Bulimia Nervosa

Author: sara tambini
Date: 02/04/2012



Bulimia nervosa (BN) is an eating disorder characterized by a cycle of binge eating (bulimia or bingeing) followed by inappropriate acts (purging) to avert weight gain. Purging methods often include self-induced vomiting, use of laxatives or diuretics, excessive exercise, and fasting.
( http://www.diseasesdatabase.com/:hobix)


The term bulimia comes from Greek βουλιμία (boulīmia; ravenous hunger), a compound of βους (bous), ox + λιμός (līmos), hunger. This eating disorder was first named and described by the British psychiatric G. Russell in 1979.

Most studies conducted thus far have been on convenience samples from hospital patients, high school or university students. These have yielded a wide range of results: between 0.1% and 1.4% of males and between 0.3 and 9.4% of females suffers from this eating disorder.

People who suffers from BN eats in out-of-control manner until his/her stomach hurts from over-extension followed by several forms of purging. This cycle is repeated several times a day, and it may directly cause:
* Chronic gastric reflux after eating
* Dehydration and hypokalemia caused by frequent vomiting
* Electrolyte imbalance, which can lead to cardiac arrhythmia, cardiac arrest, and even death
* Esophagitis, or inflammation of the esophagus
* Oral trauma, in which repetitive insertion of fingers or other objects causes lacerations to the lining of the mouth or throat
* Gastroparesis or delayed emptying
* Constipation
* Infertility
* Peptic ulcers
* Calluses or scars on back of hands due to repeated trauma from incisors
* Constant weight++fluctuations are common

The frequent contact between teeth and gastric acid, in particular, may cause:
* Severe dental erosion
* Perimolysis, or the erosion of tooth enamel
* Constant vomiting can lead to gastroesophageal reflux

As with many psychiatric illnesses, delusions can occur with other signs and symptoms leaving the person with a false belief that is not ordinarily accepted by others. The person may also suffer physical complications such as tetany, epileptic seizures, cardiac arrhythmias and muscle weakness.


The onset of bulimia nervosa is often during adolescence, between 13 and 20 years old and in many cases people have previous suffered obesity. Bulimic adolescents have self-imposed perfectionism and compulsivity issues in eating compared to their peers.
BN can be difficult to detect, due to the fact that bulimics tend to be of average or slightly above or below average weight. The Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR) published by the American Psychiatric Association includes:

  • a repetetive episodes of binge eating ( a discrete episode of overeating during which the individual feels out of control of consumption) almost twice a day
  • measures taken to avoid to gaining weight
  • preoccupation with body size and shape, food, eating and fear of gain weight even when eating small amounts of food
  • self-esteem influenced by physical mass and appearance

The initial evaluation should include a complete history of weight, eating behavior, psychological functioning, including perception of weight and shape, depression, a complete medical history and developmental history.

  • Body weight : it’s important to document weight at the time of initiation of puberty and onset of the eating disorder. For the adult patient, it’s important to know weight at specific time points including puberty, graduation from high school, college, marriage or childbirth.
  • Menstrual and sexual history: menstrual dysfunction occurs in 50% of normal weight bulimics, it’s important to determine periods of time during which amenorrhea or oligomenorrhea occur. Loss of menstrual function or onset of irregular menstrual bleeding coincides with an increase in frequency of binge eat and purge. Sexual abuse and sexual dysfunction are commonly reported in patients with eating disorders because a traumatic event could have an impact on patient self-esteem.
  • Comorbid psychiatric syndromes and mental status examination: several psychiatric illnesses occur frequently in patients with eating disorder, including depression, alcohol and substance abuse, obsessive compulsive disorder and panic disorder. ( Handbook of psychological treatment protocols for children and adolescents , Vincent B. Van Hasselt, Michel Hersen)

We can also describe two sub-types of bulimia nervosa:

  • Purging type : people affected by this form of BN rapidly remove food from the body so that it can’t be digested.
  • Non purging type : 6-8% of cases, bulimics exercise after a binge in order to offset caloric intake after eating.


Media portrayals of an “ideal” body shape are widely considered to be contributing factor to bulimia. Social environment is not the only one factor that contributes to the insurgence of BN.

Neurochemistry and Bulimia:

Several neurotransmitter systems that modulate feeding and behavior may contribute to the insurgence of eating disorders.

Insulin has an important role in the control of blood glucose and it also has a central effect, in particular on two hypothalamic areas that control food intake: the lateral hypothalamic area ( hunger center ) and the ventromedial hypothalamic area ( the satiety center). Insulin, secreted by endocrine pancreas after an increased blood glucose, binds receptors located in a hypothalamic nucleus called the arcuate nucleus. This area has connections with both areas that control food intake, and the insulin effect, mediated by the arcuate nucleus, is to inhibit the hunger center and stimulate that of the satiety. This mechanism allows to have a feeling of satiety after a meal. When operating properly these two areas operate to keep the body at a specific body weight, termed the set point. Damage to either of these regions causes the set point to be altered. Eating will then reflect the new set point, thus, if it is lower than normal the animal can literally starve themselves to death.
The development of type 1 diabets in preadolescence or adolescence seems to place girls at risk for the subsequent development of BN. ( The relationship between the age of onset of type 1 diabets and the subsequent development of a severe eating disorder by female patients ; 2011 Takii M, Uchigata Y, Kishimoto J, Morita C, Hata T, Nozaki T, Kawai K, Iwamoto Y, Sudo N, Kubo C.)

