Personality and Anxiety
Anxiety is a negative affective state that occurs in response to perceived threat and includes an attentional bias toward potential threat, physiological responses including sympathetic nervous system activation, and action-tendencies motivated to cope with the negative affect and/or threat cues. Trait anxiety is a disposition to experience frequent anxious states.
Anxiety can be characterized as a collection of subjective experiences, physiological responses, and motivated action-tendencies that occur in response to the perception of a threatening stimulus. Subjectively, anxiety involves heightened negative affect, attentional biases toward threat, and a future-oriented state that may prepare a person to respond to negative events (Barlow 2000). Physiologically, anxiety includes heightened sympathetic nervous system activity prompted by activation of the behavioral inhibition system (BIS; Gray and McNaughton 2000), a neurobiological structure that may in part underpin individual differences in personality. A variety of action tendencies may arise in the context of an anxious state, including overt behavioral avoidance of the threatening stimulus, as well as cognitive responses such as worry or problem-solving. While this collection of experiences composes an anxious state, anxiety can also be understood from a personality perspective, in which trait anxiety refers to a disposition to experience state anxiety (Spielberger 1966, 1985). This review will briefly describe the role of anxiety across various models of temperament and personality, identify factors hypothesized to contribute to the development of anxiety, and discuss the relationship between anxiety and psychopathology, with a specific focus on the development and maintenance of anxiety and related disorders.
Anxiety Within Contemporary Models of Personality
While an exhaustive review of anxiety’s position within the various theories and models of personality is beyond the scope of this review, a brief review of the role of anxiety in three contemporary models of personality and temperament is in order.
Reinforcement Sensitivity Theory (RST). Reinforcement sensitivity theory (RST; Gray and McNaughton 2000) is a neurobiological model of personality that suggests individual differences in personality can be understood in terms of three distinct affective-motivational neural systems. The fight-flight-freeze system (FFFS) activates in response to perceived threat and is experienced as fear; the behavioral approach system (BAS) motivates reactions to reward and is associated with positive affect and extraversion; and the behavioral inhibition system (BIS) is responsible for resolving conflict between goals. In this model, BIS activation is subjectively experienced as anxiety and results in the inhibition of prepotent responses and the initiation of risk assessment processes (Gray and McNaughton 2000). The BIS is hypothesized to be distributed across several neural structures that are hierarchically organized, including the periaqueductal gray, medial hypothalamus, amygdala, septo-hippocampal system, posterior cingulate, and the prefrontal dorsal stream. The personality dimension of trait anxiety has been suggested to be underpinned by individual differences in the BIS, and the symptom structure and prospective risk factors for anxiety disorders are largely consistent with predictions based on RST (see Zinbarg and Yoon 2008). Together, the three systems of RST are suggested to underlie the two higher-order affective dimensions of positive and negative affect, with more frequent activation of FFFS and BIS resulting in more negative affective states.
Big Two Dimensions of Temperament. Considerable empirical research supports the existence of two broad dimensions of affective experience, positive affect (PA) and negative affect (NA; Watson and Tellegen 1985). Anxiety is a lower-order facet of NA, a broad temperamental dimension that is attributable in part to biological factors, is present early in life, and exhibits substantial temporal stability (Clark and Watson 1999). Given that anxiety is a NA state, NA explains considerable variance in anxious symptomology (Watson et al. 1988), as well as a range of clinical constructs relevant to the development and maintenance of anxiety disorders, such as anxiety sensitivity, rumination, and perfectionism (see Watson et al. 2006). Further, NA is important in understanding broadband trait models of personality, as it has been suggested to be fundamentally equal to neuroticism (Barlow 2000; Watson and Clark 1992; Watson et al. 2006).
Five-Factor Model. The five-factor model (FFM; see McCrae and John 1992), the personality taxonomy that has received the most empirical attention over the past several decades, emphasizes five broad trait dimensions: extraversion, agreeableness, conscientiousness, neuroticism, and openness. Anxiety is considered a lower-order facet of neuroticism, or the tendency to experience negative affective states. Similar to studies on NA, a wealth of empirical research supports the association between neuroticism and difficulties with effective coping (Watson and Hubbard 1996), as well as the fear/distress cluster of psychopathology (Kotov et al. 2010; Lahey 2009).
Taken together, these models of temperament and personality may build off one another, in that the neurobiological systems postulated in RST may give rise to the higher-order affective dimensions of temperament, which in turn may form the basis of broadband personality traits outlined in taxonomies such as the FFM. Accordingly, the dimension of anxiety is well-represented in each model.
Biological and Environmental Contributors to Anxiety
Research from the field of behavioral genetics and elsewhere has demonstrated support for the genetic basis of NA/neuroticism broadly and anxiety specifically. Results from twin studies suggest heritability estimates of NA/neuroticism generally are in the range of 0.40–0.60, indicating that 40–60% of the variance in these traits can be accounted for by genetic contributions (Clark and Watson 1999). Further, research in the field of developmental psychology has shown that children can be categorized based on temperamental differences very early in life, again speaking to the notion of temperament as being attributable to innate biological factors. This line of research has demonstrated that behaviorally inhibited children, who exhibit an anxious temperament characterized by timidity around people, objects, and unfamiliar situations, are more likely to develop anxiety disorders years later (Schwartz et al. 1999) as well as exhibit increased amygdala activation in response to novelty as adults (Schwartz et al. 2003). Overall, research supports the biological origins of anxiety. Considerable variance in NA/neuroticism is explained by genetic factors, and early temperamental profiles that are likely largely influenced by biology exhibit both long-term stability and predictive validity regarding outcomes associated with anxiety.
While behavioral genetic research consistently demonstrates the genetic underpinnings of anxiety, heritability estimates simultaneously demonstrate that approximately 40% to 60% of NA/neuroticism is likely also determined by environmental factors. Early stressors and trauma have been linked to increased anxious apprehension and other negative affective states in both animals and humans (Barlow 2002). Further, frequent and recurrent anxiety has been linked to early experiences that promote a diminished sense of control (Barlow 2002). For example, an external locus of control (i.e., decreased perceptions of personal control and agency) was found to mediate the relationship between a family environment that promotes limited control over one’s environment and later anxiety in childhood (Chorpita et al. 1998). Together, early experiences may give rise to a sense that the world is unpredictable and uncontrollable, resulting in more frequent and intense experiences of anxiety (Barlow 2000).
Anxiety and Psychopathology
The biological and environmental contributors to anxiety have been suggested to be part of a group of diatheses that confer vulnerability for the development of anxiety and related disorders. In the triple vulnerability model developed by Barlow (2000, 2002), three interacting but distinct vulnerabilities contribute in the etiology of anxiety disorders. The generalized biological vulnerability refers to a relatively nonspecific genetic contribution to stable dispositions of heightened anxiety and NA/neuroticism; and the generalized psychological vulnerability includes early life experiences such as adverse childhood events and learning histories that promote a limited sense of control over one’s environment, which further increase anxiety and NA/neuroticism. While the combined diathesis of these vulnerabilities may heighten risk for depressive disorders or generalized anxiety disorder, a third vulnerability factor, known as a specific psychological vulnerability, is posited to result in focused anxiety on an object, event, or internal state and accounts for the expression of specific anxiety and related disorders. For example, in the context of combined generalized biological and psychological vulnerabilities, early learning experiences that teach an individual that physical sensations are dangerous and unpredictable may result in the development of later panic disorder (Barlow 2000, 2002).
Beyond the triple vulnerability model, trait anxiety has consistently demonstrated associations with a range of psychological constructs and mechanisms purported to underlie psychopathology. To illustrate, three constructs warrant specific review, as they are central to our understanding of various forms of psychopathology. Worry, which involves future-focused thoughts and images that are negatively affective laden, is present across all anxiety disorders and is a core process of generalized anxiety disorder. Not surprisingly, frequency of worry is significantly elevated among participants classified as high in trait anxiety (Eysenck and Van Berkum 1992), and self-reported worry exhibits moderate to strong correlations with self-report measures of anxiety (Molina and Borkovec 1994). Next, experiential avoidance, defined as the unwillingness to experience private events and engage in efforts to escape, avoid, or minimize these events, is a pathological process that underlies a range of psychological disorders (Hayes et al. 1996) and has been suggested to be a core vulnerability factor in the development of psychopathology (Kashdan et al. 2006). Across samples and measures, experiential avoidance exhibits moderate to large associations with trait anxiety, neuroticism, and negative affectivity (Boelen and Reijntjes 2008; Gámez et al. 2011). Finally, emotion dysregulation refers to difficulties with the experience, expression, and modulation of emotional responses (Gratz and Roemer 2004) and is a putative transdiagnostic risk factor across diverse forms of psychopathology (Kring and Sloan 2009). Numerous studies have demonstrated associations between trait anxiety and various emotion regulatory deficits across clinical and non-clinical samples (Cisler et al. 2010; Mennin et al. 2005). In sum, while the scope of this review is necessarily limited, anxiety is clearly inextricably linked with a range of psychological constructs and processes that are critical to the development and maintenance of psychopathology.
Since the days of Freud, anxiety has been a central component of theories of personality and psychopathology. While often described as a transient state-like experience, decades of empirical research support the notion that anxiety is also an individual difference variable, reflecting an enduring disposition to experience anxious states. Neurobiological accounts of personality describe the structures of the behavioral inhibition system (BIS) as the neural substrates of anxiety; variation in the BIS and other systems give rise to the higher-order dimension of negative affectivity; and negative affectivity encompasses a core dimension of personality (i.e., neuroticism) in major trait models of personality such as the FFM. Trait anxiety (and its higher-order factors of NA/neuroticism) is in part genetically determined, demonstrating stability over time, and research across the fields of developmental, personality, and clinical psychology has begun to elucidate relevant environmental contributors. Further, elevations in anxiety and NA/neuroticism are considered personality characteristics that are important in understanding the onset and maintenance of anxiety and related disorders. Whether the discussion be the biology of personality, the traits and affective experiences common to all people, or dimensions of personality that predict psychopathology, anxiety is central to the conversation.
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