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Anorexia nervosa as an anxiety management tool

Anorexia nervosa as an anxiety management tool



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Talking to people with anorexia nervosa, I noticed that some of them have actually much bigger problems than their aforementioned condition.

In some cases it looked as if the person was spending daily an insane amount of time on food, having no time left to deal with other more serious issues in his life. Removing his anorexia, would leave him "helpless" against his real fear, so why would he want that? He would rather keep postponing facing his fear… indefinitely.


Question:

Are there any studies related to the above conditions being used by a person, as a way to divert his attention away from other events that are actually even more stressful?


Note:
I'm not implying that distraction is always the only (or even the main) reason these conditions appear; I'm simply wondering if they are sometimes used subconsciously as another anxiety management tool.


If I'm understanding your question, you're wondering if anorexia nervosa is a symptom of other underlying problems in a person's life.

This is a current theory being supported by "Mental disorders as complex networks: An introduction and overview of a network approach to psychopathology" written by Nuijten et. al. The paper describes how instead of seeing a disorder as a single "latent variable" connecting all the symptoms, all the symptoms should just be considered as a network reinforcing themselves. This is demonstrated in the figure below taken from the paper:

For a discussion of the paper, see "Mental Disorders As Networks" by SlateStarCodex.


Types of Anxiety

Specific types of anxiety disorders are as follows:

  • Generalized anxiety disorder (GAD): This state entails undue and excessive uneasiness and tension, even when little has been done to provoke anxiety.
  • Social anxiety disorder (SAD): This condition is associated with tremendous apprehension concerning social situations.
  • Panic Disorders: Feelings of fear or alarm that occur suddenly and repeatedly without warning
  • Specific phobias: This can include an extreme fear correlated with a specific object or situation

Social anxiety in anorexia and bulimia nervosa: the mediating role of shame

Objective: The close relationship between social anxiety and eating disorders has attracted considerable scholarly attention in recent years. Shame has been identified as the key emotional symptom in the link between social anxiety and social phobia. While shame is commonly recognized as a meaningful construct for understanding eating disorders, empirical research into this issue has been lacking. Thus, the objective of this study was to determine the strength of influence shame and social anxiety have in the psychopathology of anorexia nervosa and bulimia nervosa compared with other clinical groups. Furthermore, the issue of whether shame can account for clinical group differences in the experienced levels of social anxiety was examined.

Method: The sample consisted of 120 female inpatients, divided into four groups of 30 according to individual diagnoses: anorexia nervosa, bulimia nervosa, anxiety disorders and depression. The Social Interaction Anxiety Scale (SIAS), the Social Phobia Scale (SPS) and the Internalized Shame Scale (ISS) were used to measure the target constructs for this investigation.

Results: Patients with anorexia and bulimia nervosa have higher scores in internalized global shame than patients with anxiety disorders and depressions. In contrast to anorectic patients, however, patients with bulimia also have higher scores than the other two groups in the area of social performance anxiety they also differ significantly from the anxiety disorders in terms of interaction anxiety. Once shame was partialled out, group differences of social anxiety were shown to disappear.

Discussion: Both shame and social anxiety have to be regarded as important influencing factors in anorexia and bulimia nervosa, with shame making a significant contribution to the explanation of social anxieties. The interaction between shame and social anxiety as well as its relevance for eating disorders are discussed. With regards to the therapeutic implications, it would seem reasonable not only to focus on treating shame affect but also to specifically adopt a therapeutic strategy targeting social anxiety fears. Copyright © 2006 John Wiley & Sons, Ltd.


6.4. Management of physical aspects

6.4.1. Introduction

Identification of those patients with short-term risk of serious harm or death is clearly important in clinical practice. Recommendations as to how to assess, what to monitor and when to intervene are, therefore, vital.

The vast majority of longer-term follow-up studies indicate that people with anorexia nervosa have an almost 10-fold risk of dying compared to healthy people the same age and sex. Standardised mortality rates range between 4.71 and 12.82 (Nielsen et al., 1998). Mortality in eating disorders is predominately related to malnutrition, methods of weight control and suicide. Among studies in which cause of death is documented, 54 per cent died of eating disorder complications, 27 per cent committed suicide and the remaining 19 per cent died of unknown or other causes (Nielsen, 2001).

6.4.2. Current practice

There is limited evidence as to how and where risk should be managed. Opinion and practice varies between (and within) countries, centres and clinicians. This is the case both in terms of threshold for hospital admission and the goals of the admission. For example, the APA guidelines (American Psychiatric Association, 2000) recommend admission to hospital when a BMI is less than 16 kg/m 2 or weight loss greater than 20 per cent. In both the US and Australia, patients are generally admitted for short-term medical stabilisation on a medical or paediatric ward. In the UK, patients at low weight are frequently managed in an outpatient setting in specialist eating disorder services. In these instances there is a higher threshold for inpatient treatment with admission often not occurring until the patient’s BMI falls below 13 kg/m 2 . However, managing these low weight patients in an outpatient setting can be hazardous and should rarely be done without specialist advice. In the majority of inpatient specialist services in the UK, the goal is full weight recovery and so admissions are longer term. Admission to either a medical/paediatric or general psychiatric unit may occur but this varies with availability of services.

6.4.3. Physical risk reduction and monitoring

Applying information about the best evidence to a specific patient’s problem is not easy as the clinical picture is diverse physically, psychologically and socially. The patient’s problems have to be clearly defined and placed within the context of a clinical risk assessment. This needs to include an assessment both of the acute risk and the longer-term prognosis.

Decisions on short-term risk involve a combined assessment of the physical risk and the person’s psychological capacity to consent to treatment, taking into account the possible resources of motivation and psychosocial support. A diagram is provided (see Appendix 7) as a simple guide to medical practitioners and other members of the multidisciplinary team as a decision aid when evaluating this acute risk. Body mass index is a better marker than weight alone as a proxy measure of physical risk but a rigid cut off point is less good for the extremes of height as the relationship is non-linear. Children have smaller fat stores than mature women and so medical complications occur with less weight loss. Bulimic features or refusal to drink also increase the risk. In turn, these medical markers interact with a variety of clinical and psychosocial factors. High physical risk is often associated with an impairment of capacity for the consent to treatment.

Because of the paucity of data and the nature of the issue under review, the GDG chose to use an informal consensus process (see Chapter 3, Section 3.4.7. for details) to address questions related to risk reduction and monitoring. The review team conducted a systematic search for all available evidence relating to the issue. A number of studies met the GDG’s eligibility criteria, including two systematic reviews of anorexia nervosa and mortality, and outcome at follow-up (Nielsen, 2001 Steinhassuen, 2002). Long-term follow-up studies on patients suffering from anorexia nervosa were also considered, and where possible predictors and causes of death were noted. This is an area in which there is limited research. Exact causes of death are rarely described. The majority of studies documented cause of death as being as a result of starvation in anorexia nervosa. In those studies where death certificates were examined, again the exact precipitant of death was not always established. There are few post-mortem results documented.

Physical factors associated with higher mortality include severity of weight loss, over-activity and vomiting, bulimia and purging (Nielsen, 2000 Steinhausen, 2002). A BMI less than 13 kg/m 2 in adults is of prognostic significance as it indicates a greater risk for mortality (Casper, 1996 Hebebrand et al., 1997). In the latter study, only seven out of the 14 patients with a BMI of 11 kg/m 2 at referral survived (Hebebrand, 1997). Data on malnourished females in famine indicate that with a BMI less than 11 kg/m 2 , risk of mortality increases sharply (Collins, 1995). Prolonged QT intervals may predispose a person to life-threatening arrhythmias, and might be responsible for cases of sudden death. Furthermore, prolonged QT intervals in ECG were recorded seven days before sudden death (Isner, 1985). Abnormally low serum albumin levels and low weight are the best variables to predict a lethal course (Herzog et al., 1997).

In the studies documenting mortality in patients with anorexia nervosa, causes of death vary. Causes include dehydration, electrolyte (particularly hypokalaemia) and metabolic complications, infections (bronchopneumonia and sepsis) and cardiac complications (see Neumarker, 1997, for review). Comorbid alcoholism has also been shown to be associated with increased mortality (Keel et al., 2003). Rupture/perforation of the gastrointestinal tract has been less frequently described (Zipfel, 2000)

Few studies have reported exclusively on the mortality in adolescents. There is a suggestion that the mortality rate is lower. This may reflect the fact that chronicity and mortality increase with increasing age (Steinhausen, 2002). BMI measures in children and younger adolescents are an inadequate reflection of physical reserve. Weight centiles or percentage weight for height give a more accurate guide to the degree of weight loss. Rapid weight loss in children is potentially more dangerous than in adults, and children are known to dehydrate more quickly (Irwin, 1984). Clinical judgement and physical examination may be a better indicator than serum electrolyte levels as to the need for rehydration (Nicholls & Stanhope, 2000).

6.4.4. Clinical summary

Low weight (BMI less than 13 kg/m 2 ), dehydration and electrolyte abnormalities indicate an increased risk of mortality. Cardiac arrhythmias and low serum albumin and glucose are of particular concern.

6.4.5. Clinical practice recommendations

Managing weight gain

In most patients with anorexia nervosa an average weekly weight gain of 0.5 to 1 kg in inpatient settings and 0.5 kg in outpatient settings should be an aim of treatment. This requires about 3500 to 7000 extra calories a week. [C]

Regular physical monitoring and in some cases treatment with a multi-vitamin/multi-mineral supplement in oral form is recommended for people with anorexia nervosa during both inpatient and outpatient weight restoration. [C]

Health care professionals should advise people with eating disorders and osteoporosis or related bone disorders to refrain from physical activities that significantly increase the likelihood of falls. [C]

In children and adolescents with eating disorders, growth and development should be closely monitored. Where development is delayed or growth is stunted despite adequate nutrition, paediatric advice should be sought. [C]

6.4.6. Long-term risk and its management

Apart from the concern of immediate physical risk in patients with anorexia nervosa, the long-term physical consequences are considerable. For the purposes of this section, the GDG chose to focus on the effects on the skeletal system, on reproduction and the associated hormonal abnormalities, including low oestradiol, low IGF-I, and high serum cortisol that may contribute to the bone loss. Gastrointestinal and dental complications are largely as a result of vomiting and laxative abuse. These are described in the chapter on bulimia nervosa. It should be noted however that many of these complications are exacerbated in patients with low weight and muscle weakness. Other consequences have also been described (e.g. cardiac, dermatological, haematological), but these will not be covered in this guideline.

The development of osteopenia and osteoporosis is a serious and long-term consequence of starvation. Oestrogen deficiency, malnutrition, low body mass and hyperactivity all play a part in this development. This section will consider evidence for the effect of weight gain and medication in the management of this complication. In children and adolescents, weight loss has particularly serious implications. Sixty per cent of bone accretion occurs during puberty (Golden, 1992). Gain in bone mass is most pronounced between 11 and 14 years of age and falls significantly after 16 years of age (Soyka et al., 2002). Therefore, it would be expected that the failure of bone mineral accrual in girls with anorexia nervosa would differ depending on the maturation age.

Failure of this accretion thus compounds bone loss in children and adolescents with anorexia nervosa. Growth retardation is a further complication in children and adolescents (Russell, 1985 Danziger, 1994) and failure to grow may indicate nutritional deficiencies. It is thought that with weight gain �tch-up growth’ can occur up until fusion of the epiphyses (Nicholls & Stanhope, 2000). Regular monitoring of height as well as weight is important in children and adolescents with anorexia nervosa. Recommended weight ranges have to be regularly adjusted to take into account changes in height and age. Hormonal treatments, although used, have not been evaluated in adolescents with anorexia nervosa. There is a risk that oestrogen administration may cause premature epiphyseal fusion and growth stunting (Nicholls & Stanhope, 2000).

With regard to the reproductive system, there are several areas of concern: infertility, persistent amenorrhoea and oligomenorrhoea, and polycystic ovaries. In adolescent anorexia nervosa there is a risk of pubertal delay and ultimately arrested pubertal development (Russell, 1985). The effect on fertility and pregnancy will be described below.

Dental erosion is the most common oral problem in patients with eating disorders who engage in self-induced vomiting. A discussion of the issues concerning dental complications can be found in the chapter on bulimia nervosa (Section 7.5.2).

