The Physiology and Psychology of Bulimia




Bulimia is a disorder centered around an individual’s obsession with food and weight. This obsession involves eating large quantities of food, feeling guilty about the food consumption, and taking drastic measures to prevent caloric/fat absorption. Measures vary with each individual and include one or all of the following: forced vomiting, abuse of laxatives or diuretics, or excessive exercise. This disease affects one to three percent of adolescent and young women in the United States, and bulimic behaviors are displayed by ten to twenty percent of adolescent and young women in the United States (http://dcs.engr.widener.edu/galla/gal la.htm).

In the studies of bulimia nervosa there is a continuing debate concerning the underlying cause of the disease - whether it is physiological or psychological. Studies have found convincing results for both theories. Numerous links have been found between eating regulation and neurotransmitters. However, there is no clear evidence that neurotransmitter dysfunction is the underlying cause of bulimia nervosa. Of the neurotransmitters that have been tested, serotonin has had one of the largest roles in the regulation of food intake among patients with bulimia. Progress has also come through treating bulimia as a psychological disorder. Treatment under this theory often involves psychotherapy and the use of antidepressants. However, it is widely accepted that the path to the best results involves the combination of both physiological and psychological methods of treatment.

First, the physiological aspect will be explored. Assuming that eating regulation is controlled primarily by the brain, disturbances could exist in several places: (1) the brain may not respond appropriately to food-induced changes in plasma because of an abnormality in the blood-brain barrier transport system; (2) the increase in brain tryptophan that follows a carbohydrate-rich meal may not have an adequate effect on serotonin-mediated neurotransmission because the individual has too few serotoninergic neurons; (3) the functional activity of the serotoninergic neurons might be disturbed by pathological processes located elsewhere in the brain (Stunkard 84).

One hypothesis suggests that bulimia nervosa is the behavioral manifestation of the underactivity of serotonin. Serotonin is one of the hormones/neurotransmitters that regulates vital functions, such as eating, in the central nervous system. It is also thought to be responsible for controlling states of consciousness and mood. Serotonin is special: its own synthesis and release is enhanced by some foods, suppressed by others, and unaffected by yet others. The effects are all dependent on nutritional content. Transmitters are also affected by not eating. The brain easily detects how long an individual has gone without food. These qualities enable serotonin-releasing neurons to control one type of appetite: that for eating the appropriate amounts of carbohydrates and proteins. However, these same neurons can cause food consumption to affect other behaviors linked with serotonin such as sleepiness and environmental stimuli. They may also allow mood disturbances to override appetite control mechanisms, causing an individual to eat unnecessarily (Winik 27-34).

Food should produce chemical changes in the brain. These neurochemical responses should cause the release of specific chemicals that the brain needs to carry instructions from one neuron to another. The consumption of a meal that is rich in carbohydrates causes the release of the serotonin neurotransmitter; this signal reduces the likelihood that the person will consume large amounts of carbohydrates in his/her next meal. Instead, the next meal should be rich in protein. The amino acid responsible for this serotonin synthesis and release is called tryptophan (Winik 82-83). Tyrptophan is an essential amino acid and cannot be made in the brain. Therefore, tryptophan consumed as part of dietary protein is the only source of precursor for brain serotonin synthesis. Tryptophan is absorbed from the stomach and is circulated in the blood where it is distributed (Wurtman 121).

The process of carbohydrate-serotonin interaction is described as follows: the carbohydrate-rich meal accelerates the synthesis and secretion of serotonin from neurons for one to two hours; the carbohydrates elicit insulin secretion which reduces plasma levels of most large neutral amino acids (LNAA) but not tryptophan (this means that tryptophan is taken up in the brain); this increases the saturation of tyrptophan hydroxylase - the enzyme responsible for serotonin synthesis; therefore, less serotonin is synthesized resulting in the individual’s lack of craving for carbohydrate rich foods. In patients with bulimia, the ratio of carbohydrate to protein consumption is often severely altered with the carbohydrate intake being much larger (Wurtman 2-8). In this sense, it is not surprising that a decrease in the ratio of tryptophan and LNAA helps the bulimic patient control the urges for inappropriate or excess carbohydrate consumption. The one major hindrance to understanding the relationship of mood, appetite, and serotonin is the failure to measure actual feeding patterns in eating disorders (Beumont 31).

