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. Author manuscript; available in PMC: 2025 Sep 19.
Published in final edited form as: Eat Disord. 2024 Sep 19;33(5):666–680. doi: 10.1080/10640266.2024.2405290

Cognitive Flexibility and Emotion Regulation in Eating Disorder Patients with Comorbid Generalized Anxiety and Posttraumatic Stress Symptoms

Connor J Thompson 1, Caitlin A Martin-Wagar 1
PMCID: PMC11920903  NIHMSID: NIHMS2023604  PMID: 39300694

Abstract

Research has found that difficulties in emotion regulation negatively impact mental health, whereas cognitive flexibility may promote stress resilience and positive mental health. Little is known about cognitive flexibility and emotion regulation in people with comorbid eating disorder (ED) and anxiety and stress disorders. A transdiagnostic ED population (N = 227) at an outpatient ED treatment facility completed several self-report instruments that measured cognitive flexibility, emotion regulation difficulties, posttraumatic stress disorder (PTSD) symptoms, and generalized anxiety disorder (GAD) symptoms upon admission. We investigated cognitive flexibility and emotion regulation differences for those with an ED without comorbidity and those with various combinations of comorbidity. In a one-way between-groups ANOVA, we investigated differences in cognitive flexibility for those with GAD, PTSD, neither, and both comorbidities. We found a statistically significant difference between these groups, with mean cognitive flexibility inventory scores being the lowest in the group with both comorbidities. However, when controlling for emotion regulation, a one-way between-groups ANCOVA indicated no significant differences in cognitive flexibility between comorbidity groups F(3, 222) = 1.20, p = .31 Partial η2 = .02. Though self-reported cognitive flexibility levels differ among ED patients with and without comorbidities, it appears that these differences are better explained by emotion regulation. Therefore, addressing emotion regulation early in treatment for all individuals with EDs, regardless of comorbidity, is recommended as a future research focus to enhance treatment outcomes. Further research is needed to understand the impact of treating emotion regulation on ED treatment engagement, dropout, and effectiveness.

Keywords: Eating Disorders, emotion regulation, cognitive flexibility, generalized anxiety disorder, posttraumatic stress disorder

Introduction

Individuals with an eating disorder (ED) are highly likely to have at least one psychiatric comorbidity (Hudson et al., 2007; Momen et al., 2023). For EDs, common psychiatric comorbidities include anxiety disorders and posttraumatic stress disorder (PTSD; Hambleton et al., 2022), among others. To date, while effective for many individuals, treatment effectiveness for adults with EDs is generally inadequate for a sizeable proportion of those with EDs (Linardon et al., 2017). As such, improved identification of ED maintenance and recovery mechanisms is needed. With clinicians frequently encountering patients with multiple presenting concerns, comorbidities, and functional impairments, improved treatment uptake and symptom remission may be facilitated by investigating which symptoms are most essential to target early in treatment. For example, though integrating PTSD treatments into ED treatments has been shown to be effective, the nature of this relationship is not well understood, and treatment for these concurrent disorders has yet to be consolidated into an evidence-based treatment protocol (Mitchell et al., 2021; Trottier et al., 2022; Claudat et al., 2022). While the directionality of these comorbid diagnoses is not fully understood, it might be that for some, ED symptoms serve as a coping strategy to help mitigate symptoms of generalized anxiety disorder (GAD) and PTSD (Mitchell & Wolf, 2016).

Though comorbidity predicts the severity of ED psychopathology, comorbidity itself has not been found to predict or moderate ED treatment outcomes (Lydecker & Grilo, 2021; Mitchell et al., 2021). Avoidance and coping functions of ED symptomology may help to partially explain co-occurring generalized anxiety disorder (GAD) or PTSD with EDs; however, a deficiency in cognitive flexibility has also been shown in each of these diagnostic groups (Grant & Chamberlain, 2023; Miranda-Olivos et al., 2021; Tchanturia et al., 2012). It may be that comorbidity itself is not the most important factor when considering treatment outcomes, but rather non-ED-specific deficits, such as cognitive inflexibility. Indeed, cognitive inflexibility was high among individuals with AN with severe non-ED psychopathology (Miranda-Olivos et al., 2021).

