Eating Disorders and Self–Harm: A Chaotic Intersection

There is clear empirical evidence that a subgroup of individuals with eating disorders (ED) engage in self-harm behavior (SHB). Individually these disorders are difficult to treat; in combination they represent a chaotic intersection. SHB ranges from various non-lethal forms of self-injury to genuine suicide attempts. Some examples of non-lethal self-injury include hitting, burning, scratching, or cutting oneself; pulling out one’s hair and eyelashes; purposefully precipitating harmful “accidents,” and participating in physically abusive relationships.

SHB may also manifest as overt eating disorder symptoms, such as abusing laxatives, inducing vomiting, or exercising excessively with the expressed or primary intent to experience pain or cause self-injury. Therefore, when assessing ED symptoms, it is essential to determine the intent or function of the symptoms (i.e., food, body, and weight issues vs. purposeful self-harm).

The Prevalence of SHB Among Eating Disorders Patients

The prevalence of non-lethal self-injury among ED patients is approximately 25%, regardless of the type of eating disorder or the treatment setting (Eating Disorders 2002; 10:205). As for suicide attempts, the prevalence rates appear to vary, depending on the ED diagnostic subgroup and study setting. The prevalence of suicide attempts is lowest among outpatients with anorexia nervosa (16%). Prevalence rates are higher for bulimic individuals treated as outpatients (23%) and inpatients (39%). The highest rates of suicide attempts are reported among bulimic individuals who have comorbid alcohol abuse (54%) (Eating Disorders 2002; 10:205).

Causes of SHB Among Those with ED

The precise etiology of self-harm behavior among those with ED is unknown, but it is suspected to be complex, with many underlying causes. It is also known to vary between individuals. About 25% of self-harming individuals with ED appear to meet the criteria for borderline personality disorder (BPD).

Variables that contribute to BPD include temperament, traumatic triggering events, family-of-origin dysfunction (e.g., inconsistent treatment by a caretaker, a negative family environment, or “biparental failure”), and various biological abnormalities, including possible aberrations in serotonin levels. Because BPD is frequently associated with a history of abuse during childhood (e.g., sexual, physical, and emotional abuse and witnessing violence), it is difficult to ascertain if associated biological findings are the causes of and/or outcomes of early developmental trauma. However, early violation of body boundaries appears to foster dissociative defenses in young victims, as well as a separation of body self and psychological self (“You can hurt my body, but not me”). These processes appear to subsequently lower the threshold for SHB in adulthood.

Multi-Impulsive Bulimia

A related construct, multi-impulsive bulimia, also involves impulsive SHB (e.g., suicide attempts), in addition to other forms of impulsivity such as substance abuse and sexual promiscuity. Compared with BPD, considerably less is known about multi-impulsive bulimia in terms of etiology. It may be that this syndrome is actually made up of a subset of individuals with BPD.

Assessment

When assessing an individual with suspected SHB and an eating disorder, it is crucial to explore in depth not only ED symptoms, but also the presence of concomitant SHB. These may include: (1) past suicide attempts; (2) repetitive, ongoing, non-lethal self-harm behavior; and (3) ED symptoms that do not appear to be related to concerns about food, body, and/or weight. An example of the latter could include self-injury equivalents such as inducing vomiting without food in one’s stomach.

Although proven thresholds for various symptoms have not been established, an ongoing pattern of SHB is the conceptual benchmark. Several instruments to help detect and measure self-harm are now available to clinicians, including the Self-Harm Inventory (J Clin Psychol 1998; 54:973), the Self-Injury Survey (1994; Providence, RI), and the Impulsive and Self-Harm Questionnaire (Dissert Abstr Int 1997; 58:4469).

Treatment Strategies

There is no consistent, empirically proven treatment strategy for SHB in those with ED. However, a variety of interventions, used in assorted combinations, appear to offer promise.

Psychotherapy. Many psychotherapeutic techniques for SHB have been described for years in the literature on borderline personality disorder. Here are some of the approaches:

(a) Cognitive restructuring (eliciting and restructuring faulty cognitions that promote SHB).

(b) Dynamic approaches (e.g., uncovering the deeper dynamic themes around SHB, such as self-punishment or eliciting caring responses from others, and bringing these themes into the patient’s conscious awareness).