Osteoporosis

People with anorexia nervosa have reduced bone mineral density (BMD) (Bachrach, Guido, Katzman, Litt & Marcus, 1990) which is associated with an increased fracture rate (Rigotti, Neer, Skates, Herzog & Nussbaum, 1991 Vestergaard et al., 2002 Lucas, Melton, Crowson & O�llon, 1999 Soyka, Grinspoon, Levitsky, Herzog & Klibanski, 1999) and long-term disability such as pain, kyphosis and loss of height. Osteoporosis is manifest in some people after a year of illness and the severity gradually increases over time if the illness remains untreated. Fractures may occur after a few years of illness.

The factors that predict bone density in the majority of studies include: duration of amenorrhoea (Biller et al., 1989 Seeman, Szmukler, Formica, Tsalamandris & Mestrovic, 1992), BMI, or some other variable that reflects body composition (Grinspoon et al., 2000). Some studies find that age at menarche is also a predictor (Grinspoon et al., 2000). Oestrogen use does not predict density in larger studies (Grinspoon et al., 2000).

There have been several longitudinal studies that have examined changes in bone density over time. In the majority of cases the people are also engaged with treatment, commonly nutritional and psychological interventions. In some studies additional treatments such as fluoride and hormone replacement have been added. It is difficult to compare between studies as the presentation and type of data differs between studies, as does the case mix.

Adolescents. One of the largest studies in adolescents is that of Castro and colleagues (Castro et al., 2001). They have an early intervention service with a young (mean age 14.4 years) and moderately severe (BMI 15 kg/m 2 ) group. They found that change over time depends on the severity of the osteoporosis at baseline and the degree of recovery made over the period of follow-up. The group with established osteopenia at baseline (i.e. z < 𢄡.0) had an increase in bone density of over nine per cent at spine (5.7 per cent in the femur) over the follow-up interval (1.3 years).

Adults. In adults (mean age 22 years) with a severe illness (mean BMI 13.9 kg/m 2 ) followed over two years, when BMI increased to 17.1 kg/m 2 there was an overall two per cent increase in bone density which related to weight gain. The subgroup that had full recovery (weight gain and menstruation) had the largest increase in bone density (Iketani et al., 1995).

An additional study (Zipfel et al., 2001) in adults (21 years) with BMI 14 kg/m 2 found similar results.

Current Clinical Practice. The most effective treatment/preventative agent for osteoporosis in anorexia nervosa is not yet known. Adequate nutrition and weight are the most relevant factors but in some cases this is difficult to implement in the long term. Therefore, there has been interest in replacing some factors of relevance to bone turnover. These include oestrogen (in the form of hormone replacement therapy or the contraceptive pill) which inhibits bone resorption and Vitamin D, calcium, and insulin-like growth factors (Grinspoon, 1997 & 2002) and DHEA (Gordon, 2002).

Bisphosphonates and fluoride have also been tried (Maugars et al., 1996). It is anticipated that further guidance on the management of osteoporosis will be available on the treatment and management of osteoporosis following the publication in 2005 of the NICE clinical practice guideline.

6.4.6.1. Treatments reviewed

The following treatments were included:

6.4.6.2. Studies considered

The review team conducted a new systematic search for studies examining factors associated with the management of osteoporosis in people with anorexia nervosa. Five RCTs met the eligibility criteria set by the GDG (Gordon, 1999 & 2002 Grinspoon, 1996 & 2002 Klibanski, 1995), involving 207 participants.

Of the five studies included, one compared oestrogen supplementation with assessment only (Klibanski, 1995), one compared different doses of DHEA (Gordon, 1999), one compared DHEA with hormone replacement therapy (Gordon, 2002), one compared two different doses of IGF-I with placebo (Grinspoon, 1996), and one compared IGF-I, oestrogen supplementation, placebo and the combination of IGF-I and oestrogen (Grinspoon, 2002).

6.4.6.3. Evidence statements 3

There is insufficient evidence to determine whether oestrogen supplementation improves bone density by the end of treatment. [I]

There is insufficient evidence to determine whether oral DHEA improves bone density compared to hormone replacement therapy by the end of treatment. [I]

There is limited evidence that both IGF-I alone and the combination of IGF-I and an oral contraceptive may improve bone density:

There is some evidence that the combination of rhIGF-I and an oral contraceptive is produces a better outcome than rhIGF-I alone.

There is insufficient evidence to determine whether oestrogen supplementation is more or less acceptable to people with anorexia nervosa when compared to no oestrogen supplementation. [I]

There is insufficient evidence to determine whether oral DHEA is more or less acceptable to people with anorexia nervosa when compared to hormone replacement therapy. [I]

Full recovery from anorexia nervosa with weight gain and return of menstruation leads to a marked increase in bone density (the rate depends on the initial level, but can be as much as five per cent or more a year). However in those that remain under weight with amenorrhoea bone loss continues. [III]

In adolescents with a good outcome and low initial bone density the increase in BMD is four-fold that of normal adolescents. [III]

6.4.7. Clinical summary

Bone loss is a serious problem in anorexia nervosa with serious long-term consequences. Weight restoration is associated in adolescents with important gains in bone density. Oral oestrogen and oral DHEA do not appear to have a positive impact on bone density and hormone replacement therapy is not recommended in children and adolescents as it may cause premature fusion of the bones. High impact exercise is associated with an increased risk of fracture in anorexia nervosa. rhIGF-I, alone or in combination with an oral contraceptive, is associated with improvements in bone metabolism and bone mineral density but intensive clinical monitoring is necessary and this treatment should only be given in specialist centres with appropriate skills and knowledge. The long-term effect is uncertain.

6.4.8. Clinical practice recommendations

Oestrogen administration should not be used to treat bone density problems in children and adolescents as this may lead to premature fusion of the epiphyses. [C]

6.4.9. Other physical interventions

Malnutrition is a core feature of anorexia nervosa. Refeeding is a necessary component of treatment but is not sufficient. The approach to refeeding varies between centres and countries. There is debate about the setting, means and rate of weight gain and limited evidence to support different views. In some centres the calorie deficit is made up with food, given as normal, albeit larger, meals or snacks. In other centres liquid foods can be used to supplement or replace some or all of the meals. An alternative, which is not used frequently within the UK, is nasogastric feeding. Rarely percutaneous endoscopic gastrostomy (PEG) or total parenteral nutrition (TPN) has been used. These interventions are only used when patients are not able to co-operate with oral refeeding and there is concern about physical risk. In these circumstances legal and ethical considerations need to be addressed.

A number of complications can occur during refeeding. This is a high-risk period for biochemical abnormalities. People at most risk are those with a BMI less than 12 kg/m 2 , those who vomit, abuse laxatives and binge, and those with concurrent physical conditions. Physical monitoring is necessary during periods of refeeding. A range of electrolyte disturbances can occur during refeeding, which are sometimes referred to collectively as the ‘refeeding syndrome’. Hypophosphataemia may develop rapidly during refeeding if severe, it can cause cardiac and respiratory failure, delirium and fits. Ingestion of large quantities of carbohydrates, during rapid refeeding, may result in a precipitate drop in serum phosphate levels. Therefore, in the first few days of refeeding patients who have had very low or absent intakes for long periods, no attempt should be made to achieve net weight gain. Instead they should receive energy and protein provision at levels at or less than their estimated basal requirements with generous provision of balanced multi-vitamins and minerals especially thiamine, potassium, magnesium and phosphate.

Certain vitamin or mineral deficits have come under close scrutiny. For example, the similarity between some of the symptoms of zinc deficiency and the symptoms of anorexia nervosa has led to an interest in zinc replacement. A proportion of patients with anorexia nervosa may be deficient in thiamine, riboflavin, Vitamin C and Vitamin D. The clinical significance of many of these deficiencies is unclear but it is usual for there to be a general rather than a specific deficit and therefore a multi-vitamin/multi-mineral supplement in oral form (e.g. suitable preparations include Sanatogen Gold [non-NHS], Forceval 1𠄲 or Seravit capsules daily). Care should be taken to prevent the risk of vitamin A and D toxicity from excessive use of supplements.

There has been some research into the nutritional management of anorexia nervosa but all of the studies on nutritional approaches are quasi-experimental and small, and the studies on zinc are small.

There is controversy, but little evidence, about the appropriate time course used to achieve the goals of treatment. Some argue that it is important to restore normal weight as soon as possible, others argue for a slower increase in weight. The standard rate of weight gain in the UK is 0.5 to 1 kg per week. The majority of people with anorexia nervosa are treated as outpatients but for the small number who require admission most specialist eating disorder inpatient units aim to discharge people once weight is fully recovered. However, there is an alternative view that full weight recovery can be achieved by outpatient or day patient interventions following brief inpatient refeeding, and that discharge at an intermediate weight may provide an alternative.

There is also the argument that weight gain is only one outcome of interest. Another goal is to ensure that eating behaviour is normalised and maintained after discharge, that abnormal weight and shape cognitions are normalised and that there is improved quality of life in people with anorexia nervosa.

Physical therapies have been used in some European countries (e.g. Belgium and Norway), which have a long tradition of integrating physical therapies into psychotherapy. Physical rehabilitation programmes including riding, climbing, for example, have been used. This has not been the tradition in the UK. Indeed in many programmes in the UK exercise is restricted and bed rest is prescribed.

Feeding in the context of active resistance

This section relates to those occasions where the individual requires restraining to allow the refeeding to take place. Feeding in the context of active resistance raises ethical, legal and clinical issues for all involved. The reporting of it in the general media is often inaccurate and emphasises the emotive 𠆏orce feeding’ and the suggested abuse of the individual’s rights who is fed in this way. In the UK in the treatment of people with anorexia nervosa it is a very rare event and should only be done in a specialised treatment setting with access to the skills and experience required to manage it safely and effectively. It raises complex legal issues. It is interesting to note that all requests to the courts for permission to carry out this intervention in anorexia nervosa have been granted. It is undertaken using the Mental Health Act 1983, the Children Act 1989 and parental authority. Only a small proportion of patients who are admitted and treated compulsorily require this intervention. No studies have reported on the characteristics of those who are fed in this way, or have followed them up.

Methods of delivering this intervention vary across the country, as do the circumstances under which it is used. The risks associated with nasogastric (NG) tube feeding, PEG, or spoon feeding, will be increased in the context of active physical resistance. Actions such as the pulling out the (NG) tube, interfering with or pulling out the PEG, and the physical condition of the patient increase the risk involved.

Clinical decisions as to when to start the intervention, how long to continue for, how often to repeat the intervention and when to stop are complex and difficult. There are further complications with children and adolescents where the urgency to intervene is increased because the low fat mass means that any weight loss is predominantly of lean tissue with higher medical consequences. As a result, children can become dangerously physically compromised. In addition, children and younger adolescents have a much greater tendency to restrict both fluid and food intake. The combination of these factors leads to a rapid breakdown of muscle tissue and dehydration, especially in pre-pubertal children.

6.4.9.1. Physical interventions reviewed

The following interventions were included:

6.4.9.2. Studies considered

The review team conducted a new systematic search for RCTs of physical interventions used in the treatment of anorexia nervosa. As there were few RCTs, the GDG elected to utilise lower levels of evidence where necessary. This included the APA guidelines and a recent expert review on the nutritional management of anorexia nervosa (EDSIG). Eight studies met the eligibility criteria set by the GDG (Arii, 1996 Birmingham, 1994 Hart, 2001 Katz, 1987 Lask, 1993 Pertschuk, 1981 Robb, 2002 Thien, 2000), involving 267 participants.

Of the eight studies, two involved nasogastric feeding (Arii, 1996 Robb, 2002), one TPN (Pertschuk, 1981), three zinc (Birmingham, 1994 Katz, 1987 Lask, 1993), one exercise (Thien, 2000), and one massage (Hart, 2001).

Full details of studies included in the guideline and reasons for excluding studies are given in Appendix 18.

