Symptoms of anxiety commonly co-occur in autism spectrum disorder (ASD) adding extra burden to people already suffering from this condition. According to Bejerot, Eriksson, and Mörtberg (2014), close to 50 percent of people diagnosed with ASD have reported significant levels of anxiety, which affects their day-to-day functioning. Even in cases where anxiety occurs independent of other conditions, it is strongly associated with poor quality of life. Therefore, when it co-occurs with ASD, the resulting problems are compounded, specifically affecting the socio-cognitive functioning of the affected individuals. Consequently, it is important to investigate the underlying factors that link anxiety to ASD and develop effective interventions.
Current research on this topic has highlighted some of the underlying emotional and cognitive mechanisms that could explain the strong relationship between anxiety and ASD including emotional acceptance, alexithymia, and intolerance of uncertainty (IU) (Maisel et al., 2016; Herrington, Miller, Pandey, & Schultz, 2016; South & Rodgers, 2017; Swain, Scarpa, White, & Laugeson, 2015).
Specifically, IU has been shown to be a transdiagnostic predisposing factor for the development of various anxiety disorders (Maisel et al., 2016) and in children suffering from ASD, it is a mediating factor between anxiety symptoms and ASD (Boulter, Freeston, South, & Rodgers, 2014). A theory-driven model could be used to understand the emotional and cognitive mechanisms that link anxiety symptoms to ASD. The aim of this paper is to review the available literature on the cognitive and emotional factors that mediate anxiety symptoms in people with ASD, specifically focusing on IU, alexithymia, and emotional acceptance.
Understanding Anxiety in ASD
Robust theoretical frameworks have been put forward to understand the unusually high co-occurrence of anxiety and ASD. The different underlying mechanisms could be investigated to understand why and how anxiety symptoms are common in people with ASD. However, given the complexity of anxiety and heterogeneity of autism, establishing the nature of this relationship has been problematic. Nevertheless, research studies have emerged in the recent past to address this problem using theoretical and clinical models. Some studies have investigated brain morphology and found out that the amygdala may play a critical role in the presentation of anxiety symptoms in ASD (Gibbard, Ren, Skuse, Clayden, & Clark, 2018; Weston, 2018; Herrington et al., 2016).
Other studies have focused on different emotional aspects that could trigger anxious tendencies in ASD, especially how such individuals handle threatening situations (South & Rodgers, 2017; Maisel et al., 2016; Boulter et al., 2016; Swain et al., 2015). Specifically, the role of IU, poor emotional avoidance, and alexithymia has been studied extensively and the available literature shows that these emotional and cognitive conditions have mediating effects in the occurrence of anxiety in ASD.
The Role of Emotional Regulation (ER) in Anxiety Symptoms in ASD
According to White et al. (2014), anxiety is essentially an emotional response having both physiologic and affective aspects. Therefore, the ability to control and regulate one’s emotions plays a central role in determining whether anxiety symptoms will present in ASD. ER allows individuals to control both experienced and expressed emotions to achieve a set goal. However, “impoverished ability to cope with and control intense, especially negative, emotions is associated with a range of psychiatric conditions and symptoms” (White et al., 2014, p. 22). This assertion could easily explain the almost ubiquitous occurrence of anxiety with ASD because studies have shown that ER impairments are some of the common characteristics of ASD (Mazefsky & White, 2014; White et al., 2014).
The ability to control or regulate emotions is different from experiencing the same emotions. For example, people can cope with anxiety associated with public speaking by affirming to themselves that the audience is made up of individuals with the same fears and life concerns. The ability to apply this coping mechanism is a key determinant of whether someone will handle emotions effectively. In other words, emotional experience happens automatically and people have little control over it, but ER is a set of strategies that can be used as coping mechanisms to down-regulate negative emotions.
However, in people with ASD, ER capabilities are impaired leading to emotional dysregulation. The inability to regulate emotional responses has been associated with reduced activity or functioning of the amygdala (Gibbard et al., 2018; Weston, 2018; Herrington et al., 2016). White et al. (2014) add that one of the explanations that account for impaired ER leading to elevated levels of anxiety in ASD is that people with this condition may “experience heightened levels of basal or reactive arousal.
Arousal is regulated by connections between the reticular formation in the brainstem and the limbic system, including the amygdala and the thalamus and parietal lobes” (p. 25). Therefore, based on the arguments made in this section, it is clear that emotional dysregulation plays a central role as a causal factor of anxiety in ASD. The next section uses the available literature to establish the link between anxiety and ASD focusing on IU, alexithymia, and poor emotional avoidance as the underlying mechanisms.
