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Binge eating: ADHD, borderline personality disorder, and obesityJohn Morgan

Abstractrecent research in genomics, attention deficit/hyperactivity disorder (aDHD),

autistic spectrum disorders (aSDs), and cognitive processing deficits has

advanced our understanding of the relevance of personality, neurodevelop-

ment, and binge eating to the ‘eating disorder spectrum’. causal relations

between eating disorders and personality disorders remain unclear. Family

studies suggest an increase in ‘cluster B’ personality disorders in bulimia

nervosa. Treatment models for bulimia and co-morbid borderline personality

disorder (BpD) address the problem of ‘symptom substitution’ of bulimia

with self-harm or addiction. cognitive processing deficits link both condi-

tions, and may be helped by cognitive remediation therapy and problem-

solving therapy. aDHD and aSD are common neurodevelopmental disorders

affecting impulse control and interpersonal relations. preliminary studies

suggest that 23% of patients with an eating disorder show features of aSD,

and 17% have aDHD, although this may be a reflection of nutritional sta-

tus. if confirmed, these findings have clinical implications and may explain

treatment resistance. a mediating role for aDHD should be considered as a

differential diagnosis in co-morbid BpD. Binge eating disorder (BeD) may

affect one in four obese patients, with a distinction between obesity and

purging bulimia nervosa. Family studies suggest some shared vulnerabil-

ity factors for obesity and BeD, including genotype, but also divergence.

National institute for Health and clinical excellence guidelines on bariat-

ric surgery for obesity require eating disorders to be addressed, and re-

search indicates that eating disorders may predict the outcome of surgery.

research into cognitive processing, impulsivity, neurodevelopmental dis-

orders, and genomics may help us better to match treatment to the patient.

Keywords anorexia nervosa; autistic spectrum disorders; binge eating

disorder; bulimia; eating disorders; neurodevelopment; personality

disorder

Issues of impulse control have pervaded the literature on eating disorders for the past three decades. However, recent research developments have shifted the focus towards genomics, neuro-developmental disorders, and cognitive processing. Placing the ‘eating disorder’ literature squarely within this framework has the potential to help us develop new treatments, individually tailored to patients who have previously been regarded as ‘treat-ment resistant’. In particular, models of eating disorders as devel-opmental disorders open the door to treatment innovations.

John Morgan MD (Cantab) is Head of the Yorkshire Center for Eating

Disorders and is Senior Lecturer at St George’s University Hospital,

London, where he runs a research team developing new manualized

treatment approaches for eating disorders.

pSYcHiaTrY 7:4 18

Co-morbidity of borderline personality disorder and eating disorders

Because of the relatively low incidence of eating disorders, it has been difficult to carry out the prospective studies of eating disorders and personality necessary to explore the direction of association between maladaptive personality traits and eating disorders. It is possible that certain personality traits represent vulnerability factors for the development of an eating disorder. Alternatively, it may be that ostensible abnormalities of personal-ity are simply sequelae of the underlying eating disorder.

The literature concerning bulimia nervosa and personality disorder has focused principally on personality disorders within the Diagnostic and Statistical Manual of Mental Disorders (DSM) ‘cluster B’ category, whereas overlap with personality traits has focused on impulse control and ‘rejection sensitivity’. Causal relations remain unclear within the limits of the cross-sectional or retrospective study designs utilized. However, family studies suggest an increment in cluster B personality disorders, not only among people with bulimia nervosa, but also in their relatives, raising the possibility of impulsivity and emotional instability as existing within the same phenotypic cluster as bulimia nervosa.

The literature on personality disorder and eating disorders raises more questions than it answers, with a tendency for specific stud-ies to fish for specific personality traits, based on a preconceived model of causation. What is needed is a tabula rasa approach in which a broader variety of personality traits is examined prospec-tively, in relation to the antecedents of ‘disordered eating’, and their implications for treatment are addressed pragmatically.

