4.1. How are eating disorders defined and classified? What are the shared and specific clinical features of each type?
4.2. Etiopathogeny of eating disorders: What are the main risk factors?
4.3. What are the most frequent comorbidities of eating disorders?
Eating disorders are a group of mental disorders characterised by disordered eating behaviour and the development of behaviours aimed at managing weight. These behaviours lead to physical problems and deteriorated psychosocial functioning of the patient. Current classifications of eating disorders include AN, BN and other less specific disorders known as EDNOS (See chapter 7, “Diagnosis”).
The first descriptions of AN date back to the 17th century, when Morton determined that the origin of this disorder, in contrast to other states of malnutrition, was a disturbance of the nervous system accompanied by sadness and pre-occupation. In the 19th century, it was described as an individual psychopathological picture similar to the one observed today, though it was believed to be a mood disease. Although the history of BN is much younger, the number of affected patients has been growing significantly in the past few years, possibly due to its less dramatic evolution and the ease with which affected individuals go undetected.
AN is an eating disorder that manifests itself as an uncontrollable desire to be thin, accompanied by the voluntary practice of procedures to achieve this goal: a strict, restrictive diet and purging behaviour (self-induced vomiting, laxative abuse, use of diuretics, etc). Despite gradual weight loss, patients present an extreme fear of becoming obese. They present body image distortion and an extreme pre-occupation with diet, figure and weight, and thus engage in food avoidance behaviour by means of compensatory actions to compensate for what they have ingested (extreme physical hyperactivity, purging behaviour, etc). Patients are not usually aware of the disease or the risks their behaviour entails. Their attention is focused on ponderal loss, leading to deficient nutritional states and ultimately to life-threatening risks. Usually there are previous personality traits that tend towards conformism, the need for approval, hyperresponsibility, perfectionism and poor response to internal needs.
BN is an eating disorder characterised by binge-eating episodes (voracious and uncontrolled eating), in which a large amount of food is consumed in a short period of time and usually in secret. Affected individuals attempt to counteract the effects of over-eating by means of self-induced vomiting and/or other purging methods (misuse of laxatives and diuretics, etc.) and physical hyperactivity. These individuals present pathological concern about weight and figure. BN does not necessarily lead to weight changes. Patients can present normal, low or excess weight. BN tends to be a hidden disorder given that it goes easily undetected and patients deal with feelings of shame and guilt. Patients usually seek help when the problem has progressed to advanced stages. EDNOS are usually incomplete AN or BN pictures that do not constitute a complete picture. They are not, however, less serious.
EDNOS include disorders such as the frequent use of inappropriate compensatory behaviour (after eating, chewing and spitting out small amounts of food) and recurrent compulsive eating episodes without compensatory behaviour. BED is a disorder that is currently in the study phase to determine if it is a disorder different from other EDNOS or simply a light form of BN. The main difference with BN is the absence of compensatory mechanisms, which eventually lead the patient to inevitably become overweight or obese.
At a psychopathological level, AN and BN share an excessive pre-occupation with image and weight, which reaches irrational extremes in AN (not in BN). At a physical level, malnourishment and its potential complications are always present in AN and possible in the case of BN. There are also mixtures of anorexic and bulimic behaviour that are hard to differentiate, although ponderal loss and secondary malnutrition point to AN.
Like other mental disorders, eating disorders have a multiple and somewhat uncertain ethiology (yet unclear). According to studies, its ethiopathogeny involves several biological-genetic and vulnerability factors, psychological characteristics, sociocultural aspects and stressors.
The specific impact of each one of them is yet to be determined. Eating disorders tend to begin in adolescence, although we are seeing a gradual increase in the frequency of cases beginning in adulthood and childhood. These disorders usually affect the female population (for every 9 cases of eating disorders in women, there is 1 in men, approximately).
At present, several risk factors have been determined for these disorders. The designs of some of the studies used have been cross-sectional and enable us to establish associations and not causal relationships.