6.4.9.3. Evidence statements 3
Effect of treatment on weight gain

There is limited evidence suggesting that there is a clinically significant difference between nasogastric feeding and ‘standard care’ with nasogastric feeding being superior in terms of weight gain by the end of multi-modal inpatient treatment (n = 116 Arii, 1996 Robb, 2002). [II]

There is insufficient evidence to determine whether zinc supplementation has any impact on weight compared with placebo during multi-modal inpatient treatment. [I]

There is insufficient evidence to determine whether TPN has any impact on weight compared with placebo during multi-modal inpatient treatment. [II]

There is insufficient evidence to determine whether massage or exercise given in addition to ‘standard care’ have any impact on weight compared with ‘standard care’ alone by the end of treatment. [I]

Effect of treatment on symptoms of anorexia nervosa

There is limited evidence suggesting that there is a clinically significant difference between massage and ‘standard care’ with massage being superior on EDI scores by the end of treatment (N = 1 n = 16 SMD = 1.06 95 per cent CI, 0.02 to 2.09). [I]

Acceptability of treatment

There is insufficient or no evidence to determine whether nasogastric feeding or TPN are more, or less, acceptable to people with anorexia nervosa when compared to placebo or ‘standard care’. [II]

There is insufficient evidence to determine whether zinc supplementation is more, or less, acceptable to people with anorexia nervosa when compared to placebo or ‘standard care’. [I]

There is insufficient evidence to determine whether massage or exercise are more, or less, acceptable to people with anorexia nervosa when compared with ‘standard care’. [I]

Tolerability of treatment

There is evidence from a retrospective chart review that TPN may produce a greater risk of side effects than ‘standard care’:

6.4.10. Clinical summary

Nasogastric feeding can confer some benefit in terms of increased rate of weight gain or actual weight gain, as part of a treatment programme. There was insufficient evidence that either TPN or zinc supplementation confer any benefit in terms of weight gain. TPN appears to be associated with more adverse events in one small study. Some limited benefit, on symptoms but not on weight gain, has also been identified from one small trial investigating massage.

6.4.11. Clinical practice recommendations

Total parenteral nutrition should not be used for people with anorexia nervosa, unless there is significant gastrointestinal dysfunction. [C]

6.4.12. Concurrent physical conditions

Diabetes

There does not appear to be an increased occurrence of anorexia nervosa in Type 1 diabetes, however the statistical power of the studies may be insufficient to rule this out (Nielsen, 2002). The mortality rate in 10 years of follow-up of population-based samples was found to be 2.2 (per 1000 person years) for Type 1 diabetes, 7.3 for anorexia nervosa and 34.6 for concurrent cases (the standardised mortality rates were 4.1 for Type 1 diabetes, 8.9 for anorexia nervosa, and 14.5 in concurrent cases) (Nielsen, 2002).

Close liaison and a shared knowledge base between the eating disorder and diabetes teams is essential in the management of anorexia nervosa with diabetes and they should have intensive regular physical monitoring as they are at high risk of complications and death.

Pregnancy

It is unusual for people with anorexia nervosa to become pregnant although a small proportion have fertility treatment to conceive or relapse into anorexia nervosa during the pregnancy. In a follow-up study of people with anorexia nervosa (n = 140) fertility was reduced to one-third of the expected, the rate of prematurity was twice that expected and perinatal mortality was increased six-fold (Brinch et al., 1988). In a follow-up series of 66 women there was an increased miscarriage rate and more use of Caesarean sections and the offspring were more likely to be born prematurely and smaller (Bulik et al., 1999). On the other hand Steiner found no difference in weight gain and foetal weight in their sample (Steiner, Smith, Rosenkranz & Litt, 1991). In a study in which pregnant women with anorexia nervosa were followed prospectively the infants grew slowly in utero especially in the last trimester (Treasure & Russell, 1988).

Women with anorexia nervosa are at greater risk for premature offspring and those that are small for gestational age. There are case series that suggest that some women with anorexia nervosa have difficulty feeding their children (Russell, Treasure & Eisler, 1998 Wezel-Meijler & Wit, 1989) and that the child’s growth can be abnormal (Hodes et al., 1997).

Management of laxative abuse

The management of laxative abuse is covered in the bulimia nervosa chapter (Section 7.5.2), as the management is essentially the same for both disorders.

6.4.13. Clinical practice recommendations

Managing risk

Health care professionals should monitor physical risk in patients with anorexia nervosa. If this leads to the identification of increased physical risk, the frequency and the monitoring and nature of the investigations should be adjusted accordingly. [C]

People with anorexia nervosa and their carers should be informed if the risk to their physical health is high. [C]

The involvement of a physician or paediatrician with expertise in the treatment of physically at-risk patients with anorexia nervosa should be considered for all individuals who are physically at risk. [C]

Pregnant women with either current or remitted anorexia nervosa may need more intensive prenatal care to ensure adequate prenatal nutrition and foetal development. [C]

Feeding against the will of the patient

Feeding against the will of the patient should be an intervention of last resort in the care and management of anorexia nervosa. [C]

Feeding against the will of a patient is a highly specialised procedure requiring expertise in the care and management of those with severe eating disorders and the physical complications associated with it. This should only be done in the context of the Mental Health Act 1983 or Children Act 1989. [C]

When making the decision to feed against the will of the patient the legal basis for any such action must be clear. [C]


Results

Prevalence of Anxiety Disorders

A total of 741 individuals with eating disorders were given the SCID 97 had anorexia nervosa, 282 had bulimia nervosa, 293 had both anorexia and bulimia, and 69 had an eating disorder not otherwise specified). Because of the small number of individuals with an eating disorder not otherwise specified and the diagnostic heterogeneity inherent in that subcategory, they were excluded from analysis, leaving a total of 672 participants. The vast majority of individuals in each group were women (94 [96.9%] of the subjects with anorexia nervosa, 278 [98.6%] of those with bulimia nervosa, and 290 [99.0%] of those with anorexia and bulimia ). Age did not differ across the three diagnostic groups however, body mass index was significantly lower for individuals in the group with anorexia nervosa and the group with anorexia and bulimia than for the group with bulimia nervosa. Of the entire sample, 427 (63.5%) were diagnosed with at least one lifetime anxiety disorder (Table 1). The most common anxiety disorder was OCD, which occurred in approximately 40% of individuals, followed by social phobia (20%) other anxiety disorders were somewhat less common.

Prevalence of Anxiety Disorders by Eating Disorder Subtype

The prevalence of OCD, panic disorder, social phobia, specific phobia, agoraphobia, and generalized anxiety disorder did not differ significantly across the three eating disorder subtypes (Table 1). PTSD was significantly less common among individuals with anorexia nervosa than among those with bulimia nervosa and those with both anorexia and bulimia. A nonsignificantly greater number of individuals with anorexia nervosa than those with bulimia with or without anorexia had no lifetime anxiety disorders (χ 2 =4.96, df=2, p=0.08) (data not included).

Age at Onset

Age at onset of the eating disorder was available for all participants. The age at onset of anxiety disorder was available for between 78% (specific phobia) and 98% (PTSD) of the individuals who had an anxiety disorder. If an individual stated that the anxiety disorder was present during childhood “as long as she or he could remember,” we set the age at onset as 5 years old, assuming childhood recollections were limited before this age. For each eating disorder subtype, we determined whether the age at onset of the anxiety disorder was before or either concurrent with or subsequent to the onset of the eating disorder (Table 2). Eating disorder onset was defined as the age at which all of the symptoms necessary to make the diagnosis were present concurrently. Because there were no significant differences in patterns of onset of anxiety or eating disorder for any eating disorder subtype, the groups were combined. When all eating disorder subtypes were considered together, the onset of OCD, social phobia, specific phobia, and generalized anxiety disorder usually preceded the onset of the eating disorder. In contrast, PTSD, panic disorder, and agoraphobia most often developed after the onset of the eating disorder.

When the entire sample of individuals with eating disorders was considered, 23% had an onset of OCD, 13% had an onset of social phobia, and 10% had an onset of specific phobia in childhood, before the onset of an eating disorder (Table 2). Other anxiety disorders were less common. Overall, 282 (42%) of the entire sample had the onset of one or more anxiety disorders in childhood, before the onset of an eating disorder.

Relationship of Lifetime Anxiety Disorder and State of Eating Disorder Illness on Self-Report Assessments

Previous studies suggested that being ill with an eating disorder exacerbates anxiety-related symptoms in individuals with eating disorders (18). To determine how the state of the eating disorder was associated with anxiety symptoms, we compared individuals with eating disorders stratified by current illness state (currently ill versus symptom free for at least 12 months) (Table 3). In addition, to determine whether anxiety symptoms were present in the absence of an anxiety disorder diagnosis, we stratified participants by the presence versus absence of one or more lifetime anxiety disorder(s). Thus, the four cells for this analysis were characterized by current eating disorder and lifetime history of one or more anxiety disorders.

The four groups of eating disorder subjects were relatively similar in terms of age and weight. Age at the time of study differed significantly across the four groups, but the mean age span of the four groups was less than 5 years (high 20s to low 30s). Current body mass index was higher in the subjects without an anxiety disorder, regardless of state of eating disorder illness. However, body mass index differed by about one unit between groups. The four groups had similar ages at onset of their eating disorders.

In general, scores for anxiety, harm avoidance, perfectionism, and obsessionality tended to be highest in the individuals who had a lifetime anxiety disorder diagnosis and were ill with an eating disorder. Scores tended to be somewhat lower in those who either were currently ill with an eating disorder or had a lifetime anxiety disorder diagnosis. Individuals with eating disorders who had not been symptomatic with an eating disorder in the past 12 months and who never had a lifetime diagnosis of an anxiety disorder still had scores for anxiety, harm avoidance, and perfectionism that were significantly higher than those of the comparison women in the community. For subjects who were not currently ill with an eating disorder, the ratio of having no anxiety disorder to having an anxiety disorder was 0.74. In comparison, for people ill with an eating disorder, the ratio was 0.52 (χ 2 =3.85, df=1, p=0.05). Although this could reflect some bias in terms of recall, it may also suggest that not having an anxiety disorder has a modest association with recovery.


Comorbidity of Anxiety Disorders With Anorexia and Bulimia Nervosa

OBJECTIVE: A large and well-characterized sample of individuals with anorexia nervosa and bulimia nervosa from the Price Foundation collaborative genetics study was used to determine the frequency of anxiety disorders and to understand how anxiety disorders are related to state of eating disorder illness and age at onset. METHOD: Ninety-seven individuals with anorexia nervosa, 282 with bulimia nervosa, and 293 with anorexia nervosa and bulimia were given the Structured Clinical Interview for DSM-IV Axis I Disorders and standardized measures of anxiety, perfectionism, and obsessionality. Their ratings on these measures were compared with those of a nonclinical group of women in the community. RESULTS: The rates of most anxiety disorders were similar in all three subtypes of eating disorders. About two-thirds of the individuals with eating disorders had one or more lifetime anxiety disorder the most common were obsessive-compulsive disorder (OCD) (N=277 [41%]) and social phobia (N=134 [20%]). A majority of the participants reported the onset of OCD, social phobia, specific phobia, and generalized anxiety disorder in childhood, before they developed an eating disorder. People with a history of an eating disorder who were not currently ill and never had a lifetime anxiety disorder diagnosis still tended to be anxious, perfectionistic, and harm avoidant. The presence of either an anxiety disorder or an eating disorder tended to exacerbate these symptoms. CONCLUSIONS: The prevalence of anxiety disorders in general and OCD in particular was much higher in people with anorexia nervosa and bulimia nervosa than in a nonclinical group of women in the community. Anxiety disorders commonly had their onset in childhood before the onset of an eating disorder, supporting the possibility they are a vulnerability factor for developing anorexia nervosa or bulimia nervosa.


Obsessive Compulsive Disorder Eating Disorders

Individual counts the number of mouthfuls chewed or pieces of food in a meal according to some fixed or magical number that is “correct” or “just right.” Individual counts mouthfuls or pieces of food as a means of limiting portions, and thus effectively losing more weight. Individual repeatedly washes hands due to a fear of germs, contact with waste products, or a number of other sources of possible contamination that exist. Individual excessively washes hands to remove trace amounts of oil that might cause weight gain if ingested. Individual throws out food in a can that has been slightly dented for fear that it might contain food poisoning and later cause serious illness to someone. Individual throws out food in a can because it was discovered to contain too many calories after reading the label. Individual repeatedly asks a waiter in a restaurant about different dishes on menu doubtful that he or she has enough knowledge to make the perfect meal decision. Individual constantly asks same waiter about contents of dishes so as to stay away from having any butter oil or fat. Individual refuses to enter the kitchen in order to eat due to fear of accidentally mixing cleaning items with the food. Individual refuses to enter the same room for it will only lead to the temptation to eat and thus get fat. Individual repeatedly checks refrigerator shelves or other parts of house in order to make sure that every piece of food bought is in its proper designated place. Individual constantly checks same locations in search of food to eat in an extensive bulimic binge period.

Thus in order to differentiate between the two disorders and make the proper diagnosis, it is crucial for the clinician to more closely examine the specific behaviors that are being observed and the motivations behind those behaviors. Whereas patients with eating disorders are primarily driven by concerns of physical appearance, and consequently alter their eating patterns in order to lose weight accordingly. OCD patients may be restricting their eating for reasons very different than body image concerns. Furthermore, for cases in which an individual qualifies for both diagnoses, such as an anorexic or bulimic who also experiences non-food related OCD symptoms, like checking or contamination, it is still imperative to consider whether or not their symptoms are being motivated by both disorders simultaneously. For example, consider a patient washing his/her groceries due to the fear of contamination as well as the fear that the products may contain high fat ingredients.

