Preamble

Anger Countering-Based Implementation Intentions Reduce Fear Reinstatement and Avoidance Tendency

Hongbo Wang¹*, Yingzhu Zeng¹
¹ (Henan Key Laboratory of Psychology and Behavior; Faculty of Education, Henan University, Kaifeng 475004, China)

Abstract:
[Objective] To explore whether anger countering-based implementation intentions (II) can reduce fear reinstatement and avoidance behavior in individuals with fear-related disorders.
[Methods] A differential fear conditioning paradigm was employed. Participants in the II group formed anger countering-based II prior to extinction training ("If I feel afraid when viewing fish/bird images, I will recognize how irrational it is to fear animal pictures. I will clench my fists and feel intensely angry with myself!!"). The control group received no II intervention. Subjective measures (fear, anger, threat expectancy, avoidance distance) and skin conductance response (SCR) were recorded during the extinction and reinstatement phases.
[Results] During the late extinction phase, the II group showed a significantly shorter avoidance distance towards the CS+ compared to the control group. During the reinstatement phase, the II group reported significantly lower levels of fear, anger, threat expectancy, and avoidance distance. No significant between-group differences were observed in SCR.
[Limitations] The sex ratio was unbalanced, and SCR was unable to distinguish between anger and fear.
[Conclusion] Forming anger countering-based II prior to extinction requires repeated practice and can automatically reduce fear reinstatement and avoidance tendencies.

Keywords: Anger; Implementation intention; Fear extinction; Emotion regulation
Classification Number: B845

1 Introduction

Fear is an evolutionarily fundamental emotion that prepares organisms for potential threats by activating defensive response systems \cite{Lang & Davis, 2000}. However, maladaptive fear responses can lead to psychiatric disorders such as anxiety disorders, phobias, and post-traumatic stress disorder (PTSD) \cite{Lebois et al., 2019}. Differential fear conditioning serves as a crucial model for investigating the pathogenesis of these disorders, helping to explain how maladaptive fear, anxiety, and avoidance are learned and maintained \cite{Vervliet et al., 2013}. During fear acquisition, an aversive unconditioned stimulus (US) is repeatedly paired with one neutral stimulus (CS+) but never with another (CS−), leading participants to develop specific fear responses to the danger-predicting CS+. Strategies for modulating fear responses include fear extinction, cognitive emotion regulation, avoidance strategies, and disrupting fear memory reconsolidation. However, memory reconsolidation is constrained by boundary conditions related to memory characteristics and retrieval methods \cite{Kindt, 2018; Lee et al., 2017; Monfils & Holmes, 2018; Vaverková et al., 2020; Zuccolo & Hunziker, 2019}. For instance, high-intensity memories are more resistant to reconsolidation processes \cite{Wang et al., 2009}, and the intense fear memories in PTSD are difficult to treat through memory reconsolidation interventions \cite{Dębiec et al., 2011; Roger, 2011; Steckler & Risbrough, 2012}. While avoidance strategies can prevent harm, excessive avoidance generalization interferes with threat verification and leads to functional disability \cite{Meulders et al., 2024}.

Cognitive behavioral therapy (CBT) based on fear extinction is a common treatment for anxiety and fear-related disorders. Fear extinction refers to the gradual reduction and disappearance of fear responses to a CS (including both CS+ and CS−) through repeated exposure without US reinforcement \cite{Britton et al., 2014}. Nevertheless, because extinction does not destroy the original fear memory but rather forms a new CS-no US safety memory, successfully extinguished fear can return through multiple pathways, including spontaneous recovery over time, renewal when the CS appears in a context different from the extinction context, and reinstatement after stress exposure \cite{Vervliet et al., 2013}. The ease with which fear returns after extinction represents a pressing challenge. Additionally, CBT is only effective for 50% to 60% of anxious children and adults, with limited efficacy for others \cite{Loerinc et al., 2015}. This may be because fear extinction requires exposure to the CS, yet some patients avoid environments or cues associated with anxiety/fear events even when they are harmless. Maladaptive avoidance constitutes a core feature of anxiety and fear-related disorders \cite{American Psychiatric Association, 2013}, hinders fear extinction \cite{Lovibond et al., 2009; O’Malley & Waters, 2018; Rattel et al., 2017; Vervliet & Indekeu, 2015}, and plays a central role in the development and maintenance of anxiety disorders \cite{Pittig et al., 2018}. For example, O’Malley and Waters (2018) used eye-tracking technology to instruct participants to either attend to (monitor group) or avoid (avoidance group) the CS+ during fear extinction, finding that avoidance impaired extinction outcomes. Other research shows that avoidance predicts worse treatment outcomes better than anxiety does \cite{Pittig et al., 2015}. Therefore, addressing this "costly" avoidance behavior is urgent.

The heterogeneity of symptoms in trauma-exposed individuals suggests that regulating abnormal responses to CSs is central to treatment. Emotion regulation—the process by which we influence our emotions and how we experience and express them—is crucial for mental health and psychopathology \cite{McRae & Gross, 2020}. It can be achieved through conscious effort (cognitive reappraisal) or automatic processes \cite{Gross, 2014}. The former is limited by prefrontal sensitivity to stress \cite{Raio et al., 2013; Raio & Phelps, 2015}, making the latter more clinically promising. Recent research has increasingly explored automatic or implicit forms of emotion regulation at behavioral and neural levels \cite{Chen et al., 2020, 2021; Gomez et al., 2015; Lutz & Krahé, 2018; Zhan et al., 2015, 2017, 2018}, primarily including emotional counteraction and implementation intentions. Traditional Chinese philosophy and medicine posit that emotions have mutual promotion and counteraction relationships (MPMC) \cite{Zhan et al., 2015}. The incompatible response hypothesis similarly suggests that inducing incompatible emotions can moderate the behavioral impact of a given emotion \cite{Baron, 1984}. Research shows that inducing sadness can reduce anger-driven aggressive behavior \cite{Lutz & Krahé, 2018; Zhan et al., 2015, 2018}, and this regulatory efficiency is unaffected by stress \cite{Zhan, Wu, et al., 2017}. Greenberg and Pascual-Leone (2024) propose that the best way to change an emotion is to use an opposite-valence, more intense emotion. However, Pavlovian counterconditioning, which replaces the fear US with reward/positive stimuli, can alleviate fear avoidance \cite{Hulsman et al., 2024} but is limited by valence differences between positive and negative emotions \cite{Ito et al., 1998; N. K. Smith et al., 2003} and cannot block fear relapse. This raises the question: Might using anger—a similar-valence but opposite-action-tendency emotion—be more effective for reducing fear avoidance and fear return?

