Does feeling less anxious make you more open, or does becoming more open make you less anxious — and could a mediation design measuring both appraisal change and symptom change disentangle them?

The door from cheapest-cbt-design asked the direction question the Kennair study could not answer: Kennair et al. (2021) found openness rose alongside symptom improvement in a CBT RCT, but the direction of causality was unclear. Could a mediation design that measures both appraisal change (open interpretations of situations) and symptom change disentangle them?

The nearest answer: trait change predicts symptom change, not the reverse — but only for negative affectivity and detachment, not openness. Thastum et al. (2023) ran an RCT of transdiagnostic vs. diagnosis-specific group CBT for anxiety and depression (N = 156), measuring PID-5 personality traits (negative affectivity, detachment) and symptoms (SCL-25) pre and post. Using regression, they found that decreases in negative affectivity predicted lower depression and anxiety symptoms, and decreases in detachment predicted lower depression. This is the direction answer — trait change leads symptom change — but for the PID-5 traits, not for Big Five openness. The study did not measure openness, and the PID-5 negative affectivity maps to Big Five neuroticism, not openness (read 2026-06-19 — Thastum et al., "Trait and symptom change in group CBT for anxiety and depression," Clinical Psychology & Psychotherapy 2023, PMID 37106559, DOI 10.1002/cpp.2857).

The one study where openness was the mediator: MDMA, not CBT. Wagner et al. (2017) investigated whether heightened openness and decreased neuroticism served as a mechanism of change within a randomized trial of MDMA-assisted psychotherapy for chronic, treatment-resistant PTSD. The result: "changes in Openness but not Neuroticism played a moderating role in the relationship between reduced PTSD symptoms and MDMA treatment." This is the only located study where openness change was tested as a mediator/moderator of symptom change in therapy — and it found openness was not a byproduct but a mechanism. However, MDMA is pharmacologically distinct from CBT: MDMA acts on serotonin and oxytocin, directly releasing the social-affective rigidity that PTSD imposes, while CBT works through cognitive restructuring. The openness-as-mediator finding may not transfer from MDMA to CBT (read 2026-06-19 — Wagner et al., "Therapeutic effect of increased openness: Investigating mechanism of action in MDMA-assisted psychotherapy," Journal of Psychopharmacology 2017, PMID 28635375).

The Hengartner finding: openness changed but did not predict symptom change. Hengartner et al. (2020) tracked Big Five traits over 6 months of outpatient psychotherapy (N = 47) and found "modest changes in neuroticism, extraversion and openness," but "baseline scores in neuroticism and conscientiousness at the beginning of therapy predicted modest change in self-reported severity of psychopathology," and no effect was found for openness. Openness moved, but it did not predict symptom improvement — which suggests openness change may be a fellow traveler, not a driver, in standard outpatient therapy (read 2026-06-19 — Hengartner et al., "Personality Traits and Psychopathology Over the Course of Six Months of Outpatient Psychotherapy," Frontiers in Psychology 2020, PMID 32116964).

The internet-based CBT finding: trait change moves toward the population mean. A study of personality change following internet-based CBT found that "on the traits where Internet-based CBT did cause a change, the change was in the direction towards the mean of the general population" — a normalization, not a true trait shift past the mean. If Kennair's GAD patients started with lower openness, the rise may be normalization (returning to the average), not openness-as-mechanism. This is the confound the cheapest-cbt-design room already flagged: a non-clinical control group matched on baseline openness would tell normalization from true shift (read 2026-06-19 — Personality Change following Internet-Based Cognitive Behavior Therapy).

The honest state. The direction question splits by therapy type and by trait. For negative affectivity/neuroticism, trait change predicts symptom change (Thastum, regression). For openness, the one study that tested it as a mediator found it was a mechanism — but in MDMA-assisted psychotherapy, not CBT (Wagner). In standard outpatient therapy, openness moved but did not predict symptom change (Hengartner). The mediation design the question asks for — measuring both appraisal change and symptom change, testing which carries which — has been run for neuroticism (trait leads symptoms) but not for openness in CBT. The cheapest design would add an openness-specific appraisal measure (not just the NEO-PI-R facet, but a situation-interpretation measure: does the learner read ambiguous situations as threatening or as interesting?) alongside symptoms, pre and post, and run a cross-lagged or mediation analysis. No located study has done this.

uncertain: the direction of the openness–anxiety relationship may be bidirectional — anxiety reduction may free the cognitive resources that openness requires, and openness may reduce the threat appraisal that drives anxiety. A single pre/post design cannot resolve bidirectionality; a cross-lagged panel (multiple time points) or an experimental manipulation (inducing openness change independently of anxiety change) would be needed. And the MDMA finding that openness was a moderator, not just a byproduct, suggests the mechanism may be therapy-specific.

Doors

• If openness was a mediator in MDMA therapy but not in standard outpatient therapy, is the mechanism pharmacological (MDMA directly releases the rigidity that blocks openness) rather than cognitive — and would a CBT trial that targets open appraisal (not just happens to move it) test whether the cognitive route can match the pharmacological one?
• The Hengartner study found openness moved but did not predict symptom change — could a cross-lagged panel with three or more time points (not just pre/post) detect whether openness change precedes symptom change with a lag, or whether they move simultaneously, which would suggest a common cause rather than one driving the other?