2 5 43.99 918.62 228.00 41.57
Model #3 8 122.13 1815.15 586.31 549.73
Model #4 7 155.22 2662.46 814.28 424.10
Model #5 7 82.24 709.23 204.32 151.56
Model #6 6 47.76 2514.71 743.17 601.16

Δ BIC, Bayesian information criterion relative to the winning model (Model #1).

Appendix 1—table 3. Objective vs. subjective happiness models.

# of parameters Δ BIC
Healthy dataset N=1026 Clinical dataset N=116 Vanhasbroeck et al., dataset N=49 Rutledge’s dataset N=46,204
Model #1 6 0 0 0 0
Model #6 5 3305.64 601.16 118.00 4997.29
Model #1 vs 6 EP - 1.00 1.00 1.00 1.00

Δ BIC, Bayesian information criterion relative to the winning model (Model #1); EP, exceedance probability; EP greater than 0.95 was considered significant.

Appendix 1—table 4. Time effect on happiness.

Model number # of parameters Δ BIC
Healthy dataset N=1026 Clinical dataset N=116 Vanhasbroeck et al., dataset N=49 Rutledge’s dataset N=46,204
Model #1 6 0 0 0 0
Model #7 6 1883.39 84.88 98.15 4152.61
Model #8 6 1487.79 66.37 61.73 2295.40
Model #9 6 1064.22 59.53 74.40 1458.34

Δ BIC, Bayesian information criterion relative to the winning model (Model #1).

Appendix 1—table 5. Contributions to model fit.

Model number # of parameters Mean R2
Healthy dataset N=1026 Clinical dataset N=116 Vanhasbroeck et al., dataset N=49 Rutledge’s dataset N=46,204
M1: CR +EV + RPE 6 0.68 0.47 0.58 0.69
M10: No CR 5 0.62 0.42 0.52 0.60
M11: No EV 5 0.59 0.40 0.54 0.60
M12: No RPE 5 0.42 0.29 0.34 0.50

Appendix 1—table 6. Interaction between different wins and risk preference for gain on z-scored happiness.

Datasets Trial types
Certain trials Gamble trials (better outcomes; nonzero)
Healthy dataset N=1026 beta = –0.00; t=–0.07; p=0.943 95% CI = [–0.01, 0.01] beta = –0.00; t=–0.24; p=0.807 95% CI = [–0.00, 0.00]
Clinical dataset N=116 beta = –0.01; t=–0.64; p=0.524 95% CI = [–0.04, 0.02] beta = –0.00; t=–2.13; p=0.034 95% CI = [-0.01,–0.00]
Vanhasbroeck et al., dataset N=49 beta = 1.41; t=0.51; p=0.609 95% CI = [–4.00, 6.82] beta = 0.38; t=0.55; p=0.581 95% CI = [–0.96, 1.71]
Rutledge’s dataset N=46,204 beta = 0.10; t=0.84; p=0.402 95% CI = [–0.14, 0.34] beta = 0.03; t=0.82; p=0.412 95% CI = [–0.04, 0.10]

Appendix 1—table 7. Correlations of the depression-specific factor with mood variation and βRPE.

Laboratory dataset Online dataset 1 Online dataset 2 Clinical dataset
Mood variation r=–0.309 p=0.041 r=–0.191 p<0.001 r=–0.135 p=0.039 r=–0.239 p=0.009
βRPE r=–0.352 p=0.019 r=–0.142 p<0.001 r=–0.189 p=0.004 r=–0.216 p=0.020
Mediation a×b = –0.306 95% CI: [-0.547,–0.065] p=0.015 a×b = –0.096 95% CI: [-0.145,–0.047] p<0.001 a×b = –0.126 95% CI: [-0.212,–0.040] p=0.004 a×b = –0.141 95% CI: [-0.261,–0.038] p=0.021

Appendix 1—table 8. Clinical characteristics of patients with affective disorders.

Clinical variables N=116
Diagnosis (MDD/AD/MDD and AD/others) 51/22/32/11
Illness duration (months) 19.57±19.22
Medications (yes)
SSRI 96
Antipsychotics 57
BZDs 38
Mood stabilizer 14

Note that mood stabilizer refers to Lithium in this dataset.

Appendix 1—table 9. Choice model comparisons.

Model number # of parameters Δ BIC
Laboratory dataset N=44 Online dataset 1 N=747 Online dataset 2 N=235 Clinical dataset N=116
cM1 1 320.92 10959.49 3818.36 2368.27
cM2 4 62.70 3655.22 1030.07 620.85
cM3 6 0 0 0 0

Δ BIC, Bayesian information criterion relative to the winning model (cM3).

Appendix 2

Computational model of momentary mood

To quantify how different events impacted participants’ momentary moods during the gambling task, we used the classic model assuming that momentary mood depends on the recency-weighted average of the chosen certain reward (CR), expected value of the chosen gamble (EV), and reward prediction error (RPE; M1; Equation 2). RPE was defined as the difference between the obtained and expected value. We also incorporated a drift parameter to account for the gradual change in happiness over time (Rutledge et al., 2016a; Blain and Rutledge, 2020).

Happiness(t)=β0+βCR∑j=1tγt−jCRj+βEV∑j=1tγt−jEVj+βRPE∑j=1tγt−jRPEj+βtt (2)

here, t and j are trial numbers, β0 is a baseline mood parameter, other weights β capture the influence of different event types. γ ∈ [0, 1] is a decay parameter explicitly modeling the influence of previous trials on current happiness ratings, assigning greater weight to recent events and progressively diminishing influence to earlier trials. CRj is the CR if the certain option was chosen on trial j; otherwise, CRj is 0. EVj is the EV and RPEj is the RPE on trial j if the gamble was chosen. If the certain option was chosen, then EVj = 0 and RPEj = 0.

Although M1 has been shown to accurately track mood data, we also fit other candidate mood models. Specifically, to verify the notion that momentary moods depend on RPE in addition to reward expectation, we fit an alternative model in which moods are contributed by the recency-weighted average of CR and the gamble reward (GR; M2; Equation 3).

Happiness(t)=β0+βCR∑j=1tγt−jCRj+βGR∑j=1tγt−jGRj+βtt (3)

To verify that mood ratings are best explained by a shared forgetting factor (i.e. the recency-weighted history of different event types), we compared a model with a single decay parameter to an alternative model including forgetting factors for each event type, e.g., different decay parameters for CR, EV, and RPE (M3; Equation 4).

Happiness(t)=β0+βCR∑j=1tγCRt−jCRj+βEV∑j=1tγEVt−jEVj+βRPE∑j=1tγRPEt−jRPEj+βtt (4)

It has been shown that moods are influenced by automatically comparing alternative outcomes. We thus considered a component of the outcome difference (OD) between the chosen option and unchosen option (M4; Equation 5) and a regret (R) component (upward comparison; M5; Equation 6) based on M1.

Happiness(t)=β0+βCR∑j=1tγt−jCRj+βEV∑j=1tγt−jEVj+βRPE∑j=1tγt−jRPEj+βOD∑j=1tγt−jODj+βtt (5)

where OD is the outcome difference between the chosen option and the unchosen option.

Happiness(t)=β0+βCR∑j=1tγt−jCRj+βEV∑j=1tγt−jEVj+βRPE∑j=1tγt−jRPEj+βR∑j=1tγt−jRj+βtt (6)

where R represents how much better the outcome could have been if the other option had been chosen. Mathematically, R is the difference between the obtained outcome and the potential better outcome if it exists; otherwise, R=0. We also considered subjective values, rather than objective values in M1, to model mood, as to calibrate the rating scale that participants may use (see Appendix 7 for details).

In the healthy datasets, we conducted a linear mixed-effect model against decay parameter (gamma) with all three factors, with dataset as a random factor. Results did not show significant effect (common: t=0.708, p=0.479; anxiety: t=0.564, p=0.573; depression: t=1.146, p=0.252). In the clinical dataset, we conducted a linear model against decay parameter (gamma) with all three factors and found no significant effect (common: t=–0.036, p=0.972; anxiety: t=–0.047, p=0.963; depression: t=0.052, p=0.959).

Appendix 3

Calibration of rating scales

There was an important issue that individual differences in risk preference may affect the subjective calibration of mood rating scales. Specifically, individuals with nonlinear utility functions (e.g. risk-seeking participants) could display disproportionately high mood responses for large relative to small wins, potentially affecting model interpretation. To systematically address this issue, we conducted several complementary analyses:

First, we examined whether objective or subjective utility models better explained happiness ratings. To enhance statistical power and simplify interpretation, we combined our laboratory and two online datasets into a single healthy dataset. Model comparisons consistently favored the objective happiness model (M1) over the subjective model (M6), as indicated by lower Bayesian Information Criterion (BIC) values and significantly higher exceedance probabilities (EP >0.95, Appendix 1—table 3), suggesting the objective model better captured happiness ratings at both individual and group levels.

Second, within the winning model (objective one), we replicated opposed roles of RPE in mood dynamics of depression and anxiety after controlling for risk attitudes (ps <0.009).

Third, we explicitly assessed whether risk preferences moderated the relationship between wins and mood ratings. Linear mixed-effects analyses on z-scored happiness with subject as a random factor and with different wins and risk preference for gain showed no significant interaction effects between risk preference and win size on happiness ratings for either certain or gamble trials (all p-values >0.05, Appendix 1—table 6).

Fourth, we validated these findings externally by examining two open datasets using similar risk-based decision-making tasks with repeated happiness ratings: (Vanhasbroeck et al., 2021; n=49) and Rutledge’s smartphone App dataset (n=46,204). Consistent with our own data, model comparisons again favored the objective happiness model (Appendix 1—table 3), and interaction analyses revealed no meaningful moderation by risk preferences (Appendix 1—table 6).

Finally, we fitted a simple happiness model with unit wins and losses (Equation 7; mean R2=0.65 for healthy dataset and 0.43 for clinical dataset). Mood sensitivity parameters were not significantly correlated with individual differences in risk preferences, either in our healthy (wins: r=0.017, p=0.588; losses: r=0.009, p=0.765) or clinical datasets (wins: r=0.072, p=0.441; losses: r=0.014, p=0.882).

Happiness(t)=β0+βwin∑j=1tγt−jwinj+βloss∑j=1tγt−jlossj+βtt (7)

Collectively, these comprehensive analyses suggest that individual differences in risk preference did not significantly affect the calibration of mood ratings, or alter our primary findings regarding distinct mood dynamics in anxiety versus depression. Instead, these results possibly suggest dissociable processes for decision-making (i.e. value perception) and mood dynamics.