According to Cameron, Ogrodniczuk, and Hadjipavlou (2014), alexithymia is a mental condition characterized by having challenges with identifying or describing someone’s emotions. Another definition of the terminology would be the lack of emotional awareness due to limited cognitive processing of emotions (Ogłodek, Szota, Just, Araszkiewicz, & Szromek, 2016; Poquérusse, Pastore, Dellantonio, & Esposito, 2018). The etiology of alexithymia is unknown but people suffering from it have difficulties with introspection, may not differentiate emotions from bodily sensations and they struggle to explain their emotions to third parties.
Some of the risk factors for the development of this mental condition include genetics, environmental conditions, and brain injuries even though as mentioned earlier, the real clinical causes have not been identified. In addition, its role as a causative factor of anxiety in ASD is still unknown. However, different studies have shown a high prevalence of alexithymia in ASD (Poquérusse et al., 2018; Maisel et al., 2016) and robust evidence linking this condition with various other cognitive and social impairments associated with ASD (Bernhardt et al., 2014; Kinnaird, Stewart, & Tchanturia, 2019), leads to the conclusion that alexithymia might be strong mediating factor between anxiety symptoms in ASD cases.
A study by Maisel et al. (2016) found that when the core symptoms of autism (restricted behaviors and poor social skills) are not considered, an increase in the levels of alexithymia would directly cause a concomitant elevation in the levels of anxiety symptoms in people with ASD. This phenomenon could be explained by the argument that when individuals have difficulties identifying and describing their emotions, which is the effective definition of alexithymia, such emotions may become overwhelming or frightening, thus arousing anxiety. Therefore, alexithymia, which is a common occurrence in ASD, forms the nexus between anxiety symptoms and ASD.
Swain et al. (2015) made similar conclusions by linking emotional dysregulation with elevated cases of anxiety in ASD. Even in cases where anxiety occurs independent of ASD, emotional dysregulation has been shown to lead to increased symptoms of anxious feelings (Swain et al., 2015). Therefore, given that emotional dysregulation is one of the socio-cognitive factors contributing to alexithymia (Poquérusse et al., 2018; Ogłodek et al., 2016), it explains the strong link between alexithymia and anxiety in ASD as observed in the Swain et al. (2015) study.
Intolerance of Uncertainty (IU)
IU is a term used to describe the inability or decreased thresholds for the understanding of ambiguity (South & Rodgers, 2017). This condition is commonly associated with increased levels of anxiety symptoms and other related conditions, such as ASD and depression. In recent studies, it has been demonstrated that IU and anxiety co-occur in individuals suffering from ASD (Boulter et al., 2014; Neil, Olsson, & Pellicano, 2016). Specifically, in their study, Boulter et al. (2014) propose a causal meditational model whereby IU directly mediates the relationship between ASD and anxiety symptoms.
Together with anxiety disorder, IU has been shown to be the underlying factor behind the co-occurrence of difficulties in sensory processing and repetitive tendencies, which characterize ASD (Wigham, Rodgers, South, McConachie, & Freeston, 2015). In a study to understand the mediating effects of IU between anxiety and ASD, Maisel et al. (2016) found out that entering IU as the only explanatory variable in a study model resulted in increased levels of anxiety in individuals with ASD. However, the mechanism through which IU leads to anxiety symptoms in ASD has not been studied conclusively.
Dar, Iqbal, and Mushtaq (2017) conducted a study to specifically understand the underlying aspects that directly link IU with anxiety symptoms in ASD. This study found out that persons with IU are highly predisposed to worry, which contributes directly to anxiety (Dar et al., 2017). In other words, people that are intolerant to uncertainty find ambiguous situations to be frustrating and nerve-wracking, which ultimately leads to anxiety. Consequently, such individuals live in constant fear worried about meeting an ambiguous situation and ultimately they become more stressed in the attempt to avoid uncertainty.
However, other studies (South & Rodger, 2017; Maisel et al., 2016) have shown that IU is a common characteristic of ASD independent of anxiety. Several aspects should be considered at this point to understand the anxiety-IU-ASD matrix. First, Dar et al. (2017) have already established that IU is the main cause of worry, which leads to anxious thoughts and tendencies. Second, Maisel et al. (2016) and South and Rodger (2017) have shown that IU does not depend on its co-occurrence with anxiety to exert its effects on ASD. Therefore, it follows that IU, as a significant symptom of ASD, causes anxiety in people with ASD. This realization explains why Boulter et al. (2014) propose a causal meditational model with IU being a direct mediator between anxiety and ASD.
Emotional acceptance is the ability to discern and accept one’s internal emotions and experiences to be as they are without necessarily denying or silencing them by assuming that they do not exist (Maisel et al., 2016; Rodgers & Ofield, 2018). However, according to Yorke et al. (2018), individuals with ASD, especially children, have impaired psychological mindedness hence the inability or reduced capacity to accept their emotions as they are without denial. Even in cases where ASD is not a factor, the failure to acknowledge and embrace one’s internal emotional states leads to elevated anxiety cases.
Therefore, given that people with ASD already have socio-cognitive impairments, the problem of poor emotional acceptance is compounded. A study by Dan-Glauser and Gross (2015) sought to investigate the role of therapy targeting mindfulness in alleviating anxiety. The results showed that as participants increased their ability to focus on their inner thoughts and feelings through mindfulness, some symptoms associated with anxiety started to disappear (Dan-Glauser & Gross, 2015). These findings underline an important relationship between emotional acceptance and anxiety in ASD.
Different studies have indicated that poor emotional acceptance is a common occurrence among people with ASD regardless of whether they have signs of anxiety or not (Swain et al., 2015; South & Rodgers, 2017). This assertion underscores the mediating effects of poor emotional acceptance between anxiety disorder and ASD. Poor emotional acceptance presents in ASD cases then contributes directly to anxiety symptoms. This observation explains why increasing mindfulness capability through therapy to allow individuals to accept their emotions leads to decreased symptoms of anxiety. Studies have been conducted to prove this theory by showing that mindfulness techniques alleviate the overall state of ASD by reducing anxiety (Mazefsky & White, 2014; Kiep, Spek, & Hoeben, 2014).
Therefore, this model could be used to explain the emotional and cognitive mechanisms that contribute to the strong relationship between ASD and anxiety symptoms. Nevertheless, while poor emotional acceptance, IU, and alexithymia are some of the underlying mediating causes of anxiety in ASD, it is important to understand the underlying neural, socio-cognitive, and emotional mechanisms that contribute to the same as explained in the next section.
The Amygdala Factor
Different theories and neurological explanations have been put forward to explain the mechanism through which emotional and cognitive mediating factors function to contribute to anxiety symptoms in ASD. A study by Herrington et al. (2016) sought to establish the role of the amygdala function in explaining how social, cognitive, and emotional deficits relate to anxiety in ASD. The study found a strong positive correlation between anxiety and ASD caused by social cognition impairments. Herrington et al. (2016) argue that abnormal amygdala function is one of the most important (if not the only one) neurobiological markers of ASD.
Therefore, studies to assess the role of the amygdala in ASD have been conducted, specifically focusing on the deficits in social cognition and other related attributes due to decreased amygdala activity (Gibbard et al., 2018; Weston, 2018; Herrington et al., 2016). Results from these studies show that diminished amygdala function directly causes social intelligence deficits and perceptions, especially in ASD cases.
However, these studies do not establish a clear link between reduced amygdala activity and anxiety in people with ASD. Nevertheless, the relationship between the two – reduced amygdala function (hence deficits on social cognition) and anxiety can be understood using arguments made earlier in this paper backed with several studies. For instance, alexithymia, IU, and poor emotional acceptance have been shown to be mediating factors between anxiety and ASD (Poquérusse et al., 2018; Maisel et al., 2016; Bernhardt et al., 2014; Kinnaird et al., 2019; Swain et al., 2015; Boulter et al., 2014; Neil et al., 2016; Wigham et al., 2015; Dar et al., 2017; Yorke et al., 2018).
However, other studies have shown that reduced function of the amygdala causes poor social cognition (Gibbard et al., 2018; Weston, 2018; Herrington et al., 2016). Therefore, the reduced amygdala function leads to poor emotional acceptance, IU, and alexithymia (social cognition deficits), which in turn cause anxiety in ASD. It is important to note that these social cognition impairments can exist in ASD independent of anxiety disorder. Therefore, using this evidence, the relationship between the amygdala function and anxiety symptoms in ASD becomes clear.
In this review, some of the underlying cognitive and emotional factors that contribute to the high prevalence rates of anxiety disorder in ASD. Specifically, it has been shown that the mechanism underlying emotional regulation plays a central role in the presentation of anxiety symptoms in ASD. Reduced function of the amygdala causes impaired socio-cognitive capabilities, which in turn affects the capability to regulate emotions. It has also been shown that conditions associated with emotional regulation impairments, such as IU, alexithymia, and poor emotional acceptance, exist in ASD independent of anxiety.
The available literature indicates that IU, alexithymia, and poor emotional acceptance lead to elevated levels of anxiety even in the absence of ASD. Therefore, it suffices to argue that emotional regulation impairments cause anxiety. Consequently, it follows that the link between anxiety and ASD is the presence of emotional dysregulation, which is a common characteristic of IU, alexithymia, and poor emotional acceptance. These factors are the main mediating factors between anxiety symptoms and ASD as shown throughout this literature review.
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