Sensitivity to punishment and low maternal care account for the link between bulimic and social anxiety symptomology

Abstract

Objective

The current study examined the joint effect of personality and parenting factors on the prediction of bulimia nervosa (BN) and social anxiety disorder (SAD) symptomology in a sample of female college students. The study also tested whether personality and parenting factors might account for the association between BN and SAD symptoms.

Method

One-hundred twenty-eight participants completed self-report measures assessing maternal care (MC), maternal overprotection, sensitivity to punishment (SP), sensitivity to reward (SR), and BN and SAD symptomology.

Results

SP, SR, and MC each uniquely predicted BN symptoms, whereas only SP and MC predicted SAD symptoms. High SP interacted with low MC to predict BN and SAD symptoms over the main effects. In addition, SP, MC, and the interaction term SP x MC mediated the association between SAD and BN symptoms.

Conclusion

High SP and low MC appear to account for the link between BN and SAD symptomology, whereas high SR appears to distinguish the disorders.

Introduction

Research studies consistently find that individuals with bulimia nervosa (BN) exhibit elevated rates of anxiety disorders (Bulik et al., 1997, Kaye et al., 2004). This is especially true for social anxiety disorder (SAD; Bulik et al., 1997, Godart et al., 2000), a chronic and debilitating anxiety disorder characterized by excessive fear of social and performance situations (American Psychiatric Association, 2000). For example, Godart et al. (2000) reported that 59% of a sample of BN patients also met criteria for comorbid SAD, and several other studies have reported similar rates of comorbity (e.g., Bulik et al., 1997). Despite the fact that personality and parenting factors are consistently associated with both BN and SAD, no research to date has examined if these factors might account for the link between the two disorders. The objective of the current study was to fill this gap in the literature and to examine the joint effect of personality and parenting factors on the prediction of BN and SAD symptomology.

Exposure to adverse parenting has long been considered a potential risk factor for psychopathology (e.g., Bowlby, 1977). Among the many adverse parenting factors that have been examined, low levels of care and high levels of overprotection appear to be key child-rearing dimensions related to the development of psychopathology (Parker, Tupling, & Brown, 1979). Low care refers to a parental-rearing style characterized by rejection, coldness, and a lack of affection on the part of a parent, whereas overprotection refers to a parental-rearing style characterized by excessive control, intrusiveness, and little or no encouragement of autonomy on the part of the parent (Parker et al., 1979). There is some evidence which suggests that BN and SAD individuals retrospectively report low levels of care and high levels of overprotection during childhood and adolescence, although some of the evidence has been mixed.

For example, Palmer, Oppenheimer, and Marshall (1988) reported that BN patients recalled less warmth and empathy (i.e., lower care) from both parents in comparison to controls, but did not differ from controls in their recall of parental overprotection. Similarly, Calam, Waller, Slade, and Newton (1990) reported that BN patients recalled both parents as being lower on care than did controls; however, this study also reported that BN patients recalled their fathers—but not their mothers—as having been high on overprotection as well. In contrast, Kendler, Myers and Prescott (2000) reported that only maternal coldness (i.e., low maternal care) was associated with an increased odds ratio for BN among a large sample of female twins. In fact, there was no evidence of any other parenting dimension (i.e., low paternal care, high maternal overprotection, high paternal overprotection) having a significant effect upon the prediction of BN. Thus, while some of the evidence concerning overprotection and BN has been mixed, the research conducted thus far has generally found that BN patients “recall their rearing in childhood as being characterised by a lack of care from both parents and most clearly from the mother” (Vandereycken, 1994, p. 230).

Other studies suggest that SAD may also be associated with exposure to adverse parenting during childhood and adolescence. For example, both Parker, 1979, Arrindell et al., 1989 reported that SAD individuals retrospectively recalled their parents as having been lower on care and higher on overprotection than control participants. More recently, Enns, Cox, and Clara (2002) reported that low maternal care and high maternal overprotection were associated with increased risk for SAD among a large sample of females; however, neither paternal care nor paternal overprotection was associated with increased risk for SAD among this group.

Taken together, these results suggest that exposure to adverse parenting—particularly exposure to low maternal care—is associated with increased risk for a number of psychological disorders, including both BN and SAD (e.g., Enns et al., 2002, Kendler et al., 2000). Thus, it is possible that exposure to low maternal care might account for all or part of the link between these two disorders; however, given the modest effect sizes and lack of specificity associated with exposure to low maternal care, it would appear that if this parenting factor did underlie the association between BN and SAD, it would be unlikely to be due to a “main effects only” developmental model (O'Kearney, 1996). Instead, it would seem more likely that exposure to low maternal care might interact with other factors to differentially predict BN and SAD.

Among the most likely candidate factors to interact with parenting experiences to predict BN and SAD are biologically-based personality traits that “predispose the individual to greater sensitivity and vulnerability to powerful familial and social experiences” (Strober & Humphrey, 1987, p. 654). Indeed, biologically-based personality factors have been implicated in the pathogenesis of both BN (e.g., Loxton & Dawe, 2001) and SAD (e.g., Kashdan & Roberts, 2006). To date, however, there has been surprisingly little research examining the relationship between BN and SAD symptomology and Jeffrey Gray's biologically-based theory of personality, Reinforcement Sensitivity Theory (RST; Gray, 1970, Gray and McNaughton, 2000). One of the goals of the current study was to expand this literature and to use RST to examine possible links between BN and SAD.

