Anorexia nervosa (AN)

Anorexia nervosa (AN) is a disorder characterised by a distortion of body image such that the individual ‘sees’ themselves as fat when they are in fact thin; they have a ‘morbid fear of fatness’, and engage in activities to try to achieve a thin body ideal. By definition, AN is diagnosed when the individual ‘refuses to maintain a weight over a minimal norm, leading to body weight less than 85% of that expected’ (DSM–IVTR) or is under a body mass index (BMI) of 17.5 kg/m² (ICD–10) (BMI = weight in kilograms/height in metres²). In growing children, there is a failure to make expected weight gain during a period of growth. In post-pubertal girls, there is the added criterion of amenorrhoea. The criteria are summarised in Table 10.2.

TABLE 10.2 Criteria for anorexia nervosa

AN afflicts around 0.5% of young females (it is much less common in males) and onsets usually around puberty (mean age at onset 15–19 years). Patients engage in dieting behaviours, with either a purely restrictive pattern (i.e. restricting intake, especially of what are perceived of as fattening foods), or encompassing binge–purge cycles, with episodic overeating followed by guilt, self-blame and purging. Dieting becomes an obsession, with avoidance of foods perceived of as fattening (some patients will avoid even smelling or touching such foods), calorie-counting, excessive weighing, and so forth. A variety of ritualised behaviours can occur, including around food preparation and meals, excessive exercise and weighing. Patients might also employ laxatives and diuretics. Box 10.1 lists some of the medical complications associated with AN.

Treatment of AN is rather complex, partly because sufferers often resent treatment and partly because the starvation cycle sets a very powerful train into motion. Education, nutritional rehabilitation and psychotherapy are the mainstays of management; psychotropic medications play an adjuvant role. This integrated approach is best coordinated among the general practitioner, psychiatrist, dietician and other clinicians.

Although there is currently an overall lack of empirically established, evidence-based treatments for AN, this does not equate to ineffectiveness of treatment, and established key components of treatment include:

restoration to healthy weight (menstruation and ovulation in females, normal sexual hormone levels in males and restoration of physical and sexual growth and development in children and adolescents)

treatment of physical complications

enhancement of motivation to restore healthy eating patterns and engagement in treatment

education about healthy nutrition and eating patterns

psychological intervention for related maladaptive thoughts, attitudes and feelings

treatment of psychiatric comorbidity, and

relapse prevention.

Treatment should, where feasible, always include the family, at the very least in terms of provision of education and support. More formal family therapy has proven of benefit for relapse prevention in younger girls. There are a number of family therapy approaches, including structural, strategic, behavioural and the Maudsley manualised guide.

If the patient is significantly underweight, such that they are medically compromised, refeeding is required. Nutritional rehabilitation and medical monitoring during refeeding are essential features of treatment for AN patients who are significantly underweight. Nutritional rehabilitation involves normalising three meals and snacks with 4000–6400 kilojoules per day initially, and increasing to 10,000–16,500 kilojoules per day. Weight gain of 0.25–0.5 kg per week as an outpatient, and 0.5–1 kg per week as an inpatient, are appropriate trajectories for weight gain. Patients have a better prognosis and are less likely to relapse if they are discharged from inpatient settings with a BMI ≥ 16 kg/m².

Vital signs, fluid and food intake, serum electrolytes (magnesium, phosphorus and potassium), thiamine and blood glucose require monitoring during refeeding. Magnesium levels can drop over the first 5–10 days (weakness, cramps, impaired short-term memory and difficulty with visual accommodation) and intravenous replacement (20 millimoles per day over 5–10 days) may be required. Phosphorus levels also fall over the first few days of refeeding and can be life-threatening once at or below 30–50% of the lower laboratory limit; symptoms might include delirium and/or cardiac failure. Intravenous glucose can worsen hypophosphataemia and should therefore be avoided at this time, particularly when hypoglycaemia is not present. Phosphate can be supplemented at 500 mg 3 times a day, or intravenously. If serum phosphorus is low and falling, then it may be necessary to cease the refeeding in the interim, while phosphate replacement is occurring. Falls in potassium level (weakness, palpitations and polyuria) during refeeding are usually gradual; this occurs in hypovolaemic states with urinary potassium loss (> 10 mm/L) in exchange for sodium to maintain extracellular volume, and when volume status is normal while serum magnesium is low.