Although fear and anger share threat-related neurophysiological underpinnings \cite{Prather, 2016; Siegel et al., 2018} and fear can readily transform into anger \cite{Zhan et al., 2015, 2018}, they show significant behavioral divergence: fear triggers avoidance responses (freezing/escape), whereas anger drives approach behavior (resistance/attack) \cite{OToole & Mikkelsen, 2021}. Unlike fear, anger effectively enhances individuals' sense of certainty and control \cite{Lerner & Keltner, 2001; Song et al., 2021; Tiedens & Linton, 2001}, makes both others \cite{Sell et al., 2009} and oneself \cite{Tibubos et al., 2013} feel powerful, and promotes goal-directed behavior \cite{Lench et al., 2024}. An individual's sense of certainty and control represents an important factor influencing the negative effects of stress \cite{Hartley et al., 2014; Meyer et al., 2021}. Based on these anger characteristics, studies from the 1970s reported successful treatment of fear-related symptoms through anger induction \cite{Butler, 1975; Goldstein et al., 1970}. For example, Goldstein et al. (1970) instructed patients to pair fear-provoking scenes with angry imagery and vocalizations, then apply these operations to real fear stimuli. A 34-year-old woman with severe, persistent anxiety, dizziness, and leg instability had failed desensitization due to excessively intense real-scene fear. She was instructed to express anger when fear stimuli appeared, such as shouting "I'm not afraid" and hitting pillows. After three clinic sessions and 1.5 hours of daily home practice combined with thought-stopping procedures, she overcame her fear and resumed normal life within two weeks. However, these were case studies combining other interventions, leaving the pure effect of anger on fear unclear. Subsequent research has been scarce, primarily due to three concerns: (1) Anger can be a trauma outcome \cite{Connor et al., 2003} and a symptom of some anxiety and trauma-related disorders—DSM-5 PTSD criteria include anger in "alterations in cognition and mood" (Cluster D) and "irritable behavior and angry outbursts" (Cluster E) \cite{American Psychiatric Association, 2013}; (2) Anger is associated with negative consequences including impulsive aggression \cite{Teten et al., 2010} and violent behavior \cite{Chereji et al., 2012}, posing safety risks; (3) Foa et al. (1995) found that in 12 female PTSD patients, stronger fear during early exposure treatment predicted better outcomes, while anger might inhibit fear expression and impair treatment efficacy.

Recent evidence has alleviated these concerns: (1) Anger/irritability symptoms in anxiety disorders are difficult to distinguish as primary or secondary—some patients' anger may be secondary, representing defensive displacement where uncontrollable threat fear (e.g., social situations) transforms into controllable target anger (e.g., toward family) \cite{Marcus-Newhall et al., 2000}, similar to "kicking the cat" effects. Research reports that COVID-19 fear may manifest as hidden aggressive behavior in virtual social ecologies \cite{Ye et al., 2021}. Neuroimaging shows that anxious individuals' threat hypervigilance (e.g., amygdala activation) and prefrontal dysregulation may cause emotional displacement \cite{Shackman et al., 2011}. CBT for generalized anxiety disorder can improve internally and externally expressed anger even without directly targeting it \cite{Laposa & Fracalanza, 2019}, possibly because reduced emotional response to the original threat eliminates reliance on "safe targets" for unresolved anxiety discharge. This suggests anger symptoms may be byproducts of unresolved fear/avoidance rather than primary emotional dysregulation. Since both fear and anger involve amygdala-prefrontal circuits, successful fear reduction may also decrease anger's motivational expression (e.g., aggressive impulses) \cite{Blair, 2016}. (2) Anger does not always lead to aggression—it varies along a continuum from minimal anger to intense rage \cite{Deffenbacher et al., 1996}. (3) van Minnen et al. (2002) confirmed with larger samples that anger is unrelated to PTSD treatment efficacy or dropout; Forbes et al. (2008) found that fear of anger (e.g., "fearing feeling anger because of endless anger and harmful consequences") causes poor treatment outcomes. More importantly, two decades of research show that excessively high initial fear during extinction training impairs extinction learning and causes extinction deficits \cite{Maren, 2014, 2022; Maren & Chang, 2006; Merz et al., 2016; Totty et al., 2019}, challenging the old view that "more fear yields better outcomes."

Although anger is a strong negative emotion, research shows angry individuals' risk estimates are closer to those of happy individuals \cite{Lerner & Keltner, 2001}, helping break fear's avoidance cycle. According to MPMC theory, fear readily transforms into anger, and anger readily transforms into happiness \cite{Zhan et al., 2015, 2018}, suggesting a circuitous path may better achieve fear-to-happiness conversion. Greenberg and Pascual-Leone (2024) also argue that inducing adaptive anger toward threat sources (e.g., perpetrators' violations) can change trauma victims' maladaptive fear. The key lies in adjusting anger induction methods, targets, and expression forms to maximize efficacy and minimize risk.