Studies with rats have shown that drugs that enhance serotoninergic transmission affect the amount of dietary carbohydrates and proteins that is consumed. If this is the case, it is probable that the pathophysiological changes in this complex metabolic-neurochemical-behavioral feedback mechanism may be the underlying causes of some disorders of appetite regulation. Two categories can account for this disregulation: (1) the individual releases less-than-normal amounts of brain serotonin at any Trp/LNAA (tryptophan/large neutral amino acid) ratio or (2) the individual has a less-than-normal increase in this ration after eating carbohydrates (Wurtman 8-14).

The second hypothesis suggests that bulimia is more likely to be a psychological disease than a physiological disease. Though the disregulation of a hormone such as serotonin is acknowledged, it is more commonly believed to be an effect of bulimic binge-purge cycles. It is, however, an important aspect of the disease. Therefore, many drugs that are used in the treatment of the psychological element of bulimia also prove beneficial to the biological elements of the disease.

vIn the past ten years, new research has lead to the development of selective serotonin reuptake inhibitors (SSRIs) to regulate serotonin in the body while suppressing food craving and promoting weight loss. Fluoxetine (Prozac) and fluvoxamine (Luvox) are two such inhibitors. To date, fluoxetine is the only drug approved by the FDA (http://pharminfo.com/pubs/msb/seroton.html).

One study has shown that there is little difference between groups that incorporate the use of fluoxetine and psychotherapy and groups with psychotherapy alone (who were given a placebo). Both groups showed tremendous improvement in eating behaviors. The only observable difference was significant weight loss with the group receiving the fluoxetine. However, other studies have shown that when no psychotherapy is used, groups receiving fluoxetine produce dramatically different results than do groups receiving a placebo. Those receiving fluoxetine displayed improved eating behaviors and mood, while those receiving a placebo did not (http://dcs.engr.widener.edu/galla/galla.htm).

The dosages of fluoxetine also affected the patients’ progress. Fluoxetine is well absorbed after oral administration and is extensively metabolized in the liver. Therefore, greater dosages will have a longer duration in the body and will result in more dramatic effects in patients (http://www.mentalhealth.com/drug/p30-p05.html) . Studies have shown that while 20mg significantly reduced vomiting but not bingeing, 60mg greatly reduced both vomiting and bingeing while also reducing depression, carbohydrate craving, and pathological eating habits (http://pharminfo.com/pubs/msb/seroton.html). Fluoxetine is associated with a significant reduction in abnormal eating behaviors and attitudes; generally, the patient’s improvement will last at least as long as the drug treatment (http://dcs.engr.widener.edu/galla/galla.htm).

A study utilizing another SSRI, fluvoxamine, has also proved effective in treating bulimia. 50-150mg of fluvoxamine significantly reduced the patient’s number of binge eating episodes while simultaneously decreasing the patient’s body weight. The only reported adverse effect is sleep disturbance. Fluvoxamine, because it lacks cardiotoxicity, is safer for those bulimic patients whose excessive vomiting often leads to electrolyte imbalances that have detrimental effects on the heart (http://pharminfo.com/pubs/msb/seroton.html). .

The discovery of the link between body chemistry and eating disorders has provided for many new developments in the treatment of these diseases. In the past, self-control was thought to be the answer to overcoming eating disorders. Now that scientists understand that the body’s hormones play major roles in disorders, treatments are much more case-specific and successful. Likewise, patients respond in a more positive manner to treatments by realizing that willpower or the lack of willpower will not be the determinant of a cure. Patients have the ability to choose the treatment program that best suits their needs and will produce the most lasting results.