Implications for treatment

Regardless of causal relations, patients with an eating disorder and co-morbid borderline personality disorder (BPD) repre-sent a therapeutic challenge. In a catchment area study of self- damaging and addictive behaviour in bulimia nervosa, Lacey1 showed a high prevalence of co-morbid self-harming and addic-tive behaviours in patients referred to a bulimia nervosa clinic, with one-quarter of such patients consuming more than 36 units of alcohol per week, 30% misusing ‘street’ drugs, over one-fifth repeatedly stealing, and comparable numbers having overdosed on more than two occasions. One in ten engaged in regular self-cutting and, in total, it was considered likely that 10% of the clinical population had a condition that Lacey characterized as ‘multi-impulsive bulimia nervosa’.

It has been suggested, although not proven, that this group represents patients with bulimia nervosa and co-morbid BPD, and that the core maladaptive personality traits need to be treated synchronously, rather than treating the presenting ‘dis-ordered eating’ behaviour alone. It was argued2 that failure to do so runs the risk of ‘symptom substitution’, whereby a reduction in the bulimia resulting in an increase in symptoms of self-harm or addiction.

The relationship between multi-impulsive eating disorders, impulsivity as a personality trait, BPD, and their respective treat-ments requires further clarification, yet represents a significant challenge in health settings. The impact in custodial settings, such as among female prisoners, and in forensic services has not been addressed.

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Conversely, it is well established that eating disorders have a high prevalence in populations with BPD. In a 6-year study, Zanarini and colleagues3 demonstrated that more than one-third of patients with BPD fulfilled DSM IV criteria for an unidentified eating disorder, with a close association between remission of borderline traits and eating disorder symptomatology. However, such studies are clearly susceptible to Berkson’s bias. Further evidence for an association is found in treatment trials, particu-larly those examining dialectic behaviour therapy (DBT). Palmer and co-workers4 examined a series of patients presenting with severe bulimia nervosa and co-morbid BPD, and demonstrated the effectiveness of DBT in reducing symptoms of disordered eat-ing as well as synchronous symptoms of borderline traits.

Deficits in cognitive processing have increasingly been identi-fied as features of eating disorder symptomatology, and may prove to be the therapeutic bridge between observations of maladaptive personality traits and clinical interventions. For example, a body of evidence has identified deficient problem-solving skills in patients with eating disorders.5–7 Studies are under way to consider the role of BPD in this pathway and the value of a manualized variant of problem-solving therapy (RASCAL – Table 1) for bulimia nervosa. Examination of specific cognitive processing deficits in patients with eating disorders and co-morbid BPD may prove to be more useful than further prevalence studies of co-morbidities.

Neurodevelopmental disorders and eating disorders

Attention deficit/hyperactivity disorder (ADHD) and autistic spectrum disorders (ASDs) are among the most common child-hood-onset neurodevelopmental disorders. The prevalence of ASD is more than 1% among children.8 Up to 5% of children with ASD may fulfil diagnostic criteria for ADHD and, although features of ADHD lessen throughout adolescence, they do persist into adult-hood.9 Autistic disorders endure for life, and psychiatry has a growing appreciation of their relevance in adult settings. The links between anorexia nervosa, autism, and obsessive–compulsive personality disorder are addressed on pages 183–187.

People with ADHD experience deficits of impulse control and interpersonal skills, suggesting possible overlap with the ante-cedents of eating disorders. Wentz and colleagues10 examined 30 women with an eating disorder in a specialist London clinic and found that 53% had at least one diagnosis of a childhood-onset neuropsychiatric disorder, with 23% showing features of ASD, and 17% features of ADHD. The study was limited by the representativeness of the sample, reliance on subjects’

RASCAL: problem solving for bulimia nervosa

• Review – create a problem list

• Analyse – determine which problems represent priorities

• Solve – create several different solutions for each problem

• Cost – conduct a cost–benefit analysis for each solution

• Act – perform the chosen solution

• Learn – conduct an analysis of the process, in order to

repeat the cycle

Table 1

pSYcHiaTrY 7:4 189

retrospective recall of childhood symptoms without corrobora-tive information from parents, and failure to address the pos-sibility that malnutrition per se may mimic features of ADHD. Nonetheless, If confirmed, these preliminary findings have clini-cal implications and may provide an explanation for treatment non-response in some patients.