Recently, Carey and Sarma (2016) found that increasing drivers' self-efficacy through questioning, then presenting high-threat information to induce fear, reduced driving speed, but anger counteracted this effect. Elkjær et al. (2023) attempted to examine counteraction between anger and anxiety—negative emotions with different action tendencies (approach vs. avoidance)—but failed to clarify anger's counteractive effect due to experimental issues (the anger task also induced high anxiety and tension). Therefore, this study continues investigating anger's counteractive effect on conditioned fear. Given that post-conditioning fear responses to CSs become automatic \cite{Gallo et al., 2009}, implementation intentions may effectively control automatic thought processes and prevent expression bias \cite{Stewart & Payne, 2008}. To better counter fear, automatically generating anger upon CS presentation may be superior. Equipping individuals with an "implementation intention" to produce anger represents the most promising approach.

Implementation intention (II) is a self-regulation strategy formulated as "if…, then…" (e.g., "If I encounter situation X, then I will initiate response Y"), creating an automatic link between anticipated situations (if) and target behaviors (then). Once formed, encountering situation X highly activates the predetermined response, promoting goal achievement without increased conscious involvement \cite{Gallo et al., 2009; Gollwitzer & Sheeran, 2006; Webb et al., 2012}. Numerous studies confirm that strategically forming different II content can automatically regulate negative emotions \cite{Azbel-Jackson et al., 2016; Chen et al., 2020, 2021; Gallo et al., 2009; Gomez et al., 2015; Hallam et al., 2015; Huang et al., 2020; Ma et al., 2019}, primarily through avoidance ("I won't feel afraid; if I see a spider, then I'll ignore it" \cite{Gallo et al., 2009}), suppression ("If I see a weapon, I'll stay calm and relaxed" \cite{Azbel-Jackson et al., 2016}; "If I see an 'inhibit' cue, then I'll 'block all bad feelings and stay calm'" \cite{Hallam et al., 2015}), or reappraisal strategies ("If I see a 'reappraise' cue, then I'll tell myself 'the upcoming pictures are just pixels on a screen; they can't reach me'" \cite{Hallam et al., 2015}; "I won't feel disgusted; if I see blood, I'll take a doctor's perspective" \cite{Chen et al., 2020, 2021; Gomez et al., 2015; Huang et al., 2020}; "I won't feel disgusted; if I see blood, I'll view it as representing vitality and health" \cite{Ma et al., 2019}). However, existing II strategies lack exploration of emotional counteraction mechanisms, and it remains unclear how II affects conditioned fear extinction and return. Moreover, traditional exposure therapy neglects patients' active coping strategies, while the strong CS-US association formed during fear memory creation causes intense fear responses to CSs during early extinction. Forming II allows individuals to formulate goal-directed responses with less effort and higher efficiency \cite{Chen et al., 2021; Hallam et al., 2015} to actively cope and promote behavioral automation, offering potential to overcome traditional therapy limitations. Against this background, this study innovatively uses II to induce self-directed, non-verbal/non-behavioral anger expression, examining how emotion-countering II affects conditioned fear extinction and return. Specifically, the II instruction states: "If I feel afraid when seeing fish and bird pictures (the CS+ and CS− in this study), then I'll feel stupid for fearing an animal picture, and I'll clench my fists and feel very angry with myself, very angry!!" The core innovation is its "conditional triggering" mechanism: anger induction strictly depends on immediate fear perception of the CS (animal pictures). When no fear is felt, anger is not triggered. This design significantly reduces ethical risks of traditional anger induction (e.g., aggressive behavior) and meets clinical safety requirements.

Through this anger-countering II, we aim to prompt individuals to re-evaluate threat (recognizing actual safety) when encountering CSs, automatically activating safety responses, reducing fear impact, and promoting extinction training efficacy. Additionally, anger's aroused initiative and sense of power may enhance individuals' willingness and motivation to actively approach CSs, further strengthening intervention effects. Ultimately, combining anger-countering II with extinction training may achieve dual intervention on fear responses and fear memories, more comprehensively alleviating excessive fear reactions.

2 Methods

2.1 Participants

The study aimed to compare II and control conditions with repeated measures at minimum two time points. Sample size was calculated using G*Power 3.1 software \cite{Faul et al., 2007}, setting a medium effect size of f = 0.25, Type I error probability α = 0.05, power 1 − β = 0.8, and medium correlation among repeated measurements = 0.5, yielding a required sample of 34. Considering high dropout rates in fear conditioning experiments, we recruited 49 university students through posters and voluntary enrollment, aged 18–25. Participants were required to attend sessions at approximately the same time for three consecutive days. All were right-handed, had no history of physical or mental illness, had normal or corrected vision, and had not participated in similar emotion experiments within six months. The study was approved by the Ethics Committee of the School of Psychology, Henan University (approval number: 20210923002). All participants presented ID to confirm they were at least 18 years old and signed informed consent. They were informed about the experimental procedures (including questionnaires and subjective ratings). Electric shocks were individually calibrated and strictly voltage-limited to cause no harm, with the option to reduce intensity or terminate if uncomfortable. All data were kept confidential, and participants were asked to keep experimental details private. Participants received monetary compensation, with possible increases based on engagement.

Participants were randomly assigned to two groups: Group 1, traditional extinction (control group, n = 25), and Group 2, implementation intention formation (II group, n = 24). Twelve participants were excluded from analysis: three failed category learning on Day 1 (two control, one II), eight withdrew due to shock intolerance or discomfort (four per group), and one control participant experienced equipment failure during Day 3 reinstatement. The final sample comprised 37 participants (control: n = 18; II: n = 19). The groups showed no significant differences in age, sex, trait anxiety, depression, or shock intensity (Table 1 [TABLE:1]).

2.2 Stimuli

Following previous research \cite{Kroes et al., 2017}, conditioned stimuli were fish and bird pictures. The study used 148 total pictures sourced from https://pixabay.com/zh/ and Baidu. One representative fish and one bird picture were used for subjective ratings (Figure 1 [FIGURE:1]C), while the remaining 73 fish and 73 bird pictures were used for training and testing. Each picture (1280×720, 96dpi, 24bit) was presented centrally on a 21-inch LCD monitor for 5 seconds. One category was followed by electric shock on 67% of trials (CS+), while the other was never paired with shock (CS−), with categories counterbalanced across participants. The unconditioned stimulus (US; electric shock) was delivered via a constant voltage stimulator (STM200-1, BIOPAC Systems, Inc.) to the left wrist to elicit fear responses. Each shock lasted 200 ms, with intensity individually calibrated based on each participant's tolerance. Before the experiment, participants rated shock discomfort on a 1–9 scale (1 = "not uncomfortable" to 9 = "unbearably painful"), with intensity set at the level rated as 8 ("extremely uncomfortable but tolerable") for the entire experiment.

