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KeywordsIrritable Bowel Syndrome Negative Emotion Generalize Anxiety Disorder Personality Disorder Social Anxiety Disorder
The tendency to experience frequent and intense negative emotions accompanied by a perceived inability to cope with such experiences.
Temperament has been broadly described as an individual’s enduring emotional nature (Shiner et al. 2012). Neuroticism, one dimension of temperament, is defined as the tendency to experience intense negative emotions accompanied by aversive reactions to these experiences when they occur (such as a sense of uncontrollability or perceived inability to cope; Sauer-Zavala and Barlow 2014). Compared to other temperamental traits, neuroticism has received the most empirical attention, likely due to its association with a variety of psychological and physical health concerns. Previously thought to be a stable part of one’s character, there is increasing evidence to suggest that neuroticism is more malleable than previously thought, underscoring exciting developments in the treatment of common mental health conditions.
The term neuroticism was first coined by Eysenck (1947) to describe the temperamental tendency to experience frequent and intense negative emotions in response to various sources of stress. This trait has primarily referred to anxious or depressed moods, but also includes other negative emotions such as fear, irritability, and anger. Additionally, individuals high in neuroticism often demonstrate aversive reactions to their emotional experiences, which typically include efforts to suppress or control these feelings (e.g., avoiding public speaking because one finds public speaking anxiety provoking and experiences this anxiety as aversive; Barlow et al. 2014b).
The origin of the word neuroticism lies in the psychoanalytic term, neurosis, used to describe psychopathology without delusions or hallucinations. Specifically, Freud (1924) differentiated between objective anxiety signaling, an immediate threat, and neurotic anxiety, a continual state of distress stemming from the unsuccessful use of defense mechanisms (i.e., repression of early traumatic experiences). Later, the early founders of the Diagnostic and Statistical Manual of Mental Disorders (DSM), the classification system for psychological disorders used in the United States, adopted this term to refer to what we now consider to be anxiety, depression, and related disorders. Using “neuroticism” to describe classes of psychopathology has largely fallen into disuse with the field focusing more on discrete diagnostic labels (e.g., generalized anxiety disorder, panic disorder). Instead, the term is now used interchangeably with other constructs that highlight the experience of negative emotions, including negative affect/affectivity, negative emotionality, and negative affect instability (Miller and Pilkonis 2006). Today, neuroticism is considered an important dimension of personality and is represented in most models of personality, including the well-known three-factor and five-factor models.
The Development of Neuroticism
There is empirical evidence to suggest that temperament arises from interactions between genetic, biological, and environmental factors over time (Shiner et al. 2012). Barlow et al. (2014a) formulated a model to describe the development of neuroticism that takes these factors into account. Broadly, this model posits that neuroticism results from a generalized biological vulnerability and a generalized psychological vulnerability.
The generalized biological vulnerability refers to genetically inherited risk, as well as the specific neurobiological functioning associated with neuroticism. There are high heritability estimates for this trait (40–60%), suggesting that the tendency to experience negative emotions is passed down in families (e.g., Bouchard and Loehlin 2001). This heritability translates to greater amygdala excitability coupled with reduced inhibitory control by prefrontal structures (Westlye et al. 2011). The amygdala is considered an emotion-generating area of the brain, whereas the prefrontal structures provide impulse and emotion-regulatory control. Thus, the aforementioned combination can result in an individual generating negative emotions frequently and/or intensely while encountering difficulty exerting executive control over their regulation.
This generalized biological vulnerability interacts with a general psychological vulnerability to perceive the world as uncontrollable combined with the belief that one would be unable to cope with any negative outcomes that arise (Gunnar and Quevedo 2007). Basic animal and human research supports the contribution of perceived lack of control in the development of neuroticism. For example, animal and human subjects placed in uncontrollable environments (i.e., where food or punishment is distributed at irregular intervals) tend to show higher levels of negative emotions and anxious behaviors such as increased autonomic arousal or excessive motor activity (for review, see Barlow et al. 2014a). Similarly, individuals with higher external loci of control (i.e., people who believe that their life is controlled by external factors such as the environment or fate) are more likely to score higher on measures of neuroticism (e.g., Wiersma et al. 2011).
