Emotion dysregulation (ED) is defined as patterns of emotional experience or expression that interfere with goal-directed behaviour [1]. ED is recognized as a core etiological and maintenance mechanism of borderline personality disorder (BPD) [2, 3]. Recently, ED has been found to be a key transdiagnostic mechanism of psychopathology involved in the development and maintenance of several psychiatric disorders, such as depression, eating disorders and complex post-traumatic stress disorder (cPTSD) [4, 5, 6, 7, 8]. Interestingly, in recent years, ED has also become a central area of research in autism spectrum disorder (ASD) [9, 10]. Indeed, findings support that ED is more prevalent in autistic people compared to the general population [9, 10, 11, 12]. Of particular importance, recent findings have reported a high prevalence of self-harm [13, 14, 15] and suicidality in ASD [16, 17, 18], particularly in autistic adults without intellectual disability presenting with high levels of ED [19, 20, 21]. Indeed, similar to findings in BPD and in the general population [14, 22], ED has been associated with self-harm with or without suicidal intent in ASD [19, 21]. Interestingly, akin to BPD [22], self-harm and suicidal behaviour have also been found to be strongly linked in ASD [14, 23]. This suggests that ED is a risk factor for suicidality and self-harm in ASD, and that autistic people may develop capability for suicide through self-harm [14, 23]. Autistic women in particular have been reported to be at greater risk of developing severe ED compared to autistic men [24, 25, 26], which suggests that gender-related factors might be involved in ED in ASD [27].
Few studies have focused on interventions targeting ED in autistic adults. Pharmacological treatments have shown limited effectiveness in this context [28]. Therefore, there is a critical need to develop psychological interventions targeting ED in autistic people given the multitude of downstream effects on adaptive functioning and quality of life [29]. Interventions based on cognitive behavioural therapy (CBT) have shown encouraging outcomes [30]. This is particularly the case for dialectical behaviour therapy (DBT) [31, 32], the most studied treatment targeting ED in BPD [33, 22]. Recently, DBT has proved to be feasible and acceptable in autistic adults without intellectual disability, as well as potentially effective to reduce ED in the presence of self-harm and suicidal behaviour [31, 32].
Linehan’s biosocial theory, which underlies DBT, conceptualizes that biological and environmental factors in childhood are involved in the emergence of ED in BPD [33]. According to this theory, ED emerges from an interaction between: (a) emotional vulnerability that stems from biological factors impacting the functioning of brain areas (e.g., prefrontal regions and amygdala) involved in emotional processing, and (b) an invalidating environment that refers to chronic and inadequate responses of the environment to the emotional needs of the child (i.e., neglect, minimization or punishment, including physical and sexual abuse) [22, 33]. Temperamental impulsivity has been subsequently added to the model as an additional risk factor for BPD [22, 34]. According to Linehan, invalidation early in life maintains and may exacerbate the pre-existing biological vulnerability in the child [33]. It also shapes maladaptive coping responses, such as using self-harm with or without suicidal intent when experiencing emotional pain [22, 35]. Most empirical findings support the relevance of Linehan’s model to conceptualize ED in BPD [e.g., 36,37,38,39,40].
Although DBT has been adapted to and studied in clinical conditions other than BPD [e.g., 41,42,43], few studies have focused on the pertinence of Linehan's biosocial model to conceptualize ED beyond BPD. Nevertheless, there are findings that support the implication of emotional vulnerability [44], including temperamental impulsivity [45], and invalidation (e.g., childhood maltreatment) [46, 47, 48] in the development of ED across psychopathology.
In ASD, studies investigating the factors involved in the emergence of ED have mainly focused on ASD-related particularities (e.g., social cognition peculiarities, sensory sensitivity, cognitive inflexibility) [9, 49] and the role played by co-occurring disorders (e.g., anxiety, depression) [11, 20, 50, 51, 52]. Thus, to our knowledge, there is a lack of comprehensive models which integrate biological and psychosocial factors potentially involved in the emergence of ED in ASD [e.g., 21,53,54,55].