A lot of data support a link between reduced CNS serotonin (5HT) activity and bulimia nervosa. First, 5HT is one of neurotransmitters that modulate appetitive behavior. Second, the majority of clinical studies found that patients with BN have signs of reduced 5HTactivity.Third, studies suggests that reducing 5HT activity in bulimia leads to reduced satiety and increased eating in women with BN. If serotonin levels are reduced then obesity occurs. Norepinephrine administration had similar outcomes. Even though rats are far removed from humans, there are some similarities with respect to neurotransmitter functioning. A study using human subjects concluded that impaired central nervous system serotoninergic responsiveness may contribute to the onset or maintenance of abnormal eating patterns in patients with bulimia nervosa.+Norepinephrine+ administration had similar outcomes. Even though rats are far removed from humans, there are some similarities with respect to neurotransmitter functioning.

Orexin A and orexin B, are connected with feeding behavior in rats. By modulating feelings of hunger and satiety the scientists can influence how much a rat eats. Following injection of these hormones into the lateral hypothalamus the rats were found to immediately begin eating eight to ten times more food than normal. Following up on this finding they measured elevated hormone levels when the rat was starved. The hypothesis of this research is that drugs that mimic orexin may help anorexic patients overcome their disorder, while drugs which block orexin action may help bulimics.
Brain-derived neurotrophic factor (BDNF) is under investigation as a possible mechanism. It is a protein that regulates neuronal development and neuroplasticity, and it plays also a role in the hypothalamic pathway that controls eating behaviour and energy homeostasis. (Handbook of psychological treatment protocols for children and adolescents, Vincent B. Van Hasselt, Michel Hersen)


The results of a study conducted in Medical College of Virginia showed that there was comorbidity between bulimia and anorexia nervosa, alcoholism, panic disorder, generalized anxiety disorder, phobia, and major depression. This study also showed that concordance for bulimia was 22.9% in monozygotic and 8.7% in dizygotic twins.
The best-fitting model indicated that familial aggregation was due to genetic factors with a heritability of liability of 55%. A multiple threshold model indicated that narrowly defined bulimia nervosa and bulimia-like syndromes represented different levels of severity on the same continuum of liability. ( The genetic epidemiology of bulimia nervosa , Kendler KS, MacLean C, Neale M, Kessler R, Heath A, Eaves L.)


Patients with bulimia nervosa more often experience severe fluid and electrolyte abnormalities resulting in hypovolemia, secondary hyperaldosteronism, depletion of total body potassium, and cardiac arrhythmias. Immediate management of medical complication and correction of nutritional deficits are necessary before patients can benefit from psychotherapy.

  • Skin: A variety of dermatologic abnormalities can be seen in patients with eating disorders including xerosis (dry, scaly skin), languo-like body hair (fine, downy dark hair on the back, abdomen, and forearms),hair loss. Patients with anorexia nervosa and bulimia nervosa who self-induce vomiting may also demonstrate Russell’s sign (the presence of scar/callus formation over the dorsal surface of the hand, as the hand is used to stimulate the gag reflex to induce vomiting).
  • Endocrine: Gendall et al. examined childhood gastrointestinal complaints in women with bulimia nervosa. One third of the participants reported gastrointestinal complaints or constipation in childhood. Women with gastrointestinal complaints tended to be younger, to have an earlier onset of bulimia nervosa, and to have an earlier onset of self-induced vomiting, compared with women without gastrointestinal complaints. Other possible gastrointestinal problems could include parotid gland swelling , gastritis ,acute liver damage, and dental complications.(Medical complications of anorexia nervosa and bulimia nervosa, James E. Mitchell and Scott Crow)

Some researchers have hypothesized a relationship to mood disorders and clinical trials have been conducted with tricyclic antidepressants, MAO inhibitors, fluoxetine, lithium carbonate. Antidepressants like MAO inhibitors increase the level of 5HT and rduce appetite. There has also been some research characterizing bulimia nervosa as an addiction disorder, and limited clinical use of topiramate, which blocks cravings for opiates, cocaine, alcohol and food.


There are several psychosocial treatments for bulimia nervosa. Cognitive behavioral thrapy (CBT) which involves teaching clients to challenge automatic thoughts and engage in behavioral experiments has demonstrated efficacy both with and without concurrent antidepressant medication. In CBT patients record how much food they eat and periods of vomiting in oreder to identify and avoid emotional fluctuations that bring on episodes of bulimia on a regular basis.
Family based treatment (FBT) might be more helpful to adolescent patient with BN because they need more support from their families. The family can be involved in adolescent’s food choices and behaviors, and gradually let the adolescent to become more autonomous when he has learned heather eating habits.

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