Research on biological factors has focused mainly on genetic factors and neurobiological disturbances.
Studies conducted on families show a higher frequency of eating disorders among relatives of individuals with eating disorders than among control subjects, leading to the conclusion that there must be family vulnerability to these disorders.
Case-control studies using molecular genetics have found a positive association between the presence of certain polymorphisms and a greater vulnerability to developing AN. The most studied are the serotonergic system (5-HT; regulates appetite, stress response, sexual behaviour, obsessive symptomatology, mood, etc), the dopaminergic system and neurotrophins76 (especially BDNF, NTRK277 and NTRK378).
Equally positive results have also been obtained in chromosomes 1, 2 and 13. However, these results are not yet conclusive. Genes seems to account for 60% to 70% of vulnerability in the case of AN79. In the case of BN, susceptibility is found in chromosome 1080. There is discrepancy regarding the early appearance of menarche as a risk factor in girls.
The studies identified the following sociocultural factors as risk factors for eating disorders: overprotective, rigid and demanding, conflictive and poorly cohesive family models81, 82, destructured families (divorced parents), family history of mood disorders and obsessive-compulsive symptomatology83, eating disorders (especially in mothers), atypical dieting and/or eating behaviour in the family (parents concerned about weight) 84, 85, obesity (especially in mothers) 85, 86, alcoholism (especially in fathers), inconsistent eating habits during childhood81, careers and/or activities during childhood-adolescence that place too much emphasis on slimness and/or weight87-89.
The following psychological factors have been associated with eating disorders: mood disorders90, 91, personality disorders92, obsessive-compulsive disorders93, impulse control disorder94, following an anomalous and restrictive diet and pre-occupation with the body, personal history of eating difficulties85, extreme rigidity, perfectionism, social alienation and low self-esteem95.
Regarding the potentially stressful life events associated with eating disorders, the following stand out: sexual and/or physical abuse during childhood, criticism towards one’s body and a history of life crisis85.
According to a review of eating disorder risk factors, some of the previously mentioned factors have shown consistent results in the prediction of eating disorders, both in longitudinal and cross-sectional studies: gender, ethnicity (except Asians), eating problems and gastrointestinal disorders at early ages of childhood, sexual abuse and other adverse life experiences, low self-esteem, general psychiatric morbidity, high weight and bodily dissatisfaction and dieting97.
Of all the different explanatory models of AN, Garner’s (1993) 98 suggests that AN is the result of the interaction of three types of factors: predisposing, precipitating and perpetuating. Predisposing factors confer susceptibility to AN.
Some of these are determined by a genetic component, such as the female sex. Other predisposing factors are individual, family and cultural. Precipitating factors, such as dissatisfaction with body weight and shape, interact with predisposing factors in such a way that they condition affected individuals to the point where they decide they must lose weight and restrict eating. Once AN has initiated, gradual weight loss leads to complications derived from malnutrition. The disorder’s multidimensional consequences (physical, psychological and social) are both perpetuating factors of the disorder and boosters of predisposing and precipitating factors.
Current literature suggests that eating disorders are partially determined by both sociocultural83,84 and biological-genetic factors (the latter would explain 60%-70%)99-101. However, a part of the variance is not explained by any of these factors, leading to the performance of studies that assess the relevance of non-shared environmental factors which would explain why twins, who have been raised in a similar family environment, can differ in terms of eating behaviour, pathological in some cases and normal in others. Amongst these factors, the following would be included: parents treating each sibling differently, the subjects’ personality and temperament, the subjects’ relational style, experienced stressful situations and specific differential characteristics81, 86. Published scientific evidence shows that non-shared environmental factors are more relevant than shared factors. In this respect, 24% to 42% of variance in AN102 and 17% to 46% of variance in BN90 would be explained by the influence of non-shared environmental factors.
