Eating Disorders

Eating Disorders
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Eating disorders are characterized as psychiatric disturbances in eating behavior and self-body perception with psychosomatic consequences[1][15]. It is known to carry the highest mortality rate amongst all psychiatric disorders[27]. There are three main classes of eating disorders: anorexia nervosa (AN), bulimia nervosa (BN), and eating disorder not otherwise specified (EDNOS)[2]. These disorders predominantly afflict young women but can affect males as well[12]. 

The etiology of eating disorders is currently idiopathic though multifactorial models to understand these disorders and the various genetic, environmental and psychological factors that contribute to their onset are used[1]. It has been hypothesized that the vast amount of change that the body undergoes during puberty increases the vulnerability of the appetite regulation systems and the hypothalamus[11]. In addition, certain types of eating disorders are often associated with certain personality traits[1]. Both AN and BN have high psychiatric comorbidity of depressive symptoms and anxiety disorders like obsessive-compulsive disorder[15].

Anorexia Nervosa

Anorexia Nervosa
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The phenomenology of anorexia nervosa[1]

The point prevalence of anorexia nervosa in adolescents and young females is between 0.3% and 0.9% and the lifetime prevalence for 20 to 40-year-old women is between 1.2% and 2.2%[21]. The ratio between affected males and females is approximately 1:10[22].

Symptoms and Diagnosis

The list below contains the diagnostic criteria for anorexia nervosa according to DSM-IV (abbreviated form)[2]:

  1. Refusal to retain body mass appropriate for respective age and height
  2. Intense fear of weight gain
  3. Disturbed perception in one’s body weight or shape
  4. Amenorrhea

There are two forms of anorexia nervosa: restricting and binge-eating-purging types.

Restricting type
During symptomatic AN, the patient does not consistently engage in binge-eating or purging behaviour.

Binge-eating–purging type
During symptomatic AN, the patient consistently engages in binge-eating or purging behaviour.

Binge-eating and purging behaviour includes self-induced vomiting or the misuse of laxatives, diuretics, or enemas.


Nonspecific supportive clinical management treatment for adult AN patients was found to be better at treating the disorder than cognitive-behavioral therapy (CBT) or interpersonal therapy (IPT)[33]. However, it was found that CBT had greater efficacy compared to nutritional counseling after the patient was hospitalized[14].

Selective serotonin reuptake inhibitors (SSRIs) are commonly prescribed for a number of psychiatric conditions. However, a number of studies suggested that the drug did not offer AN patients significant improvements. Some patients found antipsychotic drugs helpful. There is yet to be an approved drug for AN by the Food and Drug Administration (FDA)[20].

Recently, deep-brain stimulation (DBS) has become a very plausible method of treatment for unresponsive AN patients. The target of stimulation that was proposed was the nucleus accumbens (NAcc) which may also be in conjunction with an anterior capsulotomy (lesioning of the anterior limb of the internal capsule)[4]. A video from UHNToronto and Dr. Lozano’s group documenting an AN patient testifying their positive results from DBS is placed below.

Brain surgery gives 'new life' to anorexia patient - UHNToronto[47]

Bulimia Nervosa

The point prevalence of bulimia nervosa in adolescents and young females is between 1% and 2% and the ratio between affected males and females is approximately 1:30[22].

Symptoms and Diagnosis

The list below contains the diagnostic criteria for bulimia nervosa according to DSM-IV (abbreviated form)[2]:

  1. Repeated cases binge-eating distinguished by consuming an abnormally large amount of food compared to healthy control during a similar time frame under similar circumstances; and the feeling of no control over their behaviour
Repeated inappropriate compensatory behaviour to avert weight gain (e.g., self-induced vomiting; misuse of laxatives, diuretics, enemas, or other medications; fasting; excessive exercise)
Binge-eating and inappropriate compensatory behaviours concurrently happen at least twice a week for 3 months 

  4. Body shape and weight 
inappropriately affects the evaluation of oneself
  5. Disturbances are not exclusive to episodes of AN

There are two forms of bulimia nervosa: purging and nonpurging type

Purging type

During symptomatic BN, the patient consistently engages in self-induced 
vomiting or the misuse of laxatives, diuretics, or enemas.

Nonpurging type
During symptomatic BN, the patient participates in other inappropriate compensatory behaviours (e.g., fasting or excessive exercise) but does not consistently engage in self-induced vomiting or the misuse of laxatives, diuretics, or enemas.


Cognitive Behavioural Therapy
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Unlike AN patients, BN patients found CBT to be helpful. So, CBT is the most frequently applied behavioral intervention for BN. Approximately 30-40% of BN patients were alleviated of their symptoms after treatment and these improvements persisted in the long-term[20]. A recent study showed that IPT was also as effective as CBT[40].

Another difference between AN and BN patients is that SSRIs were approved by the FDA as a drug to treat adult BN. Alternative drugs, like topiramate and ondansetron, were also found to be effective in treating adult BN but the studies illustrating this were composed on relatively small sample sizes. In addition, the clinical utility of topiramate is currently debated due to its detrimental side effects that include cognitive impairment and neurological symptoms[20].