RST (Corr, 2004, Gray, 1970, Gray and McNaughton, 2000) is a biologically-based personality theory that postulates that three major subsystems of the brain underlie many of the individual differences seen in reinforcement sensitivity, personality, and psychopathology (Pickering & Gray, 1999). These brain systems are referred to as the Behavioral Inhibition System (BIS), the Behavioral Approach System (BAS), and the Fight–Flight–Freeze System (FFFS). The BIS is proposed to be the defensive subsystem of the brain that underlies anxiety. Its primary responsibility is to resolve conflicts among competing goals (e.g., approach–avoidance conflict) by inhibiting prepotent behavior, increasing attention, increasing arousal, and by actively engaging in risk assessment behaviors (Gray & McNaughton, 2000). The BAS is proposed to be the appetitive motivational subsystem of the brain that underlies impulsivity. As such, its primary responsibility is to motivate approach behavior in response to both conditioned and unconditioned appetitive stimuli. In addition, activity in the BAS is posited to be associated with the positive emotions of elation and relief (Corr, 2004, Pickering and Gray, 1999). The FFFS is proposed to be the defensive avoidance subsystem of the brain that underlies fear and panic. Its primary responsibility is to motivate avoidance and escape behaviors in response to both conditioned and unconditioned aversive stimuli (Corr, 2004, Gray and McNaughton, 2000).

The foundation of RST is Gray's (1970) proposal that Eysenck's (1967) personality dimensions of Extraversion and Neuroticism should be rotated to better reflect the underlying biological systems (Corr, 2004). An “Anxiety” dimension was proposed to run from Eysenck's Neurotic-Introvert quadrant to the Stable-Extravert quadrant and to reflect BIS activity. An “Impulsivity” dimension was proposed to run from Eysenck's Stable-Introvert quadrant to the Neurotic-Extravert quadrant and was said to reflect BAS activity. Gray also proposed that individuals high on the BIS-Anxiety dimension would be hypersensitive to punishing stimuli, whereas individuals high on the BAS-Impulsivity dimension would be hypersensitive to rewarding stimuli (Corr, 2004). Accordingly, the BIS-Anxiety dimension is also referred to as the Sensitivity to Punishment (SP) dimension, and the BAS-Impulsivity dimension is also referred to as the Sensitivity to Reward (SR) dimension.

The relationship of the FFFS to personality has historically been more difficult to determine; however, in line with Gray & McNaughton's (2000) most recent revisions to RST, Corr (2004) has argued that the personality dimension of SP actually reflects combined activity in the overall defense system (i.e., combined BIS and FFFS functioning), whereas SR continues to reflect BAS functioning only. The current paper takes this position as well. Accordingly, the term “SP” is used throughout the paper to refer to combined BIS and FFFS sensitivity, whereas the term “SR” is used to refer to BAS sensitivity.

RST proposes that individual differences in SP and SR are normally distributed and that individuals at the far poles of the SP and SR dimensions are at increased risk for developing different forms of psychopathology (Pickering & Gray, 1999). With respect to SAD, Gray and McNaughton (2000) have hypothesized that increased activity in the BIS and FFFS underlies SAD. Accordingly, SP is predicted to be positively associated with SAD. In addition, in a recent modification of RST referred to as the “joint-subsystems hypothesis,” Corr (2002) has proposed that the effects of SP and SR are interdependent upon one another rather than independent. This is an important development with respect to SAD because it predicts that individuals high on SP and low on SR will exhibit the highest levels of social anxiety; however, to date, only limited research has examined the associations among SP, SR, and SAD symptomology.

Coplan, Wilson, Frohlick, and Zelenski (2006) examined the association between self-reported SP and SR and SAD symptoms in a community sample of children. As expected, SP was positively associated with SAD symptoms. In addition, SR was negatively associated with two of three measures of social anxiety. Kashdan and Roberts (2006) examined the association between self-reported SP and SR and social anxiety in two community samples of adults. SP was positively associated with SAD symptoms in both samples, whereas SR was unrelated to SAD symptoms. There was, however, a non-significant negative relationship between SR and SAD symptoms in both samples. Thus, the prediction that SP is positively associated with social anxiety has been consistently supported in the studies that have tested it directly. In contrast, the evidence regarding the relationship between SR and social anxiety has been more mixed.

After reviewing a number of studies suggesting that BN was associated with both anxiety and impulsivity-related personality traits, Loxton and Dawe (2001) proposed that BN symptomology might also be associated with high levels of SP and SR. In support of this proposal, they reported that both SP and SR were positively associated with symptoms of disordered eating among a sample of high school girls. More recently, Kane, Loxton, Staiger, and Dawe (2004) found that BN women (with and without comorbid alcohol problems) scored higher than control participants on self-report measures of SP and SR. In contrast, Claes, Nederkoorn, Vandereycken, Guerrieri, and Vertommen (2006) reported that individuals with BN did not differ significantly from controls on either SP or SR. Thus, there are also inconsistent findings regarding the relationship between RST and BN symptomology, and further examination of this relationship is needed as well.

Due to the paucity of studies examining the associations between RST personality traits and symptoms of BN and SAD, the first aim of the current study was to explore this relationship further using a more recently developed measure of SP and SR—the Sensitivity to Punishment and Sensitivity to Reward Questionnaire (SPSRQ; Torrubia, Avila, Molto, & Caseras, 2001). The second aim of the current study was to test Strober and Humphrey's (1987) hypothesis that “certain personality factors, which may be genetically determined, predispose individuals to greater sensitivity and vulnerability to powerful familial and social experiences” (p. 654). Specifically, because SP is proposed to be a biologically-based personality trait that increases risk for both BN and SAD, and because SP is predicted to increase sensitivity to punishing and threatening stimuli, we predicted that high levels of SP would interact with exposure to low maternal care to predict symptoms of BN and SAD. To our knowledge, this hypothesis has not been tested previously. The final aim of our study was to examine if the combination of high SP and exposure to low maternal care would account for the link between BN and SAD symptomology in a non-clinical sample. To our knowledge, this is also an untested hypothesis.