2.3 Subjective Assessments

Subjective assessments for CS+ and CS− included (using bird pictures as an example, see Figure 1D): (1) US expectancy ("Please predict the likelihood that the bird picture will be followed by a shock") as a prospective index of associative memory, rated on a 9-point scale (1 = definitely not, 5 = uncertain, 9 = definitely); (2) CS-US association ("Based on previous learning, please recall how often bird pictures were followed by shock") as a retrospective index, rated 1 = never to 9 = always; (3) fear level ("Please rate your fear when seeing bird pictures," 1 = not at all fearful to 9 = extremely fearful); (4) anger level ("Please rate your anger when seeing bird pictures," 1 = not at all angry to 9 = extremely angry); and (5) avoidance distance from the CS, rated 1–9 (higher numbers = greater distance). US expectancy was rated before CS presentation; the other four were assessed before and after each learning phase. For items 1–4, the screen displayed probe text at the top, a representative bird/fish picture in the center, and a rating scale at the bottom. For item 5, the screen showed probe text at the top, the representative picture on the lower left, and a 1–9 number line on the lower right. Participants moved a blue figure representing themselves along the number line, with larger numbers indicating greater avoidance.

Shock discomfort was measured twice: after Day 1 acquisition (followed by II training in the II group) and after Day 3 reinstatement testing (following the four CS-related assessments). After Day 3 reinstatement, participants also recalled how many shocks followed each CS category on Day 1.

2.4 Physiological Recording

Skin conductance response (SCR) was recorded using two Ag/AgCl standard electrodes (8 mm diameter) filled with 0.05 M NaCl electrolyte, attached to the index and middle fingertips of the non-dominant hand. Signals were amplified by a Biopac® MP150 electrodermal activity amplifier (Biopac Systems, Inc., Goleta, California, USA). Raw signals were filtered with a 10 Hz low-pass filter, recorded at 5 μS/V resolution, and sampled continuously at 2000 Hz. Since fear and anger are defensive responses to threat marked by sympathetic nervous system activation \cite{Damasio & Carvalho, 2013}, their peripheral physiological responses show substantial overlap, including increased heart rate and blood pressure, elevated skin conductance, and vasoconstriction \cite{Stemmler et al., 2001}. Given that Day 2 extinction training comprised 48 trials and we expected no SCR differences between groups, SCR was only recorded during Day 1 acquisition and Day 3 reinstatement.

2.5 Procedure

The experiment was programmed and run using E-Prime 2.0 software across three days: Day 1 acquisition, Day 2 extinction, and Day 3 spontaneous recovery/reinstatement testing and picture recognition. Stimulus types, presentation durations, and inter-trial intervals were identical each day. The experimental design and procedure are illustrated in Figure 1.

Day 1 Fear Conditioning: After ID verification and informed consent, participants completed the State-Trait Anxiety Inventory (STAI) \cite{Spielberger et al., 1983}, Beck Depression Inventory (BDI) \cite{A. T. Beck et al., 1996}, Trait Anger Scale \cite{Tibubos et al., 2020}, and Intolerance of Uncertainty Scale (IUS) \cite{Buhr & Dugas, 2002}. After electrode attachment, shock intensity was calibrated (30–70 V range). Participants rested 4–5 minutes before viewing instructions stating that fish and bird pictures would appear and they should learn to predict shock likelihood. Acquisition used 15 unique fish and 15 bird pictures with a 2/3 reinforcement rate. The 1st, 3rd, 5th, 10th, and 12th CS+ trials were non-reinforced (pseudorandom). The first two trials were one CS− and one non-reinforced CS+ (order counterbalanced), with US expectancy rated before CS presentation. Remaining trials were divided into two blocks of 14 trials each (5 CS+-US, 2 CS+-no US, 7 CS−). The first two trials in each block included US expectancy ratings for CS− and CS+-no US; other trials had no US expectancy rating (Figures 1A and 1B). CS order was pseudorandom. After each block, participants recalled which picture category was followed by shock and completed CS-related assessments (association, fear, anger, avoidance), then rested 1–2 minutes. After acquisition, shock discomfort was rated. The control group then left, while the II group received 3 minutes of II training, silently rehearsing: "If I feel afraid when seeing fish and bird pictures, I'll feel stupid for fearing an animal picture, and I'll clench my fists and feel very angry with myself, very angry!!" They spent two minutes visualizing this scenario with eyes closed and were told the training was important for Day 2 and should be practiced mentally. Pre-training on Day 1 ensured the II would be automatic by Day 2.

Day 2 Fear Extinction: After 4–5 minutes of quiet sitting, all participants completed the four CS-related assessments to test whether Day 1 II training had created group differences. The control group then proceeded directly to extinction, while the II group first recalled the previous day's II statement and typed it into the computer. The correct II statement then appeared, and participants rated how closely their recall matched it. If subjective similarity was ≥5, they completed 3 minutes of II training; if <5, they completed 6 minutes. The extinction phase used 24 new fish and 24 new bird pictures, each repeated twice for 96 trials across three blocks. Each block pseudorandomly presented 16 CS+ and 16 CS− trials, all without shock (Figures 1A and 1B). As in acquisition, the first two trials per block were CS− and CS+ (order counterbalanced) with US expectancy ratings; the remaining 30 trials had no US expectancy ratings. CS order was pseudorandom. After each block, participants completed the four CS-related assessments, rested 1–2 minutes, then continued.

