Informed by the conceptual model of risk proposed by Svirko and Hawton (2007) (3) and Claes and Muehlencamp (2014) (2), this study examined a novel socio-cognitive-emotional model of NSSI and ED symptoms in a clinical ED and community group. Our model provided a good fit to the data in the clinical ED sample, but a poor fit in the community sample, suggesting the model does not generalise across groups, or the spectrum of severity for EDs and NSSI. For the community sample only a revised model, which included several additional pathways (e.g., anxious attachment to affect dysregulation and self-esteem, and maladaptive Cluster C schemas directly to NSSI), achieved an acceptable fit. Therefore, the initial proposed model required an increased complexity to account for the correlations between ED and NSSI symptoms in a community sample. The significance of predictors differed between the clinical ED group and the community sample, with affect dysregulation being a unique contributor for NSSI in both the ED and community groups. The only shared factor for NSSI and bulimic symptoms found for the community, but not the ED sample, was impulsivity.
Unique and shared predictors for NSSI, bulimia, and drive for thinness
We found that affect dysregulation was a unique predictor for NSSI, but not bulimia or drive for thinness in both the ED and the community groups. Several studies have also revealed positive associations between NSSI and anxiety and depression, often regarded as proxies for affect dysregulation, in ED patients (5, 32). Claes et al. (2010) (5) for instance reported that affect dysregulation was the primary motivation for all types of NSSI in EDs except bruising. Regarding community samples, a study using path analysis found that emotion dysregulation predicted positive and negative affect after engaging in NSSI. However, positive, not negative affect was responsible for more subsequent lifetime NSSI behaviours (33). These findings indicate that future studies would benefit from assessing the distinctive roles of both negative and positive affect in predicting NSSI. Finally, in terms of the previous models that assessed parts of our proposed model, Muehlenkamp et al. (2012) (34) also revealed that NSSI was related to depression through dissociation, whereas disordered eating was motivated by body dissatisfaction.
Contradicting previous studies, which have suggested that disordered eating may also function to regulate emotions (35), in the current study affect dysregulation was not related to any of the ED symptoms. This finding might be because the measurement of affect dysregulation in the current study was more general and not specific to regulating body image dissatisfaction, which may explain why it was not a significant predictor in our path-analyses. Overall, our findings indicate that a more general emotional risk factor (i.e., affect dysregulation) may be related explicitly to NSSI in EDs, but that this factor may not be sufficiently body focused to influence ED behaviours.
Surprisingly, impulsivity was a significant unique predictor of NSSI, and it was also a shared factor for bulimic symptoms and NSSI in the community, but not in the ED group. While this finding partially supports the findings of previous non-clinical ED population studies, which revealed positive correlations between NSSI, impulsiveness, and eating pathology (36), it contradicts other studies that have reported shared contributing factors for impulsivity and NSSI in clinical ED patients, especially in binge/purging ED subtypes (1). The non-significant finding for impulsivity for the ED group might be attributable to the mainly restrictive symptomatology (i.e. AN-Restrictive) present in this group (37). It is also worth noting that apart from impulsivity being shared between NSSI and bulimic symptoms in the community group, no other shared factors between NSSI and ED symtpoms were observed.
In the community group schemas relating to Cluster C personality disorders, were directly associated with NSSI. This finding is consistent with the findings by Anderson et al. (2018) (4), which revealed that experiential avoidance, a proxy for Cluster C personality disorders, was the most influential contributing factor to NSSI in their community sample. Insecure attachment may lead individuals to be socially avoidant, and steer away from close involvement with others to protect themselves against anticipated rejection, which then contributes to the adoption of maladaptive coping strategies, such as NSSI, to manage these difficulties (38).
As regards to the ED related outcome variables, our findings indicated a direct relationship between impulsiveness and body dissatisfaction for bulimic symptoms, for the ED and community groups. Furthermore, for the community sample, self-esteem was also a significant predictor for bulimic symptoms. This finding is in accordance with other studies that have shown impulsiveness, low self-esteem and body dissatisfaction to be important triggering and maintaining factors for bulimic symptoms in both clinical (14) and community (39, 40) samples.
Finally, we observed that low self-esteem and body dissatisfaction were related to drive for thinness in the ED group, which is in line with previous research (41). However, for the community group, the only significant direct contributor to ED symptoms was body dissatisfaction. Overall body dissatisfaction appears to be the most significant factor for ED symptoms in both the clinical ED and community sample, a finding that has been supported by a previous meta-analysis of risk factors for EDs (40).
Variance accounted for in NSSI, bulimia and drive for thinness.
Results showed that our model explained a higher amount of variance for NSSI, bulimia and drive for thinness than previous studies (4, 34). This was the case for the models assessing the ED and the community samples. The variance explained for NSSI in our path-analyses was 29% for the ED group and 24% for the community group. For the ED outcome variables, the variance ranged from 33% for bulimic symptoms and 57% for drive for thinness for the ED group. For the community group, these values ranged from 39% for bulimic symptoms to 51% for drive for thinness. Our percentages are almost double the amount of variance explained for by NSSI and ED symptoms in other studies (4). Therefore, including insecure attachment and early maladaptive schemas in our model appears to enhance our understanding of the processes underlying ED symptoms and NSSI.