It should be noted that the recommended psychological treatment for both OCD and eating disorders usually involves some combination of cognitive-behavioral therapy, antidepressant medication, and family counseling. Successful treatment for bulimics in particular often entails classic exposure and response prevention, in which patients are exposed to their favorite foods, asked to eat, and then prevented with careful monitoring from vomiting using laxatives or otherwise purging. Additional techniques involve gradual alteration of eating rituals and increased flexibility in eating behaviors which may include breaking rituals such as the need to use the same utensils to measure food, to time meals, and to avoid certain restaurants. Because eating disorders typically result in numerous medical complications, we strongly encourage physicians and nutritionists to be part of the team.

Significant advancements have recently been made in both the diagnosis and treatment of OCD and eating disorders as separate entities, but ample scientific research into the connection between the two, the commonality of their symptoms, and the possible biochemical similarities behind, them is presently lacking. Fortunately, some of the most promising psychiatric investigations into the overlapping symptoms of spectrum disorders have focused on these neurophysiological similarities. One such study asked participants to engage in a task believed to activate the prefrontal cortex and caudate nucleus of the brain so as to compare the performance of participants with OCD to that of those with anorexia. The study found that both groups had difficulty with the task and had higher cerebral glucose metabolism, suggesting a connection between the two disorders and offering evidence that, “ritualized obsessive and compulsive behavior (with reference to eating disorders, as well as washing and checking OCD) could have its origin within common neurobiological abnormalities,” (Murphy, et al. 2004). Although such results are clearly signs of progress, they are still indirect and speculative at best. More work is therefore needed in order to properly isolate the clinical symptoms, biochemical factors, and genetic causes behind OCD and eating disorders. In one of our studies we found that obsessive-compulsive overeaters responded to exposure and response prevention, while another group of overeaters responded better to more traditional stimulus control methods of treatment (Mount & Nezirogulu 1991). This shows that those eating disorders that are similar to OCD may respond better to treatment strategies used to treat more typical OCD behaviors. Consequently, for the sake of all those who suffer the obsessive-compulsive related disorders need to be studied further in order to enhance our understanding of their similarities and dissimilarities. In doing so we will hopefully not only arrive at better treatment strategies but also increase our knowledge of the psychological and biological mechanisms by which the disorders develop.

Fugen Neziroglu, PhD, is a board certified Behavior and Cognitive psychologist involved in the research and treatment of OCD for 25 years. She is the Clinical Director of the Bio-Behavioral Institute in Great Neck, NY and Professor at Hofstra University.

Jonathan Sandler, BA is a research assistant at the Bio-Behavioral Institute in Great Neck, NY and he is involved in the research of Obsessive Compulsive Spectrum Disorders.

1. Kaye WH, Bulik CM, Thornton L, Barbarich N, Masters K, “Comorbidity of anxiety disorders with anorexia and bulimia nervosa.” Am J Psychiatry, 2004 161 2215-2221. 2. Yaryura-Tobias JA, & Neziroglu F (1983). “Obsessive Compulsive Disorders Pathogenesis Diagnosis and Treatment.” New York Marcel Dekker
3. Yaryura-Tobias JA, Pinto A Neziroglu F. ‘The integration of primary anorexia nervosa and obsessive-compulsive disorder.” Eating Weight Disorder Journal, 2001 6 174-180. 4. Murphy R, Nutzinger DO, Paul T, Leplow B. “Conditional-Associative Learning in Eating Disorders: A Comparison With OCD.” J Clinical and Experimental Neuropsychology, 2004 26(2) 190-199.
5. Mount R, Neziroglu F, Taylor CJ. “An obsessive-compulsive view of obesity and its treatment.” J Clinical Psychology, Jan. 1990 46 (1) 68-78.


Anorexia nervosa as an anxiety management tool - Psychology

Aim This paper considers how the three principles of evidence based practice (clinical expertise, scientific evidence, and patient preference) can be applied to the complexity of treatment for anorexia nervosa AN.

Method A narrative review of the evidence of these three domains is presented. Clinical cases are used to illustrate how the formulation and management can be put into practice at different stages of illness.

Results The management of anorexia nervosa is complex. First, individuals with the illness do not regard the manifestations of the illness as a source of concern rather they are embraced and integrated into their identity. This contrasts to the reaction of other people who are terrified by the overt signs of ill health. Thus engagement into treatment is problematic. Second, the core symptom restricted eating, produces malnutrition which impacts on brain, body, and the social network. Thus a mixture of psychological and physical problems gradually accumulates over the course of the illness. This means that the treatment targets increase over time.

Conclusion Thus treatment has to work with motivation and readiness to change and tackle the various domains of ill health.


What are the hallmarks of anorexia nervosa?

The core psychological feature of anorexia nervosa is the extreme overvaluation of shape and weight. People with anorexia also have the physical capacity to tolerate extreme self imposed weight loss. Food restriction is only one aspect of the practices used to lose weight. Many people with anorexia use overexercise and overactivity to burn calories. They often choose to stand rather than sit generate opportunities to be physically active and are drawn to sport, athletics, and dance. Purging practices include self induced vomiting, together with misuse of laxatives, diuretics, and “slimming medicines.” Patients may also practise 𠇋ody checking,” which involves repeated weighing, measuring, mirror gazing, and other obsessive behaviour to reassure themselves that they are still thin (box 1).

Box 1 ICD-10 (international classification of diseases, 10th revision) criteria for anorexia nervosa 8

All five criteria must be met for a definite diagnosis to be made

Body weight is maintained at least 15% below that expected (either lost or never achieved) or body-mass index is 17.5 or less. Prepubertal patients may fail to gain the expected amount of weight during the prepubertal growth spurt

Weight loss is self induced by avoiding �ttening foods” together with self induced vomiting, purging, excessive exercising, or using appetite suppressants or diuretics (or both)

Body image is distorted in the form of a specific psychopathology whereby a dread of fatness persists as an intrusive, overvalued idea and the patient imposes a low weight threshold on himself or herself

A widespread endocrine disorder involving the hypothalamic-pituitary-gonadal axis is manifest in women as amenorrhoea and in men as a loss of sexual interest and potency (except for the persistence of vaginal bleeds in women who are taking replacement hormonal therapy, usually the contraceptive pill). Concentrations of growth hormone and cortisol may be raised, and changes in the peripheral metabolism of thyroid hormone and abnormalities of insulin secretion may also be seen

If onset is before puberty, the sequence of pubertal events will be delayed or even arrested (growth will cease in girls the breasts will not develop and primary amenorrhoea will be present in boys the genitals will remain juvenile). After recovery, puberty will often complete normally, but the menarche will be late


Psychological treatment of pathological fear and worry using exposure therapy

Exposure therapy as a mechanism of action in psychological treatments such as CBT

Cognitive-behavioural therapy (CBT) has received considerable empirical support for the treatment of anxiety disorders and is generally the preferred approach for pathological fear and worry. One hypothesized mechanism of action that is arguably shared across empirically supported treatments for different anxiety disorders is exposure therapy (the technique in which the patient is encouraged to directly face his/her fears or worries and habituation to the anxiety). There appears to be a growing consensus that exposure is an essential ingredient of CBT for most anxiety disorders, and that it is one of the most widely used behaviour therapy techniques in the treatment of anxiety symptoms (Mineka & Thomas, 1999 Moscovitch, Antony, & Swinson, 2009 ). Evidence from the child and adolescent literature on CBT for anxious youth generally support those data found in adults regarding the benefit of exposure therapy in symptom reduction (Kendall, Flannery-Schroeder, Panichelli-Mindel, Southam-Gerow, Henin, & Warman, 1997 Silverman, Kurtines, Ginsburg, Weems, Rabian, & Serafini, 1999 Prins & Ollendick, 2003 Chu & Harrison, 2007 ).

Of note, many CBT treatments that incorporate the specific ingredient of exposure with anxious children and adolescents also have a parent component. From a clinical standpoint, anecdotal evidence suggests that parents, in addition to participating in some sessions with their anxious child, are often helpful outside of the therapy office in facilitating between-session exposure ‘homework’ assignments assigned by the CBT therapist, either by helping the reluctant and anxious child take the next ‘step’ in his/her hierarchy or by providing support when exposures are to be completed. It is not uncommon for parents to either accompany the child to an exposure practice (e.g. in the case of phobia of heights, to a high floor in a tall building) outside of the therapy office or give encouragement, praise or a functional reward when the task is completed. An example of a model that includes parent involvement in treatment for child and adolescent anxiety that has received empirical support is the ‘transfer of control’ model (i.e. a gradual transfer of knowledge, skills and methods from therapist to parent and then from parent to child). Specifically, a RCT (Khanna & Kendall, 2009 ) comparing individual CBT (ICBT), family CBT (FCBT) and a family-based education control (FESA) explored the relation between use of specific parent training strategies and outcome. Results showed that ‘transfer of control’ and parental anxiety-management techniques significantly contributed to improvement on clinician and parent ratings of child global functioning within FCBT.

Different approaches to exposure therapy

Exposure to fear

As Antony and Barlow ( 2002 ) point out, exposure to feared objects and situations is both necessary and sufficient for addressing the symptom of fear, particularly in the context of treating specific phobias. Studies have found that in vivo exposure is a more effective method in reducing fear than exposure in imagination, and that in vivo exposure is effective for treating a wide range of feared stimuli (Antony & Barlow, 2002 ). While there is variability across studies regarding the length of treatment (with some evidence that merely a single session of exposure may be effective), the extent of therapist involvement and the age of participants, the positive effects of exposure for fear reactions appear to be robust. Research suggests that exposure in multiple contexts and to varying stimuli can reduce the rate of relapse, indicating that for maximal effectiveness, individuals should be exposed to phobic stimuli in a variety of locations and situations (e.g. Mineka & Thomas, 1999 ) and to varied stimuli (Rowe & Craske, 1998 ). Thus, fear-based exposure requires accuracy in the stimulus selected as well as exposure to the stimulus in different contexts to be most potent. This may be particularly true as the feared stimuli get more complex and difficult to identify, as in OCD. In gradual exposure, a fear and avoidance hierarchy is typically created, and the rate of exposure to the feared stimulus varies depending on the nature and severity of the fear. With more complex fear reactions (e.g. OCD, post-traumatic stress disorder, etc.), items on the hierarchy may need to be approached at a slower rate and repeated practice of each level may be necessary before the next item is attempted.

There are nuanced differences in exposure-based protocols tailored for OCD which may inform an exposure-based perspective in the treatment of AN, a disorder in which rituals around food and eating are often apparent (e.g. compulsive compensatory exercise, calorie counting, measuring portions). From a clinical standpoint, treatment for OCD is typically more intensive than treatment for other anxiety disorders in that both obsessions and compulsions are targeted. Exposure and response prevention techniques (in which the patient is exposed to the feared situation that is the target of the obsession and instructed to block the ritual that s/he feels driven to perform) may be more complicated than exposure for simple phobia. More specifically, EXRP may require both greater frequency (the optimum number of exposure sessions for OCD appears to be about 20 Steketee & Barlow, 2002 ), intensity (exposures may occur as often as daily), and sessions may be longer. For example, treatment may involve doing non-sensical tasks in exposure with the patient, such as touching a dirty toilet and refraining from hand-washing this practice may need to be conducted a large number of times for habituation to occur. March and Muller ( 1998 ) suggest that satiation (an exposure-based method for habituating to obsessions by repeating them over and over again) and massed practice (similar to satiation except it is the compulsion that is practiced until performing it loses any sense of urgency) may be required when using EXRP for OCD and consequently, more time may be required to devote to these practices in and out of the therapy office.