Appendix 4

Orthogonality of happiness weights on CR, EV, and RPE

One potential concern was the orthogonality of happiness weights on CR, EV, and RPE. Indeed, we found significant correlation between them (healthy dataset: 0.348<rs < 0.625, ps <0.001; clinical dataset: 0.260<rs < 0.679, ps <0.005). Parameter recovery analysis showed high correlations between the matched simulated and real parameters (healthy dataset: 0.818<rs < 0.943, ps <0.001; clinical dataset: 0.815<rs < 0. 955, ps <0.001) and low correlations between the mismatched simulated and real parameters (healthy dataset: 0.269<rs < 0.572, ps <0.001; clinical dataset: 0.172<rs < 0. 635, ps <0.065; Figure 1—figure supplement 4), confirming the identification of these parameters. To examine whether risk preferences influence their orthogonality, correlation analyses did not show significant correlation between risk preferences and model fit (e.g. R2; healthy dataset: abs(r)<0.042, ps >0.182; clinical dataset: abs(r)<0.105, ps >0.261). When controlling for risk attitudes and model fit, our findings of opposed roles of RPE in mood dynamics of depression and anxiety can be replicable (healthy dataset: ps <0.002; clinical dataset: for depression: p=0.016). In addition, we fitted a simple happiness model with unit wins and losses (Equation 7; mean R2=0.65 for healthy dataset and 0.43 for clinical dataset). Mood sensitivity parameters were not significantly correlated with individual differences in risk preferences, either in our healthy (wins: r=0.017, p=0.588; losses: r=0.009, P=0.765) or clinical datasets (wins: r=0.072, p=0.441; losses: r=0.014, p=0.882). These results suggest that the current parameters can be identified and individual differences in risk attitudes do not influence parameter recovery.

Appendix 5

Time effect on happiness

Although we incorporated a drift parameter to account for the gradual change in happiness over time (βt: t=–5.84, p<0.001), time may also interact with event parameters, affecting mood sensitivity dynamically. Therefore, we tested three additional models explicitly incorporating interactions between time-on-task and different event parameters (Models M7–M9; see Equations 8–10), enabling us to systematically evaluate how mood responses to events might change with time.

Happiness(t)=β0+βCR∑j=1tγt−jCRj+βEV∑j=1tγt−jEVj+βRPE∑j=1tγt−jRPEj+βt∑j=1tγt−jCRjt (8)
Happiness(t)=β0+βCR∑j=1tγt−jCRj+βEV∑j=1tγt−jEVj+βRPE∑j=1tγt−jRPEj+βt∑j=1tγt−jEVjt (9)
Happiness(t)=β0+βCR∑j=1tγt−jCRj+βEV∑j=1tγt−jEVj+βRPE∑j=1tγt−jRPEj+βt∑j=1tγt−jRPEjt (10)

Model comparisons consistently favored the simpler intercept-only drift model (M1) over these interaction models (M7–M9), as indicated by lower Bayesian Information Criterion (BIC) values (Appendix 1—table 4). Furthermore, we validated these results externally using two publicly available datasets with similar paradigms (Vanhasbroeck et al., 2021; n=49; and Rutledge’s smartphone app dataset, n=46,204). These external validations also strongly favored the simpler drift model without time-event interactions (see Appendix 1—table 4). Taken together, these analyses suggest that while overall mood indeed exhibits gradual drift over time, there is minimal evidence to support time-on-task by event interactions substantially affecting mood sensitivity to event parameters in our task, supporting the robustness and generalizability of our primary findings.

Appendix 6

Contributions to model fit

To elaborate on which components (CR, EV, or RPE) contributed most to model fit, we tested three additional models. Specifically, based on the winning model (M1), we kicked out each event component separately (M10-12, see Equations 11–13).

Happiness(t)=β0+βEV∑j=1tγt−jEVj+βRPE∑j=1tγt−jRPEj+βtt (11)
Happiness(t)=β0+βCR∑j=1tγt−jCRj+βRPE∑j=1tγt−jRPEj+βtt (12)
Happiness(t)=β0+βCR∑j=1tγt−jCRj+βEV∑j=1tγt−jEVj+βtt (13)

The results showed that removing RPE led to the most substantial drop in model fit: ΔR²=0.26 in the healthy dataset and ΔR²=0.18 in the clinical dataset (Appendix 1—table 5). This indicates that RPE was the most important contributor to explaining mood dynamics. In contrast, excluding either CR or EV resulted in only modest reductions in model fit (ΔR²<0.09 in the healthy dataset and ΔR²<0.07 in the clinical dataset). We replicated this pattern in two independent, publicly available datasets (Vanhasbroeck et al., 2021, n=49; and Rutledge’s smartphone app dataset, n=46,204), further supporting the robustness and generalizability of the central role of RPE in momentary mood computations (Appendix 1—table 5). These analyses confirm that reward prediction error is the dominant predictor of trial-by-trial mood changes.

Appendix 7

Computational model of gambling choice

To quantify how different events impacted participants’ momentary moods during the gambling

In line with previous studies (Quoidbach et al., 2019; Taquet et al., 2016), our choice model space included expected value model (cM1), prospect theory model (cM2) (Broome et al., 2015), and approach-avoidance prospect theory model (cM3) (Quoidbach et al., 2019). For cM2 (Equations 14–17), there were 3 parameters, including risk aversion (α, range: [0.3, 1.3]), loss aversion (λ: [0.5, 5]), and inverse temperature (μ: [0, 10]).

Ugamble=0.5(Vgain)α−0.5λ(−Vloss)α (14)
Ucertain=(Vcertain)αifVcertain≥0 (15)
Ucertain=−λ(−Vcertain)αifVcertain<0 (16)
Pgamble=11+e−μ(Ugamble−Ucertain) (17)

where Vgain and Vloss are the objective gain and loss from a gamble, respectively. Please note that Vgain is 0 in loss trials and Vloss is 0 in gain trials. Vcertain is the objective value for the certain option. Ugamble and Ucertain denote the subjective utilities of the gamble and the certain option, respectively. Choice probability for gamble (Pgamble) is determined by the softmax rule. Building on cM2, cM3 decomposes the decision process into risk-attitude-driven valuation (e.g. loss and risk aversion) and value-insensitive motivational components (Equations 14–16; 18–20). That is, choice probability for Pgamble in cM3 is jointly determined by the softmax rule and approach/avoidance parameters (βgain: [–1, 1], βloss: [–1, 1]). Approach/avoidance parameters are not applied in mixed trials. Please note that a higher gambling rate does not imply a change in risk attitude per se: it can arise from an increased value-insensitive approach bias even when risk-attitude parameters are comparable between groups. Risk attitude is indeed conceptualized in economics as the curvature of the utility function (i.e. the subjective value) of the objective outcomes, with concave curves associated with risk aversion, and convex curves associated with risk seeking (Mason et al., 2017; Taquet et al., 2020). By contrast, the approach or avoidance bias applies to all the value. A possible interpretation of the approach bias is that participants approach the option with the highest possible gain (the lottery) in the gain frame; the avoidance bias would then reflect a tendency to systematically avoid the highest potential losses (the lottery) in the loss frame.

Pgamble=1−βval1+e−μ(Ugamble−Ucertain)+βvalifβval≥0 (18)
Pgamble=1+βval1+e−μ(Ugamble−Ucertain)ifβval<0 (19)
βval{βgain,gaintrials,βloss,losstrials. (20)

Model comparison using BIC revealed that the winning model for each dataset was the approach-avoidance prospect theory model (cM3; mean R2=0.51 for the laboratory dataset, 0.49 for the online dataset1, 0.54 for the online dataset 2, and 0.40 for the clinical dataset; Appendix 1—table 9).

Funding Statement

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Contributor Information

Yunzhe Liu, Email: yunzhe.liu@bnu.edu.cn.

Pengfei Xu, Email: pxu@bnu.edu.cn.

Andreea Oliviana Diaconescu, University of Toronto, Canada.

Jonathan Roiser, University College London, United Kingdom.

Funding Information

This paper was supported by the following grants:

  • National Natural Science Foundation of China 32371104 to Pengfei Xu.

  • National Natural Science Foundation of China 32500929 to Ting Wang.

  • National Natural Science Foundation of China 32271093 to Yunzhe Liu.

  • National Science and Technology Innovation 2030 Major Program 2022ZD0205500 to Yunzhe Liu.

  • Beijing Natural Science Foundation Z230010 to Yuejia Luo, Yunzhe Liu.

  • Ministry of Education Humanities and Social Sciences 25YJC190023 to Ting Wang.

  • Shenzhen Philosophy and Social Sciences Planning Project SZ2026C011 to Pengfei Xu.

  • Shenzhen Medical Academy of Research and Translation C2601022 to Pengfei Xu.

  • National Human Genetic Resources Sharing Service Platform 2005DKA21300 to Pengfei Xu.

  • Fundamental Research Funds for the Central Universities 2243300005 to Pengfei Xu.

  • National Natural Science Foundation of China 32671404 to Pengfei Xu.

Additional information

Competing interests

No competing interests declared.

Author contributions

Conceptualization, Data curation, Formal analysis, Investigation, Visualization, Methodology, Writing – original draft, Project administration, Writing – review and editing.

Conceptualization, Formal analysis, Funding acquisition, Validation, Investigation, Visualization, Methodology, Writing – original draft, Project administration, Writing – review and editing.

Investigation, Methodology, Project administration.

Methodology, Writing – review and editing.

Supervision, Funding acquisition, Writing – original draft, Writing – review and editing.

Supervision, Funding acquisition, Writing – original draft, Writing – review and editing.

Supervision, Methodology, Writing – review and editing.

Conceptualization, Supervision, Visualization, Writing – original draft, Writing – review and editing.

Conceptualization, Supervision, Funding acquisition, Investigation, Visualization, Writing – original draft, Writing – review and editing.

Ethics

Human subjects: The study was approved by the Ethics Committee of Beijing Normal University (approval number: ICBIR_A_0016_028). Written or electronic informed consent was obtained from all participants before participation.

Additional files

MDAR checklist

Data availability

The data and code that support the findings of this study are available from https://github.com/ZhihaoWangpsyer/depression_anxiety_mood (copy archived at Wang, 2026).