Numerous studies that place the focus on the psychological aspects of the disease have found that bulimia is related to major affective disorder, or depression. Nearly 87% of patients with bulimia have moderate to severe depressive symptoms (Stunkard 259-260). Several studies of biological tests, including the dexamethasone suppression test (DST) and the tryptophan-releasing hormone stimulation test (TRH stimulation test), have found a prevalence of abnormal laboratory results in patients with bulimia comparable to those found in patients with major depression (Kaye 122).

If, in fact, bulimia was simply a variation of depression, it would be reasonable to assume that bingeing and purging was done to reduce the depressed mood. Few studies have attempted to give definite answers to this possibility, but there is enough evidence to support the idea that depression increases either during or after a binge-purge episode (Walsh 205). Therefore, some drugs that are used to treat bulimia are antidepressants.

However, it cannot be excluded that antidepressants used in studies counteract bulimia independently of their action as antidepressants. Generally, those that respond to treatment with antidepressants show a decline in depressive symptomalogy parallel with or even ahead of the reduction in bulimic symptoms. However, those that do not respond to treatment with antidepressants show no change in either depressive symptomalogy or bulimic symptoms. In most studies that involve antidepressants, the majority of patients are not cured. Though the number of bulimic episodes may be greatly reduced, they do not become extinct. This suggests that while the depressive symptoms of bulimia can be improved and the number of bulimic episodes can be reduced, the actual disease has other underlying factors that need attention (Pope 167-179).

As shown, there are numerous results in patients treated with a single method/drug. Therefore, instead of treating bulimia with one method, several techniques are usually applied. The most effective treatment of bulimia nervosa found so far is the combination of antidepressants with psychotherapy. In this type of treatment, the individual receives attention both physiologically and psychologically. This provides for a more effective overall treatment of the patient in the sense that there is a much greater probability of response to one or both of the treatments than there would be when applying only one type of treatment.

One method of psychotherapy that is used is referred to as the therapeutic triad. The first two parts of the triad deal with the treatment of the bulimic state. This includes learning about the addictive process of bulimia and the giving up of the binge-purge behavior. The third part of the triad deals with the treatment of the bulimic trait. This involves the therapy of faulty family dynamics as well as individual therapy (Heubner 145).

In order to learn about the addictive process in bulimia, part one of the triad combines an intellectual, cognitive approach with an experimental one. The bulimic patient is asked to keep a daily log which displays several things: (1) the nature and amount of food and fluid intake, (2) the number of binge-purge episodes, (3) states of mind and (4) exercising. In this method, the psychoanalyst can see the times at which bulimic activity is highest and the emotional states that triggered this activity. The psychoanalyst can also keep track of progress. Though this method is extremely helpful in treating the bulimic, the trouble is getting the patient to comply. Many bulimics find it difficult, if not impossible, to keep such a log (Huebner 146).

In part two of the triad, the bulimic experiments with her binge-purge behavior and observes the reinforcing and addictive nature of the disease. It is in this process that the first therapeutic results are seen, because the patient feels that she has cognitive control over her experiences. The experimentation with the binge-purge behavior allows for a better understanding of the addictive qualities and therefore allows for a change in this behavior (Huebner 148).

First, the patient must be taught the difference between food as a healthy part of life and as an addictive or bad part of life. This is done by a strict diet of 1,200 to 1,400 calories served in three small meals and one snack per day. If the bulimic feels the need to binge, she is instructed to wait at least one hour after her healthy meal. This prevents her from turning a meal into a binge with the numerous consequences. In this way, the bulimic knows when she is giving in to food as an addictive substance. Once the patient is able to separate addictive and healthy food consumption, she can reduce the frequency of binge-purge episodes. This is called the withdrawal stage in which the desire for the addictive behavior is heightened. Acceptance and support are key in this stage as the bulimic enters a period of heavy emotional stress as she fights between the desire to give up her addictive behavior and her desire to return to it. It is here that antidepressants are often necessary. Since antidepressants reduce the patient’s reactivity to stressful life situations, the desire to control emotions through bingeing and purging is also reduced. (Huebner 149).