Patients who have anorexia nervosa and co-morbid neuro-developmental disorders such as attention deficit disorder (ADD) may require modification to the psychotherapies conventionally offered in the treatment of eating disorders, possibly including spe-cific psychoeducational approaches.11 ADD should be considered a possible mediator of impulsivity in some patients with anorexia and bulimia nervosa, and is an important differential diagnosis in those who might otherwise be considered as showing features of BPD. Finally, pharmacological treatment of ADD may benefit patients in whom a robust diagnosis has been made, and ADD may explain improvements in bulimic behaviour in response to methylphenidate in patients with comorbid cluster B personality disorder,12 as well as the proclivity for misuse of stimulant drugs.

Binge eating

Binge eating disorder (BED) is recognized in DSM-IV as an acknowledgement of the limits of the diagnostic categories of ‘anorexia nervosa’ and ‘bulimia nervosa’. Thus, patients with recurrent episodes of binge eating, but lacking other features of bulimia nervosa, may nonetheless present to eating disorder ser-vices for treatment.13 Similarly, as many as 1 in 4 obese patients presenting for treatment may suffer from BED.14 Diagnostic cri-teria for BED require recurrent episodes of binge eating, charac-terized by both ‘an amount of food that is definitely larger than most people would eat’ and ‘a sense of lack of control’, occurring on at least 2 days a week for 6 months, and in the absence of the compensatory behaviours found in bulimia nervosa.

Patients with BED appear to be distinct from those with the purging subtype of bulimia nervosa in terms of eating disorder psychopathology,15 but there are fewer differences in affective psychopathology.16 In a community-based study of 250 young women with binge eating, Hay and Fairburn17 found that DSM-IV criteria did not clearly distinguish non-purging bulimia ner-vosa from BED in terms of the frequency of binges or presenting features, although those with BED showed less temporal stabil-ity, better outcome, and higher weight. The treatment of BED is addressed elsewhere in this issue in the article by Van den Eynde and Schmidt.

Increasing attention has been given to BED as a public health priority, particularly in relation to morbid obesity. More ques-tions than answers have been raised by aetiological research, and familial aggregation and heritability studies have been useful in generating hypotheses. For example, Hudson et al.18 compared family members of obese subjects with and without BED, and found that people with a family member suffering from BED were more than twice as likely to have the condition them-selves, compared with obese relatives without BED. The overlap between obesity and binge eating was explored by Bulik and co-workers,19 who examined twin samples in a general population. Some degree of genetic variance was shared between obesity and binge eating, but the correlation was not strong. Obesity showed a very strong heritability, with a far lower heritability for binge

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eating, which was clearly associated with environmental factors. This suggests that obesity and binge eating share some vulner-ability factors, including genotype, but there is clearly divergence between obesity with and without binge eating.

Awareness of BED is important in relation to public health campaigns addressing the growing problem of obesity. For exam-ple, the National Institute for Health and Clinical Excellence has recommended that patients with morbid obesity be considered for bariatric surgery only where ‘specialist assessment for eating disorder’ can be offered.20 Studies have indicated an association between poor surgical outcome and BED, which can be pre-dicted both before21 and after22 surgery. Psychological input thus appears to be a prerequisite for medical and surgical approaches to obesity complicated by BED, although service developments do not always consider it as such.

Conclusion

Our understanding of the aetiology and treatment of eating disorders is advanced by research into cognitive processing, impulsivity, neurodevelopmental disorders, and genomics. The development of treatment interventions tailored to individual patient characteristics may offer hope to patients traditionally regarded as refractory. The need for obesity services to provide specialist eating disorder treatments for BED has been demon-strated, but is not reflected in the commissioning of services. ◆

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