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eLife Assessment

Andreea Oliviana Diaconescu 1

This is an important study that uses a tripartite transdiagnostic framework to separate depression-specific, anxiety-specific, and shared psychopathology dimensions and relate them to mood variability and mood reactivity to reward prediction errors across several large non-clinical cohorts and a clinical sample. The evidence is compelling: large samples, a well-characterised gambling task, rigorous computational and psychometric analyses (i.e., split-half replication of the factor structure, convergent results with non-orthogonalised factors, an explicitly specified risk-attitude model, diagnostic breakdown and power analyses for the clinical cohort) and replication of the depression-specific blunting of reward prediction error sensitivity in patients. Anxiety-specific associations emerge reliably only when data are pooled and are likely underpowered clinically given co-morbid anxious depression, a constraint the authors now state explicitly. The work advances a mechanistic account of how distinct symptom dimensions shape reward-based mood updating.

Reviewer #1 (Public review):

Anonymous

Summary of strengths:

Thank you very much for giving me the opportunity to review this very interesting paper. The research question is intriguing, allowing to address commonly observed co-morbidities between depression and anxiety and their dissociable and opposite relationship to mood fluctuations and sensitivity to reward prediction errors. The computational analyses are very in-depth, including many state of the art checks and validations. Finally, another strength is the inclusion of several large or very large samples, including a patient sample in addition to the general population sample.

Comments on revised version.

I want to thank the authors for taking the time to answer all my questions. Their answers were very thoughtful and well argued. I found the theoretical explanations very helpful for explaining their approach and ideas further. In particular, it was fascinating to see how including a single non-orthogonalized depression or anxiety scored show no effect, but including them in simultaneously revealed their previously observed patterns.

Reviewer #2 (Public review):

Anonymous

Summary:

Despite their common co-occurrence, depression and anxiety are known to alter mood fluctuations in opposite ways. Here, the authors aimed at distinguishing depression-specific from anxiety-specific from psychopathology-general effects of reward processing on mood fluctuations, focusing on reward prediction errors (RPE) which are known to be linked to mood fluctuations. This mechanistic study aims at uncovering the process through which these psychopathologies are associated with mood modulations. The authors were able to appropriately test their hypothesis and obtained results corroborating their conclusions.

This work provides a convincing demonstration of the relevance of computational psychiatry (Huys et al, 2016) and the use of decision neuroscience to shed light on the interplay of anxiety and depression and mood.

Comments on revised version.

(1) Methodological & Theoretical Framework: The authors used a tripartite model to effectively distinguish depression vs anxiety dimensions from broad psychopathology/distress.

(2) Possible theoretical confounds: This manuscript addressed adequately the concerns one would have regarding risk-attitudes.

(3) Computational Rigor: The computational model elegantly separates reward expectations (EV in the model) from outcome processing through RPE, which are two sequential cognitive processes, providing a fine-grained mechanistic account of mood fluctuations.

(4) Clear & Logical Results Structure: In response to feedback provided during the previous round of review (previously cited as a recommendation for authors), the authors re-organized the Results section into three distinct, easy-to-navigate subsections (Depression, Anxiety, and Depression vs. Anxiety), which substantially improves readability and clarity.

(5) Neurobiological Context: The Discussion has been enriched with a well-integrated overview of the neural circuits (striatal-midbrain dopaminergic, vmPFC, OFC, and anterior insula) likely underpinning RPE-driven mood updates, which is sure to improve the translational interest of this work.

(6) Transparent Reporting: The authors had already provided a trustworthy writing approach when referring to trending statistical results. In this revised manuscript, they have been exceptionally transparent regarding study limitations, data collection timelines (addressing potential AI-related artifacts), and statistical power constraints.

Status of Previous Weaknesses & Suggested Revisions

(1) Clinical Sample Size and Anxiety-Specific Effects

Previous Concern: The sample size of the clinical sample (N=116) may not be sufficient to detect anxiety-specific effects due to the high rate of comorbid anxious depression. It would be beneficial to include the number of MDD vs GAD vs anxious depression diagnoses in the clinical population as this would be likely to shine light on the power limitations.

  • Author Revision: The authors have fully addressed this point by adding a diagnostic breakdown in Table S8 which details the diagnosis, illness duration, and medication status. They also included details of the power analysis (Discussion, pages 17-18) putting into perspective their results and provided two possible literature-informed interpretations of their findings. This is also reflected in their updated Abstract.

(2) Re-organization of Results

Previous Suggestion: The results sections 2 (depression) and 3 (anxiety) could be improved by reducing the back and forth between factors throughout the results. It may be useful to split them into 3 sections: depression only, anxiety only, depression vs anxiety.

  • Author Revision: The Results section was restructured as suggested, cleanly isolating depression-specific associations, anxiety-specific associations, and direct statistical comparisons between the two ("differential associations" in the manuscript).

(3) Neurocircuitry Discussion

Previous Suggestion: In the discussion, authors could have mentioned the brain areas most likely to be involved in these processes, both cognitive and psychopathological, as previous studies (such as Cecchi et al, 2022) have aimed at identifying regions involved in RPE processing while modulating mood in health. A short section on this would be useful to the neuropsychiatric community.

  • Author Revision: A concise section was added to the Discussion mapping computational parameters onto striatal, prefrontal, and insular circuitry (see Strengths #5).

Conclusion:

The authors have satisfactorily resolved all minor-to-moderate issues raised in the previous review.

Reviewer #3 (Public review):

Anonymous

Summary:

In this submission Wang and colleagues jointly examine the association between depression and anxiety symptoms and individuals' affective reactivity to reward prediction errors in Ruttledge et al.'s gambling paradigm. Taking a bifactor approach to anxiety and depression in several non-clinical (and one clinical sample), the authors find that anxiety-specific symptoms relate to over-reactivity of mood to reward prediction errors (RPEs) as well as heightened mood variability , while depression-specific symptoms relate to blunted mood sensitivity to RPEs. These depression-, but not-anxiety specific relationships replicated in patient samples.

Strengths:

I was impressed that the data-driven, transdiagnostic approach employed by the authors uncovered specific relationships between anxiety and depression-specific factors and RPE reactivity in a well characterized task and computational model, especially in a non-clinical sample. This sheds new light on how these affective processes may be perturbed-and importantly, in different ways-by anxiety and depression symptoms. Likewise, the replication of the depression-specific finding (RPE hypo-reactivity) in a clinical sample was nice to see.

Weaknesses:

While the anxiety- and depression-specific factors had differential effects on mood variability (Fig 2A-D) and RPE reactivity (Fig 2E-G) in all samples, such that the correlations between the two factors and these mood parameters were significantly different, the anxiety factor was not consistently (significantly) associated with either mood-related parameter across samples. However, the authors resolve anxiety-specific predictive effects when they collapse across datasets. While it is intuitive that achieving a larger effective sample size would afford the power necessary to detect such individual differences, this struck me as a major caveat for this set of results.

The associations the authors observe between the 'common factor' of depression and anxiety and risk-aptitudes tendencies-presumably the alpha (exponent) parameter in a prospect theory-type subjective value model. But where is this analysis explained? (i.e. how was this model formulated and how were risk attitude parameters estimated?) And what is the interpretation of this finding-is there precedent for looking at risk attitudes in this task? And why would these predictive effects only be observed in relation to the common, but not unique factors of anxiety and depression?

Comments on revised version.

I believe the weaknesses identified in the previous round of review have been adequately addressed by the authors, and my suggestions concerning clarity of presentation have by and large been implemented by the authors.

eLife. 2026 Sep 29;15:RP110631. doi: 10.7554/eLife.110631.3.sa4

Author response

Zhihao Wang 1, Ting Wang 2, Tian Nan 3, Jiahua Xu 4, André Aleman 5, Yuejia Luo 6, Bastien Blain 7, Yunzhe Liu 8, Pengfei Xu 9

The following is the authors’ response to the original reviews.

eLife Assessment

This important study uses a tripartite transdiagnostic computational framework to distinguish depression-specific, anxiety-specific, and shared psychopathology dimensions, in their relationships to mood variability and mood reactivity to reward prediction errors across multiple large non-clinical cohorts and a clinical sample. The evidence is convincing overall because the study combines large samples, a well-characterized gambling task and in-depth computational and psychometric analyses, and it replicates the depression-specific association with blunted reward prediction error-sensitivity in a clinical sample. However, the anxiety-specific effects are less consistently supported across individual datasets, may be underpowered in the clinical cohort because of comorbidity, and some aspects of the factor-analytic, risk-attitude, and mediation analyses would benefit from clearer explanation. These findings advance a mechanistic account of how distinct symptom dimensions differentially shape reward-based mood updating and variability, providing a principled framework for future transdiagnostic modeling.

We thank the editors and reviewers for this important assessment.

Regarding inconsistent results for anxiety-related effects in healthy datasets. Although the anxiety-specific factor showed associations in the expected direction across healthy datasets, these associations were not significant in several individual datasets. Specifically, anxiety-specific scores were positively correlated with mood variation (laboratory dataset: r = 0.10, p = 0.531; online dataset 1: r = 0.08, p = 0.026; online dataset 2: r = 0.19, p = 0.004) and with RPE-related mood sensitivity (laboratory dataset: r = 0.04, p = 0.820; online dataset 1: r = 0.05, p = 0.216; online dataset 2: r = 0.19, p = 0.004; Figures 2A–C and 2E–G). This pattern may partly reflect limited statistical power at the single-dataset level. Because these datasets used comparable task and questionnaire procedures and showed positive effect directions, we conducted pooled analyses to obtain a more stable estimate. Importantly, these analyses included dataset as a random intercept in mixed-effects models to account for between-dataset differences. Thus, the pooled analysis provides an integrated estimate across samples, conceptually similar to an individual-participant-data meta-analytic approach. The pooled results provided evidence for the expected anxiety-specific associations with greater mood variability and heightened RPE-related mood sensitivity in non-clinical participants (mood variation: t = 3.46, p < 0.001; RPE-related mood sensitivity: t = 2.60, p = 0.009). In addition, we conducted a mini meta-analysis, and results support that anxiety is associated with intensified mood fluctuations and increased mood sensitivity to RPE in non-clinical participants. We have clarified this point below:

Pages 10-11:

“Correlations between the anxiety-specific factor and mood variation were positive in direction across datasets, although they were not statistically significant in several datasets (the laboratory dataset: r = 0.10, p = 0.531; the online dataset 1: r = 0.08, p = 0.026; the online dataset 2: r = 0.19, p = 0.004). Similarly, correlations between the anxiety-specific factor and βRPE were positive in direction but statistically inconsistent across datasets (the laboratory dataset: r = 0.04, p = 0.820; the online dataset 1: r = 0.05, p = 0.216; the online dataset 2: r = 0.19, p = 0.004; Figure 2A-C & 2E-G). Because these datasets used comparable task and questionnaire procedures and showed positive effect directions, and because reliable individual differences often require large samples to detect[48], we combined the laboratory dataset, online dataset 1, and online dataset 2 (total N = 1,026). This approach is analogous to an individual-participant-data meta-analytic analysis. We fitted linear mixed-effects models predicting mood variation and βRPE from the three bifactor scores, with dataset included as a random intercept to account for dataset-level variability. For mood variation, the anxiety-specific factor was positively associated with mood variation (t = 3.46, p < 0.001), whereas the depression-specific factor was negatively associated with mood variation (t = -6.13, p < 0.001). For RPE-related mood sensitivity, the anxiety-specific factor was positively associated with βRPE (t = 2.60, p = 0.009), whereas the depression-specific factor was negatively associated with βRPE (t = -5.30, p < 0.001). These associations remained significant after controlling for gender, age, task earnings, and mood drift. In addition, we performed a mini meta-analysis on these correlation coefficients[49]. Results showed significant positive correlation for both mood variation and RPE-related mood sensitivity (mood variation: Z = 3.399, 95 % CI for correlation coefficient r [0.045, 0.166]; RPE-related mood sensitivity: Z = 2.618, 95 % CI for correlation coefficient r [0.021, 0.143]), supporting that anxiety is associated with intensified mood fluctuations and increased mood sensitivity to RPE in non-clinical participants.”

We also admit that the anxiety-related effects were less robust than the depression-related effects and were detectable only in the pooled dataset (n = 1,026); therefore, they require further replication in larger samples.

Page 17:

“Notably, the anxiety-related effects were less robust than the depression-related effects and were detectable only in the pooled dataset (n = 1,026); therefore, they require further replication in larger samples.”

Regarding be underpowered sample size in the clinical cohort. We agree that the clinical sample may have been underpowered to detect anxiety-specific effects, especially given the high comorbidity between anxiety and depression in affective disorders (Table S8). Based on the effect size observed in the non-clinical datasets (r = 0.079), we estimated that a sample size of 1,226 would be required to detect this effect with 80% statistical power using a two-tailed test with α = .05. This estimate is substantially larger than the current clinical sample size (n = 116). Although these covariate analyses support the robustness of the depression-related effect, they do not resolve whether the absence of the anxiety-related effect reflects limited power or true clinical discontinuity. We also revised the Discussion to explicitly acknowledge that the anxiety-related effect observed in the pooled non-clinical dataset was not replicated in the clinical sample. We now note two possible interpretations. First, this discontinuity may reflect limited statistical power in the clinical sample. Second, and more speculatively, it may reflect a disruption of mood homeostasis in affective disorders (Paulus, 2007). In non-clinical individuals, the counterbalancing associations of depression- and anxiety-related traits with mood variation may contribute to emotional equilibrium. In contrast, affective disorders may involve a loss of this regulatory balance, reducing the ability to stabilize mood in the face of competing depression- and anxiety-related affective signals. We have revised the manuscript as follows:

Pages 12-13:

“To test whether abnormalities in RPE-driven mood fluctuations can serve as clinically relevant computational markers of depression- and anxiety-related symptom dimensions, we recruited patients with affective disorders (n = 116) to complete the same questionnaire battery and gambling task with momentary mood ratings (Figure 1). Demographic, psychological, and clinical characteristics are summarized in Table 1 and Table S8. We observed significant negative correlations between depression-specific scores and both mood variation (r = -0.239, p = 0.009) and RPE-related mood sensitivity (β_RPE; r = -0.216, p = 0.020). These associations remained significant after controlling for demographic and clinical covariates, task earnings, and mood drift (ps < 0.05). Bootstrap validation yielded consistent results. Mediation analyses further showed that reduced mood sensitivity to RPEs statistically mediated the association between depression-specific scores and lower mood fluctuations (a × b = -0.141, 95% CI = [-0.261, -0.038], p = 0.021; Figure 3). However, we did not observe significant correlation with anxiety (mood variation: r = -0.092, p = 0.327; β_RPE: r = -0.095, p = 0.311).”

Pages 17-18:

“Notably, the pattern of heightened RPE sensitivity observed in the pooled non-clinical dataset was not observed in the clinical sample. On the one hand, this discontinuity may reflect that the clinical sample was underpowered to detect anxiety-specific effects, especially given the high comorbidity between anxiety and depression in affective disorders (Table S8). Based on the effect size observed in the non-clinical datasets (r = 0.079), we estimated that a sample size of 1,226 would be required to detect this effect with 80% statistical power using a two-tailed test with α = .05. This estimate is substantially larger than the current clinical sample size (n = 116). On the other hand, it may reflect a disruption of mood homeostasis in clinical populations[41,58]. In non-clinical individuals, counterbalancing associations of depression- and anxiety-related traits with mood variation may help maintain emotional equilibrium. In contrast, affective disorders may involve a loss of such regulatory balance, reducing the ability to stabilize mood in the face of competing depression- and anxiety-related affective signals.”

Abstract:

“Results showed that depression was associated with dampened mood fluctuations due to mood hyposensitivity to RPE. Importantly, this pattern was also found in patients with affective disorders. In contrast, anxiety correlated with heightened mood fluctuations stemming from mood hypersensitivity to RPE in non-clinical participants.”

We have also revised the manuscript accordingly to make the factor-analytic, risk-attitude, and mediation analyses clear.

Reviewer #1 (Public review):

Summary:

This is a very interesting paper. The research question is intriguing, allowing the authors to address commonly observed comorbidities between depression and anxiety and their dissociable and opposite relationship to mood fluctuations and sensitivity to reward prediction errors. The computational analyses are very in-depth, including many state-of-the-art checks and validations. Another strength is the inclusion of several large or very large samples, including a patient sample in addition to the general population sample.

I have the following questions:

(1) Factor analysis

I found the hierarchical organization of the factors interesting. While this is a very common procedure in, for example, the field of intelligence (producing sub-scores and a general g factor), it is not yet very commonly used in the field of computational psychiatry (though it has been validated before for anxiety/depression, so it is used here with good reason). I was also impressed by the methodological depth. In particular, it was of note how thoroughly done it was (for example, repeating the EFA on the second half of the data set). I have one question though: is the sample size too small for the exploratory analyses, given the number of items? Given the stability across the half-split, I imagine it is not. Perhaps the authors could spell out how many items, what would be the recommended standard for a subject-to-item ratio, and comment on this. A very technical point, the authors should specify how they extracted the factor scores from the other data sets (is it using the Thurstone or Bartlett method)? From experience (though not doing a hierarchical factor analysis), Bartlett can be somewhat better compared to the default (Thurstone) - better as in the resulting factors more closely recapitulating the factor correlations in the original sample (and independence of responses of other participants in a sample for computing a person's factor score). Could you also comment on similarities or divergences in this hierarchical factor analysis approach from another one recently used transdiagnostically in Wise et al. (2026, Translational Psychiatry)?

We thank the Reviewer for the positive evaluation of our hierarchical factor-analytic approach and for recognizing the methodological depth of our analyses. We are particularly grateful for the Reviewer’s constructive suggestions regarding the participant-to-item ratio, factor score extraction, and the relation between our approach and recent transdiagnostic hierarchical factor-analytic work.

First, hierarchical organization. As the Reviewer noted, hierarchical and bifactor representations have a well-established tradition in intelligence research, where they are used to model the g factor alongside domain-specific abilities (e.g., Reise, 2012; Rodriguez et al., 2016). Crucially, the use of such hierarchical structures in the present study was motivated primarily by theory and evidence from anxiety and depression research, rather than by analogy to intelligence research alone. This tradition can be traced back to the tripartite model of anxiety and depression (Clark & Watson, 1991), which distinguished a broad shared component of general distress or negative affect from more specific anxiety- and depression-related components. Subsequent psychometric work has further supported bifactor and hierarchical representations of anxiety and depression symptoms, including models that separate a general internalizing/distress factor from symptom-specific dimensions (e.g., Simms et al., 2008). More recently, similar hierarchical symptom structures have also been adopted in computational psychiatry to relate shared and specific affective symptom dimensions to task-derived computational parameters (Gagne et al., 2020, 2022; see Wise et al., 2023 for a review). Thus, the bifactor structure used here provides a theoretically motivated way to capture both the variance shared by anxiety and depression and the symptom-specific variance relevant to our computational analyses. We have clarified this point in the revised manuscript as follows:

Pages 3-4:

“Recent work has used bifactor models of the tripartite model of depression and anxiety to clarify their distinct features and differential influences on decision-making[31,32]. The tripartite model of anxiety and depression proposes that these two symptom dimensions share a broad general distress or negative affect component while also including symptom-specific components: low positive affect/anhedonia is more specific to depression, whereas physiological hyperarousal is more specific to anxiety[30,33,34]. Bifactor analysis offers a way to model this structure statistically. In a bifactor model, symptoms load on a general factor reflecting their shared variance and on specific factors capturing residual variance in narrower symptom dimensions after accounting for the general factor. Although bifactor and hierarchical models have long been used in psychometrics, e.g., intelligence research[35,36], their application to anxiety and depression is grounded in the tripartite model and subsequent psychometric work distinguishing general internalizing/distress from symptom-specific dimensions. This framework has recently been extended to computational psychiatry, where shared and specific affective symptom dimensions have been linked to task-derived computational parameters. For example, Gagne et al. (2022) used bifactor analysis to show that depression was associated with weaker prior beliefs, whereas anxiety was associated with a stronger negative bias in belief updatin31.”

