Individuals with bulimia nervosa report elevated rates of childhood maltreatment, which appears to increase risk for co-occurring substance use problems and negatively impact clinical course. The current study sought to examine the mechanistic pathways by which specific forms of childhood maltreatment may give rise to substance use problems among individuals with bulimic-spectrum pathology. Women with bulimic-spectrum disorders (N = 204) completed measures of childhood trauma, emotion dysregulation, impulsivity, and substance use. Path analysis was used to examine emotion dysregulation and impulsivity as mediators of the relationship between distinct forms of childhood trauma (physical abuse, physical neglect, emotional abuse, emotional neglect, and sexual abuse) and the presence of problematic alcohol/drug use. In the full path model, significant pathways from childhood emotional abuse to emotion dysregulation, childhood emotional neglect to impulsivity, and emotion dysregulation to problematic substance use emerged. Further, emotion dysregulation significantly mediated the relationship between emotional abuse and substance use. Results indicate that emotion dysregulation may be an important mechanism linking a history of childhood emotional maltreatment to later eating and substance use problems, and therefore may be an important treatment target among individuals with co-occurring eating and substance use concerns. Childhood emotional abuse was related to greater emotion dysregulation. Childhood emotional neglect was related to greater impulsivity. Emotion dysregulation was related to greater problematic substance use. Emotional abuse may impact substance use through emotion dysregulation. Creating emotion dysregulation may improve substance and eating disorder symptoms.
Bibliographical noteFunding Information:
This research was supported in part by John Simon Guggenheim Foundation; [grants 1 R01-MH/DK58820, NIH 1 R01-DK61973, NIH 1 R01-MH59100, NIH 1 R01-MH66287, NIH P30-DK50456, K02 MH65919, R01 MH 59234, and NIMH T32 MH082761] from the National Institutes of Health; Walden W. and Jean Young Shaw Foundation; University of Missouri Research Council.
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