Thiamine deficiency, which can result in Wernicke’s encephalopathy, can occur during refeeding and may require thiamine and concurrent magnesium replacement. Hypoglycaemia can also occur during refeeding and result in post-prandial hypoglycaemia; the response to 1 mg intravenous glucagon should increase blood glucose to 7 millimoles/L; otherwise, there is a risk of post-prandial hypoglycaemia. The latter may require 10–20 days of refeeding to restore hepatic glycogen. Dietician advice is crucial. Adjunctive medications, notably atypical antipsychotics such as olanzapine, can be helpful

Bulimia nervosa (BN)

Bulimia nervosa (BN) shares with AN an overvalued belief in a thin ideal, but by definition sufferers are not underweight (in many cases they are actually heavier than the normal range). Again, girls are more often affected than boys. Mean onset is in the early 20s. Some bulimic activity is common in high-school girls, but BN itself has a prevalence of around 1% in such groups. BN became much more common over the latter decades of the twentieth century, and is more prevalent in so-called developed countries, and in higher socioeconomic groups.

BN usually begins with dieting behaviour, which becomes predominantly a binge–purge cycle. Thus, sufferers perennially starve themselves, but ultimately become overwhelmed by the desire.

to eat, whereupon they binge, usually on high-calorie foods such as chocolates, biscuits or bread: patients describe how once they start they simply cannot stop eating, and can consume a vast amount of food over a short period. This is often done in secret, and the person is usually ashamed of the behaviour. After the binge, there is inevitable shame and guilt, which may lead to self-induced vomiting, usually by putting a hand down the throat. They might also resort to misuse of laxatives, diuretics, enemas and appetite suppressants. Table 10.3 summarises the criteria for BN, and Box 10.2 lists some of the potential medical complications of the condition.

TABLE 10.3 Criteria for bulimia nervosa

Treatment of BN is usually done on an outpatient basis, using cognitive behaviour therapy (CBT) techniques. There is an emphasis on regular meals and snacks to break the starvation–binge–purge cycle, as well as monitoring of shape and weight concerns and the challenging of related negative thoughts. Other core components of treatment include:

addressing binge eating and related compensatory behaviours such as purging or excessive exercise

exploring and challenging underlying psychological issues (self-esteem, body image and other disturbances of thinking)

treating comorbid psychiatric conditions such as mood disorders and substance misuse

providing nutritional counselling

treating physical complications (see Box 10.2), and

planning relapse-prevention strategies.

Although CBT is the predominant psychological intervention in BN, it has evolved beyond a focus on weight and shape concerns to encompass self-esteem, tolerability of mood and interpersonal experiences (in second generation CBT), emphasis on exposure to the body (in CBT–E), and integrative approaches with greater emphasis on emotional and cultural factors.

Other effective psychological interventions in BN include: self-help, with some professional guidance; interpersonal psychotherapy, which addresses interpersonal roles, stressors and transition through them; and dialectical-behavioural therapy, focusing on behavioural change, interpersonal relationships, mindfulness and regulation of emotion with acceptance and tolerance of distress.

Antidepressants have an established place as adjunctive treatments, with reduction of binge eating and purging behaviours. There is similar efficacy among serotonergic and other antidepressants. The effect of antidepressants in BN is not as great as with CBT, and the therapeutic effect is often not maintained on cessation. The combination of CBT and antidepressants appears to be superior to either treatment alone.

Other eating disorders

The terms binge eating disorder and eating disorder not otherwise specified (EDNOS) are applied when the eating disorder does not meet criteria for AN or BN. The fact that many people with eating disorders are placed in these categories is an indication of the imperfections of the current classification systems.

Obesity

Although obesity is not considered primarily a psychiatric disorder, there is an increased incidence of obesity in some psychiatric disorders (e.g. binge eating disorder and night eating syndrome,

major depressive disorder and schizophrenia), as well as being a potential risk with psychotropic medication (such as antipsychotics). Obesity is compounded by increased mortality and morbidity, including cardiovascular disease, dyslipidaemias, diabetes mellitus, stroke, malignancy and sleep apnoea (which is also associated with depression and diurnal fatigue). The prevalence of obesity is increasing, particularly in Western countries, with a significant health–economic burden. The interaction of multiple genes, neural and hormonal regulation of appetite and activity, and the interface with environmental factors (meal size and physical activity) are significant in the aetiology of obesity. Intervention in childhood obesity may be of more enduring benefit than later in life. Box 10.3 shows the US National Heart, Lung and Blood Institute classification of obesity.

Improved eating habits, lifestyle change and exercise are the treatments of choice for overweight and moderately obese people. Psychotherapy is not a primary treatment for obesity, but may improve self-esteem and motivation for a healthier lifestyle and treatment.

Weight loss medications (such as sibutramine, or orlistat, a gastrointestinal lipase inhibitor) may be considered for a BMI > 30 kg/m² without comorbid medical conditions such as diabetes, or for a BMI > 27 kg/m² when such comorbidity is present. Such medications added to behavioural treatment of obesity may result in relatively modest weight loss of 2.5–8 kg, with weight regain highly likely on discontinuation. The safety and efficacy profile of these medications beyond 1 year is not known. Obesity surgery appears to be the most effective treatment for people with a BMI > 40 kg/m² or a BMI of 35–39.9 kg/m² with associated medical conditions, but again long-term outcomes are not clear.