Second, the participant-to-item ratio. We agree that the ratio of 450 participants to 128 items in the EFA split-half sample, approximately 3.5:1, is below some conventional sample-size recommendations for exploratory factor analysis, including the often-cited recommendation of five participants per item (Costello & Osborne, 2005). However, as the Reviewer noted, the split-half analysis showed a stable factor structure, and the independent CFA in the other split-half sample further supported the robustness of the solution. Importantly, participant-to-item ratios are only one criterion for evaluating factor recovery. De Winter, Dodou, and Wieringa (2009) demonstrated that reliable EFA solutions may be obtained even with relatively small samples when the data are well-conditioned, such as when factor loadings are high, the number of factors is small, and each factor is defined by multiple items. These conditions were largely met in our data. We have clarified this point in the revised manuscript as follows:

Supplementary Page 3:

“In addition, the ratio of 450 participants to 128 items in the EFA split-half sample, approximately 3.5:1, is below some conventional sample-size recommendations for EFA, including the often-cited recommendation of five participants per item[8]. However, the split-half EFA yielded a stable factor structure, and the independent CFA further supported the robustness of this solution. Moreover, reliable EFA solutions may be obtained even with relatively small samples when the data are well-conditioned, such as when factor loadings are high, the number of factors is small, and each factor is defined by multiple items9. These conditions were largely met in our data.”

Next, factor score extraction. We followed prior work using bifactor modeling in computational psychiatry (Gagne et al., 2020) and extracted factor scores with the Anderson–Rubin method, implemented using psych::factor.scores with method = "Anderson". This approach yields standardized and mutually orthogonal factor scores, which is particularly appropriate for our subsequent correlation analyses because it produces orthogonal scores and therefore avoids multicollinearity among the general, depression-specific, and anxiety-specific factors. In addition, as suggested by the Reviewer, we extracted factor scores using the Bartlett method from an oblique bifactor model, which allowed the depression- and anxiety-specific factors to correlate. In the combined dataset (n = 1,026), anxiety- and depression-specific scores were significantly correlated when extracted using the Bartlett method (r = 0.638, p < 0.001), whereas, as expected, they were effectively uncorrelated when extracted using the Anderson–Rubin method (r < 0.001, p = 1.000). This comparison suggests that the Anderson–Rubin method is more appropriate for our analytic aim of estimating the unique associations of shared and symptom-specific components with task-derived parameters, because it separates the general distress/internalizing factor from the statistically separable residual anxiety- and depression-specific components. For this reason, we retained the Anderson–Rubin factor scores in the main analyses. We have clarified this point in the revised manuscript as follows:

Supplementary Page 3:

“For factor score extraction, we followed prior work using bifactor modeling in computational psychiatry[10] and extracted factor scores with the Anderson–Rubin method, implemented using psych::factor.scores with method = "Anderson". This approach yields standardized and mutually orthogonal factor scores, which is particularly appropriate for our subsequent correlation analyses because it avoids multicollinearity among the general, depression-specific, and anxiety-specific factors. As a robustness check, we also extracted factor scores using the Bartlett method from an oblique bifactor model, which allowed the depression- and anxiety-specific factors to correlate. In the combined dataset (n = 1,026), anxiety- and depression-specific scores were significantly correlated when extracted using the Bartlett method (r = 0.638, p < 0.001), whereas, as expected, they were effectively uncorrelated when extracted using the Anderson–Rubin method (r < 0.001, p = 1.000). This comparison suggests that the Anderson–Rubin method is more appropriate for our analytic aim of isolating the unique contributions of shared and symptom-specific variance, because it separates the general distress/internalizing factor from residual anxiety- and depression-specific components. Thus, we retained the Anderson–Rubin factor scores in the main analyses.”

Finally, the similarities and differences between our hierarchical factor-analytic approach and the recent transdiagnostic hierarchical factor-analytic approach of Wise et al. (2026). Both approaches fit EFA models with different numbers of factors and use cross-level correlations to characterize hierarchical symptom structure. However, Wise et al. (2026) applied this framework to a broader symptom battery covering transdiagnostic and neurodevelopmental dimensions, identifying a hierarchy that included a general psychopathology factor and more specific dimensions such as internalizing, externalizing, inattentive/neurodevelopmental, mood/anxiety, and withdrawal. In contrast, our study focused more narrowly on anxiety and depression dimensions, with the goal of deriving symptom factors that could be linked to task-derived computational parameters. Accordingly, whether the current findings are specific to anxiety- and depression-related symptom dimensions or instead reflect broader transdiagnostic psychopathology or nonspecific response-related variance remains unknown. Future studies should include measures covering a wider range of psychiatric dimensions, such as internalizing, externalizing, inattentive/neurodevelopmental, mood/anxiety, and withdrawal dimensions identified by Wise et al. (2026), to better determine whether the links among symptom dimensions, RPE-related mood sensitivity, and mood variability are disorder-specific or transdiagnostic. We have discussed this point in the revised manuscript as follows:Page 19:

“Future studies should include measures covering a wider range of psychiatric dimensions, such as internalizing, externalizing, inattentive/neurodevelopmental, mood/anxiety, and withdrawal dimensions identified by Wise et al. (2026)[59], to better characterize whether links among symptom dimensions, RPE sensitivity, and mood variability are disorder-specific or transdiagnostic.”

(2) Linking factors to task parameters

As I understand it, the authors relate the orthogonalized depression/anxiety to task parameters (sensitivity to RPEs on mood and mood variations) using correlations. In order to have a better understanding of how this relates to other commonly used approaches, I would pose two questions:

(i) What are the correlations when the full (non-orthogonalized) factor scores for depression and anxiety are used? Are the signs the same?

(ii) What are the results when, instead of the independent correlations, the authors perform b_RPE ~ anxiety + depression (again using the non-orthogonalized factors)?I'm assuming all of these analyses should give the same results if the authors' hypothesis of opposing effects of anxiety and depression holds true.

We thank the Reviewer for these helpful comments. Our original analyses used orthogonalized depression- and anxiety-specific factor scores because this approach is aligned with our analytic aim of separating shared and symptom-specific variance within the tripartite/bifactor framework of anxiety and depression (Clark & Watson, 1991), and has been used in prior work (Gagne et al., 2020, 2022; see Wise et al., 2023 for a review). Orthogonalization allows us to statistically separate the shared distress component from the symptom-specific components of anxiety and depression, which was central to our hypothesis regarding their opposing associations with task-derived parameters. As expected, the orthogonalized anxiety- and depression-specific factor scores were uncorrelated in the combined dataset (r < 0.001, p = 1.000; n = 1,026). By contrast, the full non-orthogonalized depression and anxiety scores retained substantial shared variance and were highly correlated (r = 0.638, p < 0.001; n = 1,026), making their separate associations less straightforward to interpret.

Nevertheless, we agree that analyses using the full non-orthogonalized depression and anxiety scores provide an important comparison with more commonly used non-orthogonal symptom-score approaches. We therefore conducted the analyses suggested by the Reviewer. When the full depression and anxiety scores were entered separately into linear mixed-effects models predicting RPE-related mood sensitivity, with dataset included as a random intercept, the anxiety association was not significant (anxiety: b = 0.002, t = 1.130, p = 0.259; depression: b = -0.008, t = -3.732, p < 0.001). By contrast, when the full non-orthogonalized anxiety and depression scores were entered simultaneously in the same linear mixed-effects model, the original pattern was replicated: anxiety and depression showed opposing associations with RPE-related mood sensitivity (anxiety: b = 0.012, t = 4.619, p < 0.001; depression: b = -0.017, t = -5.851, p < 0.001). This pattern is consistent with a mutual suppression effect: shared variance between anxiety and depression may obscure their unique associations when examined separately, whereas the simultaneous regression model reveals their opposing symptom-specific associations.

Together, these supplementary analyses support our original interpretation that RPE-related mood sensitivity is associated with the separable anxiety- and depression-specific components in opposite directions. We have revised the manuscript as follows:

Supplementary Pages 3-4:

“We further analyzed non-orthogonalized full depression and anxiety scores to assess the robustness of our results. When full depression and anxiety scores were entered in separate linear mixed-effects models predicting RPE-related mood sensitivity, with dataset included as a random intercept, the anxiety association was not significant (anxiety: b = 0.002, t = 1.130, p = 0.259; depression: b = -0.008, t = -3.732, p < 0.001). By contrast, when the full non-orthogonalized anxiety and depression scores were entered simultaneously in the same linear mixed-effects model, the original pattern was replicated: anxiety and depression showed opposing associations with RPE-related mood sensitivity (anxiety: b = 0.012, t = 4.619, p < 0.001; depression: b = -0.017, t = -5.851, p < 0.001). This pattern is consistent with a mutual suppression effect: shared variance between anxiety and depression may obscure their unique associations when examined separately, whereas simultaneous regression reveals their opposing symptom-specific associations. These results support our interpretation that RPE-related mood sensitivity is linked to the separable anxiety- and depression-specific components.”

Minor comments:

(1) The authors should write down when the data were collected for each study. This is because AI capabilities have massively increased since ~2020 in quite specific steps (with the public release of new AI models), meaning that AI is likely to have been able to do tasks and questionnaires without detection if data were collected recently.

We thank the Reviewer for this important comment. We have now added the data collection periods for each dataset in Table 1. The laboratory and clinical dataset were collected in a controlled laboratory setting rather than through online testing. As shown in Table 1, all online experiments were conducted before November 2022, prior to the public release of ChatGPT and its broad entry into public awareness. Therefore, our data were unlikely to have been substantially affected by AI-assisted responding. We have clarified this point in the revised manuscript as follows:

Page 20:

“See Table 1 for demographic information and data collection periods. Because online data collection may raise concerns about AI-generated responses, we note that artificial intelligence tools, such as ChatGPT, became widely known to the public in November 2022, whereas all online experiments in the present study were conducted before November 2022 (see Table 1). Therefore, these data were unlikely to have been substantially affected by participants’ use of AI tools.”

(2) The authors should include a statement in the methods section that checks for AI were done. If none yet, could you do any? Recent papers (Westwood, PNAS 2025; van der Stigchel PNAS, 2026) point to the risk since at least the release of o4-mini (used in the cited paper to create very human-like behaviour).

We thank the Reviewer for this helpful comment. We have clarified this point in the revised manuscript as follows:

Page 20:

“See Table 1 for demographic information and data collection periods. Because online data collection may raise concerns about AI-generated responses, we note that artificial intelligence tools, such as ChatGPT, became widely known to the public in November 2022, whereas all online experiments in the present study were conducted before November 2022 (see Table 1). Therefore, these data were unlikely to have been substantially affected by participants’ use of AI tools.”

(3) It would have been good to collect questionnaires of other, thought to be unrelated psychiatric traits, like compulsivity or schizophrenia symptoms, to check the specificity of the results, also under the assumption that higher scores on either of these skewed questionnaires can pick up individual differences in 'bad questionnaire completion'. The authors should comment on the absence of other questionnaires in the discussion in the limitations section.