Cognitive flexibility encapsulates an individual’s ability to adjust their perspective and broaden their awareness of choices when met with unexpected or challenging environmental demands (Roberts et al., 2011). In those with EDs, cognitive inflexibility can present as difficulty with eating a wide variety of food in a variety of settings, strict food rules, and rigid behaviors. Though most of the research literature on cognitive flexibility and EDs has focused on Anorexia Nervosa samples, recent studies have identified cognitive inflexibility as associated with eating disorder severity in transdiagnostic ED samples, regardless of illness severity or body mass index (Wang et al., 2021). Additionally, individuals with PTSD frequently experience rigid and maladaptive thought patterns, including negative beliefs about the self, avoidance of traumatic memories, and overgeneralized feelings of ongoing threats (Thompson-Hollands et al., 2017; Ehlers & Clark, 2000; U.S. Department of Veterans Affairs, 2023). Cognitive inflexibility is also commonly exhibited in GAD and may impact intolerance of uncertainty, for example (Laposa et al., 2015).

However, theory and research on cognitive flexibility have yet to fully establish whether cognitive flexibility is state or trait. It might be that cognitive flexibility is an endophenotype of EDs, serving as a risk factor for ED development (Holliday et al., 2005) or cognitive inflexibility develops as a result of the ED (e.g., a scar of EDs; Friederich & Herzog, 2010). For cognitive inflexibility to be a scar of EDs, research would find that cognitive flexibility is related to illness duration and worsens over time. However, recent work has added support for cognitive flexibility being an endophenotype of EDs, with adolescents with EDs exhibiting cognitive flexibility deficits regardless of their BMI, age, or illness duration (Wang et al., 2021). Further, studies find that cognitive flexibility improves throughout typical AN treatment (Duriez et al., 2021), and cognitive flexibility was similar in weight-restored individuals with AN compared to a community sample (Miles et al., 2022).

Finally, previous research has proposed that cognitive flexibility may be an underlying mechanism of effective emotion regulation (Genet & Siemer, 2011; Oschsner & Gross, 2007). Across the spectrum of eating disorders, strong associations have been found between emotion regulation and eating pathology (Prefit et al., 2019). When considering those with a comorbid PTSD and ED diagnosis, emotion regulation deficiencies (e.g., outbursts of anger, avoidance, or impulsive behavior) are also quite common (Trottier & MacDonald, 2017). Similarly, emotion regulation difficulties are prominent in those with GAD, as generalized anxiety often coincides with emotional and cognitive avoidance (Borkovec et al., 2004). In some instances, eating pathology development and maintenance can result, in part, from general difficulties in regulating emotions and behavior in combination with other biopsychosocial factors (Leppanen et al., 2022). A recent study found an interaction between emotion regulation and cognitive flexibility in individuals with AN, impacting clinical outcomes (Dann et al., 2022). Importantly, emotion regulation difficulties, such as impulsivity, have been found to predict premature ED treatment dropout (Fassino et al., 2009). Identifying who might be at higher risk for worse clinical outcomes and premature dropout upon admission is needed.

Given the complexity of research examining cognitive flexibility and emotion regulation in those with EDs and comorbid conditions, the present study examines which factors are most pertinent to ED symptom severity in a clinical transdiagnostic ED sample. Cognitive inflexibility has been scarcely examined in transdiagnostic ED samples and has been the relevancy of comorbidity. Our goal is to expand upon the literature surrounding the role of cognitive flexibility and emotion regulation in ED comorbidity. Furthermore, if ED patients with these comorbidities experience lower levels of cognitive flexibility than those without a comorbid diagnosis, it may be key to assess comorbidities upon intake and address cognitive inflexibility, if present.

Previous studies have found inconsistent cognitive flexibility relationships with EDs, which may be partly due to the measurement of cognitive flexibility. Cognitive flexibility is typically examined through either self-report or as a neurocognitive test, and it may be that these measurements do not examine the same aspects of the construct cognitive flexibility (Johnco et al., 2014; Miles et al., 2022). Indeed, Miles and colleagues (2022) found that self-report and neurocognitive measures did not actually correlate among their AN sample.