Day 3 Fear Recovery Testing: After 4–5 minutes of quiet sitting, participants first completed the four CS-related assessments as a spontaneous recovery test (SR) to evaluate Day 2 II training effects. They then received four unsignaled shocks (200 ms each) with 20, 30, 25, and 15 s inter-shock intervals. After a 10-minute rest, the reinstatement test began. This test comprised 9 trials, each starting with expectancy rating followed by CS presentation using 9 old pictures from Day 1 (5 CS−, 4 CS+ that had been paired with shock). The first trial was CS−, followed by two blocks of 2 CS+ and 2 CS− trials each, all non-reinforced. After each block, participants completed the four CS-related assessments; blocks had no inter-block rest. Following reinstatement, shock discomfort was rated and participants recalled shock frequencies for each CS category from Day 1. The few reinstatement trials assumed group differences would appear primarily in early trials, after which both groups would rapidly extinguish due to 96 extinction trials on Day 2. We were not concerned about post-reinstatement fear because the subsequent 136-picture recognition test would also promote extinction.

Day 3 Post-Reinstatement Recognition Test: After reinstatement, participants completed an unexpected recognition test, judging whether pictures were "old" (presented on Days 1–2) or "new" (never presented) to examine whether anger-countering II regulated fear automatically without increasing cognitive effort. For "old" pictures, participants pressed keys 1, 2, or 3 (lower numbers = more certain they had seen it); for "new" pictures, they pressed 4, 5, or 6 (higher numbers = more certain they had not). The test included 136 pictures (68 fish, 68 birds): 10 old from Day 1 (excluding reinstatement pictures), 24 old from Day 2, and 34 new pictures. Pictures were divided into six groups by novelty (Day 1 old, Day 2 old, new) and CS type (CS+, CS−), with pseudorandom group order ensuring no more than two consecutive pictures from the same group, though order within groups was random. Each picture was presented with a 1–6 novelty rating scale at the bottom; it disappeared after the keypress. Inter-trial intervals were 1 s red fixation points. After recognition, participants completed the four CS-related assessments, then were compensated. This procedure followed \cite{Kroes et al., 2017}.

The overall procedure is shown in Figure 3 [FIGURE:3]. Figure 1 shows the experimental design and flow: (A) trial structure with blue arrows marking the four CS-related assessments and red arrows marking II training; (B) block 1 flowcharts for Day 1 acquisition and Day 2 extinction (example with fish as CS+); (C) representative CS pictures for subjective ratings; (D) schematic for US expectancy (left), avoidance (center), and recognition (right) assessments.

2.6 Data Analysis

All analyses used SPSS 26.0. Continuous variables are presented as mean ± standard deviation (M ± SD). Between-group baseline differences (age, trait anxiety, etc.) were compared using chi-square (χ²) or Welch's corrected independent samples t-tests. Subjective assessment data (fear, anger, association, avoidance, US expectancy) across acquisition, extinction, spontaneous recovery, and reinstatement were analyzed using repeated-measures ANOVA with CS difference scores (CS+ minus CS−) as the dependent variable, testing group (II vs. control) × time point (block or test time) interactions and main effects. SCR and recognition test results were analyzed using two-way repeated-measures ANOVA with group (II, control) × CS (CS+, CS−). Significant interactions were followed by simple effects analysis with Bonferroni correction. Effect sizes are reported as partial η². Significance was set at α = 0.05 (two-tailed).

SCR data were analyzed using AcqKnowledge 4.2. Data were low-pass filtered (Blackman −92 dB, 1 Hz) \cite{Stussi et al., 2019}. SCR to each CS was calculated as the peak skin conductance difference (in microsiemens) within a 0.5–5.5 s window post-stimulus. Raw SCR values were square-root transformed to normalize distributions, then standardized by dividing by each participant's maximum SCR value that day to facilitate group comparison \cite{Scheuermann et al., 2025}.

3 Results

3.1 Control Variables

Groups showed no significant differences in sex ratio, age, state anxiety, trait anxiety, depression, intolerance of uncertainty, trait anger, US intensity, or US aversiveness (Table 1).

Table 1 Descriptive statistics for participant grouping and questionnaire data (M ± SD)

Variable II Group (n = 19) Control Group (n = 18) χ² / t Age (years) 20.74 ± 1.91 20.78 ± 2.02 STAI-S 42.95 ± 4.64 44.56 ± 4.22 STAI-T 45.74 ± 4.70 44.00 ± 3.63 BDI 37.21 ± 7.08 37.33 ± 8.16 IUS 19.84 ± 4.71 20.94 ± 4.61 Trait Anger 52.40 ± 4.75 54.71 ± 10.62 Shock Discomfort 7.53 ± 0.77 7.50 ± 0.79

Note: II = implementation intention group; STAI-S = state anxiety; STAI-T = trait anxiety; BDI = Beck Depression Inventory; IUS = Intolerance of Uncertainty Scale.

3.2 Subjective Assessments

CS difference scores (CS+ minus CS−) for fear, anger, association, avoidance, and US expectancy across phases are shown in Figure 2 [FIGURE:2].

Day 1 Fear Acquisition: Two-way repeated-measures ANOVA (group [II, control] × block [B1, B2]) on CS difference scores revealed no significant group main effects for any measure (fear: F(1, 35) = 0.041, p = 0.841; anger: F(1, 35) = 0.088, p = 0.769; association: F(1, 35) = 3.782, p = 0.06; avoidance: F(1, 35) = 0.952, p = 0.336; US expectancy: F(1, 35) = 0.564, p = 0.458). Block main effects were significant: all CS difference scores were higher in Block 2 than Block 1 (fear: F(1, 35) = 25.524, p < 0.001, η_p² = 0.465; association: F(1, 35) = 24.466, p < 0.001, η_p² = 0.422; anger: F(1, 35) = 30.448, p < 0.001, η_p² = 0.445; US expectancy: F(1, 35) = 24.356, p < 0.001, η_p² = 0.410; avoidance: F(1, 35) = 28.013, p < 0.001, η_p² = 0.410). No significant group × block interactions emerged (all ps > 0.147), indicating both groups successfully acquired conditioned fear without differences.