We thank the Reviewer for this helpful comment. We agree that the absence of broader psychiatric trait measures limits our ability to evaluate the specificity of the observed associations. Our symptom assessment focused specifically on anxiety and depression because the study was motivated by hypotheses about their potentially opposing links with RPE sensitivity and mood variability. Although previous research has shown intact mood sensitivity to RPEs in individuals with suicidal thoughts and behaviors (Wang et al., 2026), we cannot determine whether the current findings are specific to anxiety- and depression-related symptom dimensions or instead reflect broader transdiagnostic psychopathology or nonspecific response-style variance.

Regarding the concern that higher scores on symptom questionnaires with skewed score distributions may partly capture individual differences in poor-quality questionnaire responding, we note that we implemented strict data-quality procedures for both questionnaire and task data. Four attention-check items were embedded throughout the questionnaire battery, requiring participants to select a prespecified response, for example, “Please select the second option for this item.” Similarly, four attention-check trials were embedded throughout the gambling task. For example, participants were asked to choose between a certain gain of 20 points and a gamble with possible outcomes of 35 and 55 points, for which the dominant response was to choose the gamble option. Participants who failed any of these attention checks were excluded. In addition, our behavioral and mood data reproduced key patterns reported in previous studies (Rutledge et al., 2014 & 2015) using momentary mood ratings during gambling tasks, including higher mood following gains than following losses and systematic mood drift over time (all ps < 0.001). These procedures and validation checks reduce the likelihood that the present findings were driven by poor questionnaire or task completion. We have clarified this point in the revised manuscript as follows:

Page 19:

“Second, our symptom assessment focused specifically on anxiety and depression. This choice was motivated by our primary hypotheses, but it limits our ability to evaluate the specificity of the observed associations. Recent work has shown that individuals with suicidal thoughts and behaviors exhibit reduced mood sensitivity to certain rewards (CR), but not to RPEs[49], suggesting that the current RPE-related effects are not driven by suicide-related processes. However, because we did not assess other psychiatric dimensions, such as compulsivity or schizophrenia-spectrum symptoms, we cannot determine whether the current findings are specific to anxiety- and depression-related symptom dimensions or instead reflect broader transdiagnostic psychopathology or nonspecific response-related variance. Future studies should include measures covering a wider range of psychiatric dimensions, such as internalizing, externalizing, inattentive/neurodevelopmental, mood/anxiety, and withdrawal dimensions identified by Wise et al. (2026)[59], to better characterize whether links among symptom dimensions, RPE sensitivity, and mood variability are disorder-specific or transdiagnostic.”

Page 20:

“Participants were excluded if (1) they failed any of the attentional checks (4 items); (2) they made the same choices for all items; (3) they responded with extreme inconsistency in two similar questionnaires (difference in z-scores out of ±2).”

Page 21:

“There were four items for attentional checks, which required the participants to make a specific choice and were embedded in the entire measurements, e.g., ‘please select the second option for this item’.”

Page 22:

“We also set 4 trials embedded in the entire task for attentional checks. For example, participants were asked to make a choice between a certain gain 20 and a gamble 35/55, where the correct response for this trial was the gamble choice.”

Page 5:

“Choice data (e.g., gambling rates) and mood data (e.g., initial mood, mean mood, and mood variation) showed patterns similar to those reported in previous studies measuring momentary mood during gambling tasks (Figure S2 & S3)[10,45]. We also replicated established effects on momentary mood: mood was higher following gains than following losses, and mood drifted over time (all ps < 0.001; Figure S4).”

(4) The authors could include a more explicit sentence in the abstract stating that the anxiety result did not hold up in the clinical population.

We thank the Reviewer for this helpful comment. We have clarified this point in the revised manuscript as follows:

Abstract:

“Results showed that depression was associated with dampened mood fluctuations due to mood hyposensitivity to RPE. Importantly, this pattern was also found in patients with affective disorders. In contrast, anxiety correlated with heightened mood fluctuations stemming from mood hypersensitivity to RPE in non-clinical participants.”

Reviewer #2 (Public review):

Summary:

Despite their common co-occurrence, depression and anxiety are known to alter mood fluctuations in opposite ways. Here, the authors aimed at distinguishing depression-specific from anxiety-specific from psychopathology-general effects of reward processing on mood fluctuations, focusing on reward prediction errors (RPEs), which are known to be linked to mood fluctuations. This mechanistic study aims at uncovering the process through which these psychopathologies are associated with mood modulations. The authors were able to appropriately test their hypothesis and obtained results corroborating their conclusions.

This work provides a convincing demonstration of the relevance of computational psychiatry (Huys et al, 2016) and the use of decision neuroscience to shed light on the interplay of anxiety, depression, and mood.

Strengths:

The authors used a tripartite model to distinguish depression vs anxiety, as well as a computational model distinguishing reward expectation (EV in the model) from outcome processing through RPE, which are two sequential cognitive processes.

The manuscript adequately addresses the concerns one would have regarding risk-attitudes and regarding referring to trending statistical results.

Weaknesses:

The sample size of the clinical sample (N=116) may not be sufficient to detect anxiety-specific effects due to the high rate of comorbid anxious depression. It would be beneficial to include the number of MDD vs GAD vs anxious depression diagnoses in the clinical population, as this would likely shine light on the power limitations.

We thank the Reviewer for this helpful comment. We agree that the clinical sample may have been underpowered to detect anxiety-specific effects, especially given the high comorbidity between anxiety and depression in affective disorders (see Table S8 for diagnosis, illness duration, and medication status). Based on the effect size observed in the non-clinical datasets (r = 0.079), we estimated that a sample size of 1,226 would be required to detect this effect with 80% statistical power using a two-tailed test with α = .05. This estimate is substantially larger than the current clinical sample size (n = 116). Although these covariate analyses support the robustness of the depression-related effect, they do not resolve whether the absence of the anxiety-related effect reflects limited power or true clinical discontinuity.

We also revised the Discussion to explicitly acknowledge that the anxiety-related effect observed in the pooled non-clinical dataset was not replicated in the clinical sample. We now note two possible interpretations. First, this discontinuity may reflect limited statistical power in the clinical sample. Second, and more speculatively, it may reflect a disruption of mood homeostasis in affective disorders (Paulus, 2007). In non-clinical individuals, the counterbalancing associations of depression- and anxiety-related traits with mood variation may contribute to emotional equilibrium. In contrast, affective disorders may involve a loss of this regulatory balance, reducing the ability to stabilize mood in the face of competing depression- and anxiety-related affective signals. We have revised the manuscript as follows:

Pages 12-13:

“To test whether abnormalities in RPE-driven mood fluctuations can serve as clinically relevant computational markers of depression- and anxiety-related symptom dimensions, we recruited patients with affective disorders (n = 116) to complete the same questionnaire battery and gambling task with momentary mood ratings (Figure 1). Demographic, psychological, and clinical characteristics are summarized in Table 1 and Table S8. We observed significant negative correlations between depression-specific scores and both mood variation (r = -0.239, p = 0.009) and RPE-related mood sensitivity (βRPE; r = -0.216, p = 0.020). These associations remained significant after controlling for demographic and clinical covariates, task earnings, and mood drift (ps < 0.05). Bootstrap validation yielded consistent results. Mediation analyses further showed that reduced mood sensitivity to RPEs statistically mediated the association between depression-specific scores and lower mood fluctuations (a × b = -0.141, 95% CI = [-0.261, -0.038], p = 0.021; Figure 3). However, we did not observe significant correlation with anxiety (mood variation: r = -0.092, p = 0.327; β_RPE: r = -0.095, p = 0.311).”

Pages 17-18:

“Notably, the pattern of heightened RPE sensitivity observed in the pooled non-clinical dataset was not observed in the clinical sample. On the one hand, this discontinuity may reflect that the clinical sample was underpowered to detect anxiety-specific effects, especially given the high comorbidity between anxiety and depression in affective disorders (Table S8). Based on the effect size observed in the non-clinical datasets (r = 0.079), we estimated that a sample size of 1,226 would be required to detect this effect with 80% statistical power using a two-tailed test with α = .05. This estimate is substantially larger than the current clinical sample size (n = 116). On the other hand, it may reflect a disruption of mood homeostasis in clinical populations[41,58]. In non-clinical individuals, counterbalancing associations of depression- and anxiety-related traits with mood variation may help maintain emotional equilibrium. In contrast, affective disorders may involve a loss of such regulatory balance, reducing the ability to stabilize mood in the face of competing depression- and anxiety-related affective signals.”

Abstract:

“Results showed that depression was associated with dampened mood fluctuations due to mood hyposensitivity to RPE. Importantly, this pattern was also found in patients with affective disorders. In contrast, anxiety correlated with heightened mood fluctuations stemming from mood hypersensitivity to RPE in non-clinical participants.”

Reviewer #3 (Public review):

Summary:

In this submission, Wang and colleagues jointly examine the association between depression and anxiety symptoms and individuals' affective reactivity to reward prediction errors in Ruttledge et al.'s gambling paradigm. Taking a bifactor approach to anxiety and depression in several non-clinical (and one clinical sample), the authors find that anxiety-specific symptoms relate to over-reactivity of mood to reward prediction errors (RPEs) as well as heightened mood variability, while depression-specific symptoms relate to blunted mood sensitivity to RPEs. These depression- but not anxiety-specific relationships replicated in patient samples.

Strengths:

I was impressed that the data-driven, transdiagnostic approach employed by the authors uncovered specific relationships between anxiety and depression-specific factors and RPE reactivity in a well characterized task and computational model, especially in a non-clinical sample. This sheds new light on how these affective processes may be perturbed-and importantly, in different ways-by anxiety and depression symptoms. Likewise, the replication of the depression-specific finding (RPE hypo-reactivity) in a clinical sample was nice to see.

Weaknesses:

(1) While the anxiety- and depression-specific factors had differential effects on mood variability (Figure 2A-D) and RPE reactivity (Figure 2E-G) in all samples, such that the correlations between the two factors and these mood parameters were significantly different, the anxiety factor was not consistently (significantly) associated with either mood-related parameter across samples. However, the authors resolve anxiety-specific predictive effects when they collapse across datasets. While it is intuitive that achieving a larger effective sample size would afford the power necessary to detect such individual differences, this struck me as a major caveat for this set of results.

