Anorexia nervosa and bulimia nervosa affect millions of people each year in the United States (1). Popular thought holds that these disorders are caused by women trying to fulfill a culturally imposed ideal body image which stresses thinness. As anorexia and bulimia have proven difficult to treat solely with a psychological-based treatment plan it is likely that there are many factors contributing to these disorders. Research has shown, however, that there is a significant biological component which leads to a manifestation of these disorders (2). Current ideas on the biological origins of anorexia and bulimia will be explored in this paper. These include areas ranging from genetic factors to neurotransmitter and hormone imbalances. Genetics appears to play a significant role in predisposing a person to developing an eating disorder. Abnormal neurotransmitter levels have been shown to exist in people with both bulimia and anorexia. Hormone functioning and levels are also atypical in people with eating disorders. While most studies focus on one area, and usually on just one neurotransmitter or hormone, the different biological causes of eating disorders seem to be related to one another. How these possible biological causes influences the I-function (which is the term for the components of the nervous system which give a sense of being oneself) will be examined as well in this paper. Anorexia nervosa is described as a disorder in which women and men intentionally starve themselves, losing at least fifteen percent of their normal body weight. This self imposed emaciation usually begins during puberty and is most common among middle to upper class Caucasian women, affecting one percent of the US population (1). Amenorrhea, the cessation of the normal menstrual cycle is a common occurrence among anorexic women. There is a tremendous discord between actual weight and perceived body weight. While the woman may feel fat she is actually excessively underweight. "When she came in for consultation she looked like a walking skeleton. Alma insisted that she looked fine and that there was nothing wrong with her being so skinny. 'I enjoy having this disease and I want it. I cannot convince myself that I am sick and that there is anything from which I have to recover." (3)
Bulimia nervosa is a related disorder which affects two to three percent of young American women (1). This disease is most commonly described as the cycle of eating huge quantities of food, thousands of calories in one sitting, then ridding the body of this food through some form of self purging. Purging is accomplished through excessive exercise, abuse of laxatives or diuretics, enemas, or vomiting. Many of these methods are often incorporated simultaneously. The bulimic frequently thinks this practice of bingeing and purging is disgusting and does so in private, making it hard to detect and treat.
"Lisa would eat pounds of candy and cake at a time, and often not stop until she was exhausted or in severe pain. Then, overwhelmed with guilt and disgust, she would make herself vomit." (1)
Studies have shown genetic predisposition for developing an eating disorder. Females in a family which has a member with an eating disorders are more likely then average women to develop an eating disorder themselves (1). According to one study, cited on numerous web pages, "about half the risk of developing this (anorexia) eating disorder is inherited."(4) It was found that identical twin sisters were more prone to both developing an eating disorder then non-identical twins. DNA samples of affected siblings are now being analyzed to determine if they share genetic characteristics different from those of non-eating disorder siblings. While lay people blame the media and society for portraying ideal beauty as dangerously thin, these studies suggests that that is only part of the reason for these eating disorders. Genetic causes may explain the difficulty in treating these disorders. One difficulty with the argument of a genetic predisposition for bulimia and anorexia is that these disorders are most common among upper and middle class women. The genetic predisposition toward an eating disorder may be present in other socioeconomic classes, but other factors which are needed for the disease to be fully manifested are not present. Environmental conditions were also noted in studies discussing genetic links. It appears that mothers and fathers who worry or comment about their daughters beauty and weight were providing a risky environment which could lead to an eating disorder. Possibly this happens more often in households of the higher economic classes. Other behavioral studies have shown that parental disorders (depression, spouse abuse, etc.) are often passed on to their children in part through this environmental, yet genetically intertwined fashion. (4,1)
Neurotransmitter links to these eating disorders stem from studies done primarily on the hypothalamus. Specifically, the ventromedial and lateral hypothalamus have been shown to govern eating behavior in humans, as well as in many laboratory animals. The ventromedial hypothalamus has been called the satiety center. When this part of the brain is stimulated eating behavior stops, correlating to a feeling of being satiated. Conversely the lateral hypothalamus, when stimulated, correlates to eating behavior. 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 then normal the animal can literally starve themselves to death. (5,6)
Decreasing the level of epinephrine in the ventromedial hypothalamus of rats was correlated with their exhibiting anorexic type behaviors. That is, they would adopt a low rate of eating, increase their rate of activity, reduce their carbohydrate intake, and rebound with overeating. (7)
Serotonin, norepinephrine, and dopamine have all been found to exist at abnormal levels in individuals with anorexia and bulimia. Experiments done on laboratory animals with serotonin show that when it is released into either the ventromedial hypothalamus or the lateral hypothalamus eating is stopped and starvation results. 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. (5) A study using human subjects concluded that "impaired central nervous system serotonergic responsiveness may contribute to the onset or maintenance of abnormal eating patterns in patients with bulimia nervosa."(8) These researchers linked serotonin to feelings of well being and satiation. After ingestion of a carbohydrate-rich diet the body converts these sugars, through a multi-step process, into tryptophan which is the precursor of serotonin. Thus, it is suggested that the binge behavior of bulimics may be in response to a chemical imbalance in the brain, that of low serotonin levels.