Exposure to worry

Given that worry and its accompanying features may be present across the anxiety disorders, a wide variety of cognitive-behavioural interventions have been developed to address this specific symptom, particularly in the context of Generalized Anxiety Disorder (GAD). This may be due to the complexity of the symptom of worry, which is future-oriented and potentially abstract in nature. Treatments for GAD/worry vary in terms of the specific CBT elements they contain, and Roemer et al., 2002 have identified certain common elements to these approaches. These include self-monitoring of worry, applied relaxation, imaginal exposure, in vivo exposure, coping skills rehearsal, engagement in pleasurable activities, mindfulness-based strategies and cognitive restructuring. Worry exposure (WE) is considered to be a core element of CBT for GAD. This approach involves imaginal exposure to feared catastrophic outcomes and is certainly a component of many treatment packages for worry-based disorders. For example, Craske ( 1999 ) and Zinbarg, Craske, and Barlow, ( 1993 ) have produced a cognitive-behavioural protocol that includes WE the exposure is then followed by a management phase in which cognitive and other coping strategies are employed in response to the imagined scene. The comprehensive treatment proposed by these authors also includes additional cognitive techniques, problem-solving and self-monitoring. Although one study to date suggests that WE may be as effective as applied relaxation as a stand-alone (e.g. no other CBT interventions used) treatment for GAD (Hoyer, Beesdo, Gloster, Runge, Hofler, & Becker, 2009 ), it is unclear whether exposure in isolation is sufficient to address worry as a symptom due to the abstract nature of cognitions and associated sequelae. In summary, it appears that exposure therapy may need to be either amplified or accompanied by adjunctive interventions as the precise emotional symptom becomes more complex, with simple fear considered the least complex and concrete to treat and worry the most complex and abstract.


What are the hallmarks of anorexia nervosa?

The core psychological feature of anorexia nervosa is the extreme overvaluation of shape and weight. People with anorexia also have the physical capacity to tolerate extreme self imposed weight loss. Food restriction is only one aspect of the practices used to lose weight. Many people with anorexia use overexercise and overactivity to burn calories. They often choose to stand rather than sit generate opportunities to be physically active and are drawn to sport, athletics, and dance. Purging practices include self induced vomiting, together with misuse of laxatives, diuretics, and “slimming medicines.” Patients may also practise 𠇋ody checking,” which involves repeated weighing, measuring, mirror gazing, and other obsessive behaviour to reassure themselves that they are still thin (box 1).

Box 1 ICD-10 (international classification of diseases, 10th revision) criteria for anorexia nervosa 8

All five criteria must be met for a definite diagnosis to be made

Body weight is maintained at least 15% below that expected (either lost or never achieved) or body-mass index is 17.5 or less. Prepubertal patients may fail to gain the expected amount of weight during the prepubertal growth spurt

Weight loss is self induced by avoiding �ttening foods” together with self induced vomiting, purging, excessive exercising, or using appetite suppressants or diuretics (or both)

Body image is distorted in the form of a specific psychopathology whereby a dread of fatness persists as an intrusive, overvalued idea and the patient imposes a low weight threshold on himself or herself

A widespread endocrine disorder involving the hypothalamic-pituitary-gonadal axis is manifest in women as amenorrhoea and in men as a loss of sexual interest and potency (except for the persistence of vaginal bleeds in women who are taking replacement hormonal therapy, usually the contraceptive pill). Concentrations of growth hormone and cortisol may be raised, and changes in the peripheral metabolism of thyroid hormone and abnormalities of insulin secretion may also be seen

If onset is before puberty, the sequence of pubertal events will be delayed or even arrested (growth will cease in girls the breasts will not develop and primary amenorrhoea will be present in boys the genitals will remain juvenile). After recovery, puberty will often complete normally, but the menarche will be late


Types of Anxiety

Specific types of anxiety disorders are as follows:

  • Generalized anxiety disorder (GAD): This state entails undue and excessive uneasiness and tension, even when little has been done to provoke anxiety.
  • Social anxiety disorder (SAD): This condition is associated with tremendous apprehension concerning social situations.
  • Panic Disorders: Feelings of fear or alarm that occur suddenly and repeatedly without warning
  • Specific phobias: This can include an extreme fear correlated with a specific object or situation

Social anxiety in anorexia and bulimia nervosa: the mediating role of shame

Objective: The close relationship between social anxiety and eating disorders has attracted considerable scholarly attention in recent years. Shame has been identified as the key emotional symptom in the link between social anxiety and social phobia. While shame is commonly recognized as a meaningful construct for understanding eating disorders, empirical research into this issue has been lacking. Thus, the objective of this study was to determine the strength of influence shame and social anxiety have in the psychopathology of anorexia nervosa and bulimia nervosa compared with other clinical groups. Furthermore, the issue of whether shame can account for clinical group differences in the experienced levels of social anxiety was examined.

Method: The sample consisted of 120 female inpatients, divided into four groups of 30 according to individual diagnoses: anorexia nervosa, bulimia nervosa, anxiety disorders and depression. The Social Interaction Anxiety Scale (SIAS), the Social Phobia Scale (SPS) and the Internalized Shame Scale (ISS) were used to measure the target constructs for this investigation.

Results: Patients with anorexia and bulimia nervosa have higher scores in internalized global shame than patients with anxiety disorders and depressions. In contrast to anorectic patients, however, patients with bulimia also have higher scores than the other two groups in the area of social performance anxiety they also differ significantly from the anxiety disorders in terms of interaction anxiety. Once shame was partialled out, group differences of social anxiety were shown to disappear.

Discussion: Both shame and social anxiety have to be regarded as important influencing factors in anorexia and bulimia nervosa, with shame making a significant contribution to the explanation of social anxieties. The interaction between shame and social anxiety as well as its relevance for eating disorders are discussed. With regards to the therapeutic implications, it would seem reasonable not only to focus on treating shame affect but also to specifically adopt a therapeutic strategy targeting social anxiety fears. Copyright © 2006 John Wiley & Sons, Ltd.


Results

Prevalence of Anxiety Disorders

A total of 741 individuals with eating disorders were given the SCID 97 had anorexia nervosa, 282 had bulimia nervosa, 293 had both anorexia and bulimia, and 69 had an eating disorder not otherwise specified). Because of the small number of individuals with an eating disorder not otherwise specified and the diagnostic heterogeneity inherent in that subcategory, they were excluded from analysis, leaving a total of 672 participants. The vast majority of individuals in each group were women (94 [96.9%] of the subjects with anorexia nervosa, 278 [98.6%] of those with bulimia nervosa, and 290 [99.0%] of those with anorexia and bulimia ). Age did not differ across the three diagnostic groups however, body mass index was significantly lower for individuals in the group with anorexia nervosa and the group with anorexia and bulimia than for the group with bulimia nervosa. Of the entire sample, 427 (63.5%) were diagnosed with at least one lifetime anxiety disorder (Table 1). The most common anxiety disorder was OCD, which occurred in approximately 40% of individuals, followed by social phobia (20%) other anxiety disorders were somewhat less common.

Prevalence of Anxiety Disorders by Eating Disorder Subtype

The prevalence of OCD, panic disorder, social phobia, specific phobia, agoraphobia, and generalized anxiety disorder did not differ significantly across the three eating disorder subtypes (Table 1). PTSD was significantly less common among individuals with anorexia nervosa than among those with bulimia nervosa and those with both anorexia and bulimia. A nonsignificantly greater number of individuals with anorexia nervosa than those with bulimia with or without anorexia had no lifetime anxiety disorders (χ 2 =4.96, df=2, p=0.08) (data not included).

Age at Onset

Age at onset of the eating disorder was available for all participants. The age at onset of anxiety disorder was available for between 78% (specific phobia) and 98% (PTSD) of the individuals who had an anxiety disorder. If an individual stated that the anxiety disorder was present during childhood “as long as she or he could remember,” we set the age at onset as 5 years old, assuming childhood recollections were limited before this age. For each eating disorder subtype, we determined whether the age at onset of the anxiety disorder was before or either concurrent with or subsequent to the onset of the eating disorder (Table 2). Eating disorder onset was defined as the age at which all of the symptoms necessary to make the diagnosis were present concurrently. Because there were no significant differences in patterns of onset of anxiety or eating disorder for any eating disorder subtype, the groups were combined. When all eating disorder subtypes were considered together, the onset of OCD, social phobia, specific phobia, and generalized anxiety disorder usually preceded the onset of the eating disorder. In contrast, PTSD, panic disorder, and agoraphobia most often developed after the onset of the eating disorder.

When the entire sample of individuals with eating disorders was considered, 23% had an onset of OCD, 13% had an onset of social phobia, and 10% had an onset of specific phobia in childhood, before the onset of an eating disorder (Table 2). Other anxiety disorders were less common. Overall, 282 (42%) of the entire sample had the onset of one or more anxiety disorders in childhood, before the onset of an eating disorder.

Relationship of Lifetime Anxiety Disorder and State of Eating Disorder Illness on Self-Report Assessments

Previous studies suggested that being ill with an eating disorder exacerbates anxiety-related symptoms in individuals with eating disorders (18). To determine how the state of the eating disorder was associated with anxiety symptoms, we compared individuals with eating disorders stratified by current illness state (currently ill versus symptom free for at least 12 months) (Table 3). In addition, to determine whether anxiety symptoms were present in the absence of an anxiety disorder diagnosis, we stratified participants by the presence versus absence of one or more lifetime anxiety disorder(s). Thus, the four cells for this analysis were characterized by current eating disorder and lifetime history of one or more anxiety disorders.

The four groups of eating disorder subjects were relatively similar in terms of age and weight. Age at the time of study differed significantly across the four groups, but the mean age span of the four groups was less than 5 years (high 20s to low 30s). Current body mass index was higher in the subjects without an anxiety disorder, regardless of state of eating disorder illness. However, body mass index differed by about one unit between groups. The four groups had similar ages at onset of their eating disorders.

In general, scores for anxiety, harm avoidance, perfectionism, and obsessionality tended to be highest in the individuals who had a lifetime anxiety disorder diagnosis and were ill with an eating disorder. Scores tended to be somewhat lower in those who either were currently ill with an eating disorder or had a lifetime anxiety disorder diagnosis. Individuals with eating disorders who had not been symptomatic with an eating disorder in the past 12 months and who never had a lifetime diagnosis of an anxiety disorder still had scores for anxiety, harm avoidance, and perfectionism that were significantly higher than those of the comparison women in the community. For subjects who were not currently ill with an eating disorder, the ratio of having no anxiety disorder to having an anxiety disorder was 0.74. In comparison, for people ill with an eating disorder, the ratio was 0.52 (χ 2 =3.85, df=1, p=0.05). Although this could reflect some bias in terms of recall, it may also suggest that not having an anxiety disorder has a modest association with recovery.


Psychological treatment of pathological fear and worry using exposure therapy

Exposure therapy as a mechanism of action in psychological treatments such as CBT

Cognitive-behavioural therapy (CBT) has received considerable empirical support for the treatment of anxiety disorders and is generally the preferred approach for pathological fear and worry. One hypothesized mechanism of action that is arguably shared across empirically supported treatments for different anxiety disorders is exposure therapy (the technique in which the patient is encouraged to directly face his/her fears or worries and habituation to the anxiety). There appears to be a growing consensus that exposure is an essential ingredient of CBT for most anxiety disorders, and that it is one of the most widely used behaviour therapy techniques in the treatment of anxiety symptoms (Mineka & Thomas, 1999 Moscovitch, Antony, & Swinson, 2009 ). Evidence from the child and adolescent literature on CBT for anxious youth generally support those data found in adults regarding the benefit of exposure therapy in symptom reduction (Kendall, Flannery-Schroeder, Panichelli-Mindel, Southam-Gerow, Henin, & Warman, 1997 Silverman, Kurtines, Ginsburg, Weems, Rabian, & Serafini, 1999 Prins & Ollendick, 2003 Chu & Harrison, 2007 ).

Of note, many CBT treatments that incorporate the specific ingredient of exposure with anxious children and adolescents also have a parent component. From a clinical standpoint, anecdotal evidence suggests that parents, in addition to participating in some sessions with their anxious child, are often helpful outside of the therapy office in facilitating between-session exposure ‘homework’ assignments assigned by the CBT therapist, either by helping the reluctant and anxious child take the next ‘step’ in his/her hierarchy or by providing support when exposures are to be completed. It is not uncommon for parents to either accompany the child to an exposure practice (e.g. in the case of phobia of heights, to a high floor in a tall building) outside of the therapy office or give encouragement, praise or a functional reward when the task is completed. An example of a model that includes parent involvement in treatment for child and adolescent anxiety that has received empirical support is the ‘transfer of control’ model (i.e. a gradual transfer of knowledge, skills and methods from therapist to parent and then from parent to child). Specifically, a RCT (Khanna & Kendall, 2009 ) comparing individual CBT (ICBT), family CBT (FCBT) and a family-based education control (FESA) explored the relation between use of specific parent training strategies and outcome. Results showed that ‘transfer of control’ and parental anxiety-management techniques significantly contributed to improvement on clinician and parent ratings of child global functioning within FCBT.