We thank the Reviewer for this important comment. Although the anxiety-specific factor showed associations in the expected direction across datasets, these associations were not significant in several individual datasets. Specifically, anxiety-specific scores were positively correlated with mood variation (laboratory dataset: r = 0.10, p = 0.531; online dataset 1: r = 0.08, p = 0.026; online dataset 2: r = 0.19, p = 0.004) and with RPE-related mood sensitivity (laboratory dataset: r = 0.04, p = 0.820; online dataset 1: r = 0.05, p = 0.216; online dataset 2: r = 0.19, p = 0.004; Figures 2A–C and 2E–G). This pattern may partly reflect limited statistical power at the single-dataset level.

Because these datasets used comparable task and questionnaire procedures and showed positive effect directions, we conducted pooled analyses to obtain a more stable estimate. Importantly, these analyses included dataset as a random intercept in mixed-effects models to account for between-dataset differences. Thus, the pooled analysis provides an integrated estimate across samples, conceptually similar to an individual-participant-data meta-analytic approach. The pooled results provided evidence for the expected anxiety-specific associations with greater mood variability and heightened RPE-related mood sensitivity (mood variation: t = 3.46, p < 0.001; RPE-related mood sensitivity: t = 2.60, p = 0.009). In addition, we conducted a mini meta-analysis, and results support that anxiety is associated with intensified mood fluctuations and increased mood sensitivity to RPE.

However, we have clarified in the revised manuscript that the anxiety-related effects were less robust than the depression-related effects and require further replication in larger samples.

Pages 10-11:

“Correlations between the anxiety-specific factor and mood variation were positive in direction across datasets, although they were not statistically significant in several datasets (the laboratory dataset: r = 0.10, p = 0.531; the online dataset 1: r = 0.08, p = 0.026; the online dataset 2: r = 0.19, p = 0.004). Similarly, correlations between the anxiety-specific factor and βRPE were positive in direction but statistically inconsistent across datasets (the laboratory dataset: r = 0.04, p = 0.820; the online dataset 1: r = 0.05, p = 0.216; the online dataset 2: r = 0.19, p = 0.004; Figure 2A-C & 2E-G). Because these datasets used comparable task and questionnaire procedures and showed positive effect directions, and because reliable individual differences often require large samples to detect[48], we combined the laboratory dataset, online dataset 1, and online dataset 2 (total N = 1,026). This approach is analogous to an individual-participant-data meta-analytic analysis. We fitted linear mixed-effects models predicting mood variation and βRPE from the three bifactor scores, with dataset included as a random intercept to account for dataset-level variability. For mood variation, the anxiety-specific factor was positively associated with mood variation (t = 3.46, p < 0.001), whereas the depression-specific factor was negatively associated with mood variation (t = -6.13, p < 0.001). For RPE-related mood sensitivity, the anxiety-specific factor was positively associated with βRPE (t = 2.60, p = 0.009), whereas the depression-specific factor was negatively associated with βRPE (t = -5.30, p < 0.001). These associations remained significant after controlling for gender, age, task earnings, and mood drift. In addition, we performed a mini meta-analysis on these correlation coefficients[49]. Results showed significant positive correlation for both mood variation and RPE-related mood sensitivity (mood variation: Z = 3.399, 95 % CI for correlation coefficient r [0.045, 0.166]; RPE-related mood sensitivity: Z = 2.618, 95 % CI for correlation coefficient r [0.021, 0.143]), supporting that anxiety is associated with intensified mood fluctuations and increased mood sensitivity to RPE.”

Page 17:

“Notably, the anxiety-related effects were less robust than the depression-related effects and were detectable only in the pooled dataset (n = 1,026); therefore, they require further replication in larger samples.”

(2) The authors observe associations between the 'common factor' of depression and anxiety and risk-attitude tendencies, presumably the alpha (exponent) parameter in a prospect theory-type subjective value model. But where is this analysis explained? (i.e. how was this model formulated and how were risk attitude parameters estimated?) And what is the interpretation of this finding - is there precedent for looking at risk attitudes in this task? And why would these predictive effects only be observed in relation to the common, but not unique, factors of anxiety and depression?

We apologize for the unclear statement. We have added a description of the computational modeling of choice behavior. Please see our revisions below:

Page 13:

“Choice parameters were estimated using an established approach–avoidance prospect theory model[10,45,49], which included loss aversion, domain-specific risk attitude parameters in the gain and loss domains, and value-independent Pavlovian approach and avoidance parameters (see Supplementary Note 7 for details of the computational choice models). In this model, risk attitude was quantified by the exponent parameter α in a prospect-theory-inspired subjective value function. Lower α values reflect greater risk aversion, whereas values closer to or above 1 reflect more linear or risk-seeking valuation.”

Supplementary Pages 8-9:

Note 7: Computational model of gambling choice

To quantify how different events impacted participants’ momentary moods during the gamblingIn line with previous studies[14,15], our choice model space included expected value model (cM1), prospect theory model (cM2)[16], and approach-avoidance prospect theory model (cM3)[14]. For cM2 (Equations 6-9), there were 3 parameters, including risk aversion (α, range: [0.3, 1.3]), loss aversion (λ: [0.5, 5]), and inverse temperature (μ: [0, 10]).

Ugamble=0.5(Vgain)α−0.5λ(−Vloss)α
Ucertain=(Vcertain)a if Vcertain≥0
Ucertain=−λ(−Vcertain)αifVcertain<0
Pgamble=11+e−μ(Ugamble−Ucertain)

Where Vgain and Vloss are the objective gain and loss from a gamble, respectively. Please note thatVgain is 0 in loss trials and Vloss is 0 in gain trials. Vcertain is the objective value for the certain option. Ugamble and Ucertain denote the subjective utilities of the gamble and the certain option, respectively. Choice probability for gamble (Pgamble) is determined by the softmax rule. Building on cM2, cM3 decomposes the decision process into risk-attitude-driven valuation (e.g., loss and risk aversion) and value-insensitive motivational components (Equations 6-8 & 10-12). That is, choice probability for Pgamble in cM3 is jointly determined by the softmax rule and approach/avoidance parameters (βgain: [-1, 1], βloss: [-1, 1]). Approach/avoidance parameters are not applied in mixed trials. Please note that a higher gambling rate does not imply a change in risk attitude per se: it can arise from an increased value-insensitive approach bias even when risk-attitude parameters are comparable between groups. Risk attitude is indeed conceptualized in economics as the curvature of the utility function (i.e., the subjective value) of the objective outcomes, with concave curves associated with risk aversion, and convex curves associated with risk seeking[17,18]. By contrast, the approach or avoidance bias apply to all the value. A possible interpretation of the approach bias is that participant approach the option with the highest possible gain (the lottery) in the gain frame; the avoidance bias would then reflect a tendency to systematically avoid the highest potential losses (the lottery) in the loss frame.

Pgamble=1−βval1+e−μ(Ugamble−Ucertain)+βvalifβval≥0
Pgamble=1+βval1+e−μ(Ugamble−Ucertain)ifβval<0
βval{βgain,gain trials,βloss,loss trials.

Model comparison using BIC revealed that the winning model for each dataset was the approach-avoidance prospect theory model (cM3; mean R2 = 0.51 for the laboratory dataset, 0.49 for the online dataset1, 0.54 for the online dataset 2, and 0.40 for the clinical dataset; Table S9).

Please also see our interpretation of this finding below:

Page 18:

“With respect to decision-making, prior literature using risky decision-making tasks without feedback has linked pathological anxiety to greater risk aversion[58]. In line with this, our results from a risky decision-making task with feedback suggest that the common factor, rather than anxiety-specific variance per se, is more consistently associated with risk aversion. This suggests that heightened gain-domain risk aversion may be a transdiagnostic feature of internalizing psychopathology, rather than being uniquely attributable to anxiety.”

Recommendations for the authors:

Reviewer #1 (Recommendations for the authors):

Thank you very much for giving me the opportunity to review this very interesting paper.

Recommendations:

(1) Add more specific ethics information than "study was approved by ethics committee of Beijing normal university".

We thank the Reviewer for this important comment. We have added approval number. Please see our revision below:

Page 20:

“The study was approved by the Ethics Committee of Beijing Normal University (approve number: ICBIR_A_0016_028). Written or electronic informed consent was obtained from all participants before participation.”

(2) Add information on how participants were recruited. I think the websites listed only hosted the experiment/questionnaires?

We thank the Reviewer for pointing this out. We have revised the relevant text as follows:

Page 20:

“A total of 2634 participants via online platforms (questionnaires from https://www.wjx.cn and tasks from https://www.naodao.com) took part in five experiments, including a psychometric experiment, a laboratory experiment, two online replication experiments. Participants were recruited through participant pools and study advertisement. For online experiments, interested participants accessed the study through an online link and completed the questionnaires and task remotely. For the laboratory experiment, participants completed the study in a controlled laboratory setting.”

(3) Typo in Figure 1A, grey panel - psychometric.

We apologize for the typo. We have corrected typographical errors throughout the manuscript.

(4) In the Discussion, there is a section on r-to-z transformations, and I was not quite sure what in the Results this links to.

We thank the Reviewer for pointing out the unclear statement. Please see our revision below:

Page 18:

“First, although anxiety- and depression-related associations differed consistently, the anxiety-specific associations themselves were less robust across datasets.”

**Reviewer #2 (Recommendations for the authors):&&

The Results sections 2 (depression) and 3 (anxiety) could be improved by reducing the back and forth between factors throughout the results. It may be useful to split them into 3 sections: depression only, anxiety only, and depression vs anxiety.

We thank the Reviewer for this helpful suggestion. As suggested, we have reorganized this part into three sections: depression, anxiety, and depression versus anxiety. Please see our revision below:

Page 12:

“Differential associations of depression and anxiety with mood fluctuations. To directly test whether depression- and anxiety-specific factors differed in their associations with mood dynamics, we compared the corresponding correlations. These comparisons showed that depression-specific associations were significantly more negative than anxiety-specific associations for both mood variation (laboratory dataset: Z = -1.84, p = 0.033; online dataset 1: Z = -5.36, p < 0.001; online dataset 2: Z = -3.42, p < 0.001) and β_RPE (laboratory dataset: Z = -1.77, p = 0.038; online dataset 1: Z = -3.67, p < 0.001; online dataset 2: Z = -4.00, p < 0.001; Figures 2A–C and 2E–G). These results support distinct associations of depression- and anxiety-specific factors with RPE-related mood dynamics.”