Eating Disorders Not Otherwise Specified

The list below contains the diagnostic criteria for EDNOS according to DSM-IV (abbreviated form)[2]:

  1. All diagnostic criteria for AN are satisfied, except the menstrual cycle is normal
  2. All diagnostic criteria for AN are satisfied, except weight is normal with respect to patient's height and age despite significant weight loss
  3. All diagnostic criteria for BN are satisfied, but patient's binge-eating behaviour is less frequent than twice per week and for a duration of less than 3 months
  4. Patient attempts to compensate by eating small amounts of food, but weight is normal with respect to patient's height and age
  5. Chewing and spitting out a lot of food frequently but no swallowing
  6. Binge-eating disorder – consistent binge eating with no effort to compensate

Due to the heterogenous nature of EDNOS, prognosis and treatment is likely to be different with respect to the particular phenomenology of EDNOS in a particular patient[43].

Binge Eating Disorder

Binge eating disorder (BED) that is listed under EDNOS is characterized to have regular episodes of binge eating, but with no recurring efforts to compensate, such as purging or excessive exercise[2]. A frequent behaviour observed is the affected individual to eat alone or late at night in concealment. Unlike AN and BN, it is more common for individuals with BED to be obese or overweight[1].

Recently, it has been suggested that BED should have its own official diagnostic that was independent of EDNOS in the upcoming DSM-V (watch video below for more information). There are a number of reasons as to why these suggestions arose. For one, a major population of EDNOS patients fit the BED diagnosis. Also, the criteria for BED is easily applicable in clinical situations since its diagnosis relies on unique clinical markers that are different of BN and obesity. And finally, there are effective treatments for BED that are currently in use[43].

What Is an Eating Disorder Not Otherwise Specified? | Eating Disorders - Howcast[48]

Structural Differences

Anorexia Nervosa

Reduced volume: hippocampus-amygdala, ant. cingulate, total grey matter

Pathological enlargements of the ventricles and/or sulci alongside cerebral atrophy in symptomatic AN were found in a number of studies. The loss of both grey and white matter appeared to happen diffusely in the brain. These changes were found to revert back to normal once the patient was asymptomatic. There is evidence to suggest exceptions to this reversion. In one study, AN patients were found to have persistent reduced volume in the hippocampus-amygdala, anterior cingulate, and total grey matter after weight recovery. In particular, the reduction in total grey matter remained after years of normalized body weight[37][25].

Another study, using proton magnetic resonance spectroscopic imaging (MRSI), showed significant metabolite changes in the grey matter of AN patients compared to healthy control. This suggested that the grey matter was distinctively vulnerable to nutrient depletion[5].

In addition, the Papez Circuit, which includes structures like the fornix and cingulate gyrus, was found to be compromised in AN patients compared to healthy control. A study, using diffusion tensor imaging, showed a reduction in white matter integrity in the bilateral fimbria-fornix, fronto-occipital and cingulum white matter association fiber tracts for AN patients[29].

Bulimia Nervosa

Asymmetry of brain glucose metabolism

Asymmetric Index Data
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Comparing AI in each brain region between BN patients and healthy control[35]

One study suggested that bulimia nervosa carried characteristic asymmetries in cerebral blood flow. Using single photon emission computed tomography (SPECT), the investigators compared the changes in cerebral blood flow (CBF) from resting state to eating behavior between BN patients and age-matched healthy control. The results included distinct differences between BN patients and control groups in the asymmetric index (AI), which illustrated the magnitude of asymmetric CBF there was between hemispheres relative to certain brain regions. The AI value of the BN group was positive in all cortical regions with the exception of the temporal region before eating. After eating, the AI values of the BN group reversed to negative, which showed greater CBF on the left hemisphere than the right[35].

Enlarged ventricles, widened cortical sulci, reduced cerebral/cranial ratios

White Matter Integrity of BN Patients
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Reduced white matter fractional anisotropy in BN patients compared to healthy control[34]

There are a number of structural differences that are observed in those afflicted with bulimia nervosa compared to healthy individuals. In one study, 40% of normal-weight patients exhibited enlarged ventricles, widened cortical sulci and reduced cerebral/cranial ratios on CT scans. Though, these changes were found to be evident only when the patient was symptomatic–they seemed to resolve back to normal with recovery. Because these patients were of normal weight, it was suggested that the changes were observed were correlated to disturbed endocrine systems or metabolic factors instead of weight loss[37]. Another study used diffusion tensor imaging to show reduction in white matter integrity of BN patients compared to healthy control women, particularly in the bilateral corona radiata extending into the posterior limb of the internal capsule, the coprus callosum, the right sub-insular white matter and right fornix[34].