Different approaches to exposure therapy

Exposure to fear

As Antony and Barlow ( 2002 ) point out, exposure to feared objects and situations is both necessary and sufficient for addressing the symptom of fear, particularly in the context of treating specific phobias. Studies have found that in vivo exposure is a more effective method in reducing fear than exposure in imagination, and that in vivo exposure is effective for treating a wide range of feared stimuli (Antony & Barlow, 2002 ). While there is variability across studies regarding the length of treatment (with some evidence that merely a single session of exposure may be effective), the extent of therapist involvement and the age of participants, the positive effects of exposure for fear reactions appear to be robust. Research suggests that exposure in multiple contexts and to varying stimuli can reduce the rate of relapse, indicating that for maximal effectiveness, individuals should be exposed to phobic stimuli in a variety of locations and situations (e.g. Mineka & Thomas, 1999 ) and to varied stimuli (Rowe & Craske, 1998 ). Thus, fear-based exposure requires accuracy in the stimulus selected as well as exposure to the stimulus in different contexts to be most potent. This may be particularly true as the feared stimuli get more complex and difficult to identify, as in OCD. In gradual exposure, a fear and avoidance hierarchy is typically created, and the rate of exposure to the feared stimulus varies depending on the nature and severity of the fear. With more complex fear reactions (e.g. OCD, post-traumatic stress disorder, etc.), items on the hierarchy may need to be approached at a slower rate and repeated practice of each level may be necessary before the next item is attempted.

There are nuanced differences in exposure-based protocols tailored for OCD which may inform an exposure-based perspective in the treatment of AN, a disorder in which rituals around food and eating are often apparent (e.g. compulsive compensatory exercise, calorie counting, measuring portions). From a clinical standpoint, treatment for OCD is typically more intensive than treatment for other anxiety disorders in that both obsessions and compulsions are targeted. Exposure and response prevention techniques (in which the patient is exposed to the feared situation that is the target of the obsession and instructed to block the ritual that s/he feels driven to perform) may be more complicated than exposure for simple phobia. More specifically, EXRP may require both greater frequency (the optimum number of exposure sessions for OCD appears to be about 20 Steketee & Barlow, 2002 ), intensity (exposures may occur as often as daily), and sessions may be longer. For example, treatment may involve doing non-sensical tasks in exposure with the patient, such as touching a dirty toilet and refraining from hand-washing this practice may need to be conducted a large number of times for habituation to occur. March and Muller ( 1998 ) suggest that satiation (an exposure-based method for habituating to obsessions by repeating them over and over again) and massed practice (similar to satiation except it is the compulsion that is practiced until performing it loses any sense of urgency) may be required when using EXRP for OCD and consequently, more time may be required to devote to these practices in and out of the therapy office.

Exposure to worry

Given that worry and its accompanying features may be present across the anxiety disorders, a wide variety of cognitive-behavioural interventions have been developed to address this specific symptom, particularly in the context of Generalized Anxiety Disorder (GAD). This may be due to the complexity of the symptom of worry, which is future-oriented and potentially abstract in nature. Treatments for GAD/worry vary in terms of the specific CBT elements they contain, and Roemer et al., 2002 have identified certain common elements to these approaches. These include self-monitoring of worry, applied relaxation, imaginal exposure, in vivo exposure, coping skills rehearsal, engagement in pleasurable activities, mindfulness-based strategies and cognitive restructuring. Worry exposure (WE) is considered to be a core element of CBT for GAD. This approach involves imaginal exposure to feared catastrophic outcomes and is certainly a component of many treatment packages for worry-based disorders. For example, Craske ( 1999 ) and Zinbarg, Craske, and Barlow, ( 1993 ) have produced a cognitive-behavioural protocol that includes WE the exposure is then followed by a management phase in which cognitive and other coping strategies are employed in response to the imagined scene. The comprehensive treatment proposed by these authors also includes additional cognitive techniques, problem-solving and self-monitoring. Although one study to date suggests that WE may be as effective as applied relaxation as a stand-alone (e.g. no other CBT interventions used) treatment for GAD (Hoyer, Beesdo, Gloster, Runge, Hofler, & Becker, 2009 ), it is unclear whether exposure in isolation is sufficient to address worry as a symptom due to the abstract nature of cognitions and associated sequelae. In summary, it appears that exposure therapy may need to be either amplified or accompanied by adjunctive interventions as the precise emotional symptom becomes more complex, with simple fear considered the least complex and concrete to treat and worry the most complex and abstract.


Comorbidity of Anxiety Disorders With Anorexia and Bulimia Nervosa

OBJECTIVE: A large and well-characterized sample of individuals with anorexia nervosa and bulimia nervosa from the Price Foundation collaborative genetics study was used to determine the frequency of anxiety disorders and to understand how anxiety disorders are related to state of eating disorder illness and age at onset. METHOD: Ninety-seven individuals with anorexia nervosa, 282 with bulimia nervosa, and 293 with anorexia nervosa and bulimia were given the Structured Clinical Interview for DSM-IV Axis I Disorders and standardized measures of anxiety, perfectionism, and obsessionality. Their ratings on these measures were compared with those of a nonclinical group of women in the community. RESULTS: The rates of most anxiety disorders were similar in all three subtypes of eating disorders. About two-thirds of the individuals with eating disorders had one or more lifetime anxiety disorder the most common were obsessive-compulsive disorder (OCD) (N=277 [41%]) and social phobia (N=134 [20%]). A majority of the participants reported the onset of OCD, social phobia, specific phobia, and generalized anxiety disorder in childhood, before they developed an eating disorder. People with a history of an eating disorder who were not currently ill and never had a lifetime anxiety disorder diagnosis still tended to be anxious, perfectionistic, and harm avoidant. The presence of either an anxiety disorder or an eating disorder tended to exacerbate these symptoms. CONCLUSIONS: The prevalence of anxiety disorders in general and OCD in particular was much higher in people with anorexia nervosa and bulimia nervosa than in a nonclinical group of women in the community. Anxiety disorders commonly had their onset in childhood before the onset of an eating disorder, supporting the possibility they are a vulnerability factor for developing anorexia nervosa or bulimia nervosa.


6.4. Management of physical aspects

6.4.1. Introduction

Identification of those patients with short-term risk of serious harm or death is clearly important in clinical practice. Recommendations as to how to assess, what to monitor and when to intervene are, therefore, vital.

The vast majority of longer-term follow-up studies indicate that people with anorexia nervosa have an almost 10-fold risk of dying compared to healthy people the same age and sex. Standardised mortality rates range between 4.71 and 12.82 (Nielsen et al., 1998). Mortality in eating disorders is predominately related to malnutrition, methods of weight control and suicide. Among studies in which cause of death is documented, 54 per cent died of eating disorder complications, 27 per cent committed suicide and the remaining 19 per cent died of unknown or other causes (Nielsen, 2001).

6.4.2. Current practice

There is limited evidence as to how and where risk should be managed. Opinion and practice varies between (and within) countries, centres and clinicians. This is the case both in terms of threshold for hospital admission and the goals of the admission. For example, the APA guidelines (American Psychiatric Association, 2000) recommend admission to hospital when a BMI is less than 16 kg/m 2 or weight loss greater than 20 per cent. In both the US and Australia, patients are generally admitted for short-term medical stabilisation on a medical or paediatric ward. In the UK, patients at low weight are frequently managed in an outpatient setting in specialist eating disorder services. In these instances there is a higher threshold for inpatient treatment with admission often not occurring until the patient’s BMI falls below 13 kg/m 2 . However, managing these low weight patients in an outpatient setting can be hazardous and should rarely be done without specialist advice. In the majority of inpatient specialist services in the UK, the goal is full weight recovery and so admissions are longer term. Admission to either a medical/paediatric or general psychiatric unit may occur but this varies with availability of services.

6.4.3. Physical risk reduction and monitoring

Applying information about the best evidence to a specific patient’s problem is not easy as the clinical picture is diverse physically, psychologically and socially. The patient’s problems have to be clearly defined and placed within the context of a clinical risk assessment. This needs to include an assessment both of the acute risk and the longer-term prognosis.

Decisions on short-term risk involve a combined assessment of the physical risk and the person’s psychological capacity to consent to treatment, taking into account the possible resources of motivation and psychosocial support. A diagram is provided (see Appendix 7) as a simple guide to medical practitioners and other members of the multidisciplinary team as a decision aid when evaluating this acute risk. Body mass index is a better marker than weight alone as a proxy measure of physical risk but a rigid cut off point is less good for the extremes of height as the relationship is non-linear. Children have smaller fat stores than mature women and so medical complications occur with less weight loss. Bulimic features or refusal to drink also increase the risk. In turn, these medical markers interact with a variety of clinical and psychosocial factors. High physical risk is often associated with an impairment of capacity for the consent to treatment.

Because of the paucity of data and the nature of the issue under review, the GDG chose to use an informal consensus process (see Chapter 3, Section 3.4.7. for details) to address questions related to risk reduction and monitoring. The review team conducted a systematic search for all available evidence relating to the issue. A number of studies met the GDG’s eligibility criteria, including two systematic reviews of anorexia nervosa and mortality, and outcome at follow-up (Nielsen, 2001 Steinhassuen, 2002). Long-term follow-up studies on patients suffering from anorexia nervosa were also considered, and where possible predictors and causes of death were noted. This is an area in which there is limited research. Exact causes of death are rarely described. The majority of studies documented cause of death as being as a result of starvation in anorexia nervosa. In those studies where death certificates were examined, again the exact precipitant of death was not always established. There are few post-mortem results documented.

Physical factors associated with higher mortality include severity of weight loss, over-activity and vomiting, bulimia and purging (Nielsen, 2000 Steinhausen, 2002). A BMI less than 13 kg/m 2 in adults is of prognostic significance as it indicates a greater risk for mortality (Casper, 1996 Hebebrand et al., 1997). In the latter study, only seven out of the 14 patients with a BMI of 11 kg/m 2 at referral survived (Hebebrand, 1997). Data on malnourished females in famine indicate that with a BMI less than 11 kg/m 2 , risk of mortality increases sharply (Collins, 1995). Prolonged QT intervals may predispose a person to life-threatening arrhythmias, and might be responsible for cases of sudden death. Furthermore, prolonged QT intervals in ECG were recorded seven days before sudden death (Isner, 1985). Abnormally low serum albumin levels and low weight are the best variables to predict a lethal course (Herzog et al., 1997).

In the studies documenting mortality in patients with anorexia nervosa, causes of death vary. Causes include dehydration, electrolyte (particularly hypokalaemia) and metabolic complications, infections (bronchopneumonia and sepsis) and cardiac complications (see Neumarker, 1997, for review). Comorbid alcoholism has also been shown to be associated with increased mortality (Keel et al., 2003). Rupture/perforation of the gastrointestinal tract has been less frequently described (Zipfel, 2000)

Few studies have reported exclusively on the mortality in adolescents. There is a suggestion that the mortality rate is lower. This may reflect the fact that chronicity and mortality increase with increasing age (Steinhausen, 2002). BMI measures in children and younger adolescents are an inadequate reflection of physical reserve. Weight centiles or percentage weight for height give a more accurate guide to the degree of weight loss. Rapid weight loss in children is potentially more dangerous than in adults, and children are known to dehydrate more quickly (Irwin, 1984). Clinical judgement and physical examination may be a better indicator than serum electrolyte levels as to the need for rehydration (Nicholls & Stanhope, 2000).

6.4.4. Clinical summary

Low weight (BMI less than 13 kg/m 2 ), dehydration and electrolyte abnormalities indicate an increased risk of mortality. Cardiac arrhythmias and low serum albumin and glucose are of particular concern.

6.4.5. Clinical practice recommendations

Managing weight gain

In most patients with anorexia nervosa an average weekly weight gain of 0.5 to 1 kg in inpatient settings and 0.5 kg in outpatient settings should be an aim of treatment. This requires about 3500 to 7000 extra calories a week. [C]

Regular physical monitoring and in some cases treatment with a multi-vitamin/multi-mineral supplement in oral form is recommended for people with anorexia nervosa during both inpatient and outpatient weight restoration. [C]

Health care professionals should advise people with eating disorders and osteoporosis or related bone disorders to refrain from physical activities that significantly increase the likelihood of falls. [C]

In children and adolescents with eating disorders, growth and development should be closely monitored. Where development is delayed or growth is stunted despite adequate nutrition, paediatric advice should be sought. [C]

6.4.6. Long-term risk and its management

Apart from the concern of immediate physical risk in patients with anorexia nervosa, the long-term physical consequences are considerable. For the purposes of this section, the GDG chose to focus on the effects on the skeletal system, on reproduction and the associated hormonal abnormalities, including low oestradiol, low IGF-I, and high serum cortisol that may contribute to the bone loss. Gastrointestinal and dental complications are largely as a result of vomiting and laxative abuse. These are described in the chapter on bulimia nervosa. It should be noted however that many of these complications are exacerbated in patients with low weight and muscle weakness. Other consequences have also been described (e.g. cardiac, dermatological, haematological), but these will not be covered in this guideline.