In this study, we focused on self-reported cognitive flexibility because of the questionable ecological validity of neurocognitive measures of cognitive flexibility, the influence of other executive functioning required for these measures, and ease of use within a real-world clinical setting. Instead, we sought to measure how patient participants perceive their own cognitive flexibility abilities in their daily lives versus using an experimental set-shifting task common among neurocognitive measures. We compared cognitive inflexibility among GAD and PTSD comorbidity groups and hypothesized higher levels of cognitive inflexibility among ED patients with multiple comorbidities admitted to an ED specialty clinic. We also sought to clarify the role of emotion regulation and cognitive flexibility among the comorbidity groups.

Methods

Participants and Procedures

Participants were adults seeking treatment within an eating disorder specialty clinic in the Midwestern United States (N = 227). All participants completed measures as part of the intake process at the clinic and were asked for consent for their measures to be used for research purposes. They were informed that their relationships with treatment, providers, and the clinic would not be impacted by their decision to participate in research. Participants were also asked to consent for the research team to view their electronic medical records to confirm ED diagnoses and anthropometric data. During the intake procedures, participants were assessed for the presence of an eating disorder. Intake clinicians were licensed mental health providers who used diagnostic criteria from the Diagnostic and Statistical Manual of Mental Disorders – 5th Edition (American Psychological Association, 2013) and who specialized in eating disorders. A university Institution Review Board in the Midwestern United States approved all study procedures.

Participant age ranged from 18 to 67 (M = 31.91), and of the body mass indexes available from chart review (n=172), BMI ranged from 11.20–60.10 (M = 25.39) in this transdiagnostic eating disorder sample. Additional participant demographics can be found in Table 1.

Table 1.

Participant Demographics (N = 227)

n %
Race/Ethnicity
 White/European American 213 93.8
 Black/African American 4 1.8
 Asian American 2 0.9
 Hispanic/Latinx 4 1.8
 Native American 1 0.4
 Middle Eastern 1 0.4
 Bi/Multi-Racial 2 0.9
Sexual Orientation
 Heterosexual/Straight 199 87.7
 Lesbian/Gay 5 2.2
 Bisexual/Pansexual 15 6.6
 Asexual 1 0.4
 Demisexual 1 0.4
 Questioning/Curious/Uncertain 4 1.8
 Did not respond 2 0.9
Annual Household Income
 Less than 10,000 35 15.4
 10,000–49,000 75 33.0
 50,000–89,000 51 22.5
 90,000–149,000 34 15.0
 150,000 or more 24 10.6
 Did not respond 8 3.5
Eating Disorder Diagnosis
 Anorexia Nervosa 74 32.6
 Bulimia Nervosa 28 12.3
 Binge Eating Disorder 54 23.8
 Other Specified Eating Disorders 71 31.3
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Measures

Posttraumatic stress disorder symptoms.

Posttraumatic stress disorder symptoms were measured using the Posttraumatic Stress Disorder Checklist for the DSM-5 (PCL-5; Blevins et al., 2015). Participants received this measure only if they endorsed having experienced a traumatic event on the trauma history screen (THS). The PCL-5 consists of 20 items, measuring the 20 DSM-5 symptoms of posttraumatic stress disorder (PTSD). Each item of the PCL-5 is scored on a 5-point Likert scale, with participants rating how much they have been bothered by each of these symptoms in the past month, from 0 (not at all) to 4 (extremely). An overall score for the PCL-5 can be calculated by summing the scores on all 20 items (range 0–80), with a clinical cutoff score of 31 (Bovin et al., 2016). Upon its initial development, Blevins and colleagues (2015) found that PCL-5 scores exhibited strong internal consistency (α = .94), test-retest reliability (r = .82), and convergent (r = .74 to .85) and discriminant (r = .31 to .60) validity. In a network analysis of posttraumatic stress and eating disorder symptoms in a sample of adults, internal consistency was excellent (α = .95; Liebman et al., 2021). McDonald’s omega for the PCL-5 in this study was found to be 0.96, indicating good reliability (Hayes & Coutts, 2020).

Generalized Anxiety Disorder.

Generalized anxiety symptoms were measured using the Generalized Anxiety Disorder 7-item Scale (GAD-7; Spitzer et al., 2006). The measure consists of 7 items that measure for symptoms of anxiety (similar to the generalized anxiety disorder diagnostic criteria described in the DSM). The GAD-7 then asks participants to rate how often they have been bothered by these symptoms over the past two weeks (e.g., “Feeling nervous, anxious, or on edge”) on a 4-point Likert scale, ranging from 0 (Not at all) to 3 (Nearly every day). An overall score on the GAD-7 can be calculated by summing item scores of the 7 responses. The clinical cut-off score is 10, and the GAD-7 is regarded as a useful screening tool for GAD (Kroenke et al., 2007). The current study found good reliability on the GAD-7, with a McDonald’s omega value of 0.92.