Functional Differences

Changes observed from food cues

Cortico-Striatal Pathway
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With a focus on taste - illustrates how differences
in brain region activation of AN and BN patients could
influence this circuit[28]

Homeostatic regulation necessitates our brains to evaluate the sensory cues of food and decide whether to approach it if it’s desired. Though, this regulation is not solely responsible for our eating behavior where a diverse range of physiological, emotional and cognitive processes are elicited by our interactions with food[17]. In comparison to non-food objects, the sight of food normally activates our occipital, limbic and paralimbic, and prefrontal areas, which is hypothesized to activate anticipatory responses that will probably govern eating behavior[3][31][42].

A number of functional magnetic resonance imaging (fMRI) studies demonstrated that patients afflicted with an eating disorder showed greater activation in the medial prefrontal cortex (mpFC) and inhibition of the lateral prefrontal cortex[30]. AN patients also showed hypoactivity in the inferior parietal lobe and orbitofrontal cortex (oFC) compared to healthy control[23][7]. When compared to BN patients, AN patients showed increased activation of the posterior cingulate cortex, anterior cingulate cortex/mpFC, lateral oFC, and the lingual gyrus. BN patients showed increased activation in the superior and middle temporal gyrus, caudate, supplementary motor area and cerebellum in comparison to AN patients[30][7][44].The mPFC has been shown to also activate in self-referencing tasks that involved self-reflection and judgement[32][24]. It is suggested that mPFC activation in AN patients shows how they make out-of-proportion comparisons between their bodies and the bodies of others as they view the food stimulus[39].

Self-images, non-self images, and the insula

Activation When Viewing Self-Images and Non-Self Images
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(a) Control subjects and (b) AN patients show relatively the same amount of
activation when viewing non-self images. However, (d) AN patients show a significant
reduction in activation than (c) control patients when viewing self-images[39]

A unifying symptom that is characteristic of many eating disorders is the way the patient perceives themselves. For one, AN patients experience intense self-body awareness and differentially perceive their bodies from others[2]. They construct inappropriate representations of their own body images based on various information systems. These systems contribute to how they believe they look, their satisfaction of how they look and how they believe other people would perceive their bodies[9]. With AN patients, these systems work in a way to distort their body images by making these patients think they’re overweight and feel dissatisfied with their body[39].

A recent fMRI study was able to shed light on some of the neural correlates of this phenomena. AN patients were found to have reduced activation in the paracentral lobule, precuneus, superior temporal gyrus, cuneus and the lingual gyrus when viewing self-images. This lack of activation was suggested to work in an effort to suppress cognitive, perceptual and emotional processing. When viewing non-self-images, AN patients showed increased activation in the middle and inferior frontal gyri, superior parietal lobule, fusiform gyrus, inferior occipital gyrus and the thalamus compared to the control group[39].

In contrast, the control group elicited greater activation of the insula, prefrontal cortex and occipital lobe than AN patients, as well as the dorsolateral prefrontal cortex (dlpFC), thalamus and cerebellum when viewing self-images. It has been suggested that the insula played a key role in forming the representation of the body schema, which may be due to its ability to integrate sensory information from numerous modalities[6]. In addition, it is involved in the somatosensory-limbic pathway responsible for relating information to the self. The lack of insula or prefrontal cortex activation in AN patients could be a possible explanation for their self-image distorting behavior[39].

Differential EBA activation

EBA Activation
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Eating disorder patients show reduced amount of EBA activation compared to healthy control[45]

The extrastraite body area (EBA) is found in the occipito-temporal site of the visual cortex and is responsible for processing and perceiving human bodies[38]. An fMRI study investigated the differential activation of EBA between those with eating disorders and healthy control. AN patients were found to have the weakest EBA and parietal cortex activation in response to seeing body shapes compared to BN patients and healthy control. BN patients were found to have activation in the right lateral fusiform gyrus that was stronger than AN patients but weaker than healthy control[45].

In AN patients, an MRI study was conducted to show significantly reduced grey matter volume in the left lateral occipital cortex where the EBA is situated. This finding also found the overlap of activated groups of nuclei related to EBA activation and the reduction of gray matter in the same area. The behavioral data also illustrated the AN patient’s tendency to overestimate body size compared to healthy controls. As a result, a correlation between EBA density and body size misjudgment was found and provided support for a significant correlation [41].

Reward processing

Mesolimbic System
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Many aspects of this circuit may be altered in eating disorder patients[18]

The mesolimbic dopaminergic pathway that involves the ventral tegmental area and the limbic system via nucleus accumbens is responsible for reward processing[18]. It is suggested that the rewarding nature of food is of a lesser degree in AN patients, which may be linked to OFC or striatal activation. It is found that AN patients do have disrupted reward processes that, in turn, influences many behaviors[28]. For one, these patients were found to be anhedonic and able to consistently deny themselves of food and other sources of pleasure[16]. In contrast, BN patients are prone to impulsivity, and pleasure and are less concerned with consequences [8]. A number of studies show that both symptomatic and recovered AN patients display altered dopamine function, which could lead to alterations of appetitive behaviors, anhedonia, dysphoric mood, and increased motor activity[26][19][46].

See also

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