The development of osteopenia and osteoporosis is a serious and long-term consequence of starvation. Oestrogen deficiency, malnutrition, low body mass and hyperactivity all play a part in this development. This section will consider evidence for the effect of weight gain and medication in the management of this complication. In children and adolescents, weight loss has particularly serious implications. Sixty per cent of bone accretion occurs during puberty (Golden, 1992). Gain in bone mass is most pronounced between 11 and 14 years of age and falls significantly after 16 years of age (Soyka et al., 2002). Therefore, it would be expected that the failure of bone mineral accrual in girls with anorexia nervosa would differ depending on the maturation age.

Failure of this accretion thus compounds bone loss in children and adolescents with anorexia nervosa. Growth retardation is a further complication in children and adolescents (Russell, 1985 Danziger, 1994) and failure to grow may indicate nutritional deficiencies. It is thought that with weight gain �tch-up growth’ can occur up until fusion of the epiphyses (Nicholls & Stanhope, 2000). Regular monitoring of height as well as weight is important in children and adolescents with anorexia nervosa. Recommended weight ranges have to be regularly adjusted to take into account changes in height and age. Hormonal treatments, although used, have not been evaluated in adolescents with anorexia nervosa. There is a risk that oestrogen administration may cause premature epiphyseal fusion and growth stunting (Nicholls & Stanhope, 2000).

With regard to the reproductive system, there are several areas of concern: infertility, persistent amenorrhoea and oligomenorrhoea, and polycystic ovaries. In adolescent anorexia nervosa there is a risk of pubertal delay and ultimately arrested pubertal development (Russell, 1985). The effect on fertility and pregnancy will be described below.

Dental erosion is the most common oral problem in patients with eating disorders who engage in self-induced vomiting. A discussion of the issues concerning dental complications can be found in the chapter on bulimia nervosa (Section 7.5.2).

Osteoporosis

People with anorexia nervosa have reduced bone mineral density (BMD) (Bachrach, Guido, Katzman, Litt & Marcus, 1990) which is associated with an increased fracture rate (Rigotti, Neer, Skates, Herzog & Nussbaum, 1991 Vestergaard et al., 2002 Lucas, Melton, Crowson & O�llon, 1999 Soyka, Grinspoon, Levitsky, Herzog & Klibanski, 1999) and long-term disability such as pain, kyphosis and loss of height. Osteoporosis is manifest in some people after a year of illness and the severity gradually increases over time if the illness remains untreated. Fractures may occur after a few years of illness.

The factors that predict bone density in the majority of studies include: duration of amenorrhoea (Biller et al., 1989 Seeman, Szmukler, Formica, Tsalamandris & Mestrovic, 1992), BMI, or some other variable that reflects body composition (Grinspoon et al., 2000). Some studies find that age at menarche is also a predictor (Grinspoon et al., 2000). Oestrogen use does not predict density in larger studies (Grinspoon et al., 2000).

There have been several longitudinal studies that have examined changes in bone density over time. In the majority of cases the people are also engaged with treatment, commonly nutritional and psychological interventions. In some studies additional treatments such as fluoride and hormone replacement have been added. It is difficult to compare between studies as the presentation and type of data differs between studies, as does the case mix.

Adolescents. One of the largest studies in adolescents is that of Castro and colleagues (Castro et al., 2001). They have an early intervention service with a young (mean age 14.4 years) and moderately severe (BMI 15 kg/m 2 ) group. They found that change over time depends on the severity of the osteoporosis at baseline and the degree of recovery made over the period of follow-up. The group with established osteopenia at baseline (i.e. z < 𢄡.0) had an increase in bone density of over nine per cent at spine (5.7 per cent in the femur) over the follow-up interval (1.3 years).

Adults. In adults (mean age 22 years) with a severe illness (mean BMI 13.9 kg/m 2 ) followed over two years, when BMI increased to 17.1 kg/m 2 there was an overall two per cent increase in bone density which related to weight gain. The subgroup that had full recovery (weight gain and menstruation) had the largest increase in bone density (Iketani et al., 1995).

An additional study (Zipfel et al., 2001) in adults (21 years) with BMI 14 kg/m 2 found similar results.

Current Clinical Practice. The most effective treatment/preventative agent for osteoporosis in anorexia nervosa is not yet known. Adequate nutrition and weight are the most relevant factors but in some cases this is difficult to implement in the long term. Therefore, there has been interest in replacing some factors of relevance to bone turnover. These include oestrogen (in the form of hormone replacement therapy or the contraceptive pill) which inhibits bone resorption and Vitamin D, calcium, and insulin-like growth factors (Grinspoon, 1997 & 2002) and DHEA (Gordon, 2002).

Bisphosphonates and fluoride have also been tried (Maugars et al., 1996). It is anticipated that further guidance on the management of osteoporosis will be available on the treatment and management of osteoporosis following the publication in 2005 of the NICE clinical practice guideline.

6.4.6.1. Treatments reviewed

The following treatments were included:

6.4.6.2. Studies considered

The review team conducted a new systematic search for studies examining factors associated with the management of osteoporosis in people with anorexia nervosa. Five RCTs met the eligibility criteria set by the GDG (Gordon, 1999 & 2002 Grinspoon, 1996 & 2002 Klibanski, 1995), involving 207 participants.

Of the five studies included, one compared oestrogen supplementation with assessment only (Klibanski, 1995), one compared different doses of DHEA (Gordon, 1999), one compared DHEA with hormone replacement therapy (Gordon, 2002), one compared two different doses of IGF-I with placebo (Grinspoon, 1996), and one compared IGF-I, oestrogen supplementation, placebo and the combination of IGF-I and oestrogen (Grinspoon, 2002).

6.4.6.3. Evidence statements 3

There is insufficient evidence to determine whether oestrogen supplementation improves bone density by the end of treatment. [I]

There is insufficient evidence to determine whether oral DHEA improves bone density compared to hormone replacement therapy by the end of treatment. [I]

There is limited evidence that both IGF-I alone and the combination of IGF-I and an oral contraceptive may improve bone density:

There is some evidence that the combination of rhIGF-I and an oral contraceptive is produces a better outcome than rhIGF-I alone.

There is insufficient evidence to determine whether oestrogen supplementation is more or less acceptable to people with anorexia nervosa when compared to no oestrogen supplementation. [I]

There is insufficient evidence to determine whether oral DHEA is more or less acceptable to people with anorexia nervosa when compared to hormone replacement therapy. [I]

Full recovery from anorexia nervosa with weight gain and return of menstruation leads to a marked increase in bone density (the rate depends on the initial level, but can be as much as five per cent or more a year). However in those that remain under weight with amenorrhoea bone loss continues. [III]

In adolescents with a good outcome and low initial bone density the increase in BMD is four-fold that of normal adolescents. [III]

6.4.7. Clinical summary

Bone loss is a serious problem in anorexia nervosa with serious long-term consequences. Weight restoration is associated in adolescents with important gains in bone density. Oral oestrogen and oral DHEA do not appear to have a positive impact on bone density and hormone replacement therapy is not recommended in children and adolescents as it may cause premature fusion of the bones. High impact exercise is associated with an increased risk of fracture in anorexia nervosa. rhIGF-I, alone or in combination with an oral contraceptive, is associated with improvements in bone metabolism and bone mineral density but intensive clinical monitoring is necessary and this treatment should only be given in specialist centres with appropriate skills and knowledge. The long-term effect is uncertain.

6.4.8. Clinical practice recommendations

Oestrogen administration should not be used to treat bone density problems in children and adolescents as this may lead to premature fusion of the epiphyses. [C]

6.4.9. Other physical interventions

Malnutrition is a core feature of anorexia nervosa. Refeeding is a necessary component of treatment but is not sufficient. The approach to refeeding varies between centres and countries. There is debate about the setting, means and rate of weight gain and limited evidence to support different views. In some centres the calorie deficit is made up with food, given as normal, albeit larger, meals or snacks. In other centres liquid foods can be used to supplement or replace some or all of the meals. An alternative, which is not used frequently within the UK, is nasogastric feeding. Rarely percutaneous endoscopic gastrostomy (PEG) or total parenteral nutrition (TPN) has been used. These interventions are only used when patients are not able to co-operate with oral refeeding and there is concern about physical risk. In these circumstances legal and ethical considerations need to be addressed.

A number of complications can occur during refeeding. This is a high-risk period for biochemical abnormalities. People at most risk are those with a BMI less than 12 kg/m 2 , those who vomit, abuse laxatives and binge, and those with concurrent physical conditions. Physical monitoring is necessary during periods of refeeding. A range of electrolyte disturbances can occur during refeeding, which are sometimes referred to collectively as the ‘refeeding syndrome’. Hypophosphataemia may develop rapidly during refeeding if severe, it can cause cardiac and respiratory failure, delirium and fits. Ingestion of large quantities of carbohydrates, during rapid refeeding, may result in a precipitate drop in serum phosphate levels. Therefore, in the first few days of refeeding patients who have had very low or absent intakes for long periods, no attempt should be made to achieve net weight gain. Instead they should receive energy and protein provision at levels at or less than their estimated basal requirements with generous provision of balanced multi-vitamins and minerals especially thiamine, potassium, magnesium and phosphate.

Certain vitamin or mineral deficits have come under close scrutiny. For example, the similarity between some of the symptoms of zinc deficiency and the symptoms of anorexia nervosa has led to an interest in zinc replacement. A proportion of patients with anorexia nervosa may be deficient in thiamine, riboflavin, Vitamin C and Vitamin D. The clinical significance of many of these deficiencies is unclear but it is usual for there to be a general rather than a specific deficit and therefore a multi-vitamin/multi-mineral supplement in oral form (e.g. suitable preparations include Sanatogen Gold [non-NHS], Forceval 1𠄲 or Seravit capsules daily). Care should be taken to prevent the risk of vitamin A and D toxicity from excessive use of supplements.

There has been some research into the nutritional management of anorexia nervosa but all of the studies on nutritional approaches are quasi-experimental and small, and the studies on zinc are small.

There is controversy, but little evidence, about the appropriate time course used to achieve the goals of treatment. Some argue that it is important to restore normal weight as soon as possible, others argue for a slower increase in weight. The standard rate of weight gain in the UK is 0.5 to 1 kg per week. The majority of people with anorexia nervosa are treated as outpatients but for the small number who require admission most specialist eating disorder inpatient units aim to discharge people once weight is fully recovered. However, there is an alternative view that full weight recovery can be achieved by outpatient or day patient interventions following brief inpatient refeeding, and that discharge at an intermediate weight may provide an alternative.

There is also the argument that weight gain is only one outcome of interest. Another goal is to ensure that eating behaviour is normalised and maintained after discharge, that abnormal weight and shape cognitions are normalised and that there is improved quality of life in people with anorexia nervosa.

Physical therapies have been used in some European countries (e.g. Belgium and Norway), which have a long tradition of integrating physical therapies into psychotherapy. Physical rehabilitation programmes including riding, climbing, for example, have been used. This has not been the tradition in the UK. Indeed in many programmes in the UK exercise is restricted and bed rest is prescribed.

Feeding in the context of active resistance

This section relates to those occasions where the individual requires restraining to allow the refeeding to take place. Feeding in the context of active resistance raises ethical, legal and clinical issues for all involved. The reporting of it in the general media is often inaccurate and emphasises the emotive 𠆏orce feeding’ and the suggested abuse of the individual’s rights who is fed in this way. In the UK in the treatment of people with anorexia nervosa it is a very rare event and should only be done in a specialised treatment setting with access to the skills and experience required to manage it safely and effectively. It raises complex legal issues. It is interesting to note that all requests to the courts for permission to carry out this intervention in anorexia nervosa have been granted. It is undertaken using the Mental Health Act 1983, the Children Act 1989 and parental authority. Only a small proportion of patients who are admitted and treated compulsorily require this intervention. No studies have reported on the characteristics of those who are fed in this way, or have followed them up.