Part three of the triad involves the treatment of the individual and her family. In this phase, the individual learns to identify the life situation(s) that caused her bulimia. This allows her to apply an analytical approach to future life situations that may trigger her desire to return to her addictive behavior. Family therapy is a must in the treatment of bulimia. It is vital to understand the dynamics of the family in order to determine where certain pressures reside. It is also important for the family to know how to support their daughter in her struggles (Huebner 150, 98).

Another important type of psychotherapy used in the treatment of bulimia is group psychotherapy. Group psychotherapy is similar to individual psychotherapy in that it employs the same methods of self-realization and progress. However, in group psychotherapy, the individual is able to obtain a sense of belonging to and acceptance from a group with a common task. In this sense, group psychotherapy is more effective than individual psychotherapy in helping the patient to overcome guilt and frustration. It is important to the success of the group that there remain high levels of participation, risk-taking and self-disclosure and low levels of defensiveness and tension (Harper-Giuffre 37).

Group psychotherapy, individual psychotherapy and medications are all active parts in the treatment of bulimia. The objectives for the treatment of bulimia nervosa in all methods are: (1) to increase the ability to recognize signals and feelings, (2) to improve social competence and emotional expression, (3) to learn to relax physically and attain tranquillity, (4) to change depressive thought patterns, (5) to reduce excessive achievement orientation, (6) to take on responsibility and (7) to organize appropriate leisure activities (Fichter 277). Though there is still a debate between the underlying cause of bulimia - whether it is physiological or psychological - the methods that involve the use of both medications and psychotherapy have provided the best results in the treatment their patients.




Courtney E. Sanders
Vanderbilt University
December 5, 1996
Psychology 115 A
Professor: Dr. David Schlundt



References


Beumont, Pierre J.V., et al. (1987). "Neural Basis of Appetite and Food Intake." Handbook of Eating Disorders, New York: Elsevier Science Publishing Co.

Fichter, Manfred M., ed. (1990). Bulimia Nervosa: Basic Research, Diagnosis and Therapy, New York: John Wiley & Sons.

Garner, David M. and Paul E. Garfinkel, eds. (1985). Handbook of Psychotherapy for Anorexia Nervosa and Bulimia, New York: The Guilford Press.

Harper-Guiffre, Heather and K. Roy MacKenzie, eds. (1992). Group Psychotherapy for Eating Disorders, Washington, DC: American Psychiatric Press.

Huebner, Hans F., M.D. (1993). Endorphins, Eating Disorders, and Other Addictive Behaviors, New York: W.W. Norton & Co.

Kaye, Walter H. and Harry E. Gwirtsman, eds. (1985). The Treatment of Normal Weight Bulimia, Washington, DC: American Psychiatric Press.

Pope, H.G., Jr. and Hudson, J.I. (1982). "Treating Bulimia with Antidepressants." Psychopharmacology, 78, 176-179.

Stunkard, Albert J. and Eliot Stellar, eds. (1984). Eating and Its Disorders: Research Publications, 62, 84; 259-260.

Walsh, Timothy B. (1988). Eating Behavior in Eating Disorders, Washington, DC: American Psychiatric Press.

Winik, Myron, ed. (1988). Control of Appetite: Current Concepts in Nutrition, 16, 27-34; 82-83.

Wurtman, J.J. and R.J. Wurtman, et al. (1981). "Carbohydrate Craving in Obese People: Suppression of Serotoninergic Transmission." International Journal of Eating Disorders, 1, 2-14.

Wurtman, J.J. and R.J. Wurtman, eds. (1979). Disorders of Eating: Nutrition and the Brain, 3, 121.

 

 

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