Cognitive Flexibility.

Levels of cognitive flexibility were measured using the Cognitive Flexibility Inventory (CFI; Dennis & Vander Wal, 2010), as this measure has commonly been used to differentiate cognitive flexibility between clinical and non-clinical samples (Johnco et al., 2014). The CFI measures one’s ability to generate multiple alternative solutions to different situations and one’s tendency to perceive difficult situations as controllable (Johnco et al., 2014). When taking the CFI, participants are asked to rate how much they agree with 20 statements, scoring items on a 7-point Likert scale, ranging from 1 (strongly disagree) to 7 (strongly agree). A total score (ranging from 20 to 140) can be calculated by summing all 20 items, with higher scores indicating higher cognitive flexibility. Total CFI score had good reliability in this study, with a McDonald’s omega value of 0.91.

Emotion Regulation.

Self-reported emotion regulation skills were measured using the Difficulties in Emotion Regulation Scale (DERS; Gratz & Roemer, 2004). The DERS has 36 items and asks participants to indicate how often these statements apply to them (e.g., “I experience my emotions as overwhelming and out of control”) on a 5-point Likert scale, ranging from 1 (almost never, 0–10%) to 5 (almost always, 91–100%). Higher scores indicate greater problems with emotion regulation (Gratz & Roemer, 2004). The DERS had good reliability in this study, with McDonald’s omega being 0.95.

Analytic Plan

IBM SPSS Statistics 28.0 was used to examine the study hypotheses. First, we computed total GAD-7 and PCL-5 scores. We were then able to make probable comorbidity groups in each variable based on the clinical cutoff for the GAD-7 and the PCL-5 (scores of 10 and 31, respectively; Spitzer et al., 2006; Blevins et al., 2015). In doing so, we were able to compare groups that had no GAD and PTSD comorbidity, a probable GAD comorbidity, a probable PTSD comorbidity, or both comorbidities on cognitive flexibility and emotion regulation.

We conducted a one-way between-groups analysis of variance (ANOVA) to examine differences in cognitive flexibility among four groups of individuals with EDs: the GAD-only comorbidity, PTSD-only comorbidity, both comorbidities, and no GAD or PTSD comorbidities. Following this, we conducted a one-way between-groups analysis of covariance (ANCOVA) that controlled for emotion regulation. This allowed us to examine if self-reported difficulties with emotion regulation might help to explain potential differences in cognitive flexibility, which we found necessary given previous research on the interaction between the two.

Results

Using scale-level analyses of missing data, we found no missing items across the CFI, DERS, PCL-5, or GAD-7. Thus, no adjustments to the data set were needed to account for missing data.

Clinical Cutoffs in the Outpatient ED Sample

In the transdiagnostic ED outpatient sample (N = 227), 25.1% met the clinical cutoff for only GAD, 4.0% met the clinical cutoff for only PTSD, and 41.9% met clinical cutoffs for both PTSD and GAD on the PCL-5 and the GAD-7, respectively. 29.1% of the ED patients did not meet clinical cutoffs for either GAD or PTSD.

Potential Covariates

A Chi-Square Test for Independence found a significant association between ED diagnosis and meeting the GAD clinical cutoff, χ2 (3, n = 227) = 17.55, p < .001, phi = .28 (small-medium effect). On the other hand, no significant association between ED diagnosis and meeting the PTSD clinical cutoff was found, χ2 (3, n = 227) = 3.20, p = .36, phi = .12 (not significant).

Using one-way between-groups ANOVA, we next assessed if there were significant differences in cognitive flexibility for the ED diagnostic groups. There were no significant differences in cognitive flexibility between the ED diagnostic groups, F(3, 223) = 2.06, p = .11. We also examined the relationship between BMI and cognitive flexibility with a bivariate correlation, finding no significant relationship, r = −.01, p = .88. Given there were no significant relationships between our outcome variable (cognitive flexibility) and ED diagnosis and BMI, we did not control for ED diagnosis or BMI in our study analyses reported below.