(c) Sublimation (defined as rechanneling SHB into more socially acceptable alternatives, such as drawing or writing out self-destructive urges in detail).

(d) Interpersonal restructuring (using a consistent verbal phraseology at the time of a crisis that restructures the meaning and function of self-harm behavior in an interpersonal relationship).

(e) Family intervention (i.e., uncovering and translating what the patient may be trying to communicate though SHB).

(f) Various forms of contracting (i.e., encouraging personal control, establishing limits around the treatment).

(g) Group therapy.

Again, none of these approaches alone is effective, whereas combinations appear to promote some degree of stabilization in most patients.

Dialectical Behavior Therapy is a formal approach that includes a combination of techniques, including individual and group intervention, cognitive and dynamic therapy, and psychoeducation. Like other forms of combination treatment, this systematized approach holds promise for the treatment of these complex patients.

Psychotropic medication. Three clinical issues are relevant when considering whether to use psychotropic medications in this population: (1) the meaningful reduction of SHB; (2) selection of medications that are reasonably weight-neutral; and (3) avoidance of medications that are dangerous in overdose.

Most prescribing clinicians initially choose treatment with a weight-neutral selective serotonergic reuptake inhibitor (SSRI). As caveats, both sertraline (Zoloft®) and fluoxetine (Prozac®) appear to be relatively weight-neutral, whereas paroxetine (Paxil®) is frequently associated with weight gain. In addition, citalopram (Celexa®) overdose is associated with cardiac conduction changes that may foreshadow an arrhythmia, which can be lethal.

When there is no meaningful response with an SSRI, a second medication may be added. We typically choose an anticonvulsant. Gabapentin (Neurontin®; 100-600 mg per day) is seemingly weight-neutral at lower doses, and is safe in overdose. Topiramate (Topamax®) is associated with weight loss, and may be particularly helpful among those with binge eating disorder. Safety in overdose with topiramate is not well studied, but reports indicate no adverse effects.

Low-dose, atypical antipsychotic drugs may also be used as an augmentation strategy, either with the SSRI alone, or with the combination of an SSRI and anticonvulsant. Ziprasidone (Geodon®) is weight-neutral at all doses (e.g., 20 mg once or twice daily) and low-dose risperidone (Risperdal®; e.g., 0.25-0.5 mg per day) also appears to be reasonably weight-neutral. In contrast, olanzapine (Zyprexa®), quetiapine (Seroquel®), and clozapine (Clozaril®) are noted for producing weight gain in susceptible patients. These latter three atypical antipsychotics may also cause metabolic abnormalities such as elevated serum glucose, cholesterol, and triglyceride levels.

Finally, several studies indicate that eicosapentaenoic acid (EPA), an omega-3 fatty acid found in fish oil, may reduce depressive and aggressive symptoms as well as suicidal ideation (Am J Psychiatry 2003; 160:167; Am J Psychiatry 2002; 159:477). In the empirical literature, the suggested dosage of EPA has been 1000 mg/day, although this explicit formulation is not seemingly available over-the-counter (e.g., a 432- mg softgel capsule is available). EPA appears to be weight-neutral and safe, even in overdoses.

Given the preceding pharmacologic suggestions, medications appear to offer modest yet meaningful reductions in SHB (an estimated 30% reduction in symptoms). As is the case with any trauma-based syndrome, including post-traumatic stress disorder, full remission is unlikely with the use of medications alone. The outcome data for the combination of psychotherapy strategies and medications varies, of course, from moderate remissions to refractory courses.

Conclusions

Patients with SHB constitute a substantial minority of individuals with eating disorders. While our understanding of the causes for SHB in this population remain somewhat elusive, it is likely that this phenomenon has many causes. Assessment of all ED patients should include clinical inquiry into the presence of SHB. In addition, formal measures of SHB are available.

Treatment approaches need to be individualized, and consist of a combination of psychotherapeutic strategies and medications. A reduction in SHB is a reasonable expectation, but a full and sustained remission is less likely to occur in the short term. Whether full remission occurs with longer follow-up periods is unknown. Clearly, these patients remain complex enigmas in our clinical realms.