Based on the existing literature, including Mazefsky and White’s model for ED in autistic youth [49], we recently proposed an application of Linehan’s biosocial model to ED in ASD [56] to provide a comprehensive conceptualization of the biosocial factors (i.e., emotional vulnerability and invalidating environment) involved in the emergence of ED in ASD. More specifically, we considered the interplay between ASD traits and both emotional vulnerability and the experience of invalidation. Indeed, in addition to the biological vulnerability similar to that found in BPD (i.e., hypersensitivity, hyperreactivity and slow return to emotional baseline) [57], ToM peculiarities, sensory sensitivity, lack of cognitive flexibility, change-related anxiety and repetitive behaviour have been associated with ED in ASD [49, 11]. Alexithymia, prevalent in ASD, has also been reported to be linked to ED in autistic adults [20], especially in autistic women [27]. Moreover, ASD-related difficulties seem to interfere directly with the ability to self-regulate [10, 11, 49], but also contribute to high levels of anxiety and fatigue making emotion regulation costly for autistic people [11, 49, 58]. In terms of invalidating experiences, autistic children are highly exposed to different early stressful and traumatic experiences (e.g., physical and emotional maltreatment from caregivers and school bullying), because of their atypical functioning that cause misunderstanding and rejection from others [59, 60, 61]. Autistic girls seem to be particularly vulnerable to the experience of adverse events [62, 63]. Among other environmental factors potentially involved in the emergence of ED, lack of parental scaffolding and modeling (i.e., support provided by the parent to help the child regulate their emotions) have been pinpointed as risk factors for dysregulated behaviour in autistic youth [64, 65]. Additionally, recent studies have reported that autistic camouflaging, i.e., behaviour and/or strategies used to appear “less autistic”, is associated with lifetime suicidality, especially in autistic women [66, 67, 68]. Given this, our extension of the biosocial model to ASD includes excessive autistic camouflaging as a form of self-invalidation resulting from internalized invalidation from others [69].
The application of Linehan’s model to ASD requires an empirical test of its validity as well as an assessment of its specificity to ED in ASD, particularly in comparison with BPD. The latter point is crucial given that ED is highly associated with BPD [70] and that individuals with BPD may exhibit ASD-like traits that may lead to misdiagnosis with ASD [71]. For instance, some studies found that individuals with BPD might also have sensory sensitivity and social cognition peculiarities [72, 73]. Despite the overlap between ASD and BPD, studies comparing ED and its etiological factors in ASD and BPD are lacking.
The aim of the current study is to evaluate the relevance and the specificity of factors involved in Linehan’s model applied to ED in ASD [56]. To do so, autistic adults without intellectual disability (ASD group), adults with BPD (BPD group), and adults without any known diagnoses (nonclinical controls group; NC group) completed a battery of self-report scales measuring the model’s components and indicated the occurrences of the ED behavioural correlates (i.e., hospitalizations, self-harm and suicidal behaviour). We did not assess parental scaffolding as relevant measures are observational in the context of child-parent interaction [64, 74]. Specifically, we were interested in the characteristics of ED and its behavioural correlates in each clinical group. Given that ED is a core feature of BPD and that self-harm and suicidal behaviour are strongly associated with BPD [2, 3, 22], we hypothesized that ED and its behavioural correlates would be higher in the BPD group compared to the ASD group, whereas both clinical groups would have heightened ED scores compared to the NC group (H1). In addition, since self-harm has been associated with ED in BPD [22] and ASD [14, 20], we expected to find an association between self-harm and suicidal behaviour in both groups (H2). We also expected ED to be a predictor of the presence of self-harm and/or suicidal behaviour in both clinical groups (H3). Moreover, we hypothesized that ED would be heightened in the BPD group compared to the ASD group, whereas both clinical groups would have higher ED scores compared to the NC group (H4). Additionally, in the autistic group only, we expected to observe gender differences, with autistic women presenting with higher ED than autistic men (H5) [27]. Regarding the predictors of ED, we hypothesized that emotional vulnerability, impulsivity and invalidation – which are direct measures of the biosocial model – would predict ED in both clinical groups, but ASD-related factors would be specific predictors of ED in the ASD group compared to the BPD group (H6). To assess the specific load of the predictors of ED, machine learning (ML) models were used, and we expected emotional vulnerability and invalidation to emerge among the largest contributors of ED in both clinical groups, while ASD-related factors were expected to rank among the largest ED predictors for the ASD group only (H7).