Methods of delivering this intervention vary across the country, as do the circumstances under which it is used. The risks associated with nasogastric (NG) tube feeding, PEG, or spoon feeding, will be increased in the context of active physical resistance. Actions such as the pulling out the (NG) tube, interfering with or pulling out the PEG, and the physical condition of the patient increase the risk involved.

Clinical decisions as to when to start the intervention, how long to continue for, how often to repeat the intervention and when to stop are complex and difficult. There are further complications with children and adolescents where the urgency to intervene is increased because the low fat mass means that any weight loss is predominantly of lean tissue with higher medical consequences. As a result, children can become dangerously physically compromised. In addition, children and younger adolescents have a much greater tendency to restrict both fluid and food intake. The combination of these factors leads to a rapid breakdown of muscle tissue and dehydration, especially in pre-pubertal children.

6.4.9.1. Physical interventions reviewed

The following interventions were included:

6.4.9.2. Studies considered

The review team conducted a new systematic search for RCTs of physical interventions used in the treatment of anorexia nervosa. As there were few RCTs, the GDG elected to utilise lower levels of evidence where necessary. This included the APA guidelines and a recent expert review on the nutritional management of anorexia nervosa (EDSIG). Eight studies met the eligibility criteria set by the GDG (Arii, 1996 Birmingham, 1994 Hart, 2001 Katz, 1987 Lask, 1993 Pertschuk, 1981 Robb, 2002 Thien, 2000), involving 267 participants.

Of the eight studies, two involved nasogastric feeding (Arii, 1996 Robb, 2002), one TPN (Pertschuk, 1981), three zinc (Birmingham, 1994 Katz, 1987 Lask, 1993), one exercise (Thien, 2000), and one massage (Hart, 2001).

Full details of studies included in the guideline and reasons for excluding studies are given in Appendix 18.

6.4.9.3. Evidence statements 3
Effect of treatment on weight gain

There is limited evidence suggesting that there is a clinically significant difference between nasogastric feeding and ‘standard care’ with nasogastric feeding being superior in terms of weight gain by the end of multi-modal inpatient treatment (n = 116 Arii, 1996 Robb, 2002). [II]

There is insufficient evidence to determine whether zinc supplementation has any impact on weight compared with placebo during multi-modal inpatient treatment. [I]

There is insufficient evidence to determine whether TPN has any impact on weight compared with placebo during multi-modal inpatient treatment. [II]

There is insufficient evidence to determine whether massage or exercise given in addition to ‘standard care’ have any impact on weight compared with ‘standard care’ alone by the end of treatment. [I]

Effect of treatment on symptoms of anorexia nervosa

There is limited evidence suggesting that there is a clinically significant difference between massage and ‘standard care’ with massage being superior on EDI scores by the end of treatment (N = 1 n = 16 SMD = 1.06 95 per cent CI, 0.02 to 2.09). [I]

Acceptability of treatment

There is insufficient or no evidence to determine whether nasogastric feeding or TPN are more, or less, acceptable to people with anorexia nervosa when compared to placebo or ‘standard care’. [II]

There is insufficient evidence to determine whether zinc supplementation is more, or less, acceptable to people with anorexia nervosa when compared to placebo or ‘standard care’. [I]

There is insufficient evidence to determine whether massage or exercise are more, or less, acceptable to people with anorexia nervosa when compared with ‘standard care’. [I]

Tolerability of treatment

There is evidence from a retrospective chart review that TPN may produce a greater risk of side effects than ‘standard care’:

6.4.10. Clinical summary

Nasogastric feeding can confer some benefit in terms of increased rate of weight gain or actual weight gain, as part of a treatment programme. There was insufficient evidence that either TPN or zinc supplementation confer any benefit in terms of weight gain. TPN appears to be associated with more adverse events in one small study. Some limited benefit, on symptoms but not on weight gain, has also been identified from one small trial investigating massage.

6.4.11. Clinical practice recommendations

Total parenteral nutrition should not be used for people with anorexia nervosa, unless there is significant gastrointestinal dysfunction. [C]

6.4.12. Concurrent physical conditions

Diabetes

There does not appear to be an increased occurrence of anorexia nervosa in Type 1 diabetes, however the statistical power of the studies may be insufficient to rule this out (Nielsen, 2002). The mortality rate in 10 years of follow-up of population-based samples was found to be 2.2 (per 1000 person years) for Type 1 diabetes, 7.3 for anorexia nervosa and 34.6 for concurrent cases (the standardised mortality rates were 4.1 for Type 1 diabetes, 8.9 for anorexia nervosa, and 14.5 in concurrent cases) (Nielsen, 2002).

Close liaison and a shared knowledge base between the eating disorder and diabetes teams is essential in the management of anorexia nervosa with diabetes and they should have intensive regular physical monitoring as they are at high risk of complications and death.

Pregnancy

It is unusual for people with anorexia nervosa to become pregnant although a small proportion have fertility treatment to conceive or relapse into anorexia nervosa during the pregnancy. In a follow-up study of people with anorexia nervosa (n = 140) fertility was reduced to one-third of the expected, the rate of prematurity was twice that expected and perinatal mortality was increased six-fold (Brinch et al., 1988). In a follow-up series of 66 women there was an increased miscarriage rate and more use of Caesarean sections and the offspring were more likely to be born prematurely and smaller (Bulik et al., 1999). On the other hand Steiner found no difference in weight gain and foetal weight in their sample (Steiner, Smith, Rosenkranz & Litt, 1991). In a study in which pregnant women with anorexia nervosa were followed prospectively the infants grew slowly in utero especially in the last trimester (Treasure & Russell, 1988).

Women with anorexia nervosa are at greater risk for premature offspring and those that are small for gestational age. There are case series that suggest that some women with anorexia nervosa have difficulty feeding their children (Russell, Treasure & Eisler, 1998 Wezel-Meijler & Wit, 1989) and that the child’s growth can be abnormal (Hodes et al., 1997).

Management of laxative abuse

The management of laxative abuse is covered in the bulimia nervosa chapter (Section 7.5.2), as the management is essentially the same for both disorders.

6.4.13. Clinical practice recommendations

Managing risk

Health care professionals should monitor physical risk in patients with anorexia nervosa. If this leads to the identification of increased physical risk, the frequency and the monitoring and nature of the investigations should be adjusted accordingly. [C]

People with anorexia nervosa and their carers should be informed if the risk to their physical health is high. [C]

The involvement of a physician or paediatrician with expertise in the treatment of physically at-risk patients with anorexia nervosa should be considered for all individuals who are physically at risk. [C]

Pregnant women with either current or remitted anorexia nervosa may need more intensive prenatal care to ensure adequate prenatal nutrition and foetal development. [C]

Feeding against the will of the patient

Feeding against the will of the patient should be an intervention of last resort in the care and management of anorexia nervosa. [C]

Feeding against the will of a patient is a highly specialised procedure requiring expertise in the care and management of those with severe eating disorders and the physical complications associated with it. This should only be done in the context of the Mental Health Act 1983 or Children Act 1989. [C]

When making the decision to feed against the will of the patient the legal basis for any such action must be clear. [C]


Anorexia nervosa as an anxiety management tool - Psychology

Aim This paper considers how the three principles of evidence based practice (clinical expertise, scientific evidence, and patient preference) can be applied to the complexity of treatment for anorexia nervosa AN.

Method A narrative review of the evidence of these three domains is presented. Clinical cases are used to illustrate how the formulation and management can be put into practice at different stages of illness.

Results The management of anorexia nervosa is complex. First, individuals with the illness do not regard the manifestations of the illness as a source of concern rather they are embraced and integrated into their identity. This contrasts to the reaction of other people who are terrified by the overt signs of ill health. Thus engagement into treatment is problematic. Second, the core symptom restricted eating, produces malnutrition which impacts on brain, body, and the social network. Thus a mixture of psychological and physical problems gradually accumulates over the course of the illness. This means that the treatment targets increase over time.

Conclusion Thus treatment has to work with motivation and readiness to change and tackle the various domains of ill health.


Obsessive Compulsive Disorder Eating Disorders

Individual counts the number of mouthfuls chewed or pieces of food in a meal according to some fixed or magical number that is “correct” or “just right.” Individual counts mouthfuls or pieces of food as a means of limiting portions, and thus effectively losing more weight. Individual repeatedly washes hands due to a fear of germs, contact with waste products, or a number of other sources of possible contamination that exist. Individual excessively washes hands to remove trace amounts of oil that might cause weight gain if ingested. Individual throws out food in a can that has been slightly dented for fear that it might contain food poisoning and later cause serious illness to someone. Individual throws out food in a can because it was discovered to contain too many calories after reading the label. Individual repeatedly asks a waiter in a restaurant about different dishes on menu doubtful that he or she has enough knowledge to make the perfect meal decision. Individual constantly asks same waiter about contents of dishes so as to stay away from having any butter oil or fat. Individual refuses to enter the kitchen in order to eat due to fear of accidentally mixing cleaning items with the food. Individual refuses to enter the same room for it will only lead to the temptation to eat and thus get fat. Individual repeatedly checks refrigerator shelves or other parts of house in order to make sure that every piece of food bought is in its proper designated place. Individual constantly checks same locations in search of food to eat in an extensive bulimic binge period.

Thus in order to differentiate between the two disorders and make the proper diagnosis, it is crucial for the clinician to more closely examine the specific behaviors that are being observed and the motivations behind those behaviors. Whereas patients with eating disorders are primarily driven by concerns of physical appearance, and consequently alter their eating patterns in order to lose weight accordingly. OCD patients may be restricting their eating for reasons very different than body image concerns. Furthermore, for cases in which an individual qualifies for both diagnoses, such as an anorexic or bulimic who also experiences non-food related OCD symptoms, like checking or contamination, it is still imperative to consider whether or not their symptoms are being motivated by both disorders simultaneously. For example, consider a patient washing his/her groceries due to the fear of contamination as well as the fear that the products may contain high fat ingredients.

It should be noted that the recommended psychological treatment for both OCD and eating disorders usually involves some combination of cognitive-behavioral therapy, antidepressant medication, and family counseling. Successful treatment for bulimics in particular often entails classic exposure and response prevention, in which patients are exposed to their favorite foods, asked to eat, and then prevented with careful monitoring from vomiting using laxatives or otherwise purging. Additional techniques involve gradual alteration of eating rituals and increased flexibility in eating behaviors which may include breaking rituals such as the need to use the same utensils to measure food, to time meals, and to avoid certain restaurants. Because eating disorders typically result in numerous medical complications, we strongly encourage physicians and nutritionists to be part of the team.

Significant advancements have recently been made in both the diagnosis and treatment of OCD and eating disorders as separate entities, but ample scientific research into the connection between the two, the commonality of their symptoms, and the possible biochemical similarities behind, them is presently lacking. Fortunately, some of the most promising psychiatric investigations into the overlapping symptoms of spectrum disorders have focused on these neurophysiological similarities. One such study asked participants to engage in a task believed to activate the prefrontal cortex and caudate nucleus of the brain so as to compare the performance of participants with OCD to that of those with anorexia. The study found that both groups had difficulty with the task and had higher cerebral glucose metabolism, suggesting a connection between the two disorders and offering evidence that, “ritualized obsessive and compulsive behavior (with reference to eating disorders, as well as washing and checking OCD) could have its origin within common neurobiological abnormalities,” (Murphy, et al. 2004). Although such results are clearly signs of progress, they are still indirect and speculative at best. More work is therefore needed in order to properly isolate the clinical symptoms, biochemical factors, and genetic causes behind OCD and eating disorders. In one of our studies we found that obsessive-compulsive overeaters responded to exposure and response prevention, while another group of overeaters responded better to more traditional stimulus control methods of treatment (Mount & Nezirogulu 1991). This shows that those eating disorders that are similar to OCD may respond better to treatment strategies used to treat more typical OCD behaviors. Consequently, for the sake of all those who suffer the obsessive-compulsive related disorders need to be studied further in order to enhance our understanding of their similarities and dissimilarities. In doing so we will hopefully not only arrive at better treatment strategies but also increase our knowledge of the psychological and biological mechanisms by which the disorders develop.

Fugen Neziroglu, PhD, is a board certified Behavior and Cognitive psychologist involved in the research and treatment of OCD for 25 years. She is the Clinical Director of the Bio-Behavioral Institute in Great Neck, NY and Professor at Hofstra University.

Jonathan Sandler, BA is a research assistant at the Bio-Behavioral Institute in Great Neck, NY and he is involved in the research of Obsessive Compulsive Spectrum Disorders.

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