Early adversity and parenting styles have also been shown to influence children’s perceptions of control, thereby affecting their propensity to experience negative emotions. For example, parents who consistently and warmly respond to their children provide a sense of predictability in the environment. On the other hand, negative parenting behaviors, notably abuse or neglect, are associated with higher levels of neuroticism potentially because they create an environment of unpredictability or even punishment. Other parenting styles such as overprotectiveness can also contribute to neuroticism by modeling to children that emotions are dangerous and the child requires protection from experiencing them. Importantly, these early learning experiences can lead to changes in brain functioning, creating a feedback loop in which the generalized biological vulnerabilities are sensitized. That is, early adversity can augment amygdala hyperexcitability and reduced prefrontal control (Barlow et al. 2014b).
Association of Neuroticism with Physical and Mental Illness
Given neuroticism’s association with a wide range of physical and mental health concerns, the public health implications of this trait have begun to draw attention (for review, see Lahey 2009). In terms of physical health, patients high in neuroticism are more likely to report a variety of somatic complaints, including cardiovascular disease, asthma, and irritable bowel syndrome (Frølund Pedersen et al. 2016). In one study, individuals higher in neuroticism showed greater reactivity to daily stressors, which was associated with increased risk of having a chronic physical health condition at a later point in time (Piazza et al. 2013). Further, in the context of chronic diseases and cancer, neuroticism is a strong predictor of clinical deterioration and mortality. Taken together, there is accumulating evidence to suggest that neuroticism is associated with the onset, maintenance, and deterioration of a wide range of physical health problems (for review, see Lahey 2009).
Additionally, neuroticism is associated with the presence of a number of mental disorders including mood, anxiety, somatoform, psychotic, eating, substance use, and personality disorders. Further, neuroticism has been shown to predict the onset of mental disorders with the most research support drawing temporal links between high levels of neuroticism and the subsequent development depressive and anxiety disorders (for review, see Lahey 2009; Zinbarg et al. 2016). Also of note, comorbidity or co-occurrence of these disorders is common; estimates suggest that up to 55% of patients with a mood or anxiety disorder meet criteria for an additional disorder at the same time. Research indicates that higher levels of neuroticism are related to greater comorbidity among these disorders (Brown and Barlow 2009; Zinbarg et al. 2016).
There is increasing evidence to suggest that the comorbidity among common mental health conditions might be accounted for by a common, core underlying process (Brown and Barlow 2009). A functional model of anxiety, depressive, and related disorders (emotional disorders; Barlow 1991) that implicates neuroticism as a key, transdiagnostic risk factor has been articulated (Barlow et al. 2014b). In this model, emotional disorders are characterized by the frequent and intense experience of negative emotions and aversive reactions to this experience (neuroticism) combined with efforts to escape or avoid these emotional experiences. Paradoxically, such efforts tend to reduce distress in the short-term but lead to rebound effects that increase the experience of negative emotions in the long term (Sauer-Zavala and Barlow 2014). The symptoms of anxiety, depressive, obsessive-compulsive, trauma-related, and bipolar disorders, as well as borderline personality disorder, have all been conceptualized within this framework (Sauer-Zavala and Barlow 2014). Given that neuroticism has been implicated as a transdiagnostic risk factor for a range of psychopathology, it raises the question of whether this trait, itself, could be a target of intervention.
Malleability of Neuroticism
Despite longstanding beliefs that personality traits are stable and inflexible across time (APA 2013), there is increasing evidence that neuroticism may be more malleable than previously thought. For example, longitudinal studies of the general population show gradual age-related decreases in neuroticism and related constructs that continue into old age (Eaton et al. 2011). Interestingly, data indicate that these changes are largely idiosyncratic, with great variability in the degree of change over time (Helson et al. 2002). Specifically, individuals with higher initial levels of neuroticism tend to show less change in this trait over time, and conversely, individuals with lower initial levels of neuroticism tend to evidence greater change (Brown 2007).