Comorbidity in eating disorders is common, both of mental and organic origin. The next section describes the most frequent associations. The therapeutic approach required in these cases will be addressed in the chapter dealing with treatment.
Abuse of illegal substances and chemical dependence is common in eating disorders, especially in BN and similar clinical pictures. In the beginning the use of stimulants (amphetamines and cocaine) is related with attempts to decrease appetite, but later it is linked with impulsivity-associated BN pictures. Up to 40% of diagnosed patients (AN or BN) admit to abusing or having a dependence on alcohol or illegal substances103-105.
Anxiety is so present in eating disorders it is hard to decide if it is a specific clinical component of these disorders or if it is a comorbid condition. Eating disorders present specific phobia clinical pictures (phobia of certain foods, social phobia, etc.) and others such as claustrophobia or unrelated simple phobias. Panic attacks or anxiety crises present a similar situation. In some cases they are linked to eating disorders and in others they are truly comorbid. Studies report very varied anxiety prevalences that range between 10% and 40%, depending on the measurement tools and inclusion criteria used106-109 .
Patients with eating disorders, especially AN, present significant prevalence of obsessive personality traits (See personality disorders). Many of these patients are rigid, strict, organized, responsible, constant, intransigent and intolerant, personality traits that predispose and accompany eating disorders. However, in a considerable number of patients, up to 40% of them diagnosed with AN, obsessive-compulsive disorder that meets comorbidity criteria is present110-112.
Approximately 30% of eating disorder cases present personality disorders113-115. There is a high prevalence of patients who meet BN criteria and present an associated personality disorder, especially borderline and histrionic.
Depression is closely linked with eating disorders. It is hard to think of AN or BN without a depressive clinical picture. As in the case of anxiety, in some cases depression predisposes and in others it is linked with the clinical manifestation of eating disorders or presents itself as a comorbid condition. Prevalence of depression ranges between 40% and 80% and occurs more frequently in BN116,117.
Some of the behavioural disturbances of eating disorders entail a loss of self-control (overeating, purging behaviour, self-aggression, etc.). Other impulse control disorders occur with eating disorders, such as kleptomania or trichotillomania118-119.
DM is present in the genesis and evolution of eating disorders and also in treatment, which will have to be adjusted to this physical condition. Studies show very varied prevalence rates. Between 0.5% and 7% of cases of AN and BN present Type 2 DM. This percentage reaches up to 20% in EDNOS. Up to 9% of obese diabetics present an eating disorder120-122.
Type 1 DM is a risk factor for eating disorders (three times more risk in BN and two times more risk in subclinical EDNOS120 than the population without type 1 DM). Type 2 DM is a risk factor for engaging in inadequate eating behaviours. When type 1 DM and an eating disorder coincide (OR: 4.8; 95% CI: 3.0 to 7.8) physical complication such as retinopathy increase. In another 4-year longitudinal study (N=91) on a cohort of patients with both pathologies (ED and type 1 DM), 60% were associated with retinopathy123. In a further study conducted by Nielsen, 2002120, mortality in patients with type DM at 10 years follow-up was 2.2 per 1,000 inhabitants/year; in the AN population it was 7.3 and in the population with AN associated with type 1 DM it was 34.4.
Obesity as a risk factor is linked to AN and BN. It is also a mid-long term habitual state of BED and, in this case, obesity directly influences diagnosis and treatment. Up to 6% of obese children present BED124-126.
Especially in AN, malabsorbtion syndromes, gluten-intolerance or lactose-intolerance are risk factors for eating disorders, course and prognosis modifiers and pathologies that must be taken into account when planning a treatment diet aimed at ponderal recovery. There are no prevalence studies and the literature only yields descriptions and studies of alienated cases127,128.
Thyroid diseases, both hyper and hypothyroidism, are relevant in the onset, course, prognosis and treatment of eating disorders. There are no prevalence studies, only case description studies129-132.
Latest update: January 2010