This study also found that after a normal meal healthy subjects described feeling satiated more often then people with bulimia (8). This indicates that bulimics may have a faulty satiation response center. A desire to feel satiated may cause the bulimic to try to flood their brain with tryptophan, by overeating on sugars which will lead to this precursor. The successful treatment of bulimia with fluoxetine hydrochloride, Prozac, also suggests the importance of serotonin in eating disorders. This drug acts to increase the amount of serotonin in the brain by inhibiting its reuptake. Some patients find this helps them control their binge/purge behaviors (9).
Anorexic patients, on the other hand, may have overactive serotonerigic response centers, leading to a need to reduce the levels of serotonin in their brains by restricting their food intake. Actually, excessive levels of serotonin are correlated with a nervous, jittery feeling. Self-starvation may be an attempt to rid the body of this uncomfortable feeling.
Low serotonin levels have been linked to depression which is a commonly concurrent disorder in people with eating disorders. Both eating disorders and depression can be seen as disorders that occur when the I-function, a sense of self, is not in agreement with external reality. For example, the depressed person often has a feeling of helplessness, hopelessness, and exceedingly low self esteem regardless of their actual situation in life. A person suffering from anorexia or bulimia feels they are overweight when in fact they are underweight (anorexia) or of normal weight (bulimia). The I-function has somehow adopted an unhealthy self image. The body presented by the I-function to the self is not the same body which others see. Researchers looking for biological treatments for these disorders are in effect looking for ways to bring the I-function's body image into agreement with the body as seen by the outside world. Ultimately, the I-function must be a conglomeration of neurons whose arrangement was determined through genetic programming. As neurons communicate by neurotransmitters an aberrant neurotransmitter system could affect the I-function, and therefore self perception. Possible reasons for the faulty neurotransmitter system range from genetic to environmental influences.
Success of drug therapies suggest that the I-function can be positively affected by artificial augmentation of the neuro-chemical environment. Treatment with anti-depressant medication correlates with an increase in self esteem among depressed individuals. That is, an I-function which was previously supplying a poor self image can be changed, allowing for a healthier, more accurate view of the self. A bulimic's or anorexic's I-function may also be positively affected by drugs which can change its neuro-chemical environment. In this chemical fashion relief may be found for affected individuals. Numerous hormones, cortisol, orexin A, orexin B, luteinizing hormone, luteinizing-hormone-releasing factor, and follicle-stimulating hormone, have been linked to these eating disorders. These hormones are all present in healthy people, while in those affected with an eating disorder the levels or distributions are abnormal. The brain hormone, cortisol, is found to be at elevated levels in patients with anorexia. This hormone is usually released in response to stress. In these sick individuals it appears to be mis-released by malfunctions in the hypothalamus.(1)
Two newly discovered hormones, 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. These researchers have not yet been able to see if a decrease of orexin A and B result in decreased appetites, but they are planning on genetically engineering rats which will be missing the gene needed to produce them, thus allowing them to test the deficiency. 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. (10)
One common symptom of anorexia is amenorrhea, the loss of a regular menstrual cycle such that the woman does not menstruate. It appears that a result of amenhorrea is the depression of the reproductive hormones, luteinizing hormone, luteinizing-hormone-releasing factor, and follicle-stimulating hormone. The levels of these hormones usually return to a normal cyclically fluctuating pattern when weight is gained back. In some individuals, however, even when good nutrition is received their menstrual cycles do not return. This is thought to be related to function of the neuroendocrine system, particularly the hypothalamus. Likelihood of recovery from anorexia is not good for patients who do not attain a regular menstrual cycle. (7)
A few sources suggested that anorexics are addicted to fasting, apparently because of the chemical changes brought on by starvation. The opioids, enkephalins and endorphins are found to be at elevated levels in the spinal fluid of patients with anorexia. It is unclear however, whether or not the starving was caused by, or was the cause of, these elevated opioid levels. Some studies have found that drugs which inhibit the functioning of these opioids cause anorexic patients to gain weight. (11) Unusual hormones levels may also effect the I-function, causing it to once again portray an unhealthy body image to the self. Artificial manipulation of theses targeted hormones may help in the treatment of these eating disorders by bringing the I-function's self image back into consort with reality.