Comparing CFI Scores Across Comorbidity Groups

In the one-way between-groups ANOVA, we investigated differences in self-reported CFI global scores for the GAD and PTSD comorbidity group, compared to the GAD-only group, PTSD-only group, or no comorbidity group. Levene’s test of equality of error variances was significant (p = .047), indicating the data did not meet the assumption of homogeneity of variances. As such, Welch statistic was used to examine differences in CFI scores amongst the four comorbidity groups, F(3, 52.486) = 31.256, p < .001, Partial η2 = .22 (large effect).

Tukey’s HSD Test for multiple comparisons indicated that the mean CFI score of those with no comorbidities (M = 101.85, SD = 15.64) was significantly higher than those in the GAD-only group (M = 92.04, SD = 18.26, p = .009, 95% C.I. = [1.80,17.83]), and those with both comorbidities (M = 81.22, SD = 18.03, p < .001, 95% C.I. = [13.53, 27.73]). Tukey’s HSD also indicated that mean CFI scores were lower in those with both comorbidities than in both the GAD-only (p = .001, 95% C.I. = [−18.24, −3.39]) and PTSD-only groups (M = 105.33, SD = 6.02, p < .001, 95% C.I. = [−39.57, −8.65]). There were no significant differences between the no comorbidity and PTSD-only groups (p = .940) or between the GAD-only and PTSD-only groups (p = .136).

Next, we examined differences in CFI global scores for the GAD-only group, the PTSD-only group, the no comorbidity group, and the group that had both comorbidities, using self-reported emotion regulation abilities from the DERS as a covariate in a one-way between-groups ANCOVA. No significant differences in CFI scores were found between the groups after controlling for DERS score, F(3, 222) = 1.20, p = .31 Partial η2 = .02. We found a significant relationship between the CFI and DERS scores, Partial η2 = .27.

Discussion

Supporting our hypothesis on the compounded effect of having both GAD and PTSD comorbidities, total cognitive flexibility was significantly lower in individuals with both GAD and PTSD than in individuals with singular GAD or PTSD comorbidity or no comorbidities. This finding is in line with previous research on the negative implications of comorbid illness and PTSD, which can exacerbate one another, leading to further complications in both (e.g., avoidance of feared stimuli, negative coping strategies; Price et al., 2019; van Dam et al., 2013). Further, these findings build upon past research on cognitive flexibility deficiencies in those with EDs, GAD, or PTSD (Grant & Chamberlain, 2023; Tchanturia et al., 2012), elaborating on the intersection of these illnesses and the relationships that these various comorbidities have with cognitive flexibility. However, our later findings seem to suggest that these differences can be attributed to differing levels of emotion regulation ability.

These findings are somewhat consistent with prior research on emotion regulation deficiencies in those with PTSD and an ED (Trottier & MacDonald, 2017), showing that the comorbidity of the two often co-occurs with difficulty regulating one’s emotions. Similarly, these findings coincide with previous findings on emotion regulation difficulties in those with GAD, as generalized anxiety is often accompanied by avoidance of negative experiences (Borkovec et al., 2004). For instance, worry (a central characteristic of GAD) is often used as a means of emotional and experiential avoidance (e.g., utilizing worry about an external life event as a means of avoiding distressing or intense emotions that are experienced internally), further exhibiting emotion regulation difficulties in those with GAD (Hayes et al., 1996; Oathes et al., 2011; & Roemer et al., 2005). Emotion regulation deficiencies are of great importance across mental health treatment settings, as impulsivity based on emotional reactivity is a predictor of premature treatment dropout (Fassino et al., 2009). While those with comorbidity do have lower cognitive flexibility, it appears the individual’s emotion regulation abilities are more directly related to cognitive flexibility (and not comorbidity status).

Dann and colleagues (2022) measured flexibility pertaining to eating pathology, finding that flexibility was an independent predictor of eating pathology (i.e., cognitions and compensatory behaviors). In our sample, we found cognitive flexibility to be insignificant in the prevalence of potential stress and anxiety comorbidity in an ED sample, after controlling for difficulties in regulating emotions. However, we did not examine these variables in relation to ED pathology but among comorbidity groups. Additional methodologies are needed to fully examine the relationships between ED symptoms, comorbidity, emotion regulation, and cognitive flexibility. Future clinical research should focus on further attempts to tease out how these factors interact and examine the role of cognitive flexibility in the development and treatment of eating disorders and comorbid illnesses.