Despite our model accounting for significantly more variance in our primary outcome variables than other studies, a large amount of variance was still unexplained. Future studies should examine important predisposing factors including aversive childhood experiences, family characteristics (e.g., parenting styles) as well as more immediate emotional (e.g., dissociation) and cognitive (e.g., need for control) variables that have been outlined in the original theoretical models of the co-occurrence of ED symptoms and NSSI (2, 3). However, increased complexity in our theoretical understanding of these processes comes with increased statistical complexity, which makes model fitting extremely difficult.
Indirect effects of insecure attachment and maladaptive schemas
In the current study, the mediation analyses revealed that both anxious and avoidant attachment were related to both NSSI and ED symptoms through maladaptive Cluster C and B schemas as well as the emotional variables (e.g., impulsivity, affect instability, self-esteem). This finding indicates that early in illness progression, there may be a range of general risk factors that relate to both NSSI and ED symptoms. However, as the illness progresses, associations may become narrower and more specific, which can be seen in the fact that apart from impulsivity in the community sample, no other immediate factors were shared between NSSI and ED symptoms. This notion is in line with staging models for mental illnesses such as psychosis (42) and more recently also EDs (43).
NSSI and ED symptoms frequently occur in interpersonal contexts (44, 45). Caregiver neglect and traumatic events during childhood are influential risk factors for NSSI behaviours in ED populations (12, 20, 46). These difficult early experiences can lead to the development of insecure attachment styles, which manifest as either avoidant or anxious forms of attachment (47). Attachment difficulties may predispose an individual to fear negative social evaluation (9), including schemas related to Cluster B (e.g., emotional deprivation) and Cluster C (e.g., failure) personality disorders (48). In adulthood, these core beliefs remain dormant until they are activated by situations or life events that are relevant to that specific schema (13). These factors may then become central in triggering both ED and NSSI symptoms through other emotional and body image-related variables, and inevitably serve to maintain both problem sets.
Our findings may be considered in the context of the study's limitations. First, as the data is cross-sectional, future research may benefit from the use of longitudinal designs, which may include constructs such as attachment and schemas earlier in life. It is also important to highlight that our model tested for independent associations for NSSI and ED symptoms. If a variable accounted for some common, shared variance between NSSI and ED symptoms, this was unfortunately not captured by our current model. It is for instance possible that ED symptoms lead to NSSI, as individuals try to find an alternative coping style to ED behaviours or struggle with associated shame and distress. The idea that NSSI and ED symptoms may be more causally linked in this way, could not be considered in the current study due to the cross-sectional data.
Second, the ED sample differed in terms of illness status, with 35% of the sample already recovered from their ED, which may have affected our results. A mixed sample between current and recovered ED samples is common in ED populations that have not exclusively been ascertained from a tertiary setting. These studies have commonly referred to lifetime, rather than current ED statuses (49). It is also worth acknowledging that some of the current traits (i.e., attachment. impulsivity) are considered to be endophenotpyes, that have been found to be elevated, even after the recovery from an ED (50).
Third, due to the small sample size for the different ED subdiagnoses, we were not able to assess different models for ED subtypes. Future research may consider the use of a more balanced ED sample with equal distribution of participants across all ED subtypes, to determine any existing differences in the variables of interest between ED subtypes.
Fourth, the model is limited to females living in Australia, and we, therefore, do not know whether our findings are generalisable to males and individuals from other countries.
Finally, there are limitations in the conceptualisation of the model such that the current variables may not fully explain the variance in NSSI and ED symptoms indicating other contributing factors. Future research may, therefore, continue to assess variables related to both problem behaviours, including other variables that have recently been implicated in both ED and NSSI, such as rejection sensitivity (51), social rank (52), and alexithymia (53).
Withstanding these limitations, the proposed conceptual model is the first model assessing a wide range of interpersonal, cognitive, and emotional factors known to be associated with both NSSI and ED, in an ED as well as a community sample.
The current findings highlight the importance of screening for NSSI within clinical ED populations, and for clinicians to formulate the overlapping and distinct processes which contribute to both problem sets. Knowledge of the shared contributing factors between EDs and NSSI as well as the functional role self-harm and disordered eating may serve for individuals, may contribute to improved clinical decision-making regarding treatment and support. Specifically, those presenting with comorbidity may benefit from treatments that target both ED and NSSI symptoms such as dialectical behavioural therapy (54), schema therapy (24), interpersonal therapy (55), and emotion regulation training programs (56)]. Finally, there is the need to address the role of insecure attachment, both through the prevention of insecure attachment and maladaptive schemas using early intervention parenting programs (57), as well as fostering secure attachment for those already engaged in therapy. The results also highlight the importance of identifying those risk factors more pertinent for individuals with less severe disordered eating such as those participants within the community, to identify where to target prevention strategies.