There are numerous questions which still need to be addressed through further research. What is the difference between females and males which cause there to be such a disparity in the rates of acquiring these disorders? Do these differences stem from biological or societal roots? Is the relationship between neurotransmitter/hormonal imbalances and eating disorders purely a one way event? Or do the anorexic and bulimic behaviors of starving, bingeing, and purging effect the bodies chemical environment? Could the relationship be a snowball effect, chemical imbalance causing eating disorder, which in turn causes a greater chemical imbalance? How susceptible is the I-function to manipulation by medical interventions? By altering the bodies chemical state can the sense of self truly be changed as well? Is this a good idea, to change personalities, which to some extent are determined by genetics? All of these possible research topics will certainly lead to more questions about the I-function and its role in mental health. Future inquiry may enable some of these questions to be answered, but some will always remain a mystery. Many conditions ranging from biological, psychological, and psychosocial, are required for bulimia or anorexia to manifest in an individual. Ultimately, it is the sum of all these influences which effect the I-function, causing it to malfunction. If it becomes possible through modern medicine to positively influence the I-function the biological component of these disorders may one day be brought under control.
List of web sites used for this paper:
1. NIMH: Eating Disorders.
This page was an online information packet provided by the National Institutes of Mental Health. It contained a lot of information about the eating disorders in an easy to understand format.
2. Research Re: Cause of Bulimia Nervosa.
A lengthy list of abstracts from papers about Bulimia. It was a good source for getting a general sense of current research on the causes of bulimia.
3. Understanding Eating Disorders.
A comprehensive page on anorexia and bulimia. It talks briefly about the history of these disorders then goes into the causes and course of the illnesses.
4. Mental Health Net.
A short news article reviewing a study done which links anorexia to genetic roots.
5. Bulimia Nervosa.
A comprehensive review of bulimia. It was used primarily for its biological section. The other sections were interesting as well.
6. Hunger and Satiety.
A very brief page on the areas of the hypothalmus which govern feelings of hunger and satiety.
7. Eating Disorders. This page is devoted entirely to the biological causes of eating disorders. It discusses studies which look at various biological origins.
8. Decreased Serotonin Function in Bu...
This was an actual scientific research paper in which the researchers looked at the relationship between serotonin and bulimia. Parts of it were hard to understand. The conclusion, however was very useful.
9. Research Re: Treatment of Bulimia Nervosa.
This page is a list of absrtacts from research articles centered on the treatment of bulimia. It is good for a quick overview on what is being done currently in this field. The anstracts were generally easy to understand and follow.
10. Scientific American: Explorations.
This page, from Scientific American, is an article from that journal. It focuses on the discovery of two new hormones related to weight control.
11. Eating Disorders.
This is an extensive web site on eating disorders from The Harvard Mental Health Letter. It is well written and very complete.
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This paper reflects the research and thoughts of a student at the time the paper was written for a course at Bryn Mawr College. Like other materials on Serendip, it is not intended to be "authoritative" but rather to help others further develop their own explorations. Web links were active as of the time the paper was posted but are not updated.