Affect dysregulation has been defined in two distinct ways (Paivio & Laurent,
2001; Taylor, Bagby, & Parker,
1997; Van Dijke,
2008; Van Dijke, Ford, et al.,
2010). In the borderline personality disorder (BPD) literature, affect dysregulation refers to a deficiency in the capacity to modulate affect such that emotions become uncontrolled, expressed in intense and unmodified forms, and overwhelm reasoning (Koeningberg et al.,
2002; Zittel Conklin, Bradley, & Westen,
2006; Zittel Conklin & Westen,
2005). These problems have been described as under-regulation of affect and include extremely intense affective distress (e.g., overwhelming rage or fear) and affectively driven behavioral disinhibition (e.g., impulsivity, aggression). Under-regulation of affect has been shown to be a common and potentially severe sequela of childhood sexual (Carey, Walker, Rossouw, Seedat, & Stein,
2008; Putnam,
2003), physical (Dodge, Lochman, Harnish, Bates, & Pettit,
1997; Ford et al.,
2000), and emotional (Goldsmith & Freyd,
2005; Teicher, Samson, Polcari, & McGreenery,
2006) abuse.
In the somatoform disorder (SoD) literature, affect dysregulation has been referred to as alexithymia (Waller & Scheidt,
2004,
2006). Alexithymia, generally understood as “no words for feelings,” encompasses: (a) difficulty identifying emotions, (b) difficulty describing emotions to others, (c)
pensée opératoire, and (d) limited imaginal capacity (e.g., Sifneos, 1973). Alexithymia has also been shown to be associated with a history of childhood abuse (Bermond, Moormann, Albach, & Van Dijke,
2008; Greenberg & Bolger,
2001; Moormann, Bermond, & Albach,
2004; Moormann, Bermond, Albach, & Van Dorp,
1997; Paivio & Laurent,
2001). In addition to involving an inhibition of the cognitive capacity to differentiate and articulate affects, alexithymia also tends to involve a suppression or numbing of affect that may be considered a form of over-regulation of affect. In posttraumatic stress disorder (PTSD; Lanius, Vermetten, et al.,
2010; Lanius, Frewen, et al.,
2010), complex PTSD (
Şar, 2011), and in SoD and BPD (Van Dijke, Ford, et al.,
2010), over-regulation of affect may represent a sub-type that is associated with negative symptoms of somatoform and psychoform dissociation (e.g., Van Dijke, Van der Hart et al.,
2010).
Affective disruptions including under-regulation and over-regulation of affect are at the heart of disturbances stemming from childhood victimization (Cook et al.,
2005; Ford,
2005), especially when this involves a caretaker (Freyd, DePrince, & Gleaves,
2007; Paivio & Laurent,
2001). Adults who have experienced childhood victimization consistently are found to be at risk for problems with under-regulation of affect, but over-regulation of affect also may be a clinically important sequela of childhood interpersonal trauma. For example, Marx and Sloan (
2002) found that among survivors of child sexual abuse, over-regulation and under-regulation of affect were significantly related to psychological distress. However, over-regulation (but not under-regulation) mediated the relationship between child sexual abuse status and distress, indicating that over-regulation also may be influential in the development of psychological symptoms in child sexual abuse survivors.
Childhood traumatization is known to be associated with psychiatric disorders such as BPD (Yen et al.,
2002; Zanarini, Yonge, & Frankenburg,
2002), SoD (Brown, Schrag, & Trimble,
2005; Teicher et al.,
2006), and dissociative disorders (Nijenhuis, Van der Hart, Kruger, & Steele,
2004; Roelofs, Keijsers, Hoogduin, Näring, & Moene,
2002; Şar, Akyuz, Kugu, Ozturk, & Ertem-Vehid,
2006).
Although contemporary researchers consider the causal association between child abuse and psychiatric disorders to be an oversimplification (e.g., Van der Kolk et al.,
1996), sexual, physical, and emotional abuse have been hypothesized to be important etiological contributors to BPD (Bradley, Jenei, & Westen,
2005), SoD (Brown et al.,
2005), and dissociative disorders (e.g., Roelofs et al.,
2002; Şar & Ross,
2006). However, relatively little is known about how child abuse contributes to the etiology of these psychiatric disorders (Verdurmen et al.,
2007). One possible factor contributing to the association of child abuse with subsequent BPD and SoD is affect dysregulation. Therefore, the present study investigated the relationship of childhood victimization and both forms of affect dysregulation in adults diagnosed with BPD, SoD, and comorbid BPD and SoD.
Childhood traumatization for which the primary caretaker was the agent has been hypothesized to have special importance in the etiology of severe psychiatric disorders (Allen,
2001). Caretaker-caused traumatic stressors are likely to occur in and contribute to result in a relational growth-inhibiting early environment in which caretakers not only play less with the infant but also evoke stress (in the case of an abusive caretaker) or fail to protect the child from post-traumatic states of enduring negative affect (Fonagy, Gergely, Jurist, & Target,
2002; Lieberman,
2007; Lieberman & Amaya-Jackson,
2005). In addition, the caretaker might provide insufficient protection against other potential abusers of the child (Lieberman,
2007). The caretaker also often is inaccessible and reacts unattuned and/or with rejection to the infants’ expressions of emotions and stress. Therefore, the caretaker shows minimal or unpredictable participation in the various types of arousal regulating processes (Lyons-Ruth, Dutra, Schuder, & Bianchi,
2006). Instead of modulating extreme levels of stimulation and arousal, the infant and caretaker tend to experience high levels of arousal episodically when abuse has occurred and/or low levels of arousal when neglect has occurred. If interactive repair from a caretaker is not available or responsive to the infant, intense negative states can persist and be experienced by the infant as unmanageable. Until these states subside, the infant must devote most or all of their available biological and affective resources to withstand this state of distress and dysregulation (Tronick & Weinberg,
1997). Thus, the combination of the psychobiological challenge posed by traumatic stressors and the absence of consistent and effective co-regulation by a responsive available caretaker might compromise the child's capacity to regulate excessive levels of high and/or low arousal negative affect; and, when this persists in early development, it may result in persistent problems with under- or over-regulation of affect in adulthood.
Although theory and research have emphasized the adverse impact of caretaker-related abuse that occurs in the earliest years of development, abuse or neglect by primary caretakers that occurs later in childhood or adolescence also may have detrimental effects. Prospective (Dodge, Pettit, Bates, & Valente,
1995) and retrospective (Teicher et al.,
2006; Zinzow et al.,
2009) studies of emotional, physical, and sexual abuse have found evidence of deleterious effects on functioning, mental health, and health in the aftermath of abuse in the school years and adolescence. However, studies that systematically examined the relationship between a history of exposure to traumatic stressors for which a primary caretaker is the agent
at differing developmental epochs with psychiatric and psychosocial morbidity were not found. Therefore, in the present study, trauma by a primary caretaker is assessed in each of three developmental epochs, early childhood (ages 0–6 years old), middle childhood (ages 7–12 years old), and adolescence (ages 13–18 years old). We hypothesized that trauma by a primary caretaker would be associated with particularly severe under-regulation of affect in adults diagnosed with BPD and over-regulation of affect in adults diagnosed with SoD. We also hypothesized that these relationships would be strongest when trauma by a primary caretaker occurred during early childhood, compared to middle-childhood or adolescence.