In the discussion, the authors could have mentioned the brain areas most likely to be involved in these processes, both cognitive and psychopathological, as previous studies (such as Cecchi et al, 2022) have aimed at identifying regions involved in RPE processing while modulating mood in health. A short section on this would be useful to the neuropsychiatric community.

We thank the Reviewer for this helpful suggestion. We agree that the Discussion would benefit from a more explicit consideration of the neural systems that may support RPE-related mood updating and their relevance to psychopathology. We have revised the Discussion accordingly, as shown below:

Page 16:

“Although the present study did not include neuroimaging, the observed computational dissociation may map onto partially distinct neural systems involved in reward learning, mood updating, and affective psychopathology. RPE processing has been consistently linked to striatal–midbrain dopaminergic reward-learning circuits[8,50]. The integration of these reward-learning signals into subjective mood and value-based decision-making may further involve the ventral medial prefrontal cortex and orbitofrontal cortex[44]. In addition, the anterior insula may be particularly relevant for integrating feedback-related signals with affective and interoceptive states[8,44], potentially linking RPE processing to anxiety- and depression-related mood dynamics. Consistent with this view, Cecchi et al. (2022)[51] used intracranial EEG to show that feedback-related neural activity tracks mood fluctuations and risky choice. Future neuroimaging studies should test whether depression-related reductions and anxiety-related increases in RPE-related mood sensitivity are associated with altered interactions among striatal, prefrontal, and insular circuits.”

Reviewer #3 (Recommendations for the authors):

(1) The authors need to present a clearer definition of the terms "bifactor analysis" and "tripartite model" in the Introduction. What does tripartite mean in this context? What are the assumptions of such bifactor analyses (e.g. as used in Gagne et al. and the present work) and how, in broad strokes, are they carried out? These are important constructs to clarify for readers outside the computational psychiatry niche.

We thank the Reviewer for this helpful suggestion. We have revised the Introduction accordingly, as shown below:

Page 3:

“Recent work has used bifactor models of the tripartite model of depression and anxiety to clarify their distinct features and differential influences on decision-making[31,32]. The tripartite model of anxiety and depression proposes that these two symptom dimensions share a broad general distress or negative affect component while also including symptom-specific components: low positive affect/anhedonia is more specific to depression, whereas physiological hyperarousal is more specific to anxiety[30,33,34]. Bifactor analysis offers a way to model this structure statistically. In a bifactor model, symptoms load on a general factor reflecting their shared variance and on specific factors capturing residual variance in narrower symptom dimensions after accounting for the general factor.”

(2) Previous examinations of depression and RPE reactivity in this task paradigm, as the authors note (e.g. Rutledge et al., 2017), observed that individuals diagnosed with depression showed an intact association between RPEs and mood. In other words, there was no previously observed relationship between depression and affective reactivity to RPEs in this task context. Here, the authors find that the "unique" depression factor identified by the authors (in a non-clinical sample) is associated with blunted RPE sensitivity - this is worth commenting on specifically.

We thank the Reviewer for this helpful suggestion. We have discussed this point in the Discussion. Please also see it below:

Pages 15-16:

“Our computational model not only replicates the important role of RPEs in mood dynamics but also highlights the divergent mediating roles of RPE-related mood sensitivity in the associations of depression and anxiety with mood fluctuations. The opposite associations of depression and anxiety with mood sensitivity to RPEs complement previous findings of apparently intact RPE-related mood sensitivity in depression[12,25,37]. These findings further underscore the necessity of decomposing shared and specific components of depression and anxiety in studies of mood dynamics, which can enhance our understanding of their distinct associations with emotion processing and cognitive flexibility. This point is consistent with bifactor-based work showing that shared and specific symptom dimensions can have different computational correlates. For example, Gagne et al. (2020) showed that bifactor-derived symptom dimensions differentially relate to maladaptation to environmental volatility[32], complementing previous findings that trait anxiety is associated with inflexible adjustment to volatility[32].”

(3) There is a note (line 247) about the interpretation of the correlations in Figure 2, which attempts to explain away the inconsistent relationships between the anxiety-specific factor and mood variability as well as RPE reactivity observed in Figure 2. I can't say I understand the authors' point here about "signs of positive correlations", so I would say the authors need to clarify their logic here. More to the point, the authors only resolve anxiety-specific predictive effects when they collapse across these datasets. As discussed above (see 'weaknesses'), this is a serious limitation in my view and needs to be discussed as such in the paper.

We apologize for the unclear statement. Although the anxiety-specific factor showed associations in the expected direction across datasets, these associations were not significant in several individual datasets. Specifically, anxiety-specific scores were positively correlated with mood variation (laboratory dataset: r = 0.10, p = 0.531; online dataset 1: r = 0.08, p = 0.026; online dataset 2: r = 0.19, p = 0.004) and with RPE-related mood sensitivity (laboratory dataset: r = 0.04, p = 0.820; online dataset 1: r = 0.05, p = 0.216; online dataset 2: r = 0.19, p = 0.004; Figures 2A–C and 2E–G). This pattern may partly reflect limited statistical power at the single-dataset level.

Because these datasets used comparable task and questionnaire procedures and showed positive effect directions, we conducted pooled analyses to obtain a more stable estimate. Importantly, these analyses included dataset as a random intercept in mixed-effects models to account for between-dataset differences. Thus, the pooled analysis provides an integrated estimate across samples, conceptually similar to an individual-participant-data meta-analytic approach. The pooled results provided evidence for the expected anxiety-specific associations with greater mood variability and heightened RPE-related mood sensitivity (mood variation: t = 3.46, p < 0.001; RPE-related mood sensitivity: t = 2.60, p = 0.009). We have revised it to make it clear. Please see our revisions below:

Pages 10-11:

“Correlations between the anxiety-specific factor and mood variation were positive in direction across datasets, although they were not statistically significant in several datasets (the laboratory dataset: r = 0.10, p = 0.531; the online dataset 1: r = 0.08, p = 0.026; the online dataset 2: r = 0.19, p = 0.004). Similarly, correlations between the anxiety-specific factor and β_RPE were positive in direction but statistically inconsistent across datasets (the laboratory dataset: r = 0.04, p = 0.820; the online dataset 1: r = 0.05, p = 0.216; the online dataset 2: r = 0.19, p = 0.004; Figure 2A-C & 2E-G). Because these datasets used comparable task and questionnaire procedures and showed positive effect directions, and because reliable individual differences often require large samples to detect, we combined the laboratory dataset, online dataset 1, and online dataset 2 (total N = 1,026). This approach is analogous to an individual-participant-data meta-analytic analysis while accounting for dataset-level variability. Because these datasets used comparable task and questionnaire procedures and showed positive effect directions, and because reliable individual differences often require large samples to detect[48], we combined the laboratory dataset, online dataset 1, and online dataset 2 (total N = 1,026). This approach is analogous to an individual-participant-data meta-analytic analysis while accounting for dataset-level variability. We fitted linear mixed-effects models predicting mood variation and βRPE from the three bifactor scores, with dataset included as a random intercept. For mood variation, the anxiety-specific factor was positively associated with mood variation (t = 3.46, p < 0.001), whereas the depression-specific factor was negatively associated with mood variation (t = -6.13, p < 0.001). For RPE-related mood sensitivity, the anxiety-specific factor was positively associated with βRPE (t = 2.60, p = 0.009), whereas the depression-specific factor was negatively associated with βRPE (t = -5.30, p < 0.001).”

Page 17:

“Notably, the anxiety-related effects were less robust than the depression-related effects and were detectable only in the pooled dataset (n = 1,026); therefore, they require further replication in larger samples.”

(4) I expected to see that the authors would also investigate relationships between anxiety/depression related factors and the decay (gamma) parameter in the 'Happiness equation', which is presumably estimated from the data here. While I don't have a strong intuition about directions of (or presence of) predictive relationships here, doesn't it stand to reason that different aspects of psychopathology examined here might map onto how long- (versus short-) lasting the effects of, say, RPEs are, upon mood?

We thank the Reviewer for this important comment. In the healthy datasets, we fitted a linear mixed-effects model predicting the decay parameter (γ) from the three bifactor scores, with dataset included as a random intercept. None of the factors showed a significant association with γ (common: t = 0.708, p = 0.479; anxiety: t = 0.564, p = 0.573; depression: t = 1.146, p = 0.252). In the clinical dataset, we fitted a linear model predicting γ from the three bifactor scores and again found no significant associations (common: t = -0.036, p = 0.972; anxiety: t = -0.047, p = 0.963; depression: t = 0.052, p = 0.959). We have clarified this point in the revised manuscript as follows:

Supplementary Page 5:

“In the healthy datasets, we conducted a linear mixed-effect model against decay parameter (gamma) with all three factors, with dataset as a random factor. Results did not show significant effect (common: t = 0.708, p = 0.479; anxiety: t = 0.564, p = 0.573; depression: t = 1.146, p = 0.252). In the clinical dataset, we conducted a linear model against decay parameter (gamma) with all three factors and found no significant effect (common: t = -0.036, p = 0.972; anxiety: t = -0.047, p = 0.963; depression: t = 0.052, p = 0.959).”

(5) The rationale for and interpretation of the mediation model, which presumably aims to explain the relationships between anxiety- and depression-specific factors, RPE reactivity, and mood variability was barely explained by the authors. At present, I'm not sure what the added value of this analysis is. The authors should either remove or explain/motivate the mediation more clearly.

We thank the Reviewer for this helpful comment. The rationale for the mediation analysis is that mood variability in the task is not only a descriptive behavioral outcome, but may also arise from the degree to which momentary mood is updated by RPEs. Therefore, if depression is associated with reduced RPE-related mood sensitivity and anxiety with increased RPE-related mood sensitivity, these alterations should statistically account for their opposite associations with mood variability. The mediation model directly tested this possibility by examining whether RPE-related mood sensitivity accounted for the association between symptom-specific factors and mood variability. We have clarified this rationale in the revised manuscript as follows:

Page 10:

“Given the strong correlation between βRPE and mood variation (rs > 0.67, ps < 0.001), we further conducted a mediation analysis to examine whether individual differences in RPE-related mood sensitivity statistically accounted for the association between depression loading and mood variation. This analysis was motivated by the hypothesis that depression-related dampening of mood variability may arise, at least in part, from reduced mood sensitivity to RPEs.”

(6) This submission would benefit from extensive English language copy editing. There are many passages in the paper (in fact, too many to list here) that suffer from either grammatical errors or clarity issues.

We apologize for these mistakes. We have corrected the typographical errors throughout the manuscript.


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