From previous and current research, it is apparent that ED considerations around comorbidity, cognitive flexibility, and emotion regulation are complex and nuanced. ED clinicians are routinely faced with complex presenting concerns among their patients, making it challenging to identify which symptoms or comorbidities are most relevant to include in treatment planning, and which symptoms may elevate the risk of premature treatment dropout. Our findings provide evidence that while comorbidity may be relevant, it is more likely that emotion regulation, a common non-ED-specific symptom, is highly important in patients’ functioning. As such, measuring emotion regulation at intake is recommended rather than relying on comorbid diagnoses alone to guide treatment recommendations and targets. Many common comorbidities for those with EDs share the feature of emotion regulation difficulties (Borkovec et al., 2004; Prefit et al., 2019; Trottier & MacDonald, 2017), and one’s emotion regulation difficulties may also impact cognitive flexibility. As such, emotion regulation is a solid initial treatment target to explore within treatment as usual for EDs of any type and a good target when clinicians are triaging multiple impairing symptoms. It may be that resolving emotion regulation will have a ripple effect in supporting improved cognitive flexibility and the remission of comorbid conditions.

Limitations

Though this project contributes new knowledge about comorbid symptoms, cognitive flexibility, and emotion regulation in a clinical ED sample, several limitations exist. The first is that participants completed self-report measures of PTSD and GAD without receiving a formal diagnosis from a mental health clinician. Thus, our findings apply best to understanding comorbidity symptoms, and we cannot be sure these findings will remain in a sample that also had a clinical interview to determine all relevant comorbid diagnoses. We did use well-established clinical cut-offs for the GAD-7 and PCL-5, which have an 82% specificity and 96% specificity, respectively (Spitzer et al., 2006; Blevins et al., 2015). As such, we feel our findings provide relevant information about how comorbid GAD and PTSD symptoms function in those with EDs.

Another limitation of our sample is that it is comprised of a treatment-seeking population of those with EDs. While using a clinical sample is a strength, it is also a limitation in this case because insurance-based treatment centers like the one used in this study tend to have a more homogenous population with little racial and ethnic diversity due to inequitable access to insurance and other barriers to receiving an ED diagnosis. As such, other studies should examine the variables in other samples, such as treatment samples from grant-funded studies that do not require insurance.

Conclusions

These findings indicate the importance of emotion regulation on cognitive flexibility, regardless of comorbidity, in transdiagnostic EDs. Although emotion regulation seems to be the driver of these differences in cognitive flexibility rather than comorbidity itself, it is not to say that cognitive flexibility or comorbidity has no role in ED patients. Instead, future research should examine the best ways to address emotion regulation early in treatment and its potential for impacting ED treatment engagement, dropout, and effectiveness. Existing ED treatments are already insufficient in helping a sizable proportion of those with EDs reach and maintain recovery (Linardon, 2018). Therefore, addressing emotion regulation early in treatment for all individuals with EDs, regardless of comorbidity, is a recommended avenue for future clinical research aimed at improving ED and comorbidity treatment outcomes.

Clinical Implications.

  • Eating disorder patients with comorbidities had the lowest cognitive flexibility.

  • When accounting for emotion regulation, group differences were no longer present.

  • Addressing emotion regulation early in eating disorder treatment is recommended.

Funding:

This research was supported by the National Institute of General Medical Sciences of the National Institutes of Health Award Number P20GM130418.

Footnotes

Disclosure: The authors declare no conflict of interest.

CRediT: CT-conceptualization, formal analysis, investigation, visualization, writing-original draft, writing-review and editing; CMW-conceptualization, data curation, formal analysis, funding acquisition, investigation, methodology, project administration, resources, software, supervision, validation, visualization, writing-original draft, writing-review and editing

Data Availability Statement:

The datasets generated and/or analyzed during the current study are available in the Open Science Framework repository, https://osf.io/ksx8u.

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Associated Data

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

Data Availability Statement

The datasets generated and/or analyzed during the current study are available in the Open Science Framework repository, https://osf.io/ksx8u.

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