Day 2 Fear Extinction: Two-way repeated-measures ANOVA (group × time [preExt, B1, B2, B3]) on CS difference scores showed no significant group main effects for fear (F(1, 35) = 1.571, p = 0.218) or anger (F(1, 35) = 3.373, p = 0.075). However, the control group showed significantly higher association (F(1, 35) = 5.218, p = 0.029, η_p² = 0.128) and avoidance (F(1, 35) = 5.133, p = 0.030, η_p² = 0.124) than the II group, indicating that forming anger-countering II before extinction facilitated fear extinction and reduced CS+ avoidance. Time main effects were significant (fear: F(3, 105) = 38.151, p < 0.001, η_p² = 0.407; association: F(3, 105) = 69.916, p < 0.001, η_p² = 0.666; anger: F(3, 105) = 24.055, p < 0.001, η_p² = 0.212; avoidance: F(3, 105) = 9.415, p < 0.001, η_p² = 0.522). Bonferroni post-hoc tests showed all CS difference scores at extinction end (B3) were significantly lower than pre-extinction (preExt) (all ps < 0.007). No significant group × time interactions emerged for anger, association, or avoidance (all ps > 0.100). However, fear showed a significant group × time interaction (F(3, 105) = 4.933, p = 0.012, η_p² = 0.182). Simple effects analysis revealed no group differences at preExt or B1 (preExt: p = 0.328; B1: p = 0.088), but significant differences at B2 and B3 (both p = 0.038). The II group's fear difference scores were significantly higher at preExt than all later time points (all ps < 0.001), with no differences among B1, B2, and B3 (all ps > 0.218). The control group showed preExt > B2 and B3 (B2: p = 0.032; B3: p = 0.007), with no differences among later time points (all ps > 0.191). This indicates both groups expressed fear toward CS+ initially, but after extinction training, fear differences between CS+ and CS− decreased, with superior extinction in the II group.

Two-way repeated-measures ANOVA (group × block [B1, B2, B3]) on US expectancy difference scores revealed no significant group effect (F(1, 35) = 2.177, p = 0.149) or group × block interaction (F(2, 70) = 1.409, p = 0.251), but a significant block effect (F(2, 70) = 18.542, p < 0.001, η_p² = 0.346). Bonferroni tests showed US expectancy at B3 was significantly lower than B1 and B2 (both ps < 0.001), confirming successful extinction.

Day 3 Fear Return Testing: Two-way repeated-measures ANOVA (group × time [SR, B1, B2]) on CS difference scores showed the II group was significantly lower than controls on all four measures (fear: F(1, 35) = 6.540, p = 0.015, η_p² = 0.157; anger: F(1, 35) = 7.787, p = 0.008, η_p² = 0.182; association: F(1, 35) = 4.590, p = 0.039, η_p² = 0.116; avoidance: F(1, 35) = 6.000, p = 0.019, η_p² = 0.146). Time main effects were significant for fear (F(2, 70) = 3.661, p = 0.039, η_p² = 0.095) and association (F(2, 70) = 7.918, p = 0.001, η_p² = 0.178), marginally significant for anger (F(2, 70) = 3.650, p = 0.052, η_p² = 0.094), and non-significant for avoidance (F(2, 70) = 0.239, p = 0.747). Bonferroni tests showed fear and association difference scores at spontaneous recovery (SR) were significantly higher than at reinstatement end (B2) (both ps < 0.05). No significant group × time interactions emerged (all ps > 0.280).

Post-reinstatement US expectancy difference scores were analyzed with two-way repeated-measures ANOVA (group × trial [t1, t2, t3, t4]). A significant group effect emerged (F(1, 35) = 7.588, p = 0.009, η_p² = 0.178), with controls showing higher US expectancy than the II group. Trial effect was significant (F(3, 105) = 10.066, p < 0.001, η_p² = 0.223), with trial 4 lower than trials 1–3 (all ps < 0.029). No group × trial interaction was found (F(3, 105) = 1.892, p = 0.149). These results demonstrate that anger-countering II significantly reduces conditioned fear return.

3.3 Day 3 Unexpected Recognition Test

Group (II, control) × CS (CS+, CS−) ANOVA for recognition test showed no significant group effects (Day 1 pictures: F(1, 35) = 0.100, p = 0.921; Day 2 pictures: F(1, 35) = 0.007, p = 0.935; new pictures: F(1, 35) = 0.009, p = 0.923), CS effects (Day 1: F(1, 35) = 1.369, p = 0.25; Day 2: F(1, 35) = 0.488, p = 0.489; new: F(1, 35) = 2.193, p = 0.148), or interactions (Day 1: F(1, 35) = 0.049, p = 0.827; Day 2: F(1, 35) = 1.614, p = 0.212; new: F(1, 35) = 0.421, p = 0.521).

Figure 2 shows subjective assessment CS difference scores and Day 3 recognition results for II and control groups across phases: (A) fear, (B) anger, (C) CS-US association, (D) avoidance, (E) US expectancy, and (F) recognition test results. B1/B2/B3 = after block 1/2/3; preExt = before Day 2 extinction; SR = spontaneous recovery; B1t1/B2t1 = first trial of block 1/2; t1–t4 = reinstatement trials 1–4.

3.4 Physiological Indices

SCR results for acquisition and reinstatement are shown in Figure 3 [FIGURE:3].

Day 1 Acquisition: One control participant lacked SCR data. Two-way repeated-measures ANOVA (group × stimulus [CS+, CS−]) on the final acquisition trial revealed a significant stimulus effect (F(1, 34) = 15.256, p < 0.001, η_p² = 0.31), with higher SCR to CS+ than CS−. No group effect (F(1, 34) = 0.060, p = 0.808) or group × stimulus interaction (F(1, 34) = 0.064, p = 0.801) emerged.