Studies evaluating movement on neuroticism among individuals with DSM disorders, over time or in response to treatment, have demonstrated mixed results. For example, Eaton et al. (2011) found that neuroticism remained relatively stable in a sample of individuals with depressive disorders. Additionally, neuroticism did not appear to change significantly following a course of treatment with dialectical behavior therapy for individuals with borderline personality disorder (Davenport et al. 2010). In contrast, Brown and Barlow (2009) found that, among individuals engaged in psychological treatment, DSM-IV disorder constructs (social anxiety disorder, generalized anxiety disorder, and depression) improved significantly over time while other temperamental variables (e.g., extraversion) remained stable; neuroticism, however, evidenced the greatest amount of temporal change among such variables and was associated with the largest treatment effect.
Additionally, as high neuroticism is necessary for the development of a range of common mental disorders, one would expect that this trait would vary in accordance with the onset or remission of symptoms. In fact, a number of longitudinal studies have found that neuroticism independently predicts anxiety and mood, even when taking into account the periodic occurrence of anxious or depressive symptoms (Lahey 2009). Further, while neuroticism predicts the course of DSM anxiety, mood, and personality disorders, with higher levels of this trait reflecting less change in symptoms across time, the converse does not appear to occur; that is, initial levels of DSM disorders do not predict changes in temperament over time (Warner et al. 2004).
The aforementioned research raises questions about the mechanisms through which neuroticism changes and whether directly targeting this trait in treatment would lead to more definitive results, rather than addressing DSM disorder symptoms. Indeed, recent research in this area suggests that change in neuroticism is greater with interventions explicitly designed to target this trait. The psychopharmacology literature hosts the majority of studies directly aimed at addressing temperament. Specifically, serotonergic drug agents (i.e., selective serotonin reuptake inhibitors) hold promise in reducing neuroticism (for review, see Ilieva 2015).
In addition to pharmacological agents, behavioral interventions have also been developed to target temperament. First, an intervention designed to address behavioral inhibition (elevated distress in novel situations) in children was successful in preventing the onset of future anxiety and related disorders (Rapee et al. 2005). Additionally, a modified, intensive version of the program for higher risk children demonstrated changes in behavioral inhibition (Kennedy et al. 2009). Findings from Rapee et al. (2010) further suggest that interventions targeting temperament might produce an increasing trajectory of change in temperament with time, at least in children. Second, a pilot study by Armstrong and Rimes (2016) evaluated a modified mindfulness-based cognitive therapy (MBCT) intervention designed to specifically target levels of neuroticism. They incorporated language surrounding neuroticism-related constructs, rather than depression-related themes, and demonstrated significantly greater reductions in neuroticism than participants in an intervention that did not specifically target this trait (Armstrong and Rimes 2016). Third, the Unified Protocol for transdiagnostic treatment of emotional disorders (UP) is a cognitive-behavioral treatment for emotional disorders that was explicitly developed to address neuroticism, given its implication in the development and maintenance of these disorders (Barlow et al. 2011). The UP consists of six core treatment modules explicitly designed to extinguish distress in response to the experience of frequent, strong emotions. By doing so, dependency on maladaptive emotion regulatory strategies is reduced, which in turn leads to less frequent and less intense negative emotions over time (see Barlow et al. 2014b; Sauer-Zavala and Barlow 2014). This approach has shown efficacy for the range of anxiety and unipolar depressive disorders (e.g., Barlow et al. in preparation), and there is also preliminary support for the use of the UP with bipolar disorder (Ellard et al. 2012) and posttraumatic stress disorder (PTSD; Gallagher 2015). This growing body of literature suggests that interventions designed to target neuroticism directly may be an effective way of capitalizing on its malleability in the service of improving individuals’ health outcomes.
Neuroticism has a rich history in psychology. After drawing a great deal of attention in 1940s, it faded to the background for some time and is now regaining prominence, notably in the realm of clinical psychology. A better understanding of the nature of this trait, as well as its malleability, is contributing to exciting developments in understanding the etiology and treatment of many psychological disorders.
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