Day 3 Reinstatement: Two-way repeated-measures ANOVA (group × stimulus) on the first reinstatement trial showed no significant stimulus effect (F(1, 35) = 0.542, p = 0.467), group effect (F(1, 35) = 0.213, p = 0.647), or group × stimulus interaction (F(1, 35) = 0.314, p = 0.579).

Figure 3 SCR results for control (Ctrl) and implementation intention (II) groups during fear acquisition and reinstatement.

4 Discussion

This study explored how forming anger-countering II before extinction training affects fear extinction and return. Results showed that during extinction, the II group had significantly lower CS-US association and avoidance tendency than controls. On Day 3, during both spontaneous recovery and reinstatement tests, the II group showed significantly lower subjective ratings on all measures (except US expectancy during spontaneous recovery). This indicates that forming anger-countering II before extinction facilitates fear extinction and reduces spontaneous recovery and reinstatement. However, as reported elsewhere \cite{Haesen & Vervliet, 2015; Scheuermann et al., 2025}, subjective and SCR measures dissociated: during Day 3 reinstatement, no significant group differences, CS differences, or group × stimulus interactions emerged in SCR. Possible explanations include: (1) High-intensity extinction training (96 trials: 48 CS+, 48 CS−) sufficiently weakened physiological fear responses. (2) Novelty of CS+ and CS− pictures masked differential fear responses. SCR is an autonomic index of novelty \cite{Zimmer & Richter, 2023}; although pictures were from Day 1, each was presented only once, 48 hours earlier, retaining strong novelty and orienting responses. (3) Strong physiological arousal from the four reinstatement shocks masked CS+/CS− differences. Regardless, equivalent SCR levels indicate that anger-countering II did not increase physiological arousal. From a strategy-user perspective, this is beneficial—it aligns with the "controlled," "non-cathartic" design, showing that using anger as a tool did not introduce unintended physiological stress or burden, supporting physiological homeostasis and avoiding "robbing Peter to pay Paul" side effects, thus enhancing clinical safety. However, from a researcher perspective, SCR's failure to reflect group differences evident in subjective reports highlights a methodological challenge: verifying through peripheral physiology that the paradigm successfully induced brief, conditionally triggered, goal-directed, controlled anger is extremely difficult. The core problem is that fear and anger both activate the sympathetic nervous system \cite{Damasio & Carvalho, 2013}, showing substantial peripheral overlap \cite{Stemmler et al., 2001}. This physiological similarity makes it nearly impossible to distinguish fear-related arousal from the specific anger designed in this study. Therefore, we relied primarily on verbal reports to confirm anger experience.

The II content—"If I feel afraid when seeing fish and bird pictures, I'll feel stupid for fearing an animal picture, and I'll clench my fists and feel very angry with myself, very angry!!"—aimed to induce anger and harness its energy to overcome fear and approach the actually safe CS+. According to MPMC theory, fear catalyzes anger \cite{Zhan et al., 2015, 2018}. At acquisition end, both groups reported high fear (II: 7.06; control: 7.26) and anger (II: 6.29; control: 5.95), leading us to expect stronger anger in the II group during extinction. Unexpectedly, after the first extinction block (16 CS+, 16 CS−), II group fear (3.53) and anger (3.00) toward CS+ had already dropped to low levels, and by Day 3, II group anger was significantly lower than controls. One possibility is that the instructions actually prompted cognitive reappraisal. The phrases "feel stupid" and "angry with myself" are information participants would want to avoid. Emotion can influence certainty and thus information processing \cite{Tiedens & Linton, 2001}: high-certainty emotions like anger and happiness increase heuristic processing by promoting schematic thinking and expert knowledge use, whereas low-certainty emotions like fear may reduce heuristic processing. Anger also stimulates shallow cognitive analysis and immediate action \cite{Parker & Isbell, 2010}. Thus, the self-esteem threatening and self-annoying content may have prompted participants to restructure the situation: "I'm facing just a fish or bird picture; fearing this harmless image is completely unnecessary," thereby disarming fear and reducing anger. This differs from previous II studies focusing on non-emotional reappraisal (e.g., "I won't feel disgusted; if I see blood, I'll take a doctor's perspective" \cite{Chen et al., 2020, 2021; Gomez et al., 2015; Huang et al., 2020} or "I won't feel disgusted; if I see blood, I'll view it as vitality" \cite{Ma et al., 2019}). Another possibility is that practicing the II during extinction induced anger that enabled brave CS confrontation without adverse consequences, promoting safety recognition, enhancing extinction, and weakening Day 3 fear return. The control group extinguished fear through safe CS repetition on Day 2, reducing anger, but fear return on Day 3 also caused anger return. Our results show that skillful anger utilization can reduce rather than increase anger while diminishing fear.

Previous research shows II formation enables automatic negative emotion regulation \cite{Azbel-Jackson et al., 2016; Chen et al., 2020, 2021; Gallo et al., 2009; Gomez et al., 2015; Hallam et al., 2015; Huang et al., 2020; Ma et al., 2019}. However, these studies have two key limitations: (1) Minimal time between II training and application, relying on averaged effects across many trials, leaving unclear when the automatic regulation process establishes (immediately vs. after practice) and how; (2) Few examined delayed effects. Our results provide new evidence: (1) Participants formed II after Day 1 acquisition and could recall it well, but Day 2 baseline assessments showed no group differences, indicating II did not take immediate effect. During extinction, groups remained similar through the first two blocks (48 trials), with II group showing significantly shorter CS avoidance only at the final block end (near trial 72). This suggests II's automatic regulation does not form immediately post-training but requires substantial practice, first manifesting in behavioral avoidance improvement. (2) Although no II training occurred on Day 3, the II group showed significantly lower fear, anger, avoidance, and threat expectancy during fear return testing, indicating that repeated practice during Day 2 extinction had automated the emotional regulation, producing robust delayed effects. (3) The recognition test showed no group differences, suggesting that while II formation and recall are cognitively demanding (conscious, explicit), the executed emotion regulation process itself is automatic and does not involve intentional regulatory effort toward emotional stimuli \cite{Chen et al., 2021; Gallo et al., 2009}. In summary, II initiation of target responses (e.g., emotion regulation) is not entirely "immediately automatic"—early execution may still require some cognitive engagement and multiple practice trials to become automated. This automation timeline may vary by task characteristics. Compared to weaker automatic responses in previous studies (e.g., disgust from blood pictures), the strong fear responses to CSs (fear of shock) in this study may require more practice for II to become effective.

The II group's shorter avoidance distance (lower avoidance tendency) during late extinction and fear return testing constitutes important behavioral evidence that II promotes fear extinction and reduces fear return. This has methodological significance. Traditional avoidance measurement uses: (1) No/low-cost avoidance tasks where participants press keys \cite{Klein et al., 2021} or use joysticks \cite{Glogan et al., 2023} to prevent US delivery; (2) Approach-avoidance tasks (AAT) where choosing CS+ may yield shock but wins rewards, while CS− avoids shock but loses rewards \cite{Berg et al., 2021; Pittig, 2019; Pittig et al., 2021}. Both have limitations: no/low-cost tasks often produce excessive avoidance even when ineffective \cite{De Kleine et al., 2023; Pittig & Wong, 2021}; costly tasks involve multiple motivational conflicts (approach reward vs. avoid fear) and individual differences in shock sensitivity and reward valuation, making "avoidance cost" vary across participants. Low-cost avoidance promotes avoidance and impairs extinction \cite{Rattel et al., 2017}, while high-cost avoidance drives reward approach, which may facilitate extinction if unshocked. Thus, avoidance cost indirectly affects extinction. Additionally, AAT choices evoke implicit agency (control over external events) \cite{B. Beck et al., 2017}, which itself can reduce fear \cite{Sugawara et al., 2022}. Using such tasks would confound whether extinction effects were due to II manipulation or reward reinforcement in the avoidance test. Moreover, both anger and rewards trigger approach behavior, making it difficult to disentangle their effects. To more directly measure avoidance tendency toward CSs while avoiding motivational conflict, cost differences, agency, and reward approach confounds, we modified previous avoidance paradigms \cite{Aupperle1}. We used a simplified number-line task retaining only the "avoidance" dimension. Participants moved a figure representing themselves along a 1–9 scale away from or toward the CS, with lower numbers indicating lower avoidance (greater approach willingness). This method stripped external reward/punishment associations, focusing on subjective avoidance of the CS itself. This approach clearly captured the II group's shorter avoidance distance during late extinction.

Although recent emotion-countering research exists, few have examined anger countering fear or treating PTSD symptoms, likely due to concerns about counterproductive effects. Anger countering fear may resemble a risky "fighting fire with fire" approach, but risky is not necessarily wrong. This study demonstrates that if individuals can be guided to use anger in a controlled, goal-directed manner, it may convert resistance into motivation, becoming an effective tool against fear and for restoring control. However, given anger's potential to trigger aggression, its use requires extreme caution. Research shows anger-PTSD links may be unique to impulsively aggressive individuals \cite{Teten et al., 2010}, trait anger is a PTSD risk factor \cite{McHugh et al., 2012}, and mediates PTSD's effect on aggression \cite{Bhardwaj et al., 2019}. Some propose that threat-related cognitive network activation strongly enhances anger in a positive feedback loop, and when combined with combat-related PTSD symptoms, inhibitory control over aggression is overcome, increasing violence \cite{Novaco & Chemtob, 2015}. Therefore, anger-based methods must be applied judiciously, considering the individual, context, and conditions. They should not be used indiscriminately. For individuals with high fear/avoidance but no anger symptoms who respond poorly to safe therapies, anger countering may be considered, with careful attention to induction method and intensity. For those with impulsive aggression, high trait anger, or specific populations (e.g., veterans), anger-based emotion regulation should be used cautiously to avoid potential harm. Given anger's complex role in fear-related disorders (both secondary symptom and independent risk factor), developing "personalized" interventions and targeted prevention programs is crucial \cite{Lonsdorf & Merz, 2017}.

To overcome limitations of physiological indices like SCR in distinguishing fear from specific anger states and to more comprehensively understand psychophysiological responses, future research should explore more specific measures such as heart rate variability, electromyography, and respiratory patterns, and utilize neuroscientific tools like functional near-infrared spectroscopy and fMRI to deeply explore how extinction training combined with cognitive reappraisal and II strategies affects neural activity, precisely describing the intervention's neural mechanisms. Combining these methods will enable more comprehensive, sensitive evaluation of II's functional effects in extinction training and precisely map the neural mechanisms of this anger-countering cognitive-emotion regulation strategy. This will not only advance fear extinction and emotion regulation theory but also provide more targeted, predictable biomarkers for clinical translation, guiding personalized treatment development. Additionally, \cite{Brewster et al., 2016} found that II can change behavior not only in specific situations but also in similar contexts. Recent work shows that II-based emotion regulation generalizes to target-related but unplanned situations, with broader target coverage increasing generalization \cite{Huang et al., 2020}. Future research should explore whether II's regulatory effects generalize to other conditioned stimuli and non-specific contexts. Meta-analyses show II formation helps people with mental health problems achieve various goals \cite{Toli et al., 2015}. Future studies should test whether forming anger-countering II can improve treatment outcomes for anxiety/fear disorder patients in CBT. Moreover, long-term follow-up studies assessing intervention durability are essential for validating clinical value, revealing potential delayed effects, change patterns, and influencing factors.

5 Conclusion

Forming anger-countering implementation intentions before extinction requires repeated practice to automatically initiate behavioral responses and can reduce fear reinstatement and avoidance tendency. This may offer new approaches for treating fear and anxiety-related disorders.

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Author Contributions

Hongbo Wang: Conceptualization, study design, data analysis, manuscript drafting, final revision.
Yingzhu Zeng: Study design